PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 2508560-8 1989 This mutation is theoretically equivalent to reversion of the Gly to Val transforming mutation of the cellular form of the ras gene product p21, a protein proposed to be structurally similar to EF-Tu in the GDP binding domain. Glycine 62-65 H3 histone pseudogene 16 Homo sapiens 140-143 2483936-3 1989 The mRNA expression of the transgenes was detected in two tumors obtained after introduction of the DNA fragment containing the activated human c-Ha-ras gene for p21 with valine at the 12th codon or with leucine at the 61st codon. Valine 171-177 H3 histone pseudogene 16 Homo sapiens 162-165 2692710-2 1989 We have previously assigned all five glycine resonances located in loops directly involved in binding of guanosine diphosphate in the wild-type p21 protein [Campbell-Burk, S., Papastavros, M. Z., McCormick, F., & Redfield, A. G. (1989) Proc. Glycine 37-44 H3 histone pseudogene 16 Homo sapiens 144-147 2692710-2 1989 We have previously assigned all five glycine resonances located in loops directly involved in binding of guanosine diphosphate in the wild-type p21 protein [Campbell-Burk, S., Papastavros, M. Z., McCormick, F., & Redfield, A. G. (1989) Proc. Guanosine Diphosphate 105-126 H3 histone pseudogene 16 Homo sapiens 144-147 2692710-7 1989 In this report, the corresponding glycine resonances in the p21 mutant have been assigned, and spectral differences between normal and mutant p21-guanosine diphosphate (p21.GDP) complexes have been investigated. Glycine 34-41 H3 histone pseudogene 16 Homo sapiens 60-63 2692710-7 1989 In this report, the corresponding glycine resonances in the p21 mutant have been assigned, and spectral differences between normal and mutant p21-guanosine diphosphate (p21.GDP) complexes have been investigated. Guanosine Diphosphate 146-167 H3 histone pseudogene 16 Homo sapiens 142-145 2692710-7 1989 In this report, the corresponding glycine resonances in the p21 mutant have been assigned, and spectral differences between normal and mutant p21-guanosine diphosphate (p21.GDP) complexes have been investigated. Guanosine Diphosphate 146-167 H3 histone pseudogene 16 Homo sapiens 169-176 2692710-10 1989 Two of the five active-site glycines in wild-type p21.GDP have very slow amide proton exchange rates with water (kappa less than 2.8 x 10(-5) s-1). Glycine 28-36 H3 histone pseudogene 16 Homo sapiens 50-53 2692710-10 1989 Two of the five active-site glycines in wild-type p21.GDP have very slow amide proton exchange rates with water (kappa less than 2.8 x 10(-5) s-1). Guanosine Diphosphate 54-57 H3 histone pseudogene 16 Homo sapiens 50-53 2692710-10 1989 Two of the five active-site glycines in wild-type p21.GDP have very slow amide proton exchange rates with water (kappa less than 2.8 x 10(-5) s-1). Amides 73-78 H3 histone pseudogene 16 Homo sapiens 50-53 2692710-10 1989 Two of the five active-site glycines in wild-type p21.GDP have very slow amide proton exchange rates with water (kappa less than 2.8 x 10(-5) s-1). Water 106-111 H3 histone pseudogene 16 Homo sapiens 50-53 2692710-11 1989 The active-site glycines are located in solvent-exposed loops, so their apparent solvent inaccessibility may result from strong hydrogen bond formation between glycine amide protons and bound guanine diphosphate and/or other nearby groups in p21. Glycine 16-24 H3 histone pseudogene 16 Homo sapiens 242-245 2692710-11 1989 The active-site glycines are located in solvent-exposed loops, so their apparent solvent inaccessibility may result from strong hydrogen bond formation between glycine amide protons and bound guanine diphosphate and/or other nearby groups in p21. Hydrogen 128-136 H3 histone pseudogene 16 Homo sapiens 242-245 2692710-11 1989 The active-site glycines are located in solvent-exposed loops, so their apparent solvent inaccessibility may result from strong hydrogen bond formation between glycine amide protons and bound guanine diphosphate and/or other nearby groups in p21. glycine amide 160-173 H3 histone pseudogene 16 Homo sapiens 242-245 2692710-11 1989 The active-site glycines are located in solvent-exposed loops, so their apparent solvent inaccessibility may result from strong hydrogen bond formation between glycine amide protons and bound guanine diphosphate and/or other nearby groups in p21. guanine diphosphate 192-211 H3 histone pseudogene 16 Homo sapiens 242-245 2691018-5 1989 A point mutation at this location corresponds to a substitution of histidine for glutamine in the N-ras gene product, p21. Histidine 67-76 H3 histone pseudogene 16 Homo sapiens 118-121 2691018-5 1989 A point mutation at this location corresponds to a substitution of histidine for glutamine in the N-ras gene product, p21. Glutamine 81-90 H3 histone pseudogene 16 Homo sapiens 118-121 2561364-1 1989 Purified membrane-bound Na,K-ATPase incubated with cobalt-tetrammine-ATP [Co(NH3)4ATP], which is a stable MgATP complex analog, shows two new types of membrane crystals, a new p21 form and a p4 form. cobalt-tetrammine-atp 51-72 H3 histone pseudogene 16 Homo sapiens 176-179 2561364-1 1989 Purified membrane-bound Na,K-ATPase incubated with cobalt-tetrammine-ATP [Co(NH3)4ATP], which is a stable MgATP complex analog, shows two new types of membrane crystals, a new p21 form and a p4 form. tetraamminecobalt(III)ATP 74-85 H3 histone pseudogene 16 Homo sapiens 176-179 2561364-1 1989 Purified membrane-bound Na,K-ATPase incubated with cobalt-tetrammine-ATP [Co(NH3)4ATP], which is a stable MgATP complex analog, shows two new types of membrane crystals, a new p21 form and a p4 form. Adenosine Triphosphate 106-111 H3 histone pseudogene 16 Homo sapiens 176-179 2692710-1 1989 [15N]Glycine was biosynthetically incorporated into normal cellular N-ras p21 and a position 12 transforming mutant, in order to produce p21 proteins containing several site-specific NMR probes at or near activating positions in the guanine nucleotide binding domain. [15n]glycine 0-12 H3 histone pseudogene 16 Homo sapiens 74-77 2692710-1 1989 [15N]Glycine was biosynthetically incorporated into normal cellular N-ras p21 and a position 12 transforming mutant, in order to produce p21 proteins containing several site-specific NMR probes at or near activating positions in the guanine nucleotide binding domain. [15n]glycine 0-12 H3 histone pseudogene 16 Homo sapiens 137-140 2508560-8 1989 This mutation is theoretically equivalent to reversion of the Gly to Val transforming mutation of the cellular form of the ras gene product p21, a protein proposed to be structurally similar to EF-Tu in the GDP binding domain. Valine 69-72 H3 histone pseudogene 16 Homo sapiens 140-143 2508560-8 1989 This mutation is theoretically equivalent to reversion of the Gly to Val transforming mutation of the cellular form of the ras gene product p21, a protein proposed to be structurally similar to EF-Tu in the GDP binding domain. Guanosine Diphosphate 207-210 H3 histone pseudogene 16 Homo sapiens 140-143 2508560-10 1989 We conclude that the tertiary structure model is correct in its assignment of the pyrophosphate binding site to residues 23-27; however, there are likely to be some significant differences between the configurations of the GTPases of EF-Tu and p21. diphosphoric acid 82-95 H3 histone pseudogene 16 Homo sapiens 244-247 2668035-0 1989 Conformational changes occurring in N-ras p21 in response to binding of guanine nucleotide and metal ions probed by proteolysis performed under controlled conditions. Guanine Nucleotides 72-90 H3 histone pseudogene 16 Homo sapiens 42-45 2681210-7 1989 Furthermore, this band is sensitive to hydroxylamine treatment and shows specific incorporation of [3H]palmitate, strongly suggesting that it is the palmitoylated form of p21, which is the biologically active form of the protein. Hydroxylamine 39-52 H3 histone pseudogene 16 Homo sapiens 171-174 2681210-7 1989 Furthermore, this band is sensitive to hydroxylamine treatment and shows specific incorporation of [3H]palmitate, strongly suggesting that it is the palmitoylated form of p21, which is the biologically active form of the protein. [3h]palmitate 99-112 H3 histone pseudogene 16 Homo sapiens 171-174 2682005-7 1989 Glycine----arginine mutation and glycine----valine mutation of codon 12 in ras p21 was observed in 40 and 31% of colon cancers, respectively. Glycine 33-40 H3 histone pseudogene 16 Homo sapiens 79-82 2682005-7 1989 Glycine----arginine mutation and glycine----valine mutation of codon 12 in ras p21 was observed in 40 and 31% of colon cancers, respectively. Valine 44-50 H3 histone pseudogene 16 Homo sapiens 79-82 2684162-2 1989 The inhibitory activity of full-length p21s was much weaker than that of truncated p21s, however, the inhibitory activity was potentiated after denaturation with 8 M urea and 2 M NaCl followed by renaturation. Urea 166-170 H3 histone pseudogene 16 Homo sapiens 39-42 2684162-2 1989 The inhibitory activity of full-length p21s was much weaker than that of truncated p21s, however, the inhibitory activity was potentiated after denaturation with 8 M urea and 2 M NaCl followed by renaturation. Sodium Chloride 179-183 H3 histone pseudogene 16 Homo sapiens 39-42 2476675-0 1989 Structure of the guanine-nucleotide-binding domain of the Ha-ras oncogene product p21 in the triphosphate conformation. Guanine Nucleotides 17-35 H3 histone pseudogene 16 Homo sapiens 82-85 2476675-0 1989 Structure of the guanine-nucleotide-binding domain of the Ha-ras oncogene product p21 in the triphosphate conformation. triphosphoric acid 93-105 H3 histone pseudogene 16 Homo sapiens 82-85 2476675-1 1989 The crystal structure of the guanine-nucleotide-binding domain of p21 (amino acids 1-166) complexed to the guanosine triphosphate analogue guanosine-5"-(beta, gamma-imido)triphosphate (GppNp) has been determined at a resolution of 2.6 A. Guanine Nucleotides 29-47 H3 histone pseudogene 16 Homo sapiens 66-69 2476675-1 1989 The crystal structure of the guanine-nucleotide-binding domain of p21 (amino acids 1-166) complexed to the guanosine triphosphate analogue guanosine-5"-(beta, gamma-imido)triphosphate (GppNp) has been determined at a resolution of 2.6 A. Guanosine Triphosphate 107-129 H3 histone pseudogene 16 Homo sapiens 66-69 2476675-1 1989 The crystal structure of the guanine-nucleotide-binding domain of p21 (amino acids 1-166) complexed to the guanosine triphosphate analogue guanosine-5"-(beta, gamma-imido)triphosphate (GppNp) has been determined at a resolution of 2.6 A. Guanylyl Imidodiphosphate 139-183 H3 histone pseudogene 16 Homo sapiens 66-69 2476675-1 1989 The crystal structure of the guanine-nucleotide-binding domain of p21 (amino acids 1-166) complexed to the guanosine triphosphate analogue guanosine-5"-(beta, gamma-imido)triphosphate (GppNp) has been determined at a resolution of 2.6 A. LHRH (1-6) 185-190 H3 histone pseudogene 16 Homo sapiens 66-69 2502546-2 1989 The resulting G-binding domain, p21 (1-166) = p21C", can be crystallized as a complex with the slowly hydrolyzing GTP analogues guanosin-5"-[beta,gamma-imido]triphosphate, guanosin-5"-[beta,gamma-methylene]triphosphate, and guanosin-5"-O-(3-thiotriphosphate). Guanosine Triphosphate 114-117 H3 histone pseudogene 16 Homo sapiens 32-35 2502546-2 1989 The resulting G-binding domain, p21 (1-166) = p21C", can be crystallized as a complex with the slowly hydrolyzing GTP analogues guanosin-5"-[beta,gamma-imido]triphosphate, guanosin-5"-[beta,gamma-methylene]triphosphate, and guanosin-5"-O-(3-thiotriphosphate). guanosin-5"-[beta,gamma-imido]triphosphate 128-170 H3 histone pseudogene 16 Homo sapiens 32-35 2502546-2 1989 The resulting G-binding domain, p21 (1-166) = p21C", can be crystallized as a complex with the slowly hydrolyzing GTP analogues guanosin-5"-[beta,gamma-imido]triphosphate, guanosin-5"-[beta,gamma-methylene]triphosphate, and guanosin-5"-O-(3-thiotriphosphate). guanosin-5"-[beta,gamma-methylene]triphosphate 172-218 H3 histone pseudogene 16 Homo sapiens 32-35 2502546-2 1989 The resulting G-binding domain, p21 (1-166) = p21C", can be crystallized as a complex with the slowly hydrolyzing GTP analogues guanosin-5"-[beta,gamma-imido]triphosphate, guanosin-5"-[beta,gamma-methylene]triphosphate, and guanosin-5"-O-(3-thiotriphosphate). guanosin-5"-o-(3-thiotriphosphate 224-257 H3 histone pseudogene 16 Homo sapiens 32-35 2668035-0 1989 Conformational changes occurring in N-ras p21 in response to binding of guanine nucleotide and metal ions probed by proteolysis performed under controlled conditions. Metals 95-100 H3 histone pseudogene 16 Homo sapiens 42-45 2668035-4 1989 Some capacity to bind guanine nucleotide is also retained by p21 treated with 7 M urea, as evidenced by increased resistance to proteolytic degradation, but the ability to bind divalent cations is irreversibly lost following denaturation. Guanine Nucleotides 22-40 H3 histone pseudogene 16 Homo sapiens 61-64 2668035-4 1989 Some capacity to bind guanine nucleotide is also retained by p21 treated with 7 M urea, as evidenced by increased resistance to proteolytic degradation, but the ability to bind divalent cations is irreversibly lost following denaturation. Urea 82-86 H3 histone pseudogene 16 Homo sapiens 61-64 2509438-1 1989 In the cocrystal formed by 7-methylguanosine-5"-phosphate.phenylalanine.6H2O, the interactions between guanine and phenylalanine are similar to those observed in the complex of ribonuclease T1 with 2"-guanylic acids, and those of the two G-proteins, Elongation Factor-Tu and ras oncogene p21, with GDP. Phenylalanine 58-71 H3 histone pseudogene 16 Homo sapiens 288-291 2509438-1 1989 In the cocrystal formed by 7-methylguanosine-5"-phosphate.phenylalanine.6H2O, the interactions between guanine and phenylalanine are similar to those observed in the complex of ribonuclease T1 with 2"-guanylic acids, and those of the two G-proteins, Elongation Factor-Tu and ras oncogene p21, with GDP. 6h2o 72-76 H3 histone pseudogene 16 Homo sapiens 288-291 2509438-1 1989 In the cocrystal formed by 7-methylguanosine-5"-phosphate.phenylalanine.6H2O, the interactions between guanine and phenylalanine are similar to those observed in the complex of ribonuclease T1 with 2"-guanylic acids, and those of the two G-proteins, Elongation Factor-Tu and ras oncogene p21, with GDP. 7-methylguanosine-5'-monophosphate 27-57 H3 histone pseudogene 16 Homo sapiens 288-291 2509438-1 1989 In the cocrystal formed by 7-methylguanosine-5"-phosphate.phenylalanine.6H2O, the interactions between guanine and phenylalanine are similar to those observed in the complex of ribonuclease T1 with 2"-guanylic acids, and those of the two G-proteins, Elongation Factor-Tu and ras oncogene p21, with GDP. Guanine 103-110 H3 histone pseudogene 16 Homo sapiens 288-291 2509438-1 1989 In the cocrystal formed by 7-methylguanosine-5"-phosphate.phenylalanine.6H2O, the interactions between guanine and phenylalanine are similar to those observed in the complex of ribonuclease T1 with 2"-guanylic acids, and those of the two G-proteins, Elongation Factor-Tu and ras oncogene p21, with GDP. Phenylalanine 115-128 H3 histone pseudogene 16 Homo sapiens 288-291 2509438-1 1989 In the cocrystal formed by 7-methylguanosine-5"-phosphate.phenylalanine.6H2O, the interactions between guanine and phenylalanine are similar to those observed in the complex of ribonuclease T1 with 2"-guanylic acids, and those of the two G-proteins, Elongation Factor-Tu and ras oncogene p21, with GDP. 2'-guanylic acid 198-215 H3 histone pseudogene 16 Homo sapiens 288-291 2474786-7 1989 When R256 was used to test for expression of arginine-12 p21 in tissues of transgenic mice containing an MMTV/v-Harvey-ras transgene, the monoclonal antibody was able to determine that the arginine-12 p21 transgene product was present in breast tumors but not in normal tissues. arginine-12 189-200 H3 histone pseudogene 16 Homo sapiens 201-204 2474786-8 1989 The ability of R256 to react specifically with arginine-12 p21 may prove to be valuable in the study of ras oncogenesis in model systems and in determining the presence of arginine-12 p21 in human tumors. arginine-12 47-58 H3 histone pseudogene 16 Homo sapiens 59-62 2474786-5 1989 R256 binds the activated Kirsten p21 in human lung tumor cell line A2182, which contains an activated arginine-12 p21. arginine-12 102-113 H3 histone pseudogene 16 Homo sapiens 33-36 2474786-8 1989 The ability of R256 to react specifically with arginine-12 p21 may prove to be valuable in the study of ras oncogenesis in model systems and in determining the presence of arginine-12 p21 in human tumors. arginine-12 172-183 H3 histone pseudogene 16 Homo sapiens 59-62 2474786-5 1989 R256 binds the activated Kirsten p21 in human lung tumor cell line A2182, which contains an activated arginine-12 p21. arginine-12 102-113 H3 histone pseudogene 16 Homo sapiens 114-117 2467732-3 1989 An immunohistochemical study of ras p21 expression was carried out on paraffin sections of 54 human breast carcinomas using monoclonal antibodies to p21. Paraffin 70-78 H3 histone pseudogene 16 Homo sapiens 36-39 2663468-2 1989 The primary translation product pro-p21 is cytosolic and is rapidly converted to a cytosolic form (c-p21) of higher mobility on SDS-PAGE. Sodium Dodecyl Sulfate 128-131 H3 histone pseudogene 16 Homo sapiens 36-39 2785386-0 1989 Comparison of the conformation and GTP hydrolysing ability of N-terminal ras p21 protein segments. Guanosine Triphosphate 35-38 H3 histone pseudogene 16 Homo sapiens 77-80 2785386-4 1989 Results suggest that restriction of conformational adaptation may contribute to the transforming capacity of the Val-12 p21 protein. Valine 113-116 H3 histone pseudogene 16 Homo sapiens 120-123 2663468-2 1989 The primary translation product pro-p21 is cytosolic and is rapidly converted to a cytosolic form (c-p21) of higher mobility on SDS-PAGE. Sodium Dodecyl Sulfate 128-131 H3 histone pseudogene 16 Homo sapiens 101-104 2686707-0 1989 Comparison of the computed structures for the phosphate-binding loop of the p21 protein containing the oncogenic site Gly 12 with the X-ray crystallographic structures for this region in the p21 protein and EFtu. Phosphates 46-55 H3 histone pseudogene 16 Homo sapiens 76-79 2686707-0 1989 Comparison of the computed structures for the phosphate-binding loop of the p21 protein containing the oncogenic site Gly 12 with the X-ray crystallographic structures for this region in the p21 protein and EFtu. Glycine 118-121 H3 histone pseudogene 16 Homo sapiens 76-79 2686707-2 1989 The GTP-binding p21 protein encoded by the ras-oncogene can be activated to cause malignant transformation of cells by substitution of a single amino acid at critical positions along the polypeptide chain. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 16-19 2686707-7 1989 We show that many computed structures for the Gly 12-containing phosphate binding loop, segment 9-15, are superimposable on the corresponding segment of the recently determined X-ray crystallographic structure for residues 1-171 of the p21 protein. Glycine 46-49 H3 histone pseudogene 16 Homo sapiens 236-239 2686707-7 1989 We show that many computed structures for the Gly 12-containing phosphate binding loop, segment 9-15, are superimposable on the corresponding segment of the recently determined X-ray crystallographic structure for residues 1-171 of the p21 protein. Phosphates 64-73 H3 histone pseudogene 16 Homo sapiens 236-239 2686707-9 1989 Other computed conformations for the 9-15 segment were superimposable on the structure of the corresponding 18-23 segment of EFtu, the bacterial chain elongation factor having structural similarities to the p21 protein in the phosphate-binding regions. Phosphates 226-235 H3 histone pseudogene 16 Homo sapiens 207-210 2686707-10 1989 This segment contains a Val residue where a Gly occurs in the p21 protein. Valine 24-27 H3 histone pseudogene 16 Homo sapiens 62-65 2686707-10 1989 This segment contains a Val residue where a Gly occurs in the p21 protein. Glycine 44-47 H3 histone pseudogene 16 Homo sapiens 62-65 2686707-12 1989 If these structures that are superimposable on EFtu are introduced into the p21 protein structure, bad contacts occur between the sidechain of the residue (here Val) at position 12 and another phosphate binding loop region around position 61. Valine 161-164 H3 histone pseudogene 16 Homo sapiens 76-79 2686707-12 1989 If these structures that are superimposable on EFtu are introduced into the p21 protein structure, bad contacts occur between the sidechain of the residue (here Val) at position 12 and another phosphate binding loop region around position 61. Phosphates 193-202 H3 histone pseudogene 16 Homo sapiens 76-79 2686707-15 1989 In addition, such phenomena as autophosphorylation of the p21 protein by GTP can be explained with this new model structure for the activated protein which cannot be explained by the structure for the non-activated protein. Guanosine Triphosphate 73-76 H3 histone pseudogene 16 Homo sapiens 58-61 2644645-1 1989 A sample of Escherichia coli-expressed human N-RAS-encoded p21, a 21-kDa protein, was selectively labeled with 15N at each of the 14 glycine amide positions. 15n 111-114 H3 histone pseudogene 16 Homo sapiens 59-62 2471068-1 1989 We have generated deletion mutants of the H-ras p21 protein which lack residues 58 to 63 or 64 to 68 and contain either the normal glycine or an activating mutation, arginine, at position 12. Glycine 131-138 H3 histone pseudogene 16 Homo sapiens 48-51 2471068-1 1989 We have generated deletion mutants of the H-ras p21 protein which lack residues 58 to 63 or 64 to 68 and contain either the normal glycine or an activating mutation, arginine, at position 12. Arginine 166-174 H3 histone pseudogene 16 Homo sapiens 48-51 2495001-0 1989 ras p21 and other Gn proteins are detected in mammalian cell lines by [gamma-35S]GTP gamma S binding. [gamma-35s]gtp 70-84 H3 histone pseudogene 16 Homo sapiens 4-7 2669815-1 1989 Substitutions of amino acids for Gly 12 or Gly 13 in the ras oncogene-encoded P21 proteins have been demonstrated to produce unique structural changes in these proteins that correlate with their ability to produce cell transformation. Glycine 33-36 H3 histone pseudogene 16 Homo sapiens 78-81 2669815-1 1989 Substitutions of amino acids for Gly 12 or Gly 13 in the ras oncogene-encoded P21 proteins have been demonstrated to produce unique structural changes in these proteins that correlate with their ability to produce cell transformation. Glycine 43-46 H3 histone pseudogene 16 Homo sapiens 78-81 2669815-2 1989 For example, the P21 proteins with Arg 12 or Val 13 are both known to be actively transforming. Arginine 35-38 H3 histone pseudogene 16 Homo sapiens 17-20 2669815-2 1989 For example, the P21 proteins with Arg 12 or Val 13 are both known to be actively transforming. Valine 45-48 H3 histone pseudogene 16 Homo sapiens 17-20 2669815-4 1989 In this study, we examine the structural effects of these substitutions on the amino terminal hydrophobic decapeptide (Leu 6-Gly 15) of P21 using conformational energy analysis. leu 6-gly 119-128 H3 histone pseudogene 16 Homo sapiens 136-139 2644645-1 1989 A sample of Escherichia coli-expressed human N-RAS-encoded p21, a 21-kDa protein, was selectively labeled with 15N at each of the 14 glycine amide positions. glycine amide 133-146 H3 histone pseudogene 16 Homo sapiens 59-62 2535967-5 1989 GAP interacts with p21 proteins (normal and mutant) in a GTP-dependent fashion. Guanosine Triphosphate 57-60 H3 histone pseudogene 16 Homo sapiens 19-22 2535967-7 1989 It remains possible that GAP simply regulates p21-GTP levels, and binds to the same site as the true effector without transmitting a downstream signal. Guanosine Triphosphate 50-53 H3 histone pseudogene 16 Homo sapiens 46-49 2535967-10 1989 Perhaps GAP is an enzyme (or is bound to an enzyme) that acts on membrane components in a p21-GTP-dependent manner and in doing so transmits signals to other downstream effectors. Guanosine Triphosphate 94-97 H3 histone pseudogene 16 Homo sapiens 90-93 2671311-1 1989 Antisense methylphosphonate-modified oligomers (ONMP) complementary to 8 nucleotides spanning the twelfth amino acid codon of human c-Ha-ras have been synthesized to explore their inhibitory effect on ras p21 translation. methylphosphonic acid 10-27 H3 histone pseudogene 16 Homo sapiens 205-208 2642607-2 1989 To understand the structural reasons behind cell transformation arising from this single amino acid substitution, we have determined the crystal structure of the GDP-bound form of the mutant protein, p21(Val-12), encoded by this oncogene. Guanosine Diphosphate 162-165 H3 histone pseudogene 16 Homo sapiens 200-203 2642607-2 1989 To understand the structural reasons behind cell transformation arising from this single amino acid substitution, we have determined the crystal structure of the GDP-bound form of the mutant protein, p21(Val-12), encoded by this oncogene. Valine 204-207 H3 histone pseudogene 16 Homo sapiens 200-203 2642607-3 1989 We report here the overall structure of p21(Val-12) at 2.2 A resolution and compare it with the structure of the normal c-Ha-ras protein. Valine 44-47 H3 histone pseudogene 16 Homo sapiens 40-43 2462857-2 1989 Therefore, we evaluated the expression of p21 in formaldehyde-fixed, paraffin-embedded prostatic tissue using a commercially available polyclonal antiserum prepared in sheep. Formaldehyde 49-61 H3 histone pseudogene 16 Homo sapiens 42-45 2462857-2 1989 Therefore, we evaluated the expression of p21 in formaldehyde-fixed, paraffin-embedded prostatic tissue using a commercially available polyclonal antiserum prepared in sheep. Paraffin 69-77 H3 histone pseudogene 16 Homo sapiens 42-45 2550600-2 1989 To investigate the role of ras p21 product expression in human hepatocellular carcinoma (HCC), we have localized ras p21 in formalin fixed, paraffin-embedded normal and abnormal livers utilizing the avidin-biotin peroxidase method and a monoclonal antibody to ras-gene product p21. Formaldehyde 124-132 H3 histone pseudogene 16 Homo sapiens 117-120 2550600-2 1989 To investigate the role of ras p21 product expression in human hepatocellular carcinoma (HCC), we have localized ras p21 in formalin fixed, paraffin-embedded normal and abnormal livers utilizing the avidin-biotin peroxidase method and a monoclonal antibody to ras-gene product p21. Formaldehyde 124-132 H3 histone pseudogene 16 Homo sapiens 117-120 2649686-0 1989 Crystallization and preliminary X-ray analysis of the human c-H-ras-oncogene product p21 complexed with GTP analogues. Guanosine Triphosphate 104-107 H3 histone pseudogene 16 Homo sapiens 85-88 2649686-1 1989 The catalytic domain (amino acid residues 1 to 166) of the human ras-oncogene product p21 complexed with the GTP analogues beta,gamma-imido-GTP (GMPPNP), beta,gamma-methylene-GTP (GMPPCP), and guanosine-5"-(gamma-thiotriphosphate) (GTP gamma S) have been been crystallized. Guanosine Triphosphate 109-112 H3 histone pseudogene 16 Homo sapiens 86-89 2649686-1 1989 The catalytic domain (amino acid residues 1 to 166) of the human ras-oncogene product p21 complexed with the GTP analogues beta,gamma-imido-GTP (GMPPNP), beta,gamma-methylene-GTP (GMPPCP), and guanosine-5"-(gamma-thiotriphosphate) (GTP gamma S) have been been crystallized. beta,gamma-imido-gtp 123-143 H3 histone pseudogene 16 Homo sapiens 86-89 2649686-1 1989 The catalytic domain (amino acid residues 1 to 166) of the human ras-oncogene product p21 complexed with the GTP analogues beta,gamma-imido-GTP (GMPPNP), beta,gamma-methylene-GTP (GMPPCP), and guanosine-5"-(gamma-thiotriphosphate) (GTP gamma S) have been been crystallized. Guanylyl Imidodiphosphate 145-151 H3 histone pseudogene 16 Homo sapiens 86-89 2649686-1 1989 The catalytic domain (amino acid residues 1 to 166) of the human ras-oncogene product p21 complexed with the GTP analogues beta,gamma-imido-GTP (GMPPNP), beta,gamma-methylene-GTP (GMPPCP), and guanosine-5"-(gamma-thiotriphosphate) (GTP gamma S) have been been crystallized. guanosine 5'-(beta,gamma-methylene)triphosphate 154-178 H3 histone pseudogene 16 Homo sapiens 86-89 2649686-1 1989 The catalytic domain (amino acid residues 1 to 166) of the human ras-oncogene product p21 complexed with the GTP analogues beta,gamma-imido-GTP (GMPPNP), beta,gamma-methylene-GTP (GMPPCP), and guanosine-5"-(gamma-thiotriphosphate) (GTP gamma S) have been been crystallized. 5'-guanylylmethylenebisphosphonate 180-186 H3 histone pseudogene 16 Homo sapiens 86-89 2649686-1 1989 The catalytic domain (amino acid residues 1 to 166) of the human ras-oncogene product p21 complexed with the GTP analogues beta,gamma-imido-GTP (GMPPNP), beta,gamma-methylene-GTP (GMPPCP), and guanosine-5"-(gamma-thiotriphosphate) (GTP gamma S) have been been crystallized. Guanosine 5'-O-(3-Thiotriphosphate) 193-230 H3 histone pseudogene 16 Homo sapiens 86-89 2649686-1 1989 The catalytic domain (amino acid residues 1 to 166) of the human ras-oncogene product p21 complexed with the GTP analogues beta,gamma-imido-GTP (GMPPNP), beta,gamma-methylene-GTP (GMPPCP), and guanosine-5"-(gamma-thiotriphosphate) (GTP gamma S) have been been crystallized. Guanosine Triphosphate 140-143 H3 histone pseudogene 16 Homo sapiens 86-89 2689384-2 1989 The issue of whether ras is directly involved in maintaining the metastatic phenotype through the expression and action of its gene product has been examined by analyzing the relationship to ras expression and to the production of the p21 ras-GTP complex, which is thought to mediate ras-transforming activity. Guanosine Triphosphate 243-246 H3 histone pseudogene 16 Homo sapiens 235-238 2671311-1 1989 Antisense methylphosphonate-modified oligomers (ONMP) complementary to 8 nucleotides spanning the twelfth amino acid codon of human c-Ha-ras have been synthesized to explore their inhibitory effect on ras p21 translation. onmp 48-52 H3 histone pseudogene 16 Homo sapiens 205-208 3143720-5 1988 Homology search indicates that smg p21 is a novel protein with the consensus amino acid sequences for GTP/GDP-binding and GTPase domains but shares about 55% amino acid sequence homology with the human c-Ha-ras protein. Guanosine Triphosphate 102-105 H3 histone pseudogene 16 Homo sapiens 35-38 2565631-4 1989 The monoclonal antibody DWP, which is specific for a mutated form of ras p21 having a valine/cysteine at amino acid position 12, was also used. (6aS,7S,9R,10aS)-7,10a-dimethyl-8-oxo-2-(phenylamino)-5,6,6a,7,8,9,10,10a-octahydrobenzo[h]quinazoline-9-carbonitrile 24-27 H3 histone pseudogene 16 Homo sapiens 73-76 2565631-4 1989 The monoclonal antibody DWP, which is specific for a mutated form of ras p21 having a valine/cysteine at amino acid position 12, was also used. valine/cysteine 86-101 H3 histone pseudogene 16 Homo sapiens 73-76 2567085-1 1989 In this study we examined 214 cases of primary human pulmonary neoplasms for the expression of a mutated form of the ras oncogene p21 product, recognized by the monoclonal antibody (MCA) DWP. (6aS,7S,9R,10aS)-7,10a-dimethyl-8-oxo-2-(phenylamino)-5,6,6a,7,8,9,10,10a-octahydrobenzo[h]quinazoline-9-carbonitrile 187-190 H3 histone pseudogene 16 Homo sapiens 130-133 2567085-6 1989 Since one would anticipate that the valine/cysteine substitution at position 12 of the ras p21 would occur at only low frequencies in human tumors, our results with DWP are consistent with this hypothesis. Valine 36-42 H3 histone pseudogene 16 Homo sapiens 91-94 2567085-6 1989 Since one would anticipate that the valine/cysteine substitution at position 12 of the ras p21 would occur at only low frequencies in human tumors, our results with DWP are consistent with this hypothesis. Cysteine 43-51 H3 histone pseudogene 16 Homo sapiens 91-94 2567085-6 1989 Since one would anticipate that the valine/cysteine substitution at position 12 of the ras p21 would occur at only low frequencies in human tumors, our results with DWP are consistent with this hypothesis. (6aS,7S,9R,10aS)-7,10a-dimethyl-8-oxo-2-(phenylamino)-5,6,6a,7,8,9,10,10a-octahydrobenzo[h]quinazoline-9-carbonitrile 165-168 H3 histone pseudogene 16 Homo sapiens 91-94 3143720-5 1988 Homology search indicates that smg p21 is a novel protein with the consensus amino acid sequences for GTP/GDP-binding and GTPase domains but shares about 55% amino acid sequence homology with the human c-Ha-ras protein. Guanosine Diphosphate 106-109 H3 histone pseudogene 16 Homo sapiens 35-38 3136779-3 1988 Crystals of the triazene have monoclinic symmetry with a = 8.540(1), b = 6.346(4), c = 22.460(5)A, beta = 98.75(2) degrees, and space group P21/c. Triazenes 16-24 H3 histone pseudogene 16 Homo sapiens 140-145 3181143-0 1988 Structure-function relationships in the GTP binding domain of EF-Tu: mutation of Val20, the residue homologous to position 12 in p21. Guanosine Triphosphate 40-43 H3 histone pseudogene 16 Homo sapiens 129-132 3181143-7 1988 As in p21, this position in EF-Tu is critical, influencing specifically the GDP/GTP interaction as well as other functions. Guanosine Diphosphate 76-79 H3 histone pseudogene 16 Homo sapiens 6-9 3181143-7 1988 As in p21, this position in EF-Tu is critical, influencing specifically the GDP/GTP interaction as well as other functions. Guanosine Triphosphate 80-83 H3 histone pseudogene 16 Homo sapiens 6-9 3181143-9 1988 The differences observed with two homologous residues, Gly20 and Gly12 in EF-Tu and p21 respectively, show the importance of a variable residue in a consensus element in defining specific functions of GTP binding proteins. Guanosine Triphosphate 201-204 H3 histone pseudogene 16 Homo sapiens 84-87 3146693-2 1988 p21v-ras protein possessing only the first five amino acids of p60src was not myristylated, while substitution of residue 6 (serine) produced a protein p21(GSSKS) which incorporated [3H]myristic acid that was stable to hydroxylamine, sensitive to inhibitors of protein synthesis, and found in both the normally nonacylated precursor and mature forms of p21(GSSKS). Serine 125-131 H3 histone pseudogene 16 Homo sapiens 152-155 3146693-2 1988 p21v-ras protein possessing only the first five amino acids of p60src was not myristylated, while substitution of residue 6 (serine) produced a protein p21(GSSKS) which incorporated [3H]myristic acid that was stable to hydroxylamine, sensitive to inhibitors of protein synthesis, and found in both the normally nonacylated precursor and mature forms of p21(GSSKS). gssks 156-161 H3 histone pseudogene 16 Homo sapiens 152-155 3146693-2 1988 p21v-ras protein possessing only the first five amino acids of p60src was not myristylated, while substitution of residue 6 (serine) produced a protein p21(GSSKS) which incorporated [3H]myristic acid that was stable to hydroxylamine, sensitive to inhibitors of protein synthesis, and found in both the normally nonacylated precursor and mature forms of p21(GSSKS). Tritium 183-185 H3 histone pseudogene 16 Homo sapiens 152-155 3146693-2 1988 p21v-ras protein possessing only the first five amino acids of p60src was not myristylated, while substitution of residue 6 (serine) produced a protein p21(GSSKS) which incorporated [3H]myristic acid that was stable to hydroxylamine, sensitive to inhibitors of protein synthesis, and found in both the normally nonacylated precursor and mature forms of p21(GSSKS). Myristic Acid 186-199 H3 histone pseudogene 16 Homo sapiens 152-155 3142873-9 1988 Proof that p21 is tyrosine phosphorylated zeta was afforded by a number of approaches. Tyrosine 18-26 H3 histone pseudogene 16 Homo sapiens 11-14 3170578-5 1988 The sequence of the GTP-binding site is consistent with predictions from other GTP-binding proteins such as elongation factor Tu or ras p21. Guanosine Triphosphate 20-23 H3 histone pseudogene 16 Homo sapiens 136-139 3170578-5 1988 The sequence of the GTP-binding site is consistent with predictions from other GTP-binding proteins such as elongation factor Tu or ras p21. Guanosine Triphosphate 79-82 H3 histone pseudogene 16 Homo sapiens 136-139 2842690-1 1988 The plasma membrane-bound mammalian ras proteins of relative molecular mass 21,000 (ras p21) share biochemical and structural properties with other guanine nucleotide-binding regulatory proteins (G-proteins). Guanine 148-155 H3 histone pseudogene 16 Homo sapiens 88-91 3179273-1 1988 The crystal structure of a disordered 1:1 complex between the tetradeoxyoligomer d(5BrC-G-5BrC-G) and proflavin has been determined and refined to an R factor of 26.9% for 474 reflections initially in space group P6(5) and to an R factor of 22.2% for 475 reflections in space group P2(1), both at 2-A resolution with Fobsd greater than or equal to 4.0. Proflavine 102-111 H3 histone pseudogene 16 Homo sapiens 282-287 2455265-4 1988 We have been able to regenerate both localization to the plasma membrane as well as transforming activity of such mutant ras p21 proteins by fusion of the amino-terminal 15 residues of the v-p60src protein, responsible for the covalent binding of myristic acid and its membrane association. Myristic Acid 247-260 H3 histone pseudogene 16 Homo sapiens 125-128 2834050-0 1988 Cellular proliferation and ras oncogene of p21 21,000 expression in relation to the intracellular cyclic adenosine 3":5"-monophosphate levels of a human salivary gland adenocarcinoma cell line in culture. Cyclic AMP 98-134 H3 histone pseudogene 16 Homo sapiens 43-46 2834050-2 1988 In the current study, the relationship between intracellular cAMP levels and anchorage-dependent and -independent growth or ras oncogene of p21 levels was analyzed in the differentiation process toward myoepithelial cells of HSG cells cultured in the presence of dB-cAMP. Cyclic AMP 61-65 H3 histone pseudogene 16 Homo sapiens 140-143 2834050-6 1988 When HSG cells were cultured in the presence of dB-cAMP and were committed to differentiate into myoepithelial cells, it was shown by double-antibody labeling technique and/or immunoblotting that the committed cells expressed myosin with a concomitant decrease of ras p21 protein. Bucladesine 48-55 H3 histone pseudogene 16 Homo sapiens 268-271 2834050-7 1988 Moreover, intracellular cAMP levels were found to be inversely associated with ras p21 content of the cells. Cyclic AMP 24-28 H3 histone pseudogene 16 Homo sapiens 83-86 2834050-8 1988 These findings indicate that the intracellular cAMP levels regulate significantly cell proliferation and ras p21 expression in HSG cells. Cyclic AMP 47-51 H3 histone pseudogene 16 Homo sapiens 109-112 2833702-3 1988 It is assumed that an external signal is detected by a membrane molecule (or detector) that stimulates the conversion of p21.GDP to p21.GTP which then interacts with a target molecule (or effector) to generate an internal signal. Guanosine Diphosphate 125-128 H3 histone pseudogene 16 Homo sapiens 121-124 2833702-3 1988 It is assumed that an external signal is detected by a membrane molecule (or detector) that stimulates the conversion of p21.GDP to p21.GTP which then interacts with a target molecule (or effector) to generate an internal signal. Guanosine Diphosphate 125-128 H3 histone pseudogene 16 Homo sapiens 132-135 2833702-3 1988 It is assumed that an external signal is detected by a membrane molecule (or detector) that stimulates the conversion of p21.GDP to p21.GTP which then interacts with a target molecule (or effector) to generate an internal signal. Guanosine Triphosphate 136-139 H3 histone pseudogene 16 Homo sapiens 121-124 2833702-3 1988 It is assumed that an external signal is detected by a membrane molecule (or detector) that stimulates the conversion of p21.GDP to p21.GTP which then interacts with a target molecule (or effector) to generate an internal signal. Guanosine Triphosphate 136-139 H3 histone pseudogene 16 Homo sapiens 132-135 3191559-1 1988 The X-ray crystal structure of 3 beta-(p-bromobenzoyloxy)-5 beta-cholesta-8,14-diene (space group P21, a = 10.698 A, b = 9.487 A, c = 15.024 A, beta = 96.05 degrees, Z = 2) was determined by the heavy atom method and refined to R = 0.075. 3 beta-(p-bromobenzoyloxy)-5 beta-cholesta-8,14-diene 31-84 H3 histone pseudogene 16 Homo sapiens 98-101 3076451-1 1988 The effect of the substitution of Arg for Gly 13 on the structure of the transforming region decapeptide (Leu 6-Gly 15) of the ras oncogene encoded P21 protein has been investigated using conformational energy analysis. leu 6-gly 106-115 H3 histone pseudogene 16 Homo sapiens 148-151 3045276-0 1988 Optimal preservation of p21 ras immunoreactivity and morphology in paraffin-embedded tissue. Paraffin 67-75 H3 histone pseudogene 16 Homo sapiens 24-27 2844230-0 1988 Normal cellular Ha ras p21 protein causes local disruption of bilayer phospholipid. Phospholipids 70-82 H3 histone pseudogene 16 Homo sapiens 23-26 2844230-1 1988 We have investigated the interactions of the p21 protein of c-Ha ras with its phospholipid environment. Phospholipids 78-90 H3 histone pseudogene 16 Homo sapiens 45-48 2844230-3 1988 Addition of 8 M urea to p21 preparations increased the solubility of the molecule in detergent solutions upon the removal of this denaturant. Urea 16-20 H3 histone pseudogene 16 Homo sapiens 24-27 2844230-4 1988 The progressive addition of the detergent cholate appeared to increase the efficiency of p21 preparations to bind GTP. Cholates 42-49 H3 histone pseudogene 16 Homo sapiens 89-92 2844230-4 1988 The progressive addition of the detergent cholate appeared to increase the efficiency of p21 preparations to bind GTP. Guanosine Triphosphate 114-117 H3 histone pseudogene 16 Homo sapiens 89-92 2844230-5 1988 This affinity for GTP was not removed even at high detergent concentrations, when delipification of the p21 was presumably effected. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 104-107 3323889-3 1987 Our present studies demonstrate that the mitogenic activity of the H-ras oncogene in H-ras p21-microinjected quiescent cells is markedly reduced under conditions in which PKC is downregulated by chronic phorbol ester treatment. Phorbol Esters 203-216 H3 histone pseudogene 16 Homo sapiens 91-94 3277185-4 1988 However, substitution of variant amino acids from the 80 C-terminal residues (amino acids 138-218) of R-ras p23 for the corresponding p21 amino acids (residues 112-189) inactivated the transforming activity of position-12 valine-substituted p21. Valine 222-228 H3 histone pseudogene 16 Homo sapiens 134-137 3277185-4 1988 However, substitution of variant amino acids from the 80 C-terminal residues (amino acids 138-218) of R-ras p23 for the corresponding p21 amino acids (residues 112-189) inactivated the transforming activity of position-12 valine-substituted p21. Valine 222-228 H3 histone pseudogene 16 Homo sapiens 241-244 3276311-0 1988 Proton NMR studies of the GDP.Mg2+ complex of the Ha-ras oncogene product p21. Guanosine Diphosphate 26-29 H3 histone pseudogene 16 Homo sapiens 74-77 3276311-0 1988 Proton NMR studies of the GDP.Mg2+ complex of the Ha-ras oncogene product p21. magnesium ion 30-34 H3 histone pseudogene 16 Homo sapiens 74-77 3276311-3 1988 From sequence homology with the bacterial elongation factor Tu (EF-Tu) and the known X-ray structure of the EF-Tu.GDP.Mg2+ complex it may be inferred that the Phe residue in question is either Phe78 or Phe82 in the p21 sequence. magnesium ion 118-122 H3 histone pseudogene 16 Homo sapiens 215-218 3068879-1 1988 To detect mutationally activated ras oncogenes, we analyzed electrophoretic mobilities of ras p21 proteins utilizing the fact that many ras oncogenes produce abnormal p21 proteins that migrate at SDS/polyacrylamide gel electrophoresis as a fast-moving or slow-moving species in comparison to a normal p21 depending on the kind of mutation. Sodium Dodecyl Sulfate 196-199 H3 histone pseudogene 16 Homo sapiens 94-97 3068879-1 1988 To detect mutationally activated ras oncogenes, we analyzed electrophoretic mobilities of ras p21 proteins utilizing the fact that many ras oncogenes produce abnormal p21 proteins that migrate at SDS/polyacrylamide gel electrophoresis as a fast-moving or slow-moving species in comparison to a normal p21 depending on the kind of mutation. Sodium Dodecyl Sulfate 196-199 H3 histone pseudogene 16 Homo sapiens 167-170 3068879-1 1988 To detect mutationally activated ras oncogenes, we analyzed electrophoretic mobilities of ras p21 proteins utilizing the fact that many ras oncogenes produce abnormal p21 proteins that migrate at SDS/polyacrylamide gel electrophoresis as a fast-moving or slow-moving species in comparison to a normal p21 depending on the kind of mutation. Sodium Dodecyl Sulfate 196-199 H3 histone pseudogene 16 Homo sapiens 167-170 3068879-1 1988 To detect mutationally activated ras oncogenes, we analyzed electrophoretic mobilities of ras p21 proteins utilizing the fact that many ras oncogenes produce abnormal p21 proteins that migrate at SDS/polyacrylamide gel electrophoresis as a fast-moving or slow-moving species in comparison to a normal p21 depending on the kind of mutation. polyacrylamide 200-214 H3 histone pseudogene 16 Homo sapiens 94-97 3313065-7 1987 We demonstrate a reproducible increase in 1,2-diacylglycerol, in the absence of a detectable increase in inositol phosphates, in transformed cells containing Ha-ras oncogenes and with different membrane targeting signals for the ras p21 protein. 1,2-diacylglycerol 42-60 H3 histone pseudogene 16 Homo sapiens 233-236 3427588-1 1987 1,3-Dimethyl-8-beta-D-ribofuranosylxanthine monohydrate, C12H16N4O6.H2O, is monoclinic, P21, with two molecules in a unit cell having a = 8.186(1), b = 19.222(3), c = 4.7655(8) A, beta = 103.79(1) degrees, V = 728.2 A, and Dx = 1.506 g.cm-3. 1,3-dimethyl-8-beta-d-ribofuranosylxanthine monohydrate 0-55 H3 histone pseudogene 16 Homo sapiens 88-91 3427588-1 1987 1,3-Dimethyl-8-beta-D-ribofuranosylxanthine monohydrate, C12H16N4O6.H2O, is monoclinic, P21, with two molecules in a unit cell having a = 8.186(1), b = 19.222(3), c = 4.7655(8) A, beta = 103.79(1) degrees, V = 728.2 A, and Dx = 1.506 g.cm-3. (S)-6-AMINO-2-(2,4-DINITRO-PHENYLAMINO)-HEXANOIC ACID 57-67 H3 histone pseudogene 16 Homo sapiens 88-91 3427588-1 1987 1,3-Dimethyl-8-beta-D-ribofuranosylxanthine monohydrate, C12H16N4O6.H2O, is monoclinic, P21, with two molecules in a unit cell having a = 8.186(1), b = 19.222(3), c = 4.7655(8) A, beta = 103.79(1) degrees, V = 728.2 A, and Dx = 1.506 g.cm-3. Water 68-71 H3 histone pseudogene 16 Homo sapiens 88-91 3276311-3 1988 From sequence homology with the bacterial elongation factor Tu (EF-Tu) and the known X-ray structure of the EF-Tu.GDP.Mg2+ complex it may be inferred that the Phe residue in question is either Phe78 or Phe82 in the p21 sequence. Phenylalanine 159-162 H3 histone pseudogene 16 Homo sapiens 215-218 3276554-4 1988 When ras p21 was laid over vesicle proteins immobilized on a nitrocellulose sheet by transfer from the gel of SDS-polyacrylamide gel electrophoresis, ras p21 bound to bands 4.2 and 6. ras p21 binding to these proteins was reduced by prior incubation of ras p21 with the purified band 4.2 or 6 protein. Sodium Dodecyl Sulfate 110-113 H3 histone pseudogene 16 Homo sapiens 9-12 3276554-4 1988 When ras p21 was laid over vesicle proteins immobilized on a nitrocellulose sheet by transfer from the gel of SDS-polyacrylamide gel electrophoresis, ras p21 bound to bands 4.2 and 6. ras p21 binding to these proteins was reduced by prior incubation of ras p21 with the purified band 4.2 or 6 protein. Sodium Dodecyl Sulfate 110-113 H3 histone pseudogene 16 Homo sapiens 154-157 3276554-4 1988 When ras p21 was laid over vesicle proteins immobilized on a nitrocellulose sheet by transfer from the gel of SDS-polyacrylamide gel electrophoresis, ras p21 bound to bands 4.2 and 6. ras p21 binding to these proteins was reduced by prior incubation of ras p21 with the purified band 4.2 or 6 protein. Sodium Dodecyl Sulfate 110-113 H3 histone pseudogene 16 Homo sapiens 154-157 3276554-4 1988 When ras p21 was laid over vesicle proteins immobilized on a nitrocellulose sheet by transfer from the gel of SDS-polyacrylamide gel electrophoresis, ras p21 bound to bands 4.2 and 6. ras p21 binding to these proteins was reduced by prior incubation of ras p21 with the purified band 4.2 or 6 protein. Sodium Dodecyl Sulfate 110-113 H3 histone pseudogene 16 Homo sapiens 154-157 3276554-4 1988 When ras p21 was laid over vesicle proteins immobilized on a nitrocellulose sheet by transfer from the gel of SDS-polyacrylamide gel electrophoresis, ras p21 bound to bands 4.2 and 6. ras p21 binding to these proteins was reduced by prior incubation of ras p21 with the purified band 4.2 or 6 protein. polyacrylamide 114-128 H3 histone pseudogene 16 Homo sapiens 9-12 3276554-4 1988 When ras p21 was laid over vesicle proteins immobilized on a nitrocellulose sheet by transfer from the gel of SDS-polyacrylamide gel electrophoresis, ras p21 bound to bands 4.2 and 6. ras p21 binding to these proteins was reduced by prior incubation of ras p21 with the purified band 4.2 or 6 protein. polyacrylamide 114-128 H3 histone pseudogene 16 Homo sapiens 154-157 3276554-4 1988 When ras p21 was laid over vesicle proteins immobilized on a nitrocellulose sheet by transfer from the gel of SDS-polyacrylamide gel electrophoresis, ras p21 bound to bands 4.2 and 6. ras p21 binding to these proteins was reduced by prior incubation of ras p21 with the purified band 4.2 or 6 protein. polyacrylamide 114-128 H3 histone pseudogene 16 Homo sapiens 154-157 3276554-4 1988 When ras p21 was laid over vesicle proteins immobilized on a nitrocellulose sheet by transfer from the gel of SDS-polyacrylamide gel electrophoresis, ras p21 bound to bands 4.2 and 6. ras p21 binding to these proteins was reduced by prior incubation of ras p21 with the purified band 4.2 or 6 protein. polyacrylamide 114-128 H3 histone pseudogene 16 Homo sapiens 154-157 3140742-1 1988 The ras oncogene product ras p21 is structurally homologous to guanine nucleotide-binding proteins and plays an important role in transducing signals elicited by membrane receptors into intracellular metabolism. Guanine Nucleotides 63-81 H3 histone pseudogene 16 Homo sapiens 29-32 3140742-7 1988 The functions of ras p21 have not been clearly identified in mammalian cells; however recent reports reveal that cyclic AMP production is inhibited by the transfection of activated ras gene into normal cells. Cyclic AMP 113-123 H3 histone pseudogene 16 Homo sapiens 21-24 3318757-2 1987 To gain a better understanding of the role these oncogenes may play in malignant transformation, we evaluated the levels of a ras gene protein product (p21) in formaldehyde-fixed, paraffin-embedded specimens of normal human colonic mucosa, hyperplastic polyps, tubular adenomas, villous adenomas, and epithelium from a patient with ulcerative colitis. Formaldehyde 160-172 H3 histone pseudogene 16 Homo sapiens 152-155 3318757-2 1987 To gain a better understanding of the role these oncogenes may play in malignant transformation, we evaluated the levels of a ras gene protein product (p21) in formaldehyde-fixed, paraffin-embedded specimens of normal human colonic mucosa, hyperplastic polyps, tubular adenomas, villous adenomas, and epithelium from a patient with ulcerative colitis. Paraffin 180-188 H3 histone pseudogene 16 Homo sapiens 152-155 3123435-3 1987 In cells carrying a point-mutationally activated ras, p21 with abnormal mobility upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis was clearly detected. Sodium Dodecyl Sulfate 86-108 H3 histone pseudogene 16 Homo sapiens 54-57 3123435-3 1987 In cells carrying a point-mutationally activated ras, p21 with abnormal mobility upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis was clearly detected. polyacrylamide 109-123 H3 histone pseudogene 16 Homo sapiens 54-57 3328019-3 1987 Furthermore, it has been shown that residues 16, 116 and 119 in p21 played critical roles in the guanine nucleotide binding and, consequently, the ability of the protein to induce changes characteristic of cellular transformation. Guanine Nucleotides 97-115 H3 histone pseudogene 16 Homo sapiens 64-67 2821624-4 1987 In contrast, Gly12 p21 was predominantly guanosine diphosphate (GDP)-bound because of a dramatic stimulation of Gly12 p21-associated guanosine triphosphatase (GTPase) activity. Guanosine Diphosphate 41-62 H3 histone pseudogene 16 Homo sapiens 19-22 2821624-4 1987 In contrast, Gly12 p21 was predominantly guanosine diphosphate (GDP)-bound because of a dramatic stimulation of Gly12 p21-associated guanosine triphosphatase (GTPase) activity. Guanosine Diphosphate 41-62 H3 histone pseudogene 16 Homo sapiens 118-121 2823806-1 1987 An in vitro study of phosphate-transfer, from the high-energy phosphates on the phosphoenzyme (enzyme-bound high-energy phosphate intermediate) of NDP-kinase to GDP on various guanine nucleotide binding proteins (G1, elongation factor alpha 1, recombinant v-rasH p21 protein, transducin, Gi and Go), revealed that the GDP acts as a phosphate-acceptor, in the presence of divalent cations (Mg2+ and Ca2+). Phosphates 21-30 H3 histone pseudogene 16 Homo sapiens 263-266 2823806-1 1987 An in vitro study of phosphate-transfer, from the high-energy phosphates on the phosphoenzyme (enzyme-bound high-energy phosphate intermediate) of NDP-kinase to GDP on various guanine nucleotide binding proteins (G1, elongation factor alpha 1, recombinant v-rasH p21 protein, transducin, Gi and Go), revealed that the GDP acts as a phosphate-acceptor, in the presence of divalent cations (Mg2+ and Ca2+). Guanosine Diphosphate 161-164 H3 histone pseudogene 16 Homo sapiens 263-266 3328019-8 1987 The probability for the normal p21 containing glycine as residue 12 is greatest, and the cancer-associated variants show less probabilities. Glycine 46-53 H3 histone pseudogene 16 Homo sapiens 31-34 3315926-1 1987 Expression of ras p21 in human gastric cancers, benign lesions (i.e. dysplasia, intestinal metaplasia and hyperplastic polyps) and normal tissues was immunohistochemically evaluated by the avidin-biotin complex (ABC) immunoperoxidase method with anti-ras p21 monoclonal antibody(rp-28). avidin-biotin 189-202 H3 histone pseudogene 16 Homo sapiens 18-21 3313005-10 1987 R-ras p21-like proteins, made by eliminating the first 26 R-ras codons, displayed evident mobility differences between the pro form and mature form, along with a valine 12 substitution-dependent change in electrophoretic mobility. Valine 162-168 H3 histone pseudogene 16 Homo sapiens 6-9 2821624-4 1987 In contrast, Gly12 p21 was predominantly guanosine diphosphate (GDP)-bound because of a dramatic stimulation of Gly12 p21-associated guanosine triphosphatase (GTPase) activity. Guanosine Diphosphate 64-67 H3 histone pseudogene 16 Homo sapiens 19-22 2821624-4 1987 In contrast, Gly12 p21 was predominantly guanosine diphosphate (GDP)-bound because of a dramatic stimulation of Gly12 p21-associated guanosine triphosphatase (GTPase) activity. Guanosine Diphosphate 64-67 H3 histone pseudogene 16 Homo sapiens 118-121 2821624-6 1987 This protein stimulated GTP hydrolysis by purified Gly12 p21 more than 200-fold in vitro, but had no effect on Asp12 or Val12 mutants. Guanosine Triphosphate 24-27 H3 histone pseudogene 16 Homo sapiens 57-60 2821624-9 1987 Furthermore, it appears that the major effect of position 12 mutations is to prevent this protein from stimulating p21 GTPase activity, thereby allowing these mutants to remain in the active GTP-bound state. Guanosine Triphosphate 119-122 H3 histone pseudogene 16 Homo sapiens 115-118 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Triphosphate 242-245 H3 histone pseudogene 16 Homo sapiens 34-37 3035212-7 1987 At position 12 in the p21 coding region, arginine is substituted for the naturally occurring glycine present in c-ras. Arginine 41-49 H3 histone pseudogene 16 Homo sapiens 22-25 3035212-7 1987 At position 12 in the p21 coding region, arginine is substituted for the naturally occurring glycine present in c-ras. Glycine 93-100 H3 histone pseudogene 16 Homo sapiens 22-25 3298232-1 1987 p21 isolated under nondenaturing conditions is obtained as a complex with guanosine nucleotides and magnesium ions. guanosine nucleotides 74-95 H3 histone pseudogene 16 Homo sapiens 0-3 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Triphosphate 242-245 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-1 1987 p21 isolated under nondenaturing conditions is obtained as a complex with guanosine nucleotides and magnesium ions. Magnesium 100-109 H3 histone pseudogene 16 Homo sapiens 0-3 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Triphosphate 242-245 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-4 1987 The protein thus prepared is thermally much less stable than the complexed p21, but can be used for studying its interaction with nucleotides and metal ions at low temperatures. Metals 146-151 H3 histone pseudogene 16 Homo sapiens 75-78 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. magnesium ion 272-276 H3 histone pseudogene 16 Homo sapiens 34-37 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Diphosphate 42-45 H3 histone pseudogene 16 Homo sapiens 34-37 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Diphosphate 42-45 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Diphosphate 42-45 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Triphosphate 78-81 H3 histone pseudogene 16 Homo sapiens 34-37 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Triphosphate 78-81 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Triphosphate 78-81 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Diphosphate 230-233 H3 histone pseudogene 16 Homo sapiens 34-37 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Diphosphate 230-233 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. magnesium ion 272-276 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. Guanosine Diphosphate 230-233 H3 histone pseudogene 16 Homo sapiens 226-229 3298232-5 1987 The association rate constant for p21 and GDP is 1.47 X 10(6) M-1 s-1 and for GTP is 2.9 X 10(6) M-1 s-1 at 0 degree C. By using appropriately determined dissociation rate constants we have determined the binding constant for p21.GDP and p21.GTP in the presence of excess Mg2+ to be 5.7 X 10(10) M-1 and 6.0 X 10(10) M-1, respectively, at 0 degree C. magnesium ion 272-276 H3 histone pseudogene 16 Homo sapiens 226-229 3673025-3 1987 Treatment of the cells with cycloheximide and hypertonic NaCl solution, virtually depressing the radioactive label incorporation into PEK cell proteins, also inhibits the synthesis of virus-specific proteins p69, p21, p15, and p12. Cycloheximide 28-41 H3 histone pseudogene 16 Homo sapiens 213-216 3109943-1 1987 Autophosphorylation of the purified human insulin receptor tyrosyl kinase was found to be inhibited by the ras oncogene product p21 in a concentration- and GDP-dependent manner. Guanosine Diphosphate 156-159 H3 histone pseudogene 16 Homo sapiens 128-131 3105868-4 1987 Cells grown with prednisolone (1.4-2.1 microM) expressed higher Ha-p21 levels than controls. Prednisolone 17-29 H3 histone pseudogene 16 Homo sapiens 67-70 3105868-6 1987 The steroid had no detectable effect on cells in S and G2 + M. By contrast, sodium butyrate and hyperosmolality caused a marked decrease in Ha-p21 content. Butyric Acid 76-91 H3 histone pseudogene 16 Homo sapiens 143-146 2439901-0 1987 Neutralizing monoclonal antibody against ras oncogene product p21 which impairs guanine nucleotide exchange. Guanine Nucleotides 80-98 H3 histone pseudogene 16 Homo sapiens 62-65 3554231-2 1987 The G domain, whose primary structure shares homology with the eukaryotic protein p21, is capable of supporting the basic activities of the intact molecule (guanine nucleotide binding in 1:1 molar ratio and GTPase activity). Guanine Nucleotides 157-175 H3 histone pseudogene 16 Homo sapiens 82-85 3554231-5 1987 Its GTPase shows the characteristics of a slow turnover reaction (0.1 mmol X sec-1 X mol-1 of G domain), whose rate closely corresponds to the initial hydrolysis rate of EF-Tu X GTP in the absence of effectors and lies in the typical range of GTPase of the p21 protein. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 257-260 3673025-3 1987 Treatment of the cells with cycloheximide and hypertonic NaCl solution, virtually depressing the radioactive label incorporation into PEK cell proteins, also inhibits the synthesis of virus-specific proteins p69, p21, p15, and p12. nacl solution 57-70 H3 histone pseudogene 16 Homo sapiens 213-216 3115313-11 1987 These domains of homologies are also similar to those of other GTP binding proteins, such as the product of the ras gene (p21) and the initiation or elongation factors. Guanosine Triphosphate 63-66 H3 histone pseudogene 16 Homo sapiens 122-125 3546289-1 1987 We have carried out photoaffinity labeling of the ras p21 protein, a ras oncogene product, with [alpha-32P]GTP. [alpha-32p]gtp 96-110 H3 histone pseudogene 16 Homo sapiens 54-57 3546289-3 1987 The specificity of this protocol is shown by (a) sensitivity of affinity labeling of ras p21 to known inhibitors of GTP binding and (b) immunoprecipitation of affinity labeled protein with anti-ras p21 serum. Guanosine Triphosphate 116-119 H3 histone pseudogene 16 Homo sapiens 89-92 3330790-3 1987 A transversion in codon 13 (GGT----TGT) resulting in replacement of glycine13 by cysteine13 in ras p21 protein was found. glycine13 68-77 H3 histone pseudogene 16 Homo sapiens 99-102 3549386-0 1987 The role of N-ras p21 in the coupling of growth factor receptors to inositol phospholipid turnover. Phosphatidylinositols 68-89 H3 histone pseudogene 16 Homo sapiens 18-21 3028791-0 1987 Characterisation of the metal-ion-GDP complex at the active sites of transforming and nontransforming p21 proteins by observation of the 17O-Mn superhyperfine coupling and by kinetic methods. Metals 24-29 H3 histone pseudogene 16 Homo sapiens 102-105 3028791-0 1987 Characterisation of the metal-ion-GDP complex at the active sites of transforming and nontransforming p21 proteins by observation of the 17O-Mn superhyperfine coupling and by kinetic methods. Guanosine Diphosphate 34-37 H3 histone pseudogene 16 Homo sapiens 102-105 3028791-1 1987 Kinetic studies on the interaction of three Ha-ras-encoded p21 proteins with GDP and MgGDP have yielded values for the association (10(6)-10(7) M-1 s-1) and dissociation (10(-3)-10(-5) s-1) rate constants at 0 degrees C. Dramatic differences in the rate constants were not observed for the three proteins. Guanosine Diphosphate 77-80 H3 histone pseudogene 16 Homo sapiens 59-62 3028791-6 1987 The association constant of Mn(II) to p21 proteins in the absence of nucleotides was estimated to be greater than 10(5) M-1. Manganese(2+) 28-34 H3 histone pseudogene 16 Homo sapiens 38-41 3028791-8 1987 These results have been used to construct a model for the interactions of Mg X GDP with the active site of p21 proteins. Magnesium 74-76 H3 histone pseudogene 16 Homo sapiens 107-110 3028791-8 1987 These results have been used to construct a model for the interactions of Mg X GDP with the active site of p21 proteins. Guanosine Diphosphate 79-82 H3 histone pseudogene 16 Homo sapiens 107-110 3567985-1 1987 The crystal structure of L-chiro-inositol is monoclinic, P21, with a = 6.867(3), b = 9.133(4), c = 6.217(3) A, beta = 106.59(4) degrees, Z = 2. Inositol 25-41 H3 histone pseudogene 16 Homo sapiens 57-60 3330790-3 1987 A transversion in codon 13 (GGT----TGT) resulting in replacement of glycine13 by cysteine13 in ras p21 protein was found. cysteine13 81-91 H3 histone pseudogene 16 Homo sapiens 99-102 3330790-6 1987 These data identify the first base of codon 13 as a novel mutation site in ras genes and indicate that cysteine at position 13 of the ras p21 is a transforming substitution. Cysteine 103-111 H3 histone pseudogene 16 Homo sapiens 138-141 3021182-0 1986 31P-NMR studies on ATP X Mg2+, p21 X nucleotide, and adenylate kinase X nucleotide complexes. ET bromodomain inhibitor 0-3 H3 histone pseudogene 16 Homo sapiens 31-34 3490906-3 1986 Normal p21 contains glycine at position 12; the other amino acid substitutions are those which would result from a single base change in codon 12 and may therefore be the activating mutations most likely to occur in human tumors. Glycine 20-27 H3 histone pseudogene 16 Homo sapiens 7-10 3540608-0 1986 Activation of ras p21 transforming properties associated with an increase in the release rate of bound guanine nucleotide. Guanine Nucleotides 103-121 H3 histone pseudogene 16 Homo sapiens 18-21 3540608-6 1986 Mutants with the Thr-59 substitution exhibited a three- to ninefold-higher rate of GDP and GTP release than normal p21 or mutants with other activating lesions. Threonine 17-20 H3 histone pseudogene 16 Homo sapiens 115-118 3540608-9 1986 Consistent with knowledge of known G-regulatory proteins, these findings support a model in which the p21-GTP complex is the biologically active form of the p21 protein. Guanosine Triphosphate 106-109 H3 histone pseudogene 16 Homo sapiens 102-105 3540608-9 1986 Consistent with knowledge of known G-regulatory proteins, these findings support a model in which the p21-GTP complex is the biologically active form of the p21 protein. Guanosine Triphosphate 106-109 H3 histone pseudogene 16 Homo sapiens 157-160 3533923-0 1986 Reactivity of a sulfhydryl group of the ras oncogene product p21 modulated by GTP binding. Guanosine Triphosphate 78-81 H3 histone pseudogene 16 Homo sapiens 61-64 3533923-1 1986 We have studied the sensitivity of sulfhydryl groups of a highly purified p21 protein of the v-rasH oncogene to a thiol-specific reagent, N-ethylmaleimide (NEM). Sulfhydryl Compounds 114-119 H3 histone pseudogene 16 Homo sapiens 74-77 3533923-1 1986 We have studied the sensitivity of sulfhydryl groups of a highly purified p21 protein of the v-rasH oncogene to a thiol-specific reagent, N-ethylmaleimide (NEM). Ethylmaleimide 138-154 H3 histone pseudogene 16 Homo sapiens 74-77 3533923-1 1986 We have studied the sensitivity of sulfhydryl groups of a highly purified p21 protein of the v-rasH oncogene to a thiol-specific reagent, N-ethylmaleimide (NEM). Ethylmaleimide 156-159 H3 histone pseudogene 16 Homo sapiens 74-77 3533923-2 1986 Approximately 70% of GTP binding and autokinase activities of p21 were inactivated by NEM, and excessive amounts of GTP or GDP protected p21 activities. Guanosine Triphosphate 21-24 H3 histone pseudogene 16 Homo sapiens 62-65 3533923-2 1986 Approximately 70% of GTP binding and autokinase activities of p21 were inactivated by NEM, and excessive amounts of GTP or GDP protected p21 activities. Guanosine Triphosphate 116-119 H3 histone pseudogene 16 Homo sapiens 62-65 3533923-2 1986 Approximately 70% of GTP binding and autokinase activities of p21 were inactivated by NEM, and excessive amounts of GTP or GDP protected p21 activities. Guanosine Triphosphate 116-119 H3 histone pseudogene 16 Homo sapiens 137-140 3533923-2 1986 Approximately 70% of GTP binding and autokinase activities of p21 were inactivated by NEM, and excessive amounts of GTP or GDP protected p21 activities. Guanosine Diphosphate 123-126 H3 histone pseudogene 16 Homo sapiens 62-65 3533923-2 1986 Approximately 70% of GTP binding and autokinase activities of p21 were inactivated by NEM, and excessive amounts of GTP or GDP protected p21 activities. Guanosine Diphosphate 123-126 H3 histone pseudogene 16 Homo sapiens 137-140 3533923-6 1986 This is based on the comparative tryptic peptide mapping of [14C]NEM-modified p21 in the presence and absence of GTP. Peptides 41-48 H3 histone pseudogene 16 Homo sapiens 78-81 3533923-6 1986 This is based on the comparative tryptic peptide mapping of [14C]NEM-modified p21 in the presence and absence of GTP. Carbon-14 61-64 H3 histone pseudogene 16 Homo sapiens 78-81 3533923-6 1986 This is based on the comparative tryptic peptide mapping of [14C]NEM-modified p21 in the presence and absence of GTP. Guanosine Triphosphate 113-116 H3 histone pseudogene 16 Homo sapiens 78-81 3533923-8 1986 Amino acid analysis of the purified [14C]NEM-modified peptide from tryptic digests of p21 also confirmed its identity. Carbon-14 37-40 H3 histone pseudogene 16 Homo sapiens 86-89 3533923-9 1986 This region of p21 shares an extensive sequence homology with various G-proteins and appears to be in the vicinity of the GTP-binding domain of these proteins. Guanosine Triphosphate 122-125 H3 histone pseudogene 16 Homo sapiens 15-18 3022300-6 1986 The retrovirus-treated FS-2 cells (called FSK) appeared heavily granulated and expressed viral p21 but senesced during passage in culture and were not tumorigenic. fsk 42-45 H3 histone pseudogene 16 Homo sapiens 95-98 3023062-1 1986 We synthesized a set of 20-mer oligonucleotides corresponding to a sequence of seven amino acids strictly conserved in all the different ras proteins, from yeast to man, as well as in rho and YPT, two proteins distantly related to p21 ras (approximately 30% amino acid homology). Oligonucleotides 31-47 H3 histone pseudogene 16 Homo sapiens 231-234 3023062-6 1986 The GTP binding regions of p21 ras and a C-terminal cysteine involved in membrane anchoring are also present in ral; this strongly suggests that ral is a GTP binding protein with membrane localization. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 27-30 3023062-6 1986 The GTP binding regions of p21 ras and a C-terminal cysteine involved in membrane anchoring are also present in ral; this strongly suggests that ral is a GTP binding protein with membrane localization. Guanosine Triphosphate 154-157 H3 histone pseudogene 16 Homo sapiens 27-30 3537694-2 1986 The ability of the encoded p21"s to autophosphorylate, bind guanine nucleotides, and hydrolyze GTP was assessed. Guanine Nucleotides 60-79 H3 histone pseudogene 16 Homo sapiens 27-30 2431273-1 1986 The p21 products of ras proto-oncogenes are GTP-binding proteins with associated GTPase activity. Guanosine Triphosphate 44-47 H3 histone pseudogene 16 Homo sapiens 4-7 3485974-0 1986 31P-NMR spectra of the Ha-ras p21.nucleotide complexes. ET bromodomain inhibitor 0-3 H3 histone pseudogene 16 Homo sapiens 30-33 3485974-1 1986 Phosphorus nuclear magnetic resonance spectra of the Ha-ras oncogene product p21 and its nucleotide complexes have been obtained. Phosphorus 0-10 H3 histone pseudogene 16 Homo sapiens 77-80 3485974-3 1986 In particular, the chemical shift values of the beta-phosphorus resonance of enzyme-bound NTP and NDP (N = A, G) of hydrolases exhibit a downfield shift virtually identical for myosin, elongation factor Tu, and the Ha-ras oncogene product p21. beta-phosphorus 48-63 H3 histone pseudogene 16 Homo sapiens 239-242 3012529-1 1986 Recent studies have shown that the 21-kilodalton protein (p21) Ha-ras gene product shares sequence homology with and may exhibit biochemical properties similar to the mammalian guanine nucleotide-binding proteins. Guanine Nucleotides 177-195 H3 histone pseudogene 16 Homo sapiens 58-61 3012529-8 1986 These data support the hypothesis that both the normal and mutated Ha-ras p21s are related to guanine nucleotide-binding proteins. Guanine Nucleotides 94-112 H3 histone pseudogene 16 Homo sapiens 74-77 3537694-2 1986 The ability of the encoded p21"s to autophosphorylate, bind guanine nucleotides, and hydrolyze GTP was assessed. Guanosine Triphosphate 95-98 H3 histone pseudogene 16 Homo sapiens 27-30 3537694-3 1986 All versions of p21 bound GTP equivalently; the kinase activity, while dependent upon residue 12, did not correlate with the transforming potential of the polypeptide. Guanosine Triphosphate 26-29 H3 histone pseudogene 16 Homo sapiens 16-19 2869483-0 1986 ATP-binding site of adenylate kinase: mechanistic implications of its homology with ras-encoded p21, F1-ATPase, and other nucleotide-binding proteins. Adenosine Triphosphate 0-3 H3 histone pseudogene 16 Homo sapiens 96-99 3537694-4 1986 All transforming versions exhibited an impaired GTPase activity, while a novel nontransforming derivative [p21(pro-12)] possessed an enhanced GTPase activity. pro-12 111-117 H3 histone pseudogene 16 Homo sapiens 107-110 2869483-1 1986 The MgATP binding site of adenylate kinase, located by a combination of NMR and x-ray diffraction, is near three protein segments, five to seven amino acids in length, that are homologous in sequence to segments found in other nucleotide-binding phosphotransferases, such as myosin and F1-ATPase, ras p21 and transducin GTPases, and cAMP-dependent and src protein kinases, suggesting equivalent mechanistic roles of these segments in all of these proteins. Adenosine Triphosphate 4-9 H3 histone pseudogene 16 Homo sapiens 301-304 3915772-4 1985 This antibody was also shown to strikingly and specifically inhibit the guanine nucleotide-binding function of the p21 protein. Guanine Nucleotides 72-90 H3 histone pseudogene 16 Homo sapiens 115-118 3082814-1 1986 A 576 base-pair DNA encoding human c-Ha-ras protein (p21) with a valine codon at position 12 has been synthesized by ligation of chemically synthesized oligodeoxyribonucleotides. Valine 65-71 H3 histone pseudogene 16 Homo sapiens 53-56 3082814-1 1986 A 576 base-pair DNA encoding human c-Ha-ras protein (p21) with a valine codon at position 12 has been synthesized by ligation of chemically synthesized oligodeoxyribonucleotides. Oligodeoxyribonucleotides 152-177 H3 histone pseudogene 16 Homo sapiens 53-56 3321304-4 1986 Its binding to p21 is completely blocked by guanine nucleotides, even though the region of p21 to which it binds does not seem to be part of the guanine nucleotide-binding site. Guanine Nucleotides 44-63 H3 histone pseudogene 16 Homo sapiens 15-18 3321304-4 1986 Its binding to p21 is completely blocked by guanine nucleotides, even though the region of p21 to which it binds does not seem to be part of the guanine nucleotide-binding site. Guanine Nucleotides 44-63 H3 histone pseudogene 16 Homo sapiens 91-94 3321304-4 1986 Its binding to p21 is completely blocked by guanine nucleotides, even though the region of p21 to which it binds does not seem to be part of the guanine nucleotide-binding site. Guanine Nucleotides 44-62 H3 histone pseudogene 16 Homo sapiens 15-18 3321304-4 1986 Its binding to p21 is completely blocked by guanine nucleotides, even though the region of p21 to which it binds does not seem to be part of the guanine nucleotide-binding site. Guanine Nucleotides 44-62 H3 histone pseudogene 16 Homo sapiens 91-94 3321304-6 1986 Another interesting region of p21 includes amino acids 116 and 119, which seem to confer, in part, the specificity of p21 for guanine nucleotides. Guanine Nucleotides 126-145 H3 histone pseudogene 16 Homo sapiens 30-33 3321304-6 1986 Another interesting region of p21 includes amino acids 116 and 119, which seem to confer, in part, the specificity of p21 for guanine nucleotides. Guanine Nucleotides 126-145 H3 histone pseudogene 16 Homo sapiens 118-121 3321304-8 1986 We were able to refine our model for guanine nucleotide interaction with p21 and to create mutant proteins with altered specificity for purine nucleotides. Guanine Nucleotides 37-55 H3 histone pseudogene 16 Homo sapiens 73-76 3321304-8 1986 We were able to refine our model for guanine nucleotide interaction with p21 and to create mutant proteins with altered specificity for purine nucleotides. Purine Nucleotides 136-154 H3 histone pseudogene 16 Homo sapiens 73-76 3018922-5 1986 Using 35S-methionine incorporation, immunoprecipitation with anti-p21 monoclonal antibodies, SDS-PAGE and autoradiography, it was demonstrated that p21 synthesis was remarkably enhanced in 7402 cells as well as in transformed cells derived from both 7402 and PHC DNA. Sulfur-35 6-9 H3 histone pseudogene 16 Homo sapiens 148-151 3018922-5 1986 Using 35S-methionine incorporation, immunoprecipitation with anti-p21 monoclonal antibodies, SDS-PAGE and autoradiography, it was demonstrated that p21 synthesis was remarkably enhanced in 7402 cells as well as in transformed cells derived from both 7402 and PHC DNA. Methionine 10-20 H3 histone pseudogene 16 Homo sapiens 148-151 3018922-5 1986 Using 35S-methionine incorporation, immunoprecipitation with anti-p21 monoclonal antibodies, SDS-PAGE and autoradiography, it was demonstrated that p21 synthesis was remarkably enhanced in 7402 cells as well as in transformed cells derived from both 7402 and PHC DNA. Sodium Dodecyl Sulfate 93-96 H3 histone pseudogene 16 Homo sapiens 148-151 3004443-2 1986 Only in the presence of dexamethasone (a synthetic glucocorticoid), 433.3 cells exhibit an induced level of p21 transforming protein and phenotypic transformation. Dexamethasone 24-37 H3 histone pseudogene 16 Homo sapiens 108-111 3004443-4 1986 DBcAMP (5 X 10(-4)M) added 18 hr prior to the addition of dexamethasone (10(-7)M) almost completely blocked the hormone effect: cells contained levels of p21 20% of that in the cells treated with dexamethasone alone, and formed flat, contact inhibited monolayers. Bucladesine 0-6 H3 histone pseudogene 16 Homo sapiens 154-157 3333361-3 1986 The ras gene family encodes a group of closely related 21,000 dalton (p21) proteins with special affinity for guanine nucleotides. Guanine Nucleotides 110-129 H3 histone pseudogene 16 Homo sapiens 70-73 3333361-7 1986 p21 appears to have a small membrane binding domain at the C-terminus, which contains a palmitylation site at cysteine-186, four amino acid residues from the end. Cysteine 110-118 H3 histone pseudogene 16 Homo sapiens 0-3 3333361-11 1986 Studies using site-directed mutagenesis and immnochemical probes, indicate that the basic structure of the GDP binding site is conserved between p21 and EF-Tu. Guanosine Diphosphate 107-110 H3 histone pseudogene 16 Homo sapiens 145-148 3333361-12 1986 Furthermore, these studies also conclude that GTP binding is crucial for p21 ras cellular function. Guanosine Triphosphate 46-49 H3 histone pseudogene 16 Homo sapiens 73-76 3332015-4 1986 One of the two tumors thus obtained was formed after the injection of 6.3 kb DNA fragment containing the gene for p21 with valine at the twelfth position. Valine 123-129 H3 histone pseudogene 16 Homo sapiens 114-117 4092204-1 1985 Isobutyl 2,3,4-tri-O-acetyl-1-thio-beta-D-xylopyranoside is monoclinic, P21, with a = 10.134(4), b = 7.748(3), c = 11.726(4) A, beta = 96.63(3) degrees, V = 914.55 A3, Z = 2, Dm = 1.262, Dx = 1.264 g . isobutyl 2,3,4-tri-o-acetyl-1-thio-beta-d-xylopyranoside 0-56 H3 histone pseudogene 16 Homo sapiens 72-75 3915772-5 1985 The inability of p21 protein to bind guanine nucleotides was associated with a lack of autophosphorylation or GTPase activities. Guanine Nucleotides 37-56 H3 histone pseudogene 16 Homo sapiens 17-20 3915772-6 1985 These studies suggest that a region toward its carboxy terminus is directly or indirectly involved in the guanine nucleotide-binding function of the p21 molecule. Guanine Nucleotides 106-124 H3 histone pseudogene 16 Homo sapiens 149-152 3898366-7 1985 The model makes it possible to visualize how oncogenic mutations of p21 affect interaction with guanine nucleotides. Guanine Nucleotides 96-115 H3 histone pseudogene 16 Homo sapiens 68-71 3929144-7 1985 Like the guanine nucleotide regulatory proteins, Ns and Ni, which mediate stimulation and inhibition, respectively, of adenylate cyclase, p21 is a membrane-associated GTP binding protein, which exhibits GTPase activity. Guanosine Triphosphate 167-170 H3 histone pseudogene 16 Homo sapiens 138-141 3927300-3 1985 Anti-p21ser was found to immunoprecipitate v-Ki-ras p21 and to strongly inhibit its ability to autophosphorylate and to bind GTP in an immunoabsorption assay. Guanosine Triphosphate 125-128 H3 histone pseudogene 16 Homo sapiens 5-8 3927300-4 1985 Furthermore, binding of the antibody to p21 was specifically inhibited by GTP or GDP, suggesting that amino acids around position 12 are part of the GTP/GDP binding site. Guanosine Triphosphate 74-77 H3 histone pseudogene 16 Homo sapiens 40-43 3927300-4 1985 Furthermore, binding of the antibody to p21 was specifically inhibited by GTP or GDP, suggesting that amino acids around position 12 are part of the GTP/GDP binding site. Guanosine Diphosphate 81-84 H3 histone pseudogene 16 Homo sapiens 40-43 4004262-9 1985 Crystals of 6AzTH are monoclinic, space group P21/n, with unit cell parameters a = 8.861 (1), b = 13.177 (3), c = 20.662 (2) A, beta = 93.35 (1) degrees, and Z = 16. 6azth 12-17 H3 histone pseudogene 16 Homo sapiens 46-49 3927300-4 1985 Furthermore, binding of the antibody to p21 was specifically inhibited by GTP or GDP, suggesting that amino acids around position 12 are part of the GTP/GDP binding site. Guanosine Triphosphate 149-152 H3 histone pseudogene 16 Homo sapiens 40-43 3927300-4 1985 Furthermore, binding of the antibody to p21 was specifically inhibited by GTP or GDP, suggesting that amino acids around position 12 are part of the GTP/GDP binding site. Guanosine Diphosphate 153-156 H3 histone pseudogene 16 Homo sapiens 40-43 4008102-3 1985 One substitution of a thymidine for an adenosine was found at position 1069 of the 2898 nucleotide sequence in a restriction endonuclease (SacI) fragment, which corresponds to the second base of the 61st codon of the gene encoding P21 protein. Thymidine 22-31 H3 histone pseudogene 16 Homo sapiens 231-234 4008102-3 1985 One substitution of a thymidine for an adenosine was found at position 1069 of the 2898 nucleotide sequence in a restriction endonuclease (SacI) fragment, which corresponds to the second base of the 61st codon of the gene encoding P21 protein. Adenosine 39-48 H3 histone pseudogene 16 Homo sapiens 231-234 3923480-1 1985 The conformational effects of different amino acid substitutions (lysine, serine, proline, and D-valine) for glycine at position 12 in the p21 oncogene-encoded proteins have been investigated by using conformational energy calculations. D-Valine 95-103 H3 histone pseudogene 16 Homo sapiens 139-142 3923480-1 1985 The conformational effects of different amino acid substitutions (lysine, serine, proline, and D-valine) for glycine at position 12 in the p21 oncogene-encoded proteins have been investigated by using conformational energy calculations. Glycine 109-116 H3 histone pseudogene 16 Homo sapiens 139-142 3923480-2 1985 The normal cellular gene codes for a glycine at position 12 in the amino acid sequence, in the middle of a hydrophobic p21-(6-15)-decapepetide from Leu-6 to Gly-15. Glycine 37-44 H3 histone pseudogene 16 Homo sapiens 119-122 3923480-6 1985 However, we find that proline, unlike these residues but like glycine, at position 12 causes helix termination at positions 11 and 12, a result that suggests that the p21 protein product with proline at position 12 may exhibit lowered transforming potential, in agreement with the results of recent genetic recombination experiments. Proline 22-29 H3 histone pseudogene 16 Homo sapiens 167-170 3923480-6 1985 However, we find that proline, unlike these residues but like glycine, at position 12 causes helix termination at positions 11 and 12, a result that suggests that the p21 protein product with proline at position 12 may exhibit lowered transforming potential, in agreement with the results of recent genetic recombination experiments. Proline 192-199 H3 histone pseudogene 16 Homo sapiens 167-170 3884015-6 1985 Moreover, the high p21 levels in the mammary carcinomas correlated directly with high GTPase activity, as revealed by the photo-incorporation of 8-N3-[gamma-32P]GTP into the tumor lysates. 8-n3-[gamma-32p]gtp 145-164 H3 histone pseudogene 16 Homo sapiens 19-22 6096811-2 1984 The oncogene of PR371 was found to present a mutation at codon 12 of the first coding exon which substitutes cysteine for glycine in the encoded p21 protein. Cysteine 109-117 H3 histone pseudogene 16 Homo sapiens 145-148 3919305-1 1985 Mammalian ras oncogenes encode polypeptides of relative molecular mass (Mr) 21,000 (p21) which bind GTP and GDP. Guanosine Triphosphate 100-103 H3 histone pseudogene 16 Homo sapiens 84-87 3001111-3 1985 Using a known protein (3H-labeled translation initiation factor [eIF-4D]) as a standard internal marker for isoelectric point (pI), we show that p21 proteins from various cells differ only slightly in molecular weight (21-24 kDa) but express a wide variety in charge (pI 4.8 to 7) that could only be detected by the use of two-dimensional gel electrophoresis. Tritium 23-25 H3 histone pseudogene 16 Homo sapiens 145-148 3918304-4 1985 These findings imply that intramolecular disulfide bonds affect native p21 conformation. Disulfides 41-50 H3 histone pseudogene 16 Homo sapiens 71-74 2983103-4 1985 The presence of a lysine residue in position 12 of BALB/c murine sarcoma virus p21 likely accounts for its oncogenic properties. Lysine 18-24 H3 histone pseudogene 16 Homo sapiens 79-82 3919305-1 1985 Mammalian ras oncogenes encode polypeptides of relative molecular mass (Mr) 21,000 (p21) which bind GTP and GDP. Guanosine Diphosphate 108-111 H3 histone pseudogene 16 Homo sapiens 84-87 3919305-3 1985 Recently, we and others have observed that normal p21, encoded by the Ha-ras gene, has a GTP hydrolytic activity that is reduced by the oncogenic substitutions Val 12 or Thr 59. Guanosine Triphosphate 89-92 H3 histone pseudogene 16 Homo sapiens 50-53 3919305-3 1985 Recently, we and others have observed that normal p21, encoded by the Ha-ras gene, has a GTP hydrolytic activity that is reduced by the oncogenic substitutions Val 12 or Thr 59. Valine 160-163 H3 histone pseudogene 16 Homo sapiens 50-53 3919305-3 1985 Recently, we and others have observed that normal p21, encoded by the Ha-ras gene, has a GTP hydrolytic activity that is reduced by the oncogenic substitutions Val 12 or Thr 59. Threonine 170-173 H3 histone pseudogene 16 Homo sapiens 50-53 6096811-2 1984 The oncogene of PR371 was found to present a mutation at codon 12 of the first coding exon which substitutes cysteine for glycine in the encoded p21 protein. Glycine 122-129 H3 histone pseudogene 16 Homo sapiens 145-148 6148751-2 1984 The purified protein molecules possess intrinsic GTPase activity on the basis of the following criteria: (i) elution of the GTPase activity with p21 GDP-binding activity in two different chromatography systems, (ii) parallel thermal inactivation of GTPase activity and p21 GTP-binding activity, and (iii) immunoprecipitation of the GTPase activity with monoclonal antibodies to p21. Guanosine Triphosphate 49-52 H3 histone pseudogene 16 Homo sapiens 145-148 6392849-11 1984 Finally, we used anti-p21 monoclonal antibodies to detect a guanine nucleotide binding activity in yeast lysates. Guanine Nucleotides 60-78 H3 histone pseudogene 16 Homo sapiens 22-25 6148703-2 1984 In vitro, ras proteins bind GTP, and p21 mutants with treonine at position 59 autophosphorylate at that residue. treonine 54-62 H3 histone pseudogene 16 Homo sapiens 37-40 6148703-5 1984 However, mutations at position 12 in recombinant (Thr 59) p21 molecules were observed to affect autophosphorylation. Threonine 50-53 H3 histone pseudogene 16 Homo sapiens 58-61 6148751-2 1984 The purified protein molecules possess intrinsic GTPase activity on the basis of the following criteria: (i) elution of the GTPase activity with p21 GDP-binding activity in two different chromatography systems, (ii) parallel thermal inactivation of GTPase activity and p21 GTP-binding activity, and (iii) immunoprecipitation of the GTPase activity with monoclonal antibodies to p21. Guanosine Triphosphate 49-52 H3 histone pseudogene 16 Homo sapiens 269-272 6089200-3 1984 This results in substitution of aspartic acid for glycine at this position of the p21 coding sequence. Aspartic Acid 32-45 H3 histone pseudogene 16 Homo sapiens 82-85 6089200-3 1984 This results in substitution of aspartic acid for glycine at this position of the p21 coding sequence. Glycine 50-57 H3 histone pseudogene 16 Homo sapiens 82-85 6148751-2 1984 The purified protein molecules possess intrinsic GTPase activity on the basis of the following criteria: (i) elution of the GTPase activity with p21 GDP-binding activity in two different chromatography systems, (ii) parallel thermal inactivation of GTPase activity and p21 GTP-binding activity, and (iii) immunoprecipitation of the GTPase activity with monoclonal antibodies to p21. Guanosine Triphosphate 49-52 H3 histone pseudogene 16 Homo sapiens 269-272 6148751-3 1984 At 37 degrees C, the rate of GTP hydrolysis by the purified normal p21 assayed in solution was 5.3-6.6 mmol/min per mol of p21. Guanosine Triphosphate 29-32 H3 histone pseudogene 16 Homo sapiens 67-70 6148751-3 1984 At 37 degrees C, the rate of GTP hydrolysis by the purified normal p21 assayed in solution was 5.3-6.6 mmol/min per mol of p21. Guanosine Triphosphate 29-32 H3 histone pseudogene 16 Homo sapiens 123-126 6148751-2 1984 The purified protein molecules possess intrinsic GTPase activity on the basis of the following criteria: (i) elution of the GTPase activity with p21 GDP-binding activity in two different chromatography systems, (ii) parallel thermal inactivation of GTPase activity and p21 GTP-binding activity, and (iii) immunoprecipitation of the GTPase activity with monoclonal antibodies to p21. Guanosine Diphosphate 149-152 H3 histone pseudogene 16 Homo sapiens 145-148 6148751-4 1984 The rate of GTP hydrolysis by a form of p21 [Val12] encoded by a human oncogene was significantly lower (1.4-1.9 mmol/min per mol of p21). Guanosine Triphosphate 12-15 H3 histone pseudogene 16 Homo sapiens 40-43 6148751-4 1984 The rate of GTP hydrolysis by a form of p21 [Val12] encoded by a human oncogene was significantly lower (1.4-1.9 mmol/min per mol of p21). Guanosine Triphosphate 12-15 H3 histone pseudogene 16 Homo sapiens 133-136 6148751-5 1984 The presence of a threonine phosphate acceptor site at residue 59 also decreased p21 GTPase activity. Phosphothreonine 18-37 H3 histone pseudogene 16 Homo sapiens 81-84 6147754-2 1984 In addition to the guanine nucleotide binding activity, normal p21 displays a GTPase activity which is selectively impaired by a mutation which activates its oncogenic potential. Guanine Nucleotides 19-37 H3 histone pseudogene 16 Homo sapiens 63-66 6148751-7 1984 The observation that oncogenic forms of p21 lose GTPase activity suggests that GTP hydrolysis may be a biochemical event that inactivates the growth-promoting effects of a p21 X GTP complex. Guanosine Triphosphate 49-52 H3 histone pseudogene 16 Homo sapiens 40-43 6148751-7 1984 The observation that oncogenic forms of p21 lose GTPase activity suggests that GTP hydrolysis may be a biochemical event that inactivates the growth-promoting effects of a p21 X GTP complex. Guanosine Triphosphate 49-52 H3 histone pseudogene 16 Homo sapiens 172-175 6148751-7 1984 The observation that oncogenic forms of p21 lose GTPase activity suggests that GTP hydrolysis may be a biochemical event that inactivates the growth-promoting effects of a p21 X GTP complex. Guanosine Triphosphate 79-82 H3 histone pseudogene 16 Homo sapiens 40-43 6148751-7 1984 The observation that oncogenic forms of p21 lose GTPase activity suggests that GTP hydrolysis may be a biochemical event that inactivates the growth-promoting effects of a p21 X GTP complex. Guanosine Triphosphate 79-82 H3 histone pseudogene 16 Homo sapiens 172-175 7401119-2 1980 Crystals of nafoxidine hydrochloride-ethanol are monoclinic with cell dimensions a = 17.040, b = 7.967, c = 25.260 A, beta = 123.7 degrees, and space group P21/c with four formula units per cell. Nafoxidine 12-36 H3 histone pseudogene 16 Homo sapiens 156-159 6610834-7 1984 We report here the evidence that epidermal growth factor enhances the guanine nucleotide binding activity of activated c-Ha-ras or v-Ha-ras p21, and phosphorylation of v-Ha-ras p21, suggesting that some mitogenic growth factors may regulate those activities. Guanine Nucleotides 70-88 H3 histone pseudogene 16 Homo sapiens 140-143 6609071-0 1984 Homologies in the primary structure of GTP-binding proteins: the nucleotide-binding site of EF-Tu and p21. Guanosine Triphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 102-105 6422257-8 1984 The p21 of v-Ha-ras and the 30K proteins from S. cerevisiae share methionine-labeled peptides as detected by two-dimensional tryptic peptide maps. Methionine 66-76 H3 histone pseudogene 16 Homo sapiens 4-7 6422257-8 1984 The p21 of v-Ha-ras and the 30K proteins from S. cerevisiae share methionine-labeled peptides as detected by two-dimensional tryptic peptide maps. Peptides 85-93 H3 histone pseudogene 16 Homo sapiens 4-7 6311615-1 1983 The transforming proteins (p21) of Harvey and Kirsten sarcoma viruses threonine kinase activity, which phosphorylates threonine 59 of the p21 proteins themselves. Threonine 70-79 H3 histone pseudogene 16 Homo sapiens 27-30 6311615-1 1983 The transforming proteins (p21) of Harvey and Kirsten sarcoma viruses threonine kinase activity, which phosphorylates threonine 59 of the p21 proteins themselves. Threonine 70-79 H3 histone pseudogene 16 Homo sapiens 138-141 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Arginine 18-21 H3 histone pseudogene 16 Homo sapiens 101-104 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Arginine 22-25 H3 histone pseudogene 16 Homo sapiens 101-104 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Threonine 36-39 H3 histone pseudogene 16 Homo sapiens 101-104 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Glycine 46-49 H3 histone pseudogene 16 Homo sapiens 101-104 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Glutamine 50-53 H3 histone pseudogene 16 Homo sapiens 101-104 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Glutamic Acid 54-57 H3 histone pseudogene 16 Homo sapiens 101-104 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Tyrosine 58-61 H3 histone pseudogene 16 Homo sapiens 101-104 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Serine 62-65 H3 histone pseudogene 16 Homo sapiens 101-104 6311615-2 1983 A tridecapeptide: Arg-Arg-Leu56-Asp-Thr-Thr59-Gly-Gln-Glu-Tyr-Ser-Ala66 containing residues 56-66 of p21 is phosphorylated solely on tyrosine by the epidermal growth factor (EGF)-stimulated tyrosine kinase of A431 cell membranes. Tyrosine 133-141 H3 histone pseudogene 16 Homo sapiens 101-104 7216622-4 1980 Threo-beta-hydroxy-N-acetyl-L-tryptophanamide (C13H15N3O3) crystallizes in space group P21 with cell parameters a = 13.572(4) A, b = 6.296(1) A, c = 13.796(4) A and beta = 148.10(2) degrees. threo-beta-hydroxy-n-acetyl-l-tryptophanamide 0-45 H3 histone pseudogene 16 Homo sapiens 87-90 7216622-4 1980 Threo-beta-hydroxy-N-acetyl-L-tryptophanamide (C13H15N3O3) crystallizes in space group P21 with cell parameters a = 13.572(4) A, b = 6.296(1) A, c = 13.796(4) A and beta = 148.10(2) degrees. c13h15n3o3 47-57 H3 histone pseudogene 16 Homo sapiens 87-90 7216622-5 1980 Erythro-beta-hydroxy-N-acetyl-DL-tryptophanamide (C13H15N3O3.1/2C6H6) crystallizes in space group P21/c with cell parameters a = 23.178(15) A, b = 7.202(3) A, c = 9.218(4) A and beta = 91.13(5) degrees. erythro-beta-hydroxy-n-acetyl-dl-tryptophanamide 0-48 H3 histone pseudogene 16 Homo sapiens 98-101 7216622-5 1980 Erythro-beta-hydroxy-N-acetyl-DL-tryptophanamide (C13H15N3O3.1/2C6H6) crystallizes in space group P21/c with cell parameters a = 23.178(15) A, b = 7.202(3) A, c = 9.218(4) A and beta = 91.13(5) degrees. c13h15n3o3.1 50-62 H3 histone pseudogene 16 Homo sapiens 98-101 6092927-5 1984 The intracellular half-life of p21 proteins was determined by pulse-labeling and chasing in the presence of excess unlabeled methionine. Methionine 125-135 H3 histone pseudogene 16 Homo sapiens 31-34 6100635-4 1984 Antibodies to synthetic peptides inferred from the nucleotide sequence of the env gene of HTLV-IATK were also raised and used to identify and purify env precursor gPr62-68, surface glycoprotein gp46-51 and transmembrane protein p21. Peptides 24-32 H3 histone pseudogene 16 Homo sapiens 228-231 6308640-3 1983 These findings predicted that the resulting oncogene would code for a structurally altered p21 protein containing valine instead of glycine as its 12th amino acid residue. Valine 114-120 H3 histone pseudogene 16 Homo sapiens 91-94 6308640-3 1983 These findings predicted that the resulting oncogene would code for a structurally altered p21 protein containing valine instead of glycine as its 12th amino acid residue. Glycine 132-139 H3 histone pseudogene 16 Homo sapiens 91-94 6308640-7 1983 These results predict that the p21 protein coded for by the spontaneously activated c-has/bas gene will incorporate aspartic acid as its 12th amino acid residue. Aspartic Acid 116-129 H3 histone pseudogene 16 Homo sapiens 31-34 6308640-8 1983 Computer analysis of the secondary structure of c-has/bas encoded p21 proteins indicates that substitution of the glycine residue located at position 12, not only by aspartic acid or valine but also by any other amino acid, would result in the same structural alteration. Glycine 114-121 H3 histone pseudogene 16 Homo sapiens 66-69 6308640-8 1983 Computer analysis of the secondary structure of c-has/bas encoded p21 proteins indicates that substitution of the glycine residue located at position 12, not only by aspartic acid or valine but also by any other amino acid, would result in the same structural alteration. Aspartic Acid 166-179 H3 histone pseudogene 16 Homo sapiens 66-69 6308640-8 1983 Computer analysis of the secondary structure of c-has/bas encoded p21 proteins indicates that substitution of the glycine residue located at position 12, not only by aspartic acid or valine but also by any other amino acid, would result in the same structural alteration. Valine 183-189 H3 histone pseudogene 16 Homo sapiens 66-69 6843652-2 1983 The point mutation consists of the conversion of guanine into thymine, which results in the replacement of a glycine by a valine at position 12 of the p21 protein encoded by the EJ and T24 genes. Guanine 49-56 H3 histone pseudogene 16 Homo sapiens 151-154 6843652-2 1983 The point mutation consists of the conversion of guanine into thymine, which results in the replacement of a glycine by a valine at position 12 of the p21 protein encoded by the EJ and T24 genes. Thymine 62-69 H3 histone pseudogene 16 Homo sapiens 151-154 6843652-3 1983 Sequence data of retroviral analogues of the p21 protein also indicate the importance for a glycine residue at position 12 in normal p21. Glycine 92-99 H3 histone pseudogene 16 Homo sapiens 45-48 6843652-3 1983 Sequence data of retroviral analogues of the p21 protein also indicate the importance for a glycine residue at position 12 in normal p21. Glycine 92-99 H3 histone pseudogene 16 Homo sapiens 133-136 6843652-4 1983 Comparison of the sequence of the 37 N-terminal residues of the normal human p21 protein with the sequence of the dinucleotide-binding beta alpha beta unit in a group of structurally related enzymes, suggests that these residues of p21 fold into a very similar unit which is also involved in binding a nucleotide. Dinucleoside Phosphates 114-126 H3 histone pseudogene 16 Homo sapiens 77-80 6843652-4 1983 Comparison of the sequence of the 37 N-terminal residues of the normal human p21 protein with the sequence of the dinucleotide-binding beta alpha beta unit in a group of structurally related enzymes, suggests that these residues of p21 fold into a very similar unit which is also involved in binding a nucleotide. Dinucleoside Phosphates 114-126 H3 histone pseudogene 16 Homo sapiens 232-235 6843652-5 1983 We present here a three-dimensional model of the p21 beta alpha beta unit which explains directly why glycine at position 12 cannot be replaced by another residue without altering the nucleotide-binding properties of p21. Glycine 102-109 H3 histone pseudogene 16 Homo sapiens 49-52 6296696-3 1983 The oncogene is activated by a single point mutation (guanine to thymine) resulting in the change glycine to valine at position 12 of p21 (refs 3, 4). Guanine 54-61 H3 histone pseudogene 16 Homo sapiens 134-137 6296696-3 1983 The oncogene is activated by a single point mutation (guanine to thymine) resulting in the change glycine to valine at position 12 of p21 (refs 3, 4). Thymine 65-72 H3 histone pseudogene 16 Homo sapiens 134-137 6296696-5 1983 Thus, p21 may form part of an enzyme that uses purine nucleotides in catalysis. Purine Nucleotides 47-65 H3 histone pseudogene 16 Homo sapiens 6-9 7133135-2 1982 This substitution results in the incorporation of valine instead of glycine as the twelfth amino acid residue of the T24 oncogene-encoded p21 protein. Valine 50-56 H3 histone pseudogene 16 Homo sapiens 138-141 7133135-2 1982 This substitution results in the incorporation of valine instead of glycine as the twelfth amino acid residue of the T24 oncogene-encoded p21 protein. Glycine 68-75 H3 histone pseudogene 16 Homo sapiens 138-141 6277498-3 1981 The levels of p21 RNA and protein in these transformants are regulated by physiological concentrations of dexamethasone, a synthetic glucocorticoid hormone. Dexamethasone 106-119 H3 histone pseudogene 16 Homo sapiens 14-17 7401119-2 1980 Crystals of nafoxidine hydrochloride-ethanol are monoclinic with cell dimensions a = 17.040, b = 7.967, c = 25.260 A, beta = 123.7 degrees, and space group P21/c with four formula units per cell. Ethanol 37-44 H3 histone pseudogene 16 Homo sapiens 156-159 420851-1 1979 8-Methyladenosine 3"-monophosphate dihydrate was synthesized and crystallized in the monoclinic space group P21 with the unit cell dimensions: a = 9.095(2) A, b = 16.750(3) A, c = 5.405(2) A and beta = 97.61(3) degrees. 8-methyladenosine 3"-monophosphate dihydrate 0-44 H3 histone pseudogene 16 Homo sapiens 108-111 33964346-10 2021 Moreover, overexpression of miR-130a in D-galactose (D-gal)-induced SH-SY5Y cell senescence model attenuated D-gal-induced impaired autophagy and cell senescence, demonstrated by decreased levels of LC3, Ac-p53, p21 and increased p62, suggesting that voluntary wheel running can alleviate brain aging in natural aging rats by up-regulating miR-130a-mediated autophagy. Galactose 40-51 H3 histone pseudogene 16 Homo sapiens 212-215 1166722-1 1975 Acetylcholine beta-resorcylate, C14H21NO6, crystallizes in space group P21/c with a unit cell having dimensions a=14.562(6), b=14.109(4), c=15.096(6) A, and beta=106.90(3) degrees. acetylcholine beta-resorcylate 0-30 H3 histone pseudogene 16 Homo sapiens 71-74 1166722-1 1975 Acetylcholine beta-resorcylate, C14H21NO6, crystallizes in space group P21/c with a unit cell having dimensions a=14.562(6), b=14.109(4), c=15.096(6) A, and beta=106.90(3) degrees. c14h21no6 32-41 H3 histone pseudogene 16 Homo sapiens 71-74 11945362-1 1970 The nucleoside was crystallized from aqueous methanol as its iodide monohydrate in space group P2(1). Nucleosides 4-14 H3 histone pseudogene 16 Homo sapiens 95-100 11945362-1 1970 The nucleoside was crystallized from aqueous methanol as its iodide monohydrate in space group P2(1). Methanol 45-53 H3 histone pseudogene 16 Homo sapiens 95-100 11945362-1 1970 The nucleoside was crystallized from aqueous methanol as its iodide monohydrate in space group P2(1). iodide monohydrate 61-79 H3 histone pseudogene 16 Homo sapiens 95-100 660592-2 1978 MeCCNU crystallizes in monoclinic space group P21/c, with cell dimensions a = 12.387, b = 10.810, and c = 10 .198 A , beta = 102.62 degrees , and Z = four molecules per unit cell. Semustine 0-6 H3 histone pseudogene 16 Homo sapiens 46-51 626748-2 1978 Crystals of 8-(alpha-hydroxyisopropyl)-adenosine dihydrate, C13H19N5O5.2H2O, belong to the monoclinic space group P21. 8-(alpha-hydroxyisopropyl)-adenosine dihydrate 12-58 H3 histone pseudogene 16 Homo sapiens 114-117 626748-2 1978 Crystals of 8-(alpha-hydroxyisopropyl)-adenosine dihydrate, C13H19N5O5.2H2O, belong to the monoclinic space group P21. c13h19n5o5.2h2o 60-75 H3 histone pseudogene 16 Homo sapiens 114-117 32196298-4 1976 The low temperature form of K2O 2Sb2O5 was found to be monoclinic P21/c with a = 7.178, b = 13.378, c = 11.985 A, beta = 124 10". k2o 2sb2o5 28-40 H3 histone pseudogene 16 Homo sapiens 68-71 1137835-2 1975 Crystals of the salt are monoclinic, space group P21, having a = 6.410 (1), b = 10.784 (2), c = 8.879 (1) A, betta = 92.07 (1)degrees, and Z = 2. Salts 16-20 H3 histone pseudogene 16 Homo sapiens 49-52 31927823-1 1965 Tetracalcium phosphate, Ca4O(PO4)2, has a monoclinic modification with the parameters a= 11.99, b = 9.48, and c = 6.97 A, alpha = 90.8 , z = 4, and space group P21 or P21/m. tetracalcium phosphate 0-22 H3 histone pseudogene 16 Homo sapiens 160-163 31927823-1 1965 Tetracalcium phosphate, Ca4O(PO4)2, has a monoclinic modification with the parameters a= 11.99, b = 9.48, and c = 6.97 A, alpha = 90.8 , z = 4, and space group P21 or P21/m. tetracalcium phosphate 0-22 H3 histone pseudogene 16 Homo sapiens 167-172 31927823-1 1965 Tetracalcium phosphate, Ca4O(PO4)2, has a monoclinic modification with the parameters a= 11.99, b = 9.48, and c = 6.97 A, alpha = 90.8 , z = 4, and space group P21 or P21/m. beta-tricalcium phosphate 24-34 H3 histone pseudogene 16 Homo sapiens 160-163 33964346-10 2021 Moreover, overexpression of miR-130a in D-galactose (D-gal)-induced SH-SY5Y cell senescence model attenuated D-gal-induced impaired autophagy and cell senescence, demonstrated by decreased levels of LC3, Ac-p53, p21 and increased p62, suggesting that voluntary wheel running can alleviate brain aging in natural aging rats by up-regulating miR-130a-mediated autophagy. Galactose 40-45 H3 histone pseudogene 16 Homo sapiens 212-215 34057209-11 2021 Long-term exposure of HGFs to nicotine or CSC significantly suppressed their cellular proliferation and migration and upregulated type I collagen, type III collagen, interleukin (IL)-6, IL-8, p16, p21, and p53 mRNA expression, and IL-6 and IL-8 protein expression. Nicotine 30-38 H3 histone pseudogene 16 Homo sapiens 197-200 32008465-7 2021 In cancer cells, Vit C, in a pharmacological dose, decreased cell proliferation through an inhibitory effect on cyclin-dependent kinase 2 (CDK2) (4.4-fold; p < 0.01), mainly due to the stimulatory effect on the expression of cyclin-dependent kinase (CDK) inhibitors, such as p21 and p53 (3.2- and 2.8-fold, respectively; p < 0.001), but not caspase pathway. Ascorbic Acid 17-22 H3 histone pseudogene 16 Homo sapiens 278-281 33839250-1 2021 The solvatochromic amino-acids 4-DMNA or 4-DAPA, were separately introduced at position 147, 150 or 151 of a short p21 peptide (141-155) known to bind sliding clamp protein PCNA. 4-dmna 31-37 H3 histone pseudogene 16 Homo sapiens 115-118 33839250-1 2021 The solvatochromic amino-acids 4-DMNA or 4-DAPA, were separately introduced at position 147, 150 or 151 of a short p21 peptide (141-155) known to bind sliding clamp protein PCNA. 4-N,N-Dimethylaminophthalimido-alanine 41-47 H3 histone pseudogene 16 Homo sapiens 115-118 34028092-0 2021 The p53/p21/p16 and PI3K/Akt signaling pathways are involved in the ameliorative effects of maltol on D-galactose-induced liver and kidney aging and injury. maltol 92-98 H3 histone pseudogene 16 Homo sapiens 8-11 34031191-9 2021 The index SNP of 1p21 is an eQTL (Plowest=1.74x10-58) for RWDD3 involved in SUMOlation and is associated with platelet distribution width (1.15x10-9) and 18-carbon fatty acid metabolism (P=7.36x10-12). 18-carbon fatty acid 154-174 H3 histone pseudogene 16 Homo sapiens 18-21 34028092-0 2021 The p53/p21/p16 and PI3K/Akt signaling pathways are involved in the ameliorative effects of maltol on D-galactose-induced liver and kidney aging and injury. Galactose 102-113 H3 histone pseudogene 16 Homo sapiens 8-11 34028092-3 2021 Interestingly, 4-weeks maltol treatment at 50 and 100 mg/kg activated aging-associated proteins including p53, p21, and p16 followed by inhibiting malondialdehyde (MDA)"s over-production and increasing the levels of antioxidant enzymes. maltol 23-29 H3 histone pseudogene 16 Homo sapiens 111-114 34002651-8 2021 Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 24-29 H3 histone pseudogene 16 Homo sapiens 201-204 33992720-0 2021 Aspartame induces cancer stem cell enrichment through p21, NICD and GLI1 in human PANC-1 pancreas adenocarcinoma cells. Aspartame 0-9 H3 histone pseudogene 16 Homo sapiens 54-57 33987937-0 2021 Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross-talk with p53 to activate p21. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 141-144 33987937-4 2021 At molecular level, Lovastatin by dephosphorylating STAT3, induced ERK1/2 activation that inhibited autophagy and phosphorylated p53ser15 that in turn maintained ERK1/2 activated and up-regulated p21. Lovastatin 20-30 H3 histone pseudogene 16 Homo sapiens 196-199 33992720-8 2021 In the aspartame group, T1R1 silencing further increased the CSC population but decreased cell viability and suppressed the p21, NICD and GLI activation. Aspartame 7-16 H3 histone pseudogene 16 Homo sapiens 124-127 33992720-10 2021 In conclusion, the present study demonstrated that long-term aspartame exposure increases CSC population and tumor cell aggressiveness through p21, NICD, GLI1. Aspartame 61-70 H3 histone pseudogene 16 Homo sapiens 143-146 33987937-5 2021 However, p21 played a pro-survival role in this setting, as its inhibition by UC2288 further reduced cell survival in PEL cells undergoing Lovastatin treatment. UC2288 78-84 H3 histone pseudogene 16 Homo sapiens 9-12 33755722-4 2021 At the molecular level, DEK recruits the corepressor NCoR1 to repress acetylation of histone 3 at lysine 27 (H3K27ac) and restricts the chromatin accessibility of HSCs, governing the expression of quiescence-associated genes (e.g., Akt1/2, Ccnb2, and p21). Lysine 98-104 H3 histone pseudogene 16 Homo sapiens 251-254 33987937-5 2021 However, p21 played a pro-survival role in this setting, as its inhibition by UC2288 further reduced cell survival in PEL cells undergoing Lovastatin treatment. Lovastatin 139-149 H3 histone pseudogene 16 Homo sapiens 9-12 33987937-6 2021 In conclusion, this study suggests that Lovastatin may represent a valid therapeutic alternative against PEL cells, especially if used in combination with p21 inhibitors. Lovastatin 40-50 H3 histone pseudogene 16 Homo sapiens 155-158 33982403-6 2021 Supportive evidence indicated that MTX administration induced senescence and apoptosis of human GCs in vitro, and the effects were consistent with the high levels of p21, p53, and oxidative stress (OS). Methotrexate 35-38 H3 histone pseudogene 16 Homo sapiens 166-169 33666815-0 2021 Urolithin A induces cell cycle arrest and apoptosis by inhibiting Bcl-2, increasing p53-p21 proteins and reactive oxygen species production in colorectal cancer cells. 3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one 0-11 H3 histone pseudogene 16 Homo sapiens 88-91 33995088-6 2021 TB treatment caused the downregulating of c-myc, cyclin D, CDK2, and CDK4 and upregulating of p21 and p27 in the HOG cell, while TB increased P53, p21, and p27 levels and decreased the levels of cell cycle regulator proteins such as CDK and cyclin A/B in the U251 cells. theabrownin 0-2 H3 histone pseudogene 16 Homo sapiens 94-97 33995088-6 2021 TB treatment caused the downregulating of c-myc, cyclin D, CDK2, and CDK4 and upregulating of p21 and p27 in the HOG cell, while TB increased P53, p21, and p27 levels and decreased the levels of cell cycle regulator proteins such as CDK and cyclin A/B in the U251 cells. theabrownin 0-2 H3 histone pseudogene 16 Homo sapiens 147-150 33995088-6 2021 TB treatment caused the downregulating of c-myc, cyclin D, CDK2, and CDK4 and upregulating of p21 and p27 in the HOG cell, while TB increased P53, p21, and p27 levels and decreased the levels of cell cycle regulator proteins such as CDK and cyclin A/B in the U251 cells. theabrownin 129-131 H3 histone pseudogene 16 Homo sapiens 147-150 33923162-5 2021 In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation. Pentamidine 28-39 H3 histone pseudogene 16 Homo sapiens 137-140 33913241-0 2021 Vanadium oxides modify the expression levels of the p21, p53, and Cdc25C proteins in human lymphocytes treated in vitro. vanadium oxides 0-15 H3 histone pseudogene 16 Homo sapiens 52-55 33925873-4 2021 Flow cytometric and Western blot analysis showed that ilimaquinone induced S-phase arrest by modulating the expression of p-CDC-2 and p21. ilimaquinone 54-66 H3 histone pseudogene 16 Homo sapiens 134-137 33923162-5 2021 In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation. Pentamidine 173-184 H3 histone pseudogene 16 Homo sapiens 137-140 33894272-8 2021 KEY FINDINGS: Upon treatment with oleuropein, the expression of P21, P53, and TNFRSF10B increased while that of Bcl-2 and Mcl1 decreased. oleuropein 34-44 H3 histone pseudogene 16 Homo sapiens 64-67 33953834-10 2021 Western blotting analysis showed that acetylshikonin treatment induced increase of cleaved PARP, gammaH2AX, FOXO3, Bax, Bim, Bad, p21, p27, and active forms of caspase-3, caspase-7, caspase-9, caspase-6, and caspase-8 protein levels, while those of inactive forms were decreased. acetylshikonin 38-52 H3 histone pseudogene 16 Homo sapiens 130-133 33876818-11 2021 Moreover, butyric acid alleviated CIH-induced cell proliferation, lipid formation and inflammatory status and promoted cell apoptosis through regulating related genes including p21, PPARgamma, C/EBPa, IL-1beta, IL-6, TLR4, caspase-8 and caspase-3. Butyric Acid 10-22 H3 histone pseudogene 16 Homo sapiens 177-180 33953676-6 2021 The results showed that astragalin significantly inhibited the proliferation and diffusion of HCT116 cells by induced apoptosis (by modulation of Bax, Bcl-2, P53, caspase-3, caspase 6, caspase 7, caspase 8, caspase 9 protein express) and cell cycle arrest (by modulation of Cyclin D1, Cyclin E, P21, P27, CDK2, CDK4 protein express). astragalin 24-34 H3 histone pseudogene 16 Homo sapiens 295-298 33868388-12 2021 Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment. Ketoglutaric Acids 80-94 H3 histone pseudogene 16 Homo sapiens 12-15 33850004-8 2021 Idasanutlin treatment induced BAX-mediated apoptosis in venetoclax-resistant neuroblastoma cells in the presence of venetoclax, while it caused p21-mediated growth arrest in control cells. RG7388 0-11 H3 histone pseudogene 16 Homo sapiens 144-147 33537802-8 2021 Treatment of U251 cells with PSH induced the upregulation of p21 and p27, and the downregulation cyclin D1 and S-phase kinase associated protein 2 protein expression levels, which induced cell cycle arrest at the G1 phase. paris saponin H 29-32 H3 histone pseudogene 16 Homo sapiens 61-64 33883905-8 2021 Calycosin downregulated the cell cycle proteins cyclin-dependent kinase 2 (CDK2), CDK4, CDK6, cyclin D1, and cyclin E; upregulated p21 and p27; and arrested cells in the G0/G1 phase. 7,3'-dihydroxy-4'-methoxyisoflavone 0-9 H3 histone pseudogene 16 Homo sapiens 131-134 33710861-8 2021 At the molecular level, Olmesartan inhibits the elevated expression of senescence biomarkers (p16 and p21). olmesartan 24-34 H3 histone pseudogene 16 Homo sapiens 102-105 33710861-11 2021 In conclusion, Olmesartan prevents oligomerized Abeta-induced cellular senescence in neuronal cells by downregulating p16 and p21 through a SIRT1 dependent deacetylation of p53; our finding indicates that Olmesartan has a protective effect in Abeta-induced neurotoxicity. olmesartan 15-25 H3 histone pseudogene 16 Homo sapiens 126-129 33868388-0 2021 Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate. Cisplatin 80-89 H3 histone pseudogene 16 Homo sapiens 35-38 33868388-0 2021 Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate. Ketoglutaric Acids 145-159 H3 histone pseudogene 16 Homo sapiens 35-38 33868388-0 2021 Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate. Glutamic Acid 160-169 H3 histone pseudogene 16 Homo sapiens 35-38 33868388-12 2021 Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment. NADP 126-132 H3 histone pseudogene 16 Homo sapiens 12-15 33868388-5 2021 Our work focuses on dependence of the action of the DNA damaging anticancer drug cisplatin on metabolic regulation through p53/p21 axes and cellular thiamine status in human lung adenocarcinoma cells A549. Cisplatin 81-90 H3 histone pseudogene 16 Homo sapiens 127-130 33868388-7 2021 Compared to wild type (A549WT), a stable line with a 60% knockdown of p21 (A549p21-) is less sensitive to antiproliferative action of cisplatin. Cisplatin 134-143 H3 histone pseudogene 16 Homo sapiens 70-73 33868388-12 2021 Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment. Ketoglutaric Acids 157-171 H3 histone pseudogene 16 Homo sapiens 12-15 33868388-9 2021 Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Ketoglutaric Acids 119-133 H3 histone pseudogene 16 Homo sapiens 77-80 33868388-12 2021 Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment. Thiamine 217-225 H3 histone pseudogene 16 Homo sapiens 12-15 33868388-9 2021 Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Glutamic Acid 138-147 H3 histone pseudogene 16 Homo sapiens 77-80 33868388-12 2021 Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment. Cisplatin 240-249 H3 histone pseudogene 16 Homo sapiens 12-15 33868388-13 2021 Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination. Thiamine 9-17 H3 histone pseudogene 16 Homo sapiens 128-131 33868388-13 2021 Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination. Cisplatin 76-85 H3 histone pseudogene 16 Homo sapiens 128-131 33868388-9 2021 Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Tricarboxylic Acids 187-205 H3 histone pseudogene 16 Homo sapiens 77-80 33868388-13 2021 Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination. Glutamic Acid 171-180 H3 histone pseudogene 16 Homo sapiens 128-131 33868388-9 2021 Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Tricarboxylic Acids 207-210 H3 histone pseudogene 16 Homo sapiens 77-80 33868388-9 2021 Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Cisplatin 233-242 H3 histone pseudogene 16 Homo sapiens 77-80 33868388-9 2021 Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Cisplatin 343-352 H3 histone pseudogene 16 Homo sapiens 77-80 33868388-9 2021 Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Cisplatin 343-352 H3 histone pseudogene 16 Homo sapiens 77-80 33868388-9 2021 Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Cisplatin 343-352 H3 histone pseudogene 16 Homo sapiens 77-80 33482188-7 2021 MG-132 dose-dependently inhibited the growth of HPFs, induced G2/M phase arrest of cell cycle at a certain dose, and also caused cell apoptosis, with the levels of cleaved caspase3, cleaved PARP, Bax and p21 increased. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-6 H3 histone pseudogene 16 Homo sapiens 204-207 33868388-10 2021 Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH). Thiamine 96-104 H3 histone pseudogene 16 Homo sapiens 132-135 33868388-10 2021 Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH). Thiamine Pyrophosphate 105-109 H3 histone pseudogene 16 Homo sapiens 132-135 33868388-12 2021 Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment. Glutamic Acid 56-65 H3 histone pseudogene 16 Homo sapiens 12-15 33649826-7 2021 It was also demonstrated that curcumin regulated the cell cycle- and apoptosis-related proteins (cyclin D1, p21, Bcl2, cleaved-caspase-3 and cleaved-PARP), leading to cell cycle arrest and apoptosis in both ML-2 and OCI-AML5 cells. Curcumin 30-38 H3 histone pseudogene 16 Homo sapiens 108-111 33484789-4 2021 Exposure to E2 and Fen induced the cell growth and survival ability of MCF-7 cells by increasing the S-phase cells and regulating the cell cycle-related proteins (Cyclin D1 and E1, p21 and p27). Estradiol 12-14 H3 histone pseudogene 16 Homo sapiens 181-184 33732382-10 2021 Western blotting results also revealed the upregulation of p53 acetylation and p21, as well as the downregulation of Bcl-2 and cyclin D1 in cells treated with cambinol. cambinol 159-167 H3 histone pseudogene 16 Homo sapiens 79-82 33710818-11 2021 PD166866 and RG7112, an MDM2/p53 inhibitor, cooperatively inhibited the colony formation and distal seeding of LSCC cells (P < 0.01), and upregulated the expression of p53 and p21. PD 166866 0-8 H3 histone pseudogene 16 Homo sapiens 176-179 33710818-11 2021 PD166866 and RG7112, an MDM2/p53 inhibitor, cooperatively inhibited the colony formation and distal seeding of LSCC cells (P < 0.01), and upregulated the expression of p53 and p21. RG7112 13-19 H3 histone pseudogene 16 Homo sapiens 176-179 33594879-6 2021 Cellular senescence-specific genes, such as p53 and p21, were downregulated on the PDA-coated substrate, while the stemness-related gene, OCT4, was upregulated. polydopamine 83-86 H3 histone pseudogene 16 Homo sapiens 52-55 33682127-6 2021 The gels containing 15/20 mM Lys/Arg exhibited a significant increase in the proportion of immobilized water (P21 ). Lysine 29-32 H3 histone pseudogene 16 Homo sapiens 110-113 33682127-6 2021 The gels containing 15/20 mM Lys/Arg exhibited a significant increase in the proportion of immobilized water (P21 ). Arginine 33-36 H3 histone pseudogene 16 Homo sapiens 110-113 33682127-6 2021 The gels containing 15/20 mM Lys/Arg exhibited a significant increase in the proportion of immobilized water (P21 ). Water 103-108 H3 histone pseudogene 16 Homo sapiens 110-113 33682127-7 2021 CONCLUSION: The enhancement of WHC, gel strength, and P21 was closely associated with the increased solubility and the dense microstructure induced by Lys and Arg with high concentrations of 15 mM and 20 mM. Lysine 151-154 H3 histone pseudogene 16 Homo sapiens 54-57 33682127-7 2021 CONCLUSION: The enhancement of WHC, gel strength, and P21 was closely associated with the increased solubility and the dense microstructure induced by Lys and Arg with high concentrations of 15 mM and 20 mM. Arginine 159-162 H3 histone pseudogene 16 Homo sapiens 54-57 33314719-15 2021 The expression of P21 and P53 significantly decreased in SNPC-exo-treated NPC after siRNA transfection (P < 0.05), followed by a higher growth rate (2 times higher on the 5th day and 1.5 times higher on the 7th day) and lower percentage of SA-beta-gal-positive NPC (22.5%). 2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine 240-242 H3 histone pseudogene 16 Homo sapiens 18-21 33314719-15 2021 The expression of P21 and P53 significantly decreased in SNPC-exo-treated NPC after siRNA transfection (P < 0.05), followed by a higher growth rate (2 times higher on the 5th day and 1.5 times higher on the 7th day) and lower percentage of SA-beta-gal-positive NPC (22.5%). cyclohexenoesculetin-beta-galactoside 247-251 H3 histone pseudogene 16 Homo sapiens 18-21 33131875-0 2021 Epigenetic alterations induced by aflatoxin B1: An in vitro and in vivo approach with emphasis on enhancer of zeste homologue-2/p21 axis. Aflatoxin B1 34-46 H3 histone pseudogene 16 Homo sapiens 128-131 33131875-5 2021 We demonstrated a significant reduction in the expression of p21 with a remarkable increase in the expression of cyclin D1 that correlated with increased methylation of CpG dinucleotides in p21 proximal promoter, while cyclin D1 promoter remained unmethylated. cytidylyl-3'-5'-guanosine 169-186 H3 histone pseudogene 16 Homo sapiens 61-64 33131875-5 2021 We demonstrated a significant reduction in the expression of p21 with a remarkable increase in the expression of cyclin D1 that correlated with increased methylation of CpG dinucleotides in p21 proximal promoter, while cyclin D1 promoter remained unmethylated. cytidylyl-3'-5'-guanosine 169-186 H3 histone pseudogene 16 Homo sapiens 190-193 33663585-10 2021 RPPA and IHC demonstrated an increase in p21 expression in both combinatorial and single agent ALRN-6924 in vivo treatment groups. alrn-6924 95-104 H3 histone pseudogene 16 Homo sapiens 41-44 33484789-4 2021 Exposure to E2 and Fen induced the cell growth and survival ability of MCF-7 cells by increasing the S-phase cells and regulating the cell cycle-related proteins (Cyclin D1 and E1, p21 and p27). N-(2,3-dichloro-4-hydroxyphenyl)-1-methylcyclohexanecarboxamide 19-22 H3 histone pseudogene 16 Homo sapiens 181-184 33482334-9 2021 Ubiquinol was also more efficient compared to ubiquinone in reverting the expression of the senescent phenotype, quantified in terms of beta-galactosidase positivity, p21, collagen type 1, and elastin at the gene and protein expression levels. ubiquinol 0-9 H3 histone pseudogene 16 Homo sapiens 167-170 33461161-8 2021 RESULTS: As a result of oxidative stress, MiR-494-3p was increased via the p38MAPK-c-myc signaling pathway in the lung tissues and cells of patients with COPD, and the increase in miR-494-3p was accompanied by increases in senescence markers (p27, p21 and p16) and SASP proteins (IL-1beta, TNF-alpha, MMP2 and MMP9). mir-494-3p 42-52 H3 histone pseudogene 16 Homo sapiens 248-251 33271245-0 2021 Methoxyeugenol regulates the p53/p21 pathway and suppresses human endometrial cancer cell proliferation. 4-allyl-2,6-dimethoxyphenol 0-14 H3 histone pseudogene 16 Homo sapiens 33-36 33073684-3 2021 Our results showed that GMSC-EVs robustly abrogated oxidative stress-induced upregulation in the expression of cellular senescence-related genes, such as beta-galactosidase, p21, p53, and gammaH2AX, and mTOR/pS6 signaling pathway, in human umbilical vein endothelial cells (HUVECs) and skin fibroblasts. gmsc-evs 24-32 H3 histone pseudogene 16 Homo sapiens 174-177 33271245-9 2021 Probably triggered by the higher ROS levels and mitochondrial dysfunction, the gene expression of p53 and p21 increased and the gene expression of CDK4/6 decreased in response to the methoxyeugenol treatment. 4-allyl-2,6-dimethoxyphenol 183-197 H3 histone pseudogene 16 Homo sapiens 106-109 33118830-9 2021 Furthermore, Bim and p21 were upregulated in OS cells following apcin treatment. apcin 64-69 H3 histone pseudogene 16 Homo sapiens 21-24 33580595-4 2021 Resveratrol supplementation significantly increased mRNA expression levels of p53 and p21 genes, compared with the placebo group (fold change of p53 = 1.29, p = .04; fold change of p21 = 1.46, p = .006). Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 86-89 33427831-5 2021 The Bax/Bcl2 expression ratio was increased up to 11-fold in cells pre-treated with 60 muM limonoids for 48 h. Apart from this, the limonoids also induced the expression of p21, and exhibited anti-inflammatory activity through decreasing the expression of cox-2, NF-kappaB and IL-6. Limonins 91-100 H3 histone pseudogene 16 Homo sapiens 173-176 33981481-9 2021 Also, miR-199a-5p inhibited SIRT1, promoted p21 acetylation, and upregulated p21 expression, thus accelerating nucleus pulposus cell apoptosis and IVDD. -199a-5p 9-17 H3 histone pseudogene 16 Homo sapiens 44-47 33981481-9 2021 Also, miR-199a-5p inhibited SIRT1, promoted p21 acetylation, and upregulated p21 expression, thus accelerating nucleus pulposus cell apoptosis and IVDD. -199a-5p 9-17 H3 histone pseudogene 16 Homo sapiens 77-80 33427831-5 2021 The Bax/Bcl2 expression ratio was increased up to 11-fold in cells pre-treated with 60 muM limonoids for 48 h. Apart from this, the limonoids also induced the expression of p21, and exhibited anti-inflammatory activity through decreasing the expression of cox-2, NF-kappaB and IL-6. Limonins 132-141 H3 histone pseudogene 16 Homo sapiens 173-176 33580595-4 2021 Resveratrol supplementation significantly increased mRNA expression levels of p53 and p21 genes, compared with the placebo group (fold change of p53 = 1.29, p = .04; fold change of p21 = 1.46, p = .006). Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 181-184 33580595-7 2021 Resveratrol supplementation resulted in significant changes in p53 and p21 genes expression, while serum levels of sCD163/sTWEAK ratio also improved in the resveratrol group, without any significant change in adjusted sCD163 levels. Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 71-74 33529089-5 2021 Among the 10 resveratrol analogues, Pts and Pts nicotinate attenuated the expression of senescence-associated beta-galactosidase, downregulated p21 and p53, and increased the production of NO in both angiotensin II and H2O2-induced endothelial senescence models. Niacin 48-58 H3 histone pseudogene 16 Homo sapiens 144-147 33579350-8 2021 Western blots showed an increase in apoptotic and senescence (p21) markers in all 5-AZA-dC-treated cells. Azacitidine 82-87 H3 histone pseudogene 16 Homo sapiens 62-65 33578781-4 2021 We found that FK866 markedly inhibited the senescent characteristics of hDPCs after exposure to H2O2, as revealed by an increase in the number of senescence-associated beta-galactosidase (SA-beta-gal)-positive hDPCs and the upregulation of the p21 and p53 proteins, which acts as molecular indicators of cellular senescence. N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide 14-19 H3 histone pseudogene 16 Homo sapiens 244-247 32938226-6 2021 Liquiritigenin also upregulated two downstream genes of BRCA1 (p21 and DNA-damage-inducible 45 alpha), decreased cellular DNA methyltransferase (DNMT) activity, and reduced BRCA1 promoter methylation. liquiritigenin 0-14 H3 histone pseudogene 16 Homo sapiens 63-66 33455051-4 2021 Here, we demonstrate that the salt of lycorine, lycorine hydrochloride, significantly suppressed stress-induced premature cellular senescence (SIPS) by ~2-fold, as determined by senescence-associated beta-galactosidase (SA-beta-gal) staining and the expression of p16 and p21. lycorine 38-46 H3 histone pseudogene 16 Homo sapiens 272-275 33455051-4 2021 Here, we demonstrate that the salt of lycorine, lycorine hydrochloride, significantly suppressed stress-induced premature cellular senescence (SIPS) by ~2-fold, as determined by senescence-associated beta-galactosidase (SA-beta-gal) staining and the expression of p16 and p21. Lycorine hydrochloride 48-70 H3 histone pseudogene 16 Homo sapiens 272-275 33517274-5 2021 Flow cytometry, western blotting, and caspase-3/7 assays revealed that CCL299 induced G1-phase cell-cycle arrest followed by apoptosis that was associated with up-regulation of p-p53 (Ser15) and p21 expression and the down-regulation of p-CDK2 (Thr160) expression. ccl299 71-77 H3 histone pseudogene 16 Homo sapiens 195-198 33359023-3 2021 Besides, dioscin could inhibit the proliferation of Ishikawa cells by blocking the G0/G1 cell cycle through up-regulation of p16, p21, and p27 and down-regulation of cycle-cellular protein (Cyclin A/D/E) and cyclin-dependent kinase (CDK2/4/6). dioscin 9-16 H3 histone pseudogene 16 Homo sapiens 130-133 33486250-6 2021 Here we investigated how curcumin affects the p53-p21 pathway in fluoride toxicity. Curcumin 25-33 H3 histone pseudogene 16 Homo sapiens 50-53 32786121-7 2021 We further show that SENP1 depletion synergizes with DNA damage-inducing agent etoposide to induce p53 activation and the expression of p21, leading to synergistic growth inhibition of cancer cells. Etoposide 79-88 H3 histone pseudogene 16 Homo sapiens 136-139 33010383-6 2021 The MEK inhibitor trametinib (GSK) and PI3K/mTOR dual inhibitor dactolisib (BEZ) were shown to abrogate Nurr1-augmented tumorigenesis by upregulating p21 and p27 expression and by suppressing MMP9 and KLF4 expression. dactolisib 64-74 H3 histone pseudogene 16 Homo sapiens 150-153 33010383-6 2021 The MEK inhibitor trametinib (GSK) and PI3K/mTOR dual inhibitor dactolisib (BEZ) were shown to abrogate Nurr1-augmented tumorigenesis by upregulating p21 and p27 expression and by suppressing MMP9 and KLF4 expression. bez 76-79 H3 histone pseudogene 16 Homo sapiens 150-153 33535351-1 2021 The human epigenetic gene of SET domain containing 2 (SETD2) is located at the cytogenetic band p21.31 of chromosome 3, which encodes the histone3 lysine36 trimethyltransferase SETD2, the major enzyme that catalyzes the trimethylation of lysine 36 on histone 3 (H3K36me3) of human. lysine36 147-155 H3 histone pseudogene 16 Homo sapiens 96-99 33535351-1 2021 The human epigenetic gene of SET domain containing 2 (SETD2) is located at the cytogenetic band p21.31 of chromosome 3, which encodes the histone3 lysine36 trimethyltransferase SETD2, the major enzyme that catalyzes the trimethylation of lysine 36 on histone 3 (H3K36me3) of human. Lysine 147-153 H3 histone pseudogene 16 Homo sapiens 96-99 33438556-11 2021 P21 mRNAs expression altered in all mentioned samples except those treated with 50 (mug/ml) of resveratrol. Resveratrol 95-106 H3 histone pseudogene 16 Homo sapiens 0-3 33432584-7 2021 We found that melatonin treatment attenuated d-gal-induced cell senescence and decreased the expression of p21, p16 and pp65 proteins. Melatonin 14-23 H3 histone pseudogene 16 Homo sapiens 107-110 33010383-6 2021 The MEK inhibitor trametinib (GSK) and PI3K/mTOR dual inhibitor dactolisib (BEZ) were shown to abrogate Nurr1-augmented tumorigenesis by upregulating p21 and p27 expression and by suppressing MMP9 and KLF4 expression. trametinib 18-28 H3 histone pseudogene 16 Homo sapiens 150-153 33494463-1 2021 The crystal structures of two azobenzene derivative Schiff base metal complexes (new C44H40CuN6O2 of P-1 and known C44H38MnN6O7 of P21/c abbreviated as Cu and Mn, respectively) were (re-)determined experimentally using conventional X-ray analysis to obtain electron density using a PLATON program. azobenzene 30-40 H3 histone pseudogene 16 Homo sapiens 131-136 33494463-1 2021 The crystal structures of two azobenzene derivative Schiff base metal complexes (new C44H40CuN6O2 of P-1 and known C44H38MnN6O7 of P21/c abbreviated as Cu and Mn, respectively) were (re-)determined experimentally using conventional X-ray analysis to obtain electron density using a PLATON program. Schiff Bases 52-63 H3 histone pseudogene 16 Homo sapiens 131-136 33494463-1 2021 The crystal structures of two azobenzene derivative Schiff base metal complexes (new C44H40CuN6O2 of P-1 and known C44H38MnN6O7 of P21/c abbreviated as Cu and Mn, respectively) were (re-)determined experimentally using conventional X-ray analysis to obtain electron density using a PLATON program. Metals 64-69 H3 histone pseudogene 16 Homo sapiens 131-136 33039867-10 2021 Phosphor-p53, a downstream molecule of ATM signaling, and p21, a direct target of p53, were upregulated in NaAsO2-exposed DU145 cells. sodium arsenite 107-113 H3 histone pseudogene 16 Homo sapiens 58-61 33039867-11 2021 Unexpectedly, p21 was also elevated in NaAsO2-exposed p53-null PC-3 cells. sodium arsenite 39-45 H3 histone pseudogene 16 Homo sapiens 14-17 33520087-4 2021 Additionally, berbamine induced cell cycle arrest at S phase by a synergistic mechanism involving stimulation of P21 and P27 protein expression as well as downregulation of CyclinD, CyclinA2, and CDK2 protein expression. berbamine 14-23 H3 histone pseudogene 16 Homo sapiens 113-116 33486250-6 2021 Here we investigated how curcumin affects the p53-p21 pathway in fluoride toxicity. Fluorides 65-73 H3 histone pseudogene 16 Homo sapiens 50-53 33486250-13 2021 However, curcumin itself significantly increased Ac-p53 and upregulated p21 protein levels to suppress cell proliferation in a dose-dependent manner. Curcumin 9-17 H3 histone pseudogene 16 Homo sapiens 72-75 33486250-14 2021 Curcumin suppressed fluoride-induced phosphorylation of p21 and increased p21 levels within the nuclear fraction. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 56-59 33486250-14 2021 Curcumin suppressed fluoride-induced phosphorylation of p21 and increased p21 levels within the nuclear fraction. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 74-77 33486250-14 2021 Curcumin suppressed fluoride-induced phosphorylation of p21 and increased p21 levels within the nuclear fraction. Fluorides 20-28 H3 histone pseudogene 16 Homo sapiens 56-59 33486250-14 2021 Curcumin suppressed fluoride-induced phosphorylation of p21 and increased p21 levels within the nuclear fraction. Fluorides 20-28 H3 histone pseudogene 16 Homo sapiens 74-77 33486250-16 2021 These results suggest that curcumin-induced Ac-p53 and p21 led to cell cycle arrest, while curcumin attenuated fluoride-mediated apoptosis via activation of Akt and suppressed fluoride-mediated DNA damage. Curcumin 27-35 H3 histone pseudogene 16 Homo sapiens 55-58 32451414-7 2021 RNA-sequencing analyses revealed that avasimibe suppressed the expression of CDK2, cyclin E1, CDK4, cyclin D, CDK1, cyclin B1, Aurora A, and PLK1, while induced the expression of p53, p21, p27, and GADD45A, which was validated by Western blot analysis. avasimibe 38-47 H3 histone pseudogene 16 Homo sapiens 184-187 33428109-9 2021 The mTOR inhibitor rapamycin mitigated TGF-beta-induced expression of p21, p16, and DNA damage foci and improved replicative potential of preadipocytes, supporting the cell-specific response to this cytokine. Sirolimus 19-28 H3 histone pseudogene 16 Homo sapiens 70-73 32451414-8 2021 These results demonstrated that avasimibe induced mitochondria-dependent apoptosis in glioblastoma cells, which was associated with arresting the cell cycle at G0/G1 phase and G2/M phase by regulating the p53/p21 pathway, p53/GADD45A and Aurora A/PLK1 signaling pathways. avasimibe 32-41 H3 histone pseudogene 16 Homo sapiens 209-212 32807067-9 2021 Moreover, we found that not only pioglitazone reduced the survival rate of NB4 through the induction of p21-mediated G1 arrest, also elevated the intracellular level of reactive oxygen species (ROS) which was coupled with upregulated FOXO3a. Pioglitazone 33-45 H3 histone pseudogene 16 Homo sapiens 104-107 33129231-8 2021 RESULTS: PR-619 could inhibit ESCC cell growth and induce G2/M cell cycle arrest by downregulating cyclin B1 and upregulating p21. 2,6-diaminopyridine-3,5-bis(thiocyanate) 9-15 H3 histone pseudogene 16 Homo sapiens 126-129 33035554-5 2021 At the same time, EPZ015666 regulated cell cycle related protein (P53, P21, P27, CDK2) expression. GSK3235025 18-27 H3 histone pseudogene 16 Homo sapiens 71-74 33297115-0 2021 A prolonged exposure of human lung carcinoma epithelial cells to benzo[a]pyrene induces p21-dependent epithelial-to-mesenchymal transition (EMT)-like phenotype. Benzo(a)pyrene 65-79 H3 histone pseudogene 16 Homo sapiens 88-91 33297115-7 2021 Since BaP decreased cell proliferative rate via induction of p21 expression, we generated the A549 cell model with reduced p21 expression and exposed it to BaP for two weeks. Benzo(a)pyrene 6-9 H3 histone pseudogene 16 Homo sapiens 61-64 33035554-6 2021 In brief, our study showed that PRMT5 promoted retinoblastoma growth, the PRMT5 inhibitor EPZ015666 inhibited retinoblastoma in vitro by regulating P53-P21/P27-CDK2 signaling pathways and slowed retinoblastoma growth in a xenograft model. GSK3235025 90-99 H3 histone pseudogene 16 Homo sapiens 152-155 33131904-8 2021 The mechanism of mebendazole was associated with p53-independent induction of p21 and tubule depolymerization. Mebendazole 17-28 H3 histone pseudogene 16 Homo sapiens 78-81 33437209-7 2021 Furthermore, p-cresol and indoxyl sulfate gradually increased senescence-associated beta-galactosidase positive cells while upregulated the expression of p21 which participate in senescent process. 4-cresol 13-21 H3 histone pseudogene 16 Homo sapiens 154-157 33437209-7 2021 Furthermore, p-cresol and indoxyl sulfate gradually increased senescence-associated beta-galactosidase positive cells while upregulated the expression of p21 which participate in senescent process. Indican 26-41 H3 histone pseudogene 16 Homo sapiens 154-157 33442400-4 2021 In this study, we demonstrate that BIX-01294 triggered the inhibition of human DLBCL cell proliferation, lead to G1 phase arrest via increasing P21 level and reducing cyclin E level. BIX 01294 35-44 H3 histone pseudogene 16 Homo sapiens 144-147 33394232-10 2021 The up-regulation of p21 and down-regulation of Cyclin-A1, Cyclin-B1, and Cdk-1 revealed the G2/M phase arrest mechanism of acacetin and apigenin. acacetin 124-132 H3 histone pseudogene 16 Homo sapiens 21-24 32924682-8 2021 Finally, we observed that p21 protein expression was up regulated upon the use of ALRN-6924 (Aileron) while no significant changes were seen in p53, MDM2 and MDM4 expression. alrn-6924 82-91 H3 histone pseudogene 16 Homo sapiens 26-29 33394232-10 2021 The up-regulation of p21 and down-regulation of Cyclin-A1, Cyclin-B1, and Cdk-1 revealed the G2/M phase arrest mechanism of acacetin and apigenin. Apigenin 137-145 H3 histone pseudogene 16 Homo sapiens 21-24 33296752-6 2021 We found that ABA is produced by human marrow cells, and exogenous ABA inhibits PCa cell proliferation while increasing the expression of p27, p21, and p16 and decreasing the expression of the proliferation marker, Ki67. Abscisic Acid 67-70 H3 histone pseudogene 16 Homo sapiens 143-146 33409152-9 2020 Treatment with DSF/Cu induced oxidative stress and DNA damage response by elevating the reactive oxygen species levels; increasing the expression of P53, P21, and gamma-H2AX proteins; and inhibiting Wnt/beta-catenin signaling in vitro and in vivo. Disulfiram 15-18 H3 histone pseudogene 16 Homo sapiens 154-157 33409258-9 2020 Imatinib and GNF-5 induced G0/G1 phase cell cycle arrest by downregulating Skp2 and upregulating p27 and p21. Imatinib Mesylate 0-8 H3 histone pseudogene 16 Homo sapiens 105-108 33240430-9 2021 5-FU induced apoptosis through p53-p21 activity, while chrysin arrested the cell cycle in the G2/M phase. Fluorouracil 0-4 H3 histone pseudogene 16 Homo sapiens 35-38 33425912-9 2020 Western blot in SW780 cells also confirmed that the combined use of EGCG and DOX caused significant increase in p53, p21, and cleaved-PARP expression, and induced significant inhibition in phosphorylated NF-kappaB and MDM2. epigallocatechin gallate 68-72 H3 histone pseudogene 16 Homo sapiens 117-120 33425912-9 2020 Western blot in SW780 cells also confirmed that the combined use of EGCG and DOX caused significant increase in p53, p21, and cleaved-PARP expression, and induced significant inhibition in phosphorylated NF-kappaB and MDM2. Doxorubicin 77-80 H3 histone pseudogene 16 Homo sapiens 117-120 33409152-9 2020 Treatment with DSF/Cu induced oxidative stress and DNA damage response by elevating the reactive oxygen species levels; increasing the expression of P53, P21, and gamma-H2AX proteins; and inhibiting Wnt/beta-catenin signaling in vitro and in vivo. Copper 19-21 H3 histone pseudogene 16 Homo sapiens 154-157 33298132-0 2020 Chidamide increases the sensitivity of refractory or relapsed acute myeloid leukemia cells to anthracyclines via regulation of the HDAC3 -AKT-P21-CDK2 signaling pathway. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 0-9 H3 histone pseudogene 16 Homo sapiens 142-145 33012506-3 2020 CYZ2017 treatment led to increase of p53 levels and induced the transactivation of its target genes p21. cyz2017 0-7 H3 histone pseudogene 16 Homo sapiens 100-103 33322048-5 2020 LCTP also induced the cell cycle arrest in G2/M phase, confirmed by decrease of CDK2 protein and increase of p53 and p21. intybin 0-4 H3 histone pseudogene 16 Homo sapiens 117-120 33316776-0 2020 Postprandial triglyceride-rich lipoproteins-induced premature senescence of adipose-derived mesenchymal stem cells via the SIRT1/p53/Ac-p53/p21 axis through oxidative mechanism. Triglycerides 13-25 H3 histone pseudogene 16 Homo sapiens 140-143 33298132-0 2020 Chidamide increases the sensitivity of refractory or relapsed acute myeloid leukemia cells to anthracyclines via regulation of the HDAC3 -AKT-P21-CDK2 signaling pathway. Anthracyclines 94-108 H3 histone pseudogene 16 Homo sapiens 142-145 33298132-6 2020 We found that the HDAC3-AKT-P21-CDK2 signaling pathway was significantly upregulated in anthracycline-resistant AML cells compared to non-resistant cells. Anthracyclines 88-101 H3 histone pseudogene 16 Homo sapiens 28-31 33298132-9 2020 Chidamide increases the sensitivity of anthracycline-resistant cells to anthracycline drugs, and these effects are associated with the inhibition of the HDAC3-AKT-P21-CDK2 signaling pathway. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 0-9 H3 histone pseudogene 16 Homo sapiens 163-166 33241756-6 2021 In addition, we found that HOTAIR promoted ATRA-induced differentiation via the regulation of the cell cycle regulator p21 via miR-17-5p. Tretinoin 43-47 H3 histone pseudogene 16 Homo sapiens 119-122 33298132-9 2020 Chidamide increases the sensitivity of anthracycline-resistant cells to anthracycline drugs, and these effects are associated with the inhibition of the HDAC3-AKT-P21-CDK2 signaling pathway. Anthracyclines 39-52 H3 histone pseudogene 16 Homo sapiens 163-166 33298132-10 2020 CONCLUSION: Chidamide can increase anthracycline drug sensitivity by inhibiting HDAC3-AKT-P21-CDK2 signaling pathway, thus demonstrating the potential for application. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 12-21 H3 histone pseudogene 16 Homo sapiens 90-93 33298132-10 2020 CONCLUSION: Chidamide can increase anthracycline drug sensitivity by inhibiting HDAC3-AKT-P21-CDK2 signaling pathway, thus demonstrating the potential for application. Anthracyclines 35-48 H3 histone pseudogene 16 Homo sapiens 90-93 33291321-6 2020 We have used nanocomplexes composed of siRNA and a beta-cyclodextrin derivative, AMC6, with a very high transfection efficiency to selectively knockdown clathrin heavy chain, caveolin 1, and p21 Activated Kinase 1 to specifically block clathrin-mediated, caveolin-mediated and macropinocytosis endocytic pathways. betadex 51-68 H3 histone pseudogene 16 Homo sapiens 191-194 33291321-6 2020 We have used nanocomplexes composed of siRNA and a beta-cyclodextrin derivative, AMC6, with a very high transfection efficiency to selectively knockdown clathrin heavy chain, caveolin 1, and p21 Activated Kinase 1 to specifically block clathrin-mediated, caveolin-mediated and macropinocytosis endocytic pathways. amc6 81-85 H3 histone pseudogene 16 Homo sapiens 191-194 33276759-14 2020 Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells. 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide 162-171 H3 histone pseudogene 16 Homo sapiens 103-106 33276759-14 2020 Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells. Cytarabine 172-177 H3 histone pseudogene 16 Homo sapiens 103-106 33276759-14 2020 Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells. 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide 14-23 H3 histone pseudogene 16 Homo sapiens 103-106 33969806-4 2022 Moreover, we found the altered expression of p21, p27, c-Myc, and CDK4 upon co-treatment of the cells with panobinostat and BKM120, which was associated with a substantial blockage of cell cycle progression at G2/M phase. Panobinostat 107-119 H3 histone pseudogene 16 Homo sapiens 45-48 33276759-14 2020 Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells. Cytarabine 28-33 H3 histone pseudogene 16 Homo sapiens 103-106 33287214-6 2020 In RWPE-1 cells, arecoline increased the expression of cyclin-dependent kinase (CDK)-1, p21, and cyclins B1 and D3, decreased the expression of CDK2, and had no effects on CDK4 and cyclin D1 expression. Arecoline 17-26 H3 histone pseudogene 16 Homo sapiens 88-91 33287214-8 2020 In LNCaP cells, arecoline decreased CDK2, CDK4, and cyclin D1 expression; increased p21, p27, and cyclin D3 expression; had no effects on CDK1 and cyclin B1 expression. Arecoline 16-25 H3 histone pseudogene 16 Homo sapiens 84-87 32986180-5 2020 Microarray assay, real-time PCR and western blot results revealed that AOS was able to effectively suppress H2O2-induced apoptosis via regulated integrin-alpha/FAK/PI3K pathway by influencing the expression of integrin-alpha, FAK, PI3K, PTEN, P21, and CDK2. Hydrogen Peroxide 108-112 H3 histone pseudogene 16 Homo sapiens 243-246 32985761-10 2020 Treatment with both TCDD and PUFAs collaboratively enhanced the levels of AHR, CYP1A1, p53, p21, Rb and regucalcin. Polychlorinated Dibenzodioxins 20-24 H3 histone pseudogene 16 Homo sapiens 92-95 32985761-10 2020 Treatment with both TCDD and PUFAs collaboratively enhanced the levels of AHR, CYP1A1, p53, p21, Rb and regucalcin. Fatty Acids, Unsaturated 29-34 H3 histone pseudogene 16 Homo sapiens 92-95 33302580-7 2020 We demonstrated that the temporal treatment of HCT116 and MCF-7 cancer cells (both p53 wild-type) with DPI caused induction of senescence, that was correlated with decreased level of ROS and upregulation of p53/p21 proteins. diphenyleneiodonium 103-106 H3 histone pseudogene 16 Homo sapiens 211-214 33274583-4 2020 In vitro, cyanidin-3-rutinoside (C-3-R) and cyanidin-3-glucoside (C-3-G) inhibited the d-galactose (d-gal)-induced senescence in human endothelial cells, as indicated by reduced senescence-associated-beta-galactosidase activity, p21, and p16INK4a . cyanidin 3-rutinoside 10-31 H3 histone pseudogene 16 Homo sapiens 229-232 33274583-4 2020 In vitro, cyanidin-3-rutinoside (C-3-R) and cyanidin-3-glucoside (C-3-G) inhibited the d-galactose (d-gal)-induced senescence in human endothelial cells, as indicated by reduced senescence-associated-beta-galactosidase activity, p21, and p16INK4a . cyanidin-3-o-glucoside 44-64 H3 histone pseudogene 16 Homo sapiens 229-232 33274583-4 2020 In vitro, cyanidin-3-rutinoside (C-3-R) and cyanidin-3-glucoside (C-3-G) inhibited the d-galactose (d-gal)-induced senescence in human endothelial cells, as indicated by reduced senescence-associated-beta-galactosidase activity, p21, and p16INK4a . cyanidin-3-o-glucoside 66-71 H3 histone pseudogene 16 Homo sapiens 229-232 33274583-4 2020 In vitro, cyanidin-3-rutinoside (C-3-R) and cyanidin-3-glucoside (C-3-G) inhibited the d-galactose (d-gal)-induced senescence in human endothelial cells, as indicated by reduced senescence-associated-beta-galactosidase activity, p21, and p16INK4a . Galactose 87-98 H3 histone pseudogene 16 Homo sapiens 229-232 33274583-4 2020 In vitro, cyanidin-3-rutinoside (C-3-R) and cyanidin-3-glucoside (C-3-G) inhibited the d-galactose (d-gal)-induced senescence in human endothelial cells, as indicated by reduced senescence-associated-beta-galactosidase activity, p21, and p16INK4a . Galactose 87-92 H3 histone pseudogene 16 Homo sapiens 229-232 32985761-6 2020 Mechanistically, TCDD treatment increased the protein levels of cell growth suppressors, including p53, Rb, p21 and regucalcin, and caspase-3 implicated in apoptotic cell death, and decreased the levels of Stat3, mitogen-activated protein kinase (MAPK/Erk1/2) and phospho-MAPK/Erk1/2. Polychlorinated Dibenzodioxins 17-21 H3 histone pseudogene 16 Homo sapiens 108-111 33969806-4 2022 Moreover, we found the altered expression of p21, p27, c-Myc, and CDK4 upon co-treatment of the cells with panobinostat and BKM120, which was associated with a substantial blockage of cell cycle progression at G2/M phase. NVP-BKM120 124-130 H3 histone pseudogene 16 Homo sapiens 45-48 33002483-4 2020 T-17 showed dose-dependent cytotoxicity in SGC-7901 and AGS cell lines, it induced caspase-mediated apoptosis as well as G0/G1 phase arrest and modulation of cyclinE2 and p21 expression. t-17 0-4 H3 histone pseudogene 16 Homo sapiens 171-174 33303057-10 2020 Flow cytometry analysis and western blot showed that CG induced G2/M arrest with p21 protein upregulation and cyclinB1 protein downregulation. cg 53-55 H3 histone pseudogene 16 Homo sapiens 81-84 33303057-13 2020 In conclusion, this study indicated that CG obviously inhibited A549 cell proliferation, and its mechanism may induce autophagy of A549 cells through EGFR/MEK/ERK/LC3 pathway to upregulate the expression of P21, thus lead to G2/M phase arrest to exert an anti-tumor role. cg 41-43 H3 histone pseudogene 16 Homo sapiens 207-210 31875458-6 2020 Additionally, ML suppressed the expression of cyclin-A/B and promoted that of the cyclin-dependent kinase inhibitors p21 and p27. lucidone 14-16 H3 histone pseudogene 16 Homo sapiens 117-120 32957040-6 2020 Co-treatment with p21 inhibitor UC2288 showed an additive effect on QGP-1 and NCI-H727 cell lines indicating p21 upregulation in these two cell lines might confer resistance towards ART treatment. UC2288 32-38 H3 histone pseudogene 16 Homo sapiens 18-21 32957040-6 2020 Co-treatment with p21 inhibitor UC2288 showed an additive effect on QGP-1 and NCI-H727 cell lines indicating p21 upregulation in these two cell lines might confer resistance towards ART treatment. UC2288 32-38 H3 histone pseudogene 16 Homo sapiens 109-112 33260632-5 2020 The results showed that GSPs inhibited the viability of HepG2 cells in a time- and dose-dependent manner, induced apoptosis and G2/M phase cell cycle arrest, and regulated cell cycle-related proteins, cyclin B1, cyclin-dependent kinase 1, and p21. Grape Seed Proanthocyanidins 24-28 H3 histone pseudogene 16 Homo sapiens 243-246 33496141-10 2020 FPS and VE could both ameliorate the changes of SA-beta-gal staining characteristics and klotho, P53 and P21 protein expression levels in the HK-2 cells exposed to D-gal. Galactose 164-169 H3 histone pseudogene 16 Homo sapiens 105-108 32950500-5 2020 NA20 bound to DNA and p53 identified by a combination of drug tracking, DNA relaxation assay and coimmunoprecipitation-mass spectrometry (CoIP-MS) detection, which led to the p21 activation and the suppression of EGFR signal cascading, thereby evoking cell cycle arrest and cell apoptosis, finally leading to cancer cell inhibition both in vitro and in vivo. na20 0-4 H3 histone pseudogene 16 Homo sapiens 175-178 33312341-7 2020 Western blot analysis showed that 6,8-diprenylorobol treatment increased the expression of cleaved PARP1, cleaved caspase-3, FOXO3, Bax, Bim, p21, and p27 but decreased the expression of Bcl2 and BclXL. 6,8-Diprenylorobol 34-52 H3 histone pseudogene 16 Homo sapiens 142-145 33140956-6 2020 Furthermore, effective cellular activity is achieved by the stapled 1:1 alpha/Sulfono-gamma-AA peptides, evidenced by significantly enhanced p53 transcriptional activity and much more induced level of MDM2 and p21. alpha/sulfono-gamma-aa 72-94 H3 histone pseudogene 16 Homo sapiens 210-213 33173023-10 2020 Treatment of U251 and C6 cells with PP-4-one markedly enhanced p21 expression relative to the control. pp-4-one 36-44 H3 histone pseudogene 16 Homo sapiens 63-66 33171937-4 2020 Knockdown of LINC0973 decreases p21 levels, activates cellular proliferation of cancer cells, and suppresses apoptosis of drug-treated cells. linc0973 13-21 H3 histone pseudogene 16 Homo sapiens 32-35 33050470-6 2020 Treatment of NCCIT-R with both drugs increased acetylation, induced cell cycle arrest, reduced proliferation, decreased Ki67 index, and increased p21, while increasing cell death by apoptosis, with upregulation of cleaved caspase 3. nccit-r 13-20 H3 histone pseudogene 16 Homo sapiens 146-149 33368049-9 2020 The PI3K/Akt/ERK phosphorylation was inhibited, while p21 and p53, death receptor, expression was promoted by DPMPP treatment. dpmpp 110-115 H3 histone pseudogene 16 Homo sapiens 54-57 32934683-6 2020 Combined rAd-p53 and curcumin treatment resulted in higher p53 (P<0.01) and p21 (P<0.01) expression compared with rAd-p53 or curcumin were added alone, suggesting an additive effect on TP53 expression. Curcumin 21-29 H3 histone pseudogene 16 Homo sapiens 76-79 33017771-7 2020 Consistent with the greater anti-proliferative effect, butyrate exhibits >3-fold stronger potential for inducing cell cycle arrest at the G2 phase with a drop in S-phase fraction (including c-Myc/p21 signaling) and apoptosis when compared with acetate and propionate. Butyrates 55-63 H3 histone pseudogene 16 Homo sapiens 196-199 33101585-8 2020 Phillyrin treatment upregulated the expressions of cyclin E, cyclin-dependent kinase 2 (CDK2), and cyclin A and downregulated the expressions of p21 and p-p53, thereby reversing the G0/G1 cell cycle arrest in H2O2-treated RPE cells. phillyrin 0-9 H3 histone pseudogene 16 Homo sapiens 145-148 32901866-7 2020 Moreover, OTS514 further decreased the SIRT1 transcriptional activity decreased by H2O2, but promoted the H2O2-induced p53 or p21 transcriptional activity. Hydrogen Peroxide 106-110 H3 histone pseudogene 16 Homo sapiens 126-129 33149614-8 2020 Additionally, zeaxanthin caused cell cycle arrest at the G2/M phase by increasing the levels of p21 and p27 and reduced the levels of AKT, Cyclin A, Cyclin B1, and Cyclin-dependent kinase 1/2 (CDK1/2). Zeaxanthins 14-24 H3 histone pseudogene 16 Homo sapiens 96-99 33008277-0 2021 Kojic acid enhances the proliferation of human corneal epithelial cells via p38 and p21 signaling pathways. kojic acid 0-10 H3 histone pseudogene 16 Homo sapiens 84-87 33008277-6 2021 RESULTS: Kojic acid could enhance HCEp proliferation, characterized by promoting cell proliferation rate, decreasing the expression levels of p21, galectin 8 and ki67, and increasing that of p-p38. kojic acid 9-19 H3 histone pseudogene 16 Homo sapiens 142-145 33008277-6 2021 RESULTS: Kojic acid could enhance HCEp proliferation, characterized by promoting cell proliferation rate, decreasing the expression levels of p21, galectin 8 and ki67, and increasing that of p-p38. hcep 34-38 H3 histone pseudogene 16 Homo sapiens 142-145 33008277-8 2021 Furthermore, knockdown of p21 had similar enhancive proliferation effect to kojic acid. kojic acid 76-86 H3 histone pseudogene 16 Homo sapiens 26-29 33008277-9 2021 CONCLUSION: Kojic acid might enhance HCEp proliferation through p38 and p21 signaling pathways, potentially via reduced expression levels of galectin 8 and ki67. kojic acid 12-22 H3 histone pseudogene 16 Homo sapiens 72-75 33008277-9 2021 CONCLUSION: Kojic acid might enhance HCEp proliferation through p38 and p21 signaling pathways, potentially via reduced expression levels of galectin 8 and ki67. hcep 37-41 H3 histone pseudogene 16 Homo sapiens 72-75 32533982-6 2020 In contrast, deactivating MAPK pathway by ZXF1 silencing enhanced cisplatin-induced cell cycle arrest and apoptosis by activating p53/p21 axis. Cisplatin 66-75 H3 histone pseudogene 16 Homo sapiens 134-137 32988875-7 2020 In addition, AZT treatment induced up-regulation of p21 and p16 in the TOV21G and CaOV3 cell line, respectively. Zidovudine 13-16 H3 histone pseudogene 16 Homo sapiens 52-55 32988887-7 2020 Treatment with UC2288, a p21 inhibitor, attenuated proliferation of both cell lines, more prominently in JHOC-9, resulting in reduced viability and subsequent apoptosis. UC2288 15-21 H3 histone pseudogene 16 Homo sapiens 25-28 32768576-10 2020 Cisplatin-apigenin combination was shown to produce significantly more S phase prolongation and G2/M cell cycle arrest, and apoptosis compared with cisplatin or apigenin alone, by inducing p21 and PUMA, respectively. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 189-192 32768576-10 2020 Cisplatin-apigenin combination was shown to produce significantly more S phase prolongation and G2/M cell cycle arrest, and apoptosis compared with cisplatin or apigenin alone, by inducing p21 and PUMA, respectively. Apigenin 10-18 H3 histone pseudogene 16 Homo sapiens 189-192 32847975-4 2020 The novel histone deacetylase inhibitor OBP-801 induces p21 and has shown efficacy against various cancers. YM753 compound 40-47 H3 histone pseudogene 16 Homo sapiens 56-59 32977573-6 2020 Pre-treatment with sauchinone induced down-regulation of cyclins/CDKs and up-regulation of CDK inhibitor, p21, and p27kip1 expression. sauchinone 19-29 H3 histone pseudogene 16 Homo sapiens 106-109 31956937-4 2020 The cell cycle analysis and western blot analysis revealed that LIQ induced G2/M phase arrest through increased expression of p21 and decreased levels of p27, cyclin B, and CDK1/2. liquiritin 64-67 H3 histone pseudogene 16 Homo sapiens 126-129 32659428-12 2020 MCC2344 induced cell death in CEM/ADR5000 cells by activation of PARP, caspase-3, and p21 in addition to the downregulation of p62. mcc2344 0-7 H3 histone pseudogene 16 Homo sapiens 86-89 33040777-6 2020 MDA-MB-231 cells were treated with cisatracurium of different concentrations for 48 h. CCK-8method detected cell proliferation, Transwell detected cell migration and invasion, Western Blot method detected the expression levels of CyclinD1, p21, MMP-2andMMP-9protein in cells, RT-qPCR) detected the expression level of miR-3174in cells. cisatracurium 35-48 H3 histone pseudogene 16 Homo sapiens 240-243 33040777-8 2020 After different concentrations of Cisatracurium acted on MDA-MB-231 cells, the cell inhibition rate and p21 protein expression were significantly increased (p<0.05), the number of cell migration and invasion and the expression levels of CyclinD1, MMP-2 and MMP-9 were significantly reduced (p<0.05), and the expression of miR-3174 in cells was significantly reduced (p<0.05). cisatracurium 34-47 H3 histone pseudogene 16 Homo sapiens 104-107 33046993-8 2020 Our results showed that curcumin induced ROS accumulation, apoptosis, autophagy, cell cycle arrest, and cellular senescence accompanied by upregulation of p53 and p21 proteins in SiHa cells. Curcumin 24-32 H3 histone pseudogene 16 Homo sapiens 163-166 32419149-9 2020 14,15beta-dihydroxyklaineanone induced S cell cycle arrest by downregulating the expression levels of cyclin A, p-CDK2, cyclin B1, p21, E2F-1 and PCNA. 14,15beta-dihydroxyklaineanone 0-30 H3 histone pseudogene 16 Homo sapiens 131-134 32577785-7 2020 It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone. osimertinib 27-34 H3 histone pseudogene 16 Homo sapiens 102-105 32577785-7 2020 It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone. navitoclax 37-43 H3 histone pseudogene 16 Homo sapiens 102-105 32577785-7 2020 It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone. osimertinib 120-127 H3 histone pseudogene 16 Homo sapiens 102-105 32577785-7 2020 It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone. navitoclax 131-137 H3 histone pseudogene 16 Homo sapiens 102-105 32577785-7 2020 It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone. osimertinib 120-127 H3 histone pseudogene 16 Homo sapiens 102-105 32577785-7 2020 It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone. venetoclax 170-176 H3 histone pseudogene 16 Homo sapiens 102-105 32450006-10 2020 We also found that Entinostat caused increased acetylation histones H3 or H4, and changes in the expression of cell cycle-associated proteins such as p21. entinostat 19-29 H3 histone pseudogene 16 Homo sapiens 150-153 32982289-8 2020 The molecular data showed that TB up-regulated the gene expressions of NOXA, PUMA, P21, Bax, and Bim and up-regulated the protein expressions of ASK-1, Bax, phosphorylated JNK, and phosphorylated c-Jun with down-regulation of Bcl-2. theabrownin 31-33 H3 histone pseudogene 16 Homo sapiens 83-86 32679123-5 2020 The treatment of nifedipine dose-dependently suppressed H2O2-induced senescence by reducing Ca2+ entry, autophagy impairment and mTOR signaling, and this suppression was found to be related to senescence-associated beta-galactosidase (SA-beta-gal) activity and the expressions of senescence marker protein 30 (SMP30), p53, and p21. Nifedipine 17-27 H3 histone pseudogene 16 Homo sapiens 327-330 32679123-5 2020 The treatment of nifedipine dose-dependently suppressed H2O2-induced senescence by reducing Ca2+ entry, autophagy impairment and mTOR signaling, and this suppression was found to be related to senescence-associated beta-galactosidase (SA-beta-gal) activity and the expressions of senescence marker protein 30 (SMP30), p53, and p21. Hydrogen Peroxide 56-60 H3 histone pseudogene 16 Homo sapiens 327-330 30638055-3 2020 Valtrate induced cell cycle arrest at G2/M stage and apoptosis in MDA-MB-231 and MCF-7 cells, with reduced expression of p-Akt (Ser 473), cyclin B1 and caspase 8, and increased expression of p21, p-cdc2, cleaved-caspase 3, cleaved-caspase 7 and poly (ADP-ribose) polymerase (PARP). valtrate 0-8 H3 histone pseudogene 16 Homo sapiens 191-194 32872665-5 2020 In addition, CD treatment led to cell cycle arrest at the G0/G1 phase and inhibited expression of cyclin D1 and cyclin-dependent kinases 2 and 4 and led to increased levels of p21, p27Kip1 and p53. Cadmium 13-15 H3 histone pseudogene 16 Homo sapiens 176-179 32917321-9 2020 Western blot analysis further demonstrated that hinokitiol treatment increased the levels of p53 and p21, and concomitantly reduced the expression of cell cycle regulatory proteins, including cyclin D and cyclin E. SA-beta-gal assay showed that hinokitiol treatment significantly induced beta-galactosidase activity. beta-thujaplicin 48-58 H3 histone pseudogene 16 Homo sapiens 101-104 33164374-8 2020 Flavonoids of Sophorae Fructus significantly inhibited the proliferation, migration and invasion of Huh7 cells(P<0.05), promoted the expression of p21 protein(P<0.05), and inhibited the expressions of cyclinD1, MMP-2 and MMP-9(P<0.05) in a dose-dependent manner, and could reduce the activity of MMP-2 and MMP-9(P<0.05). Flavonoids 0-10 H3 histone pseudogene 16 Homo sapiens 147-150 32705219-8 2020 Moreover, by using western blot analysis, we determined that EA increased the protein expression of the p53 target proteins p21, p53 upregulated modulator of apoptosis (PUMA) [also known as Bcl-2-binding component 3 (BBC3)] and Phorbol-12-myristate-13-acetate-induced protein 1 (NOXA). Tetradecanoylphorbol Acetate 228-259 H3 histone pseudogene 16 Homo sapiens 124-127 32478947-3 2020 The results revealed that doxorubicin (Adriamycin [ADR]) concentrations 10 to 40 times less than commonly used in previous studies induced the DNA damage-dependent G2-checkpoint and completed apoptosis within the same time frame, regardless of the presence or absence of p53, p21, and PUMA. Doxorubicin 26-37 H3 histone pseudogene 16 Homo sapiens 276-279 32478947-3 2020 The results revealed that doxorubicin (Adriamycin [ADR]) concentrations 10 to 40 times less than commonly used in previous studies induced the DNA damage-dependent G2-checkpoint and completed apoptosis within the same time frame, regardless of the presence or absence of p53, p21, and PUMA. Doxorubicin 39-49 H3 histone pseudogene 16 Homo sapiens 276-279 32497684-5 2020 Passive dosing was applied in a novel format to expose the MCL-5 human lymphoblastoid cell line to the pro-carcinogen, benzo[a]pyrene (B[a]P) and was compared to solvent (dimethyl sulphoxide) spiked B[a]P exposures over 48 h. Passive dosing induced greater changes, at lower concentrations, to micronucleus frequency, p21 mRNA expression, cell cycle abnormalities, and cell and nuclear morphology. Phosphorus 0-1 H3 histone pseudogene 16 Homo sapiens 318-321 32843583-2 2020 Here we show that prolonged treatment of HDFs with Y-27632 decreased their growth by inducing senescence, which was associated with induction of the senescence markers p16 and p21, and downmodulation of the ERK pathways. Y 27632 51-58 H3 histone pseudogene 16 Homo sapiens 176-179 32160736-3 2020 Moreover, we suggested that the ability of BKM120 to induce its anti-proliferative properties was mediated through the induction of p21-mediated G2/M cell cycle arrest. NVP-BKM120 43-49 H3 histone pseudogene 16 Homo sapiens 132-135 32859062-4 2020 The study aim was to evaluate how the RSV or CRM associated to CisPt treatment modulated some cellular processes such as proliferation, P21 gene expression, apoptotic process, and cell cycle development in HNSCC tumor cell line (PE/CA-PJ49) compared to a normal cell line (HUVEC). Resveratrol 38-41 H3 histone pseudogene 16 Homo sapiens 136-139 32859062-4 2020 The study aim was to evaluate how the RSV or CRM associated to CisPt treatment modulated some cellular processes such as proliferation, P21 gene expression, apoptotic process, and cell cycle development in HNSCC tumor cell line (PE/CA-PJ49) compared to a normal cell line (HUVEC). cispt 63-68 H3 histone pseudogene 16 Homo sapiens 136-139 32859062-6 2020 These natural compounds act against proliferation and sustain the effects of cisplatin by cell cycle arrest, induction of apoptosis and amplification of P21 expression in tumor cells. Cisplatin 77-86 H3 histone pseudogene 16 Homo sapiens 153-156 32445704-9 2020 PRI-1203, but not PRI-1204, increased the percentage of A375 and RPMI7951 melanoma cells in the G0/G1 phase of cell cycle, possibly in a p21 and p27 independent manner. pri-1203 0-8 H3 histone pseudogene 16 Homo sapiens 137-140 32807213-8 2020 Quantitative Polymerase Chain Reaction and Western blot analysis showed increased p21 and decreased cyclin D. Quantitative Polymerase Chain Reaction and western blot analysis showed that levobupivacaine significantly increased Bax expression, accompanied by a significant decreased Bcl-2 expression and inhibition of PI3K/Akt/mTOR signalling pathway. Levobupivacaine 187-202 H3 histone pseudogene 16 Homo sapiens 82-85 32449315-0 2020 Long intergenic noncoding RNA 00021 promotes glioblastoma temozolomide resistance by epigenetically silencing p21 through Notch pathway. Temozolomide 58-70 H3 histone pseudogene 16 Homo sapiens 110-113 32913496-4 2020 MiR-1236-3p inhibited PCa cells growth and metastasis by activating p21. mir-1236-3p 0-11 H3 histone pseudogene 16 Homo sapiens 68-71 32913496-7 2020 We demonstrated that miR-1236-3p significantly suppressed the AKT pathway by inhibiting TLR2 expression while activating p21 expression in PCa cells; this influence was independent of p21 activation. mir-1236-3p 21-32 H3 histone pseudogene 16 Homo sapiens 121-124 32470748-6 2020 Remarkably, P53, P21, BAX, and SMAD4 were significantly upregulated after PL treatment whereas; BCL2 and SURVIVIN were down-regulated. piperlonguminine 74-76 H3 histone pseudogene 16 Homo sapiens 17-20 32626938-7 2020 Furthermore, ISO induced G2/M cell cycle arrest by decreasing the expression levels of cyclin B1 and CDK1/2, and increasing the expression levels of p21 and p27 in A549 cells. homoorientin 13-16 H3 histone pseudogene 16 Homo sapiens 149-152 32736525-11 2020 RESULTS: In vitro, FK506 downregulated telomerase reverse transcriptase expression, resulting in decreased telomerase activity and subsequent induction of p21 expression and cell senescence. Tacrolimus 19-24 H3 histone pseudogene 16 Homo sapiens 155-158 32627020-11 2020 Subsequently, TBMS1 inhibited DNA synthesis and induced G2/M phase arrest by targeting the PI3K/Akt/p21 and the cyclin-dependent kinase 1/cyclin B1 signaling cascades. tubeimoside I 14-19 H3 histone pseudogene 16 Homo sapiens 100-103 32705888-8 2021 Genistein increased the expression levels of p53 and p21 with decreased phosphorylated p21, but did not affect the levels of major cyclin-CDK complexes. Genistein 0-9 H3 histone pseudogene 16 Homo sapiens 53-56 32744980-11 2021 o-OHVPA acted as HDACI in HeLa cells without affecting the HDAC8 expression, arresting the cell cycle of HeLa cells in the G0/G1 phase due to the increase in p21 expression with inhibition of caspase-3 activity without exhibiting toxicity toward normal cells. o-ohvpa 0-7 H3 histone pseudogene 16 Homo sapiens 158-161 32774686-6 2020 Furthermore, GA-D markedly inhibited the generation of reactive oxygen species (ROS) and the expression of p21 and p16 proteins, relieved the cell cycle arrest, and enhanced telomerase activity in senescent hAMSCs. ganoderic acid D 13-17 H3 histone pseudogene 16 Homo sapiens 107-110 32705888-0 2021 Genistein Suppresses v-Src-Driven Proliferative Activity by Arresting the Cell-Cycle at G2/M through Increasing p21 Level in Src-Activated Human Gallbladder Carcinoma cells. Genistein 0-9 H3 histone pseudogene 16 Homo sapiens 112-115 32705888-8 2021 Genistein increased the expression levels of p53 and p21 with decreased phosphorylated p21, but did not affect the levels of major cyclin-CDK complexes. Genistein 0-9 H3 histone pseudogene 16 Homo sapiens 87-90 32705888-9 2021 Taken together, genistein would be considered as the only isoflavone component that may potentially suppress Src-driven proliferative activity by arresting at G2/M induction through increasing the p21 levels, thus providing the mechanistic rationale for the potential use of genistein for the prevention of human cancers with activated Src. Genistein 16-25 H3 histone pseudogene 16 Homo sapiens 197-200 32722075-8 2020 In addition, LY and TAM combination induced the apoptotic genes Caspase-3, Caspase-7, and p53, as well as p21 as cell cycle promotor, and significantly downregulated the anti-apoptotic genes Bcl-2 and survivin. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 13-15 H3 histone pseudogene 16 Homo sapiens 106-109 32722075-8 2020 In addition, LY and TAM combination induced the apoptotic genes Caspase-3, Caspase-7, and p53, as well as p21 as cell cycle promotor, and significantly downregulated the anti-apoptotic genes Bcl-2 and survivin. Tamoxifen 20-23 H3 histone pseudogene 16 Homo sapiens 106-109 32475643-4 2020 Berberine increased the level of p53 protein and of its target p21 both time- and dose-dependently in MCF7 cells. Berberine 0-9 H3 histone pseudogene 16 Homo sapiens 63-66 32475643-9 2020 Moreover, downregulation of RPL5 inhibited berberine-driven induction of p53 and p21 and cell death in MCF7 cells. Berberine 43-52 H3 histone pseudogene 16 Homo sapiens 81-84 32567210-4 2020 Cisplatin-treated hNP cells exhibited rapid phosphorylation of ATM and subsequent increased NF-kappaB activation, aggrecanolysis, decreased total proteoglycan production and increased expression of markers of senescence, including p21, gammaH2 AX and SA-ss-gal. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 231-234 32874469-12 2020 The exposure to hyperbaric oxygen at the pressure of 2.4 ATAand 98% oxygen wasable to produce ROS and RNS molecules, which play a role in cellular adaptive responses through increasing the expression of nfkb, p21 and mRNA of interferon alpha2 plays a role in inhibition mechanism of HIV-1 replication in cells. Oxygen 27-33 H3 histone pseudogene 16 Homo sapiens 209-212 32874469-12 2020 The exposure to hyperbaric oxygen at the pressure of 2.4 ATAand 98% oxygen wasable to produce ROS and RNS molecules, which play a role in cellular adaptive responses through increasing the expression of nfkb, p21 and mRNA of interferon alpha2 plays a role in inhibition mechanism of HIV-1 replication in cells. Oxygen 68-74 H3 histone pseudogene 16 Homo sapiens 209-212 32874469-12 2020 The exposure to hyperbaric oxygen at the pressure of 2.4 ATAand 98% oxygen wasable to produce ROS and RNS molecules, which play a role in cellular adaptive responses through increasing the expression of nfkb, p21 and mRNA of interferon alpha2 plays a role in inhibition mechanism of HIV-1 replication in cells. ros 94-97 H3 histone pseudogene 16 Homo sapiens 209-212 32874469-12 2020 The exposure to hyperbaric oxygen at the pressure of 2.4 ATAand 98% oxygen wasable to produce ROS and RNS molecules, which play a role in cellular adaptive responses through increasing the expression of nfkb, p21 and mRNA of interferon alpha2 plays a role in inhibition mechanism of HIV-1 replication in cells. Radon 102-105 H3 histone pseudogene 16 Homo sapiens 209-212 33040724-6 2020 Expression of p53 and its known target, p21, has been evaluated in cisplatin-treated and control human lung adenocarcinoma A549 cells that possess functional p53 pathway. Cisplatin 67-76 H3 histone pseudogene 16 Homo sapiens 40-43 32648126-8 2022 After treated with KAI for 48 h, the proportion of G1 phase was increased, expression level of cyclin D1 and phosphorylation-RB were down-regulated, whereas the expression of p21 was up-regulated (all P<0.01). Kainic Acid 19-22 H3 histone pseudogene 16 Homo sapiens 175-178 32044796-9 2020 The combination of C61-LNP and CDDP changed in alterations of the cell cycle regulatory proteins p53, p21, p27, cyclin D1 and cyclin E levels. AT 61 19-22 H3 histone pseudogene 16 Homo sapiens 102-105 32044796-9 2020 The combination of C61-LNP and CDDP changed in alterations of the cell cycle regulatory proteins p53, p21, p27, cyclin D1 and cyclin E levels. Cisplatin 31-35 H3 histone pseudogene 16 Homo sapiens 102-105 32647677-14 2020 Besides, Tan-I treatment can notably increase Paclitaxel-inducing cell senescence by promoting DNA damage and senescence-associated proteins such as p21 and p16. tanshinone 9-14 H3 histone pseudogene 16 Homo sapiens 149-152 32394497-5 2020 Neferine was shown to downregulate the expression of Bcl-2 and CDK4, and upregulate caspase 3, clePARP, p21, p27, and p53. neferine 0-8 H3 histone pseudogene 16 Homo sapiens 104-107 32555166-10 2020 We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization. nab 21-24 H3 histone pseudogene 16 Homo sapiens 60-63 32555166-10 2020 We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization. nab 21-24 H3 histone pseudogene 16 Homo sapiens 104-107 32555166-10 2020 We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization. Cholesterol 75-86 H3 histone pseudogene 16 Homo sapiens 60-63 32606957-12 2020 Moreover, gemcitabine-pitavastatin-mediated S phase arrest downregulated cyclin A2/CDK2 and upregulated p21/p27 in MIA PaCa-2 cells. gemcitabine 10-21 H3 histone pseudogene 16 Homo sapiens 104-107 32606957-12 2020 Moreover, gemcitabine-pitavastatin-mediated S phase arrest downregulated cyclin A2/CDK2 and upregulated p21/p27 in MIA PaCa-2 cells. pitavastatin 22-34 H3 histone pseudogene 16 Homo sapiens 104-107 32551032-11 2020 The western blot analysis revealed that nitroxoline or bortezomib treatment markedly diminished the levels of Bcl-2 and cyclin D1, and increased the levels of p21, Bax, cleaved PARP and cleaved caspase-3. nitroxoline 40-51 H3 histone pseudogene 16 Homo sapiens 159-162 32551032-11 2020 The western blot analysis revealed that nitroxoline or bortezomib treatment markedly diminished the levels of Bcl-2 and cyclin D1, and increased the levels of p21, Bax, cleaved PARP and cleaved caspase-3. Bortezomib 55-65 H3 histone pseudogene 16 Homo sapiens 159-162 32294550-11 2020 ROS might contribute to ER stress and further induce apoptosis via the JNK/p53/p21 pathway. Reactive Oxygen Species 0-3 H3 histone pseudogene 16 Homo sapiens 79-82 32208876-5 2020 Polyphyllin I dose-dependent increased the release of mitochondrial cytochrome c, and levels of Fas, p53, p21, and Bax/ Bcl-2 ratios, as well as the activation of cleaved caspase-3, -8, -9, and subsequent cleavage of the poly (ADP-ribose) polymerase (PARP). polyphyllin I 0-13 H3 histone pseudogene 16 Homo sapiens 106-109 32555166-10 2020 We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization. Cholesterol 75-86 H3 histone pseudogene 16 Homo sapiens 104-107 32555166-13 2020 In conclusion, we demonstrated that NaB prevents excessive ROS through NOX2 suppression and SOD1 upregulation by p21/NRF2 pathway, which is critical for inhibiting BACE1-dependent amyloidogenesis in neuronal cells exposed to high cholesterol environment. nab 36-39 H3 histone pseudogene 16 Homo sapiens 113-116 32647677-14 2020 Besides, Tan-I treatment can notably increase Paclitaxel-inducing cell senescence by promoting DNA damage and senescence-associated proteins such as p21 and p16. Paclitaxel 46-56 H3 histone pseudogene 16 Homo sapiens 149-152 32124141-2 2020 The results show that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and the glucose consumption, its effect on the loss of mitochondrial membrane potential, on the decreasing of lactic acid as well as ATP, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 32-45 H3 histone pseudogene 16 Homo sapiens 304-307 32124141-7 2020 CONCLUSION: The overall results of the study strongly suggest that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and metabolism in vitro, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 77-90 H3 histone pseudogene 16 Homo sapiens 236-239 31792920-7 2020 Moreover, high glucose increased the protein levels of p53, acetyl-p53 and p21. Glucose 15-22 H3 histone pseudogene 16 Homo sapiens 75-78 32468080-8 2020 This correlated with differential upregulation of p53/p21 pathway, with S and G2/M arrests by cisplatin and satraplatin in contrast to G1 arrest by oxaliplatin and DAP. Cisplatin 94-103 H3 histone pseudogene 16 Homo sapiens 54-57 32468080-8 2020 This correlated with differential upregulation of p53/p21 pathway, with S and G2/M arrests by cisplatin and satraplatin in contrast to G1 arrest by oxaliplatin and DAP. satraplatin 108-119 H3 histone pseudogene 16 Homo sapiens 54-57 32468080-8 2020 This correlated with differential upregulation of p53/p21 pathway, with S and G2/M arrests by cisplatin and satraplatin in contrast to G1 arrest by oxaliplatin and DAP. Oxaliplatin 148-159 H3 histone pseudogene 16 Homo sapiens 54-57 32468080-11 2020 CONCLUSIONS: Oxaliplatin and DAP robustly activate p53 and p21, which downregulate HR proteins to enhance drug activity. Oxaliplatin 13-24 H3 histone pseudogene 16 Homo sapiens 59-62 32130660-11 2020 After treatment with si-LINC01234 or miR-193a-5p mimic, EC cells (Eca-109 and EC9706) exhibited cyclinD1 and Bcl-2 downregulation, and caspase-3, p21, Bax and cleaved caspase-3 upregulation. Silicon 21-23 H3 histone pseudogene 16 Homo sapiens 146-149 32072678-9 2020 Specifically, the combination of ART and CBP at a lower concentration suppressed cell clone numbers, promoted cell cycle arrest at the G2 /M phase, and induced the expression of the cell cycle and apoptosis related proteins BAX, p21, p53, and Caspae-3, while decreasing Bcl-2 and CyclinB1 expression. artesunate 33-36 H3 histone pseudogene 16 Homo sapiens 229-232 32072678-9 2020 Specifically, the combination of ART and CBP at a lower concentration suppressed cell clone numbers, promoted cell cycle arrest at the G2 /M phase, and induced the expression of the cell cycle and apoptosis related proteins BAX, p21, p53, and Caspae-3, while decreasing Bcl-2 and CyclinB1 expression. Carboplatin 41-44 H3 histone pseudogene 16 Homo sapiens 229-232 32064963-8 2020 In addition, neferine treatment contributed to cell proliferation loss by upregulating p21 and p27 expression leading to cycle arrest at the G1 phase. neferine 13-21 H3 histone pseudogene 16 Homo sapiens 87-90 32633363-10 2020 Meanwhile, simvastatin treatment caused cell cycle arrest in G0/G1 phase, remarkably downregulated expression of cyclin D1, and upregulated expressions of p21 and Bim. Simvastatin 11-22 H3 histone pseudogene 16 Homo sapiens 155-158 32186736-3 2020 Neddylated-cullins, especially neddylated-cullin1 were downregulated and their substrate, p21, was accumulated in RSA samples. rabbit sperm membrane autoantigen 114-117 H3 histone pseudogene 16 Homo sapiens 90-93 31971313-5 2020 alpha-Conidendrin remarkably inhibited the proliferation of breast cancer cells through induction of cell cycle arrest by upregulating p53 and p21 and downregulating cyclin D1 and CDK4. conidendrin 0-17 H3 histone pseudogene 16 Homo sapiens 143-146 32455928-6 2020 H2O2 treatment significantly increased senescence in endothelial cells and mural cells, human neonatal dermal fibroblasts (hNDFs), as measured by increased p21 levels and reduced NOS3 expression. Hydrogen Peroxide 0-4 H3 histone pseudogene 16 Homo sapiens 156-159 32319208-7 2020 Mechanistically, DHL is capable of inhibiting Hep-2 and TU212 cell viability via promoting p53 and P21 function, meanwhile DHL dose-dependently induces Hep-2 and TU212 cells apoptosis via activating mitochondrial apoptosis by inhibiting PI3K/Akt/Bad pathway and stimulating endoplasmic reticulum stress-mediated apoptosis pathway. dehydrocostus lactone 17-20 H3 histone pseudogene 16 Homo sapiens 99-102 32186773-9 2020 The treatment of NSCLC cells with SCH 529074 resulted in a dose-dependent induction of apoptosis and G0/G1 cell cycle arrest, which was associated with the activation of caspases (3 and 7), p53-independent upregulation of p21 and PUMA as well as increased LC3II, a biomarker of autophagy. SCH 529074 34-44 H3 histone pseudogene 16 Homo sapiens 222-225 32466567-0 2020 Activation of Mitochondrial 2-Oxoglutarate Dehydrogenase by Cocarboxylase in Human Lung Adenocarcinoma Cells A549 Is p53/p21-Dependent and Impairs Cellular Redox State, Mimicking the Cisplatin Action. Cisplatin 183-192 H3 histone pseudogene 16 Homo sapiens 121-124 32466567-5 2020 Molecular mechanisms of ThDP action on cellular viability and their interplay with the cisplatin and p53-p21 pathways are characterized. Thiamine Pyrophosphate 24-28 H3 histone pseudogene 16 Homo sapiens 105-108 32466567-10 2020 Cellular levels of the catalytically competent ThDP OGDHC holoenzyme are dysregulated by p21 knockdown and correlate negatively with the A549 viability. Thiamine Pyrophosphate 47-51 H3 histone pseudogene 16 Homo sapiens 89-92 32466567-12 2020 The similarity, non-additivity, and p21 dependence of the dual actions of ThDP and cisplatin on A549 cells manifest a common OGDHC-mediated mechanism of the viability decrease. Thiamine Pyrophosphate 74-78 H3 histone pseudogene 16 Homo sapiens 36-39 32466567-12 2020 The similarity, non-additivity, and p21 dependence of the dual actions of ThDP and cisplatin on A549 cells manifest a common OGDHC-mediated mechanism of the viability decrease. Cisplatin 83-92 H3 histone pseudogene 16 Homo sapiens 36-39 32466567-13 2020 High ThDP saturation of OGDHC compromises the redox state of A549 cells under the control of p53-p21 axes. Thiamine Pyrophosphate 5-9 H3 histone pseudogene 16 Homo sapiens 97-100 32547191-11 2020 Western blot results showed that DIOS significantly suppressed the expression levels of Bcl-2, cdc2, cyclinB1, and promoted the expression levels of Bax, cleaved-caspase3, cleaved-caspase8, cleaved-PARP, Bak, P53, and P21. diosmetin 33-37 H3 histone pseudogene 16 Homo sapiens 218-221 32509176-5 2020 In MCA-SVHUC-AR cells, CpdA significantly reduced the expression levels of oncogenes (c-Fos/c-Jun/c-Myc) and induced those of tumor suppressors (UGT1A/p21/p27/p53/PTEN). CPDA 23-27 H3 histone pseudogene 16 Homo sapiens 151-154 32291269-13 2020 p21 responses to high-dose SnPP and HO-1 responses to low-dose SnPP were significantly suppressed in participants with CKD versus healthy volunteers. S-Nitroso-N-propionyl-D,L-penicillamine 27-31 H3 histone pseudogene 16 Homo sapiens 0-3 32291269-13 2020 p21 responses to high-dose SnPP and HO-1 responses to low-dose SnPP were significantly suppressed in participants with CKD versus healthy volunteers. S-Nitroso-N-propionyl-D,L-penicillamine 63-67 H3 histone pseudogene 16 Homo sapiens 0-3 32435154-9 2020 Results from western blotting showed that paclitaxel inhibited cell proliferation by decreasing the expression of PCNA and increasing the expression of p21. Paclitaxel 42-52 H3 histone pseudogene 16 Homo sapiens 152-155 32106366-6 2020 In addition, up-regulated expression of p27 and p21, as well as down-regulated expression of Cyclin-A and Cyclin-B1 was detected in Mag-treated GC cells, contributing to the S/G2 cell cycle arrest. magnoflorine 132-135 H3 histone pseudogene 16 Homo sapiens 48-51 32366419-8 2020 p53 and Bax proteins were overexpressed, while p21 and bcl2 gene expression was decreased after treatment with the ciprofloxacin derivative. Ciprofloxacin 115-128 H3 histone pseudogene 16 Homo sapiens 47-50 32369692-8 2020 RESULTS: The enhanced pro-apoptotic and anti-proliferative properties of Tacrolimus versus mTOR inhibitors were associated with increased protein kinase RNA-like endoplasmic reticulum kinase (PERK)-related ER stress, Ser15P-p53/p53 ratio and p21 protein expression that may counterbalance the risk of proliferative upregulation caused by enhanced Thr172P-Cdk4/Cdk4 activation in liver cancer cells. Tacrolimus 73-83 H3 histone pseudogene 16 Homo sapiens 242-245 32369692-13 2020 CONCLUSION: The more potent pro-apoptotic and anti-proliferative properties of Tacrolimus versus mTOR inhibitors were associated with an increased activation of PERK and p53 signaling, and p21 protein expression. Tacrolimus 79-89 H3 histone pseudogene 16 Homo sapiens 189-192 31943524-8 2020 The mechanism of the regenerative and protective effects of CS may be related to the decreased reactive oxygen species generation, improved senescent state (SA-beta-gal expression decreased), upregulated expression of Smad2 and phosphorylated Smad2, and downregulated expression of p16, p21 and p53. calcium silicate 60-62 H3 histone pseudogene 16 Homo sapiens 287-290 32504383-2 2020 It was found that the action of platinum(II) and platinum(IV) complexes induced accumulation of p53 protein with a maximum in 12 h, which was confirmed by an increase in the expression of the P21 gene, the target gene of the p53 protein. Platinum 32-40 H3 histone pseudogene 16 Homo sapiens 192-195 32504383-2 2020 It was found that the action of platinum(II) and platinum(IV) complexes induced accumulation of p53 protein with a maximum in 12 h, which was confirmed by an increase in the expression of the P21 gene, the target gene of the p53 protein. Platinum 49-57 H3 histone pseudogene 16 Homo sapiens 192-195 32504383-4 2020 Suppression of p53 protein functions with specific inhibitor alpha-piphitrin under the action of platinum complexes reduced the expression of catalase and superoxide dismutase 2 genes and the target gene P21, which attested to the p53-dependent regulation of these genes. Platinum 97-105 H3 histone pseudogene 16 Homo sapiens 204-207 32421130-6 2020 The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner. swz-4-h 14-21 H3 histone pseudogene 16 Homo sapiens 80-83 32323769-5 2020 The miR-296-3p antagonist altered the expression of a number of key genes that are involved in cell cycle control, including cyclin D1 and p21. mir-296-3p 4-14 H3 histone pseudogene 16 Homo sapiens 139-142 32323826-10 2020 Western blot analysis and RT-qPCR revealed that p53 activation and the expression of p21 were increased in glioma cells treated with lenalidomide. Lenalidomide 133-145 H3 histone pseudogene 16 Homo sapiens 85-88 32421130-6 2020 The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner. swz-4-h 14-21 H3 histone pseudogene 16 Homo sapiens 160-163 32421130-6 2020 The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner. swz-4-h 105-112 H3 histone pseudogene 16 Homo sapiens 80-83 32421130-6 2020 The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner. swz-4-h 105-112 H3 histone pseudogene 16 Homo sapiens 160-163 32421130-8 2020 To sum up, our data indicated that SWZ-4-H could induce lung cancer senescence by regulating p53, p21, p16, and p-Rb, thus providing a novel perspective on anti-cancer mechanisms of SWZ-4-H in human lung cancer A549 cells. swz-4-h 35-42 H3 histone pseudogene 16 Homo sapiens 98-101 32691575-9 2020 Meanwhile, Baicalein treatment downregulated CyclinD1 and CDK4, while upregulating P53 and P21. baicalein 11-20 H3 histone pseudogene 16 Homo sapiens 91-94 32009586-5 2020 LCC induced G1 arrest accompanied by decreased cyclin D1 expression and an increase in the levels of p21 and p27. licochalcone A 0-3 H3 histone pseudogene 16 Homo sapiens 101-104 32005903-1 2020 p21-activated kinases (PAKs) are protein serine/threonine kinases stimulated by Rho-family p21 GTPases such as CDC42 and RAC. cholecystokinin C-terminal flanking peptide 41-47 H3 histone pseudogene 16 Homo sapiens 0-3 32005903-1 2020 p21-activated kinases (PAKs) are protein serine/threonine kinases stimulated by Rho-family p21 GTPases such as CDC42 and RAC. cholecystokinin C-terminal flanking peptide 41-47 H3 histone pseudogene 16 Homo sapiens 91-94 32005903-1 2020 p21-activated kinases (PAKs) are protein serine/threonine kinases stimulated by Rho-family p21 GTPases such as CDC42 and RAC. glycyl-threonine 48-57 H3 histone pseudogene 16 Homo sapiens 0-3 32005903-1 2020 p21-activated kinases (PAKs) are protein serine/threonine kinases stimulated by Rho-family p21 GTPases such as CDC42 and RAC. glycyl-threonine 48-57 H3 histone pseudogene 16 Homo sapiens 91-94 32343512-8 2020 Additionally, the naringin abrogates the beta-catenin pathway by decreasing the protein expression as well as phosphorylation of beta-catenin (Ser576) and GSK-3beta (Ser9) and simultaneously triggers cell cycle arrest at a G0/G1 phase by increasing the expression of cell cycle checkpoint proteins p21/cip and p27/kip. naringin 18-26 H3 histone pseudogene 16 Homo sapiens 298-301 32431514-9 2020 Moreover, combination of TET and PTX obviously induced cell cycle arrest in SKOV3/PTX cells via increasing the level of p21 and decreasing the levels of c-Myc and Cyclin D1. tetrandrine 25-28 H3 histone pseudogene 16 Homo sapiens 120-123 32431514-9 2020 Moreover, combination of TET and PTX obviously induced cell cycle arrest in SKOV3/PTX cells via increasing the level of p21 and decreasing the levels of c-Myc and Cyclin D1. Paclitaxel 33-36 H3 histone pseudogene 16 Homo sapiens 120-123 31954769-5 2020 Moreover, MVC inhibited the cell cycle by down regulating the proteins of the complexes of cyclin dependent kinase (CDK) 4/6 - Cyclin D and CDK2 - Cyclin E, as well as by increasing the protein levels of CDK inhibitors p18, p21 and p27. maraviroc 10-13 H3 histone pseudogene 16 Homo sapiens 224-227 32355541-12 2020 Protein levels of the cell cycle regulators and senescence markers p21 and p53 showed opposite expression patterns in cisplatin-resistant compared with cisplatin sensitive cells. Cisplatin 118-127 H3 histone pseudogene 16 Homo sapiens 67-70 32355541-12 2020 Protein levels of the cell cycle regulators and senescence markers p21 and p53 showed opposite expression patterns in cisplatin-resistant compared with cisplatin sensitive cells. Cisplatin 152-161 H3 histone pseudogene 16 Homo sapiens 67-70 32273511-4 2020 Moreover, the removal of asparagine from culture medium or the inhibition of ASNS impairs cell proliferation and induces p53/p21-dependent senescence and cell cycle arrest. Asparagine 25-35 H3 histone pseudogene 16 Homo sapiens 125-128 32340377-7 2020 Taken together, these results show that ATG enhances the cytotoxic activity of DOX in MDA-MB-231 human breast cancer cells by inducing prolonged p21 expression and p38-mediated AIF-dependent cell death. Doxorubicin 79-82 H3 histone pseudogene 16 Homo sapiens 145-148 32277808-11 2020 Western blotting of HKULC2 cells showed that betulinic acid nanoparticles promoted the expression of p21 and p53 and downregulated CD133, ALDH, BCL2, MCL1, and c-Myc expression. betulinic acid 45-59 H3 histone pseudogene 16 Homo sapiens 101-104 32215662-4 2020 The guanine deaminase gene, which is involved in purine metabolism, was upregulated with uric acid levels and p21 in SK. purine 49-55 H3 histone pseudogene 16 Homo sapiens 110-113 31996318-7 2020 ART caused cell cycle arrest at G1 and/or G2/M phases, which was associated with decreased expression of cyclin dependent kinase 1/2/4/6, cyclin B1/D2/E and c-Myc, and increased expression of p21. artesunate 0-3 H3 histone pseudogene 16 Homo sapiens 192-195 31931353-2 2020 The structural transformation between the C2/c and the P21/c monoclinic phases has a complicated nature and is mainly driven by re-orientational motions of the FA+ cations but it is also accompanied by a significant distortion of the MnO6 octahedral units as well as steric-forced changes of the PH2 groups determining the off-center shifts of FA+ cations in the cages. Manganese 234-238 H3 histone pseudogene 16 Homo sapiens 55-78 32041778-9 2020 STUB1 expression attenuates hydrogen peroxide-induced cell senescence, indicated by a reduced signal in senescence-associated beta-galactosidase staining and decreased protein levels of two cell senescence markers, p53 and p21. Hydrogen Peroxide 28-45 H3 histone pseudogene 16 Homo sapiens 223-226 32821748-7 2020 Results: In the control group and ALL patients, p21 Ser/Arg, and MDM2 TG and GG genotypes were associated with significant 1.81-fold (95% confidence interval CI= 1.008-3.267; P < 0.05), 11.07-fold (95% CI= 5.10-24.05; P < 0.0001), and 19.41-fold (95% CI= 8.56-43.99; P < 0.0001) increased risks for ALL, respectively. Serine 52-55 H3 histone pseudogene 16 Homo sapiens 48-51 31994822-3 2020 Luteolin inhibited cell survival and induced G2/M cell-cycle arrest, p21 upregulation and downregulation of phospho(p)-S6, which is downstream of mTOR signaling. Luteolin 0-8 H3 histone pseudogene 16 Homo sapiens 69-72 31703157-1 2020 WHAT IS KNOWN AND OBJECTIVE: The 3.8-kb-long antisense non-coding RNA at the INK4 locus (ANRIL) is transcribed from the short arm of human chromosome 9 on P21 and is associated with malfunction of the vascular endothelium, vascular smooth muscle cell (VSMC) proliferation/migration/senescence/apoptosis, mononuclear cell adhesion and proliferation, glycolipid metabolism disorder and DNA damage. known 8-13 H3 histone pseudogene 16 Homo sapiens 155-158 31978617-9 2020 In addition, RSV reduced the levels of senescence-associated secretory phenotype (SASP), gene markers associated with senescence (P53, P16, and P21), intracellular ROS levels and increased gene expression of enzymes protecting cells from oxidative damage (HMOX1 and SOD3). resveratrol 13-16 H3 histone pseudogene 16 Homo sapiens 144-147 33224241-8 2020 The essential oil inhibited the growth of HeLa cells and increased the expression of p21 and p53. Oils, Volatile 4-17 H3 histone pseudogene 16 Homo sapiens 85-88 32821748-7 2020 Results: In the control group and ALL patients, p21 Ser/Arg, and MDM2 TG and GG genotypes were associated with significant 1.81-fold (95% confidence interval CI= 1.008-3.267; P < 0.05), 11.07-fold (95% CI= 5.10-24.05; P < 0.0001), and 19.41-fold (95% CI= 8.56-43.99; P < 0.0001) increased risks for ALL, respectively. Arginine 56-59 H3 histone pseudogene 16 Homo sapiens 48-51 32235535-6 2020 Norhierridin B (10) interfered with several p53 transcriptional targets, increasing p21, Bax, and MDM2, while decreasing Bcl-2 protein levels, which suggested the potential activation of a p53 pathway. norhierridin b 0-14 H3 histone pseudogene 16 Homo sapiens 84-87 32031808-5 2020 It also counteracted the cell cycle blockade induced by a low concentration of H2O2 decreasing the expression of p21 and CDKN2A (p16INK4A). Water 79-83 H3 histone pseudogene 16 Homo sapiens 113-116 31729509-3 2020 NaSr5(BO3)(SiO4)2 crystallizes in a monoclinic space group of P21/c with a 3D structure consisting of a splendid strontium 3D framework strengthened by isolated BO3 and SiO4 groups. Sodium 0-17 H3 histone pseudogene 16 Homo sapiens 62-65 31729509-3 2020 NaSr5(BO3)(SiO4)2 crystallizes in a monoclinic space group of P21/c with a 3D structure consisting of a splendid strontium 3D framework strengthened by isolated BO3 and SiO4 groups. Silicon 11-15 H3 histone pseudogene 16 Homo sapiens 62-65 32219038-11 2020 Further mechanical explorations showed that H19 knockdown resulted in alternative expressions levels of cyclin D1, CDK4, CDK6, p21 and p53 under ICA treatment. icariin 145-148 H3 histone pseudogene 16 Homo sapiens 127-130 32219038-9 2020 At molecular levels, cell cycle regulators cyclin D1, CDK4, CDK6, p21 and p53 were modulated in response to treatment with ICA. icariin 123-126 H3 histone pseudogene 16 Homo sapiens 66-69 32256113-8 2020 Oxymatrine induced cell cycle arrest in the G2/M phase by increasing the protein expression of P21 and decreasing levels of cyclin B1 and CDC2. oxymatrine 0-10 H3 histone pseudogene 16 Homo sapiens 95-98 32266102-5 2020 MLN4924 inhibits proliferation and interferes with the cell cycle checkpoint regulators, p21, p27, and phospho-histone H3. pevonedistat 0-7 H3 histone pseudogene 16 Homo sapiens 89-92 32114764-4 2020 Ba2M2(PO3F)F6 (M = Mn, Co, and Cu) are isostructural, crystallizing in the monoclinic space group P21/c, while Ba2Ni2(PO3F)F6 adopted an unpredetermined structure, crystallizing in the monoclinic space group P21/n. ba2m2 0-5 H3 histone pseudogene 16 Homo sapiens 98-103 32114764-4 2020 Ba2M2(PO3F)F6 (M = Mn, Co, and Cu) are isostructural, crystallizing in the monoclinic space group P21/c, while Ba2Ni2(PO3F)F6 adopted an unpredetermined structure, crystallizing in the monoclinic space group P21/n. ba2m2 0-5 H3 histone pseudogene 16 Homo sapiens 98-101 31990147-9 2020 We further found that the effect of Lobetyolin on HCT-116 was related to the expressions of p21 and bax, and transportation of p53 to nucleus. lobetyolin 36-46 H3 histone pseudogene 16 Homo sapiens 92-95 31751608-7 2020 Glyphosate decreased expression of P16 and TP53 as well as an increase in the expression of BCl2, CCND1 and P21. glyphosate 0-10 H3 histone pseudogene 16 Homo sapiens 108-111 31967931-7 2020 Contrastingly, for P21 neurons the main effect of (S)-Bay K8644 was to enhance burst-firing. 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester 58-63 H3 histone pseudogene 16 Homo sapiens 19-22 31967931-8 2020 (S)-Bay K8644 increased spontaneous inhibitory synaptic currents at both P7 and P21 but did not affect evoked synaptic currents at either stage. 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester 8-13 H3 histone pseudogene 16 Homo sapiens 80-83 31631444-10 2020 Furthermore, the expressions of senescence markers, such as p21 and p53, were upregulated upon bleomycin treatment, thereby intensifying the fibrotic condition. Bleomycin 95-104 H3 histone pseudogene 16 Homo sapiens 60-63 32045477-1 2020 The selective inhibitor of nuclear export (SINE) compounds selinexor (KPT-330) and eltanexor (KPT-8602) are from a novel class of small molecules that target exportin-1 (XPO1 [CRM1]), an essential nucleo-cytoplasmic transport protein responsible for the nuclear export of major tumor suppressor proteins and growth regulators such as p53, p21, and p27. selinexor 94-102 H3 histone pseudogene 16 Homo sapiens 339-342 32149078-5 2020 In addition, this bendamustine-derived drug showed both a HDACi effect as demonstrated by histone hyperacetylation and p21 transcription and a DNA-damaging effect as shown by an increase in gamma-H2AX. Bendamustine Hydrochloride 18-30 H3 histone pseudogene 16 Homo sapiens 119-122 31995555-8 2020 Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC). Reactive Oxygen Species 181-184 H3 histone pseudogene 16 Homo sapiens 95-98 31894334-6 2020 The induction of p21 and G1 arrest of the cell cycle also was revealed in niclosamide-treated CE81T cells by qPCR and flow cytometric assays, respectively. Niclosamide 74-85 H3 histone pseudogene 16 Homo sapiens 17-20 32016852-6 2020 The cells were incubated with olivacine derivatives for 18 h and then assays were carried out: measurement of the amount of p53 and p21 proteins, detection of apoptosis, cell cycle analysis, and rhodamine 123 accumulation assay (evaluation of P-glycoprotein inhibition). olivacine 30-39 H3 histone pseudogene 16 Homo sapiens 132-135 31840737-8 2020 Mechanistic analysis revealed that ISL inhibited cyclin D1 and up-regulated the proteins P21, P27 that negatively regulate the cell cycle. isoliquiritigenin 35-38 H3 histone pseudogene 16 Homo sapiens 89-92 31995555-8 2020 Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC). Acetylcysteine 196-213 H3 histone pseudogene 16 Homo sapiens 95-98 31995555-8 2020 Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC). Acetylcysteine 215-218 H3 histone pseudogene 16 Homo sapiens 95-98 32071742-1 2020 Deuterated potassium orthophosphate hepta-hydrate, K3PO4 7D2O, crystallizes in the Sohnke space group P21, and its absolute structure was determined from 2017 Friedel pairs [Flack parameter 0.004 (16)]. Phosphates 11-35 H3 histone pseudogene 16 Homo sapiens 102-105 31979361-0 2020 The Antiproliferative Activity of Oxypeucedanin via Induction of G2/M Phase Cell Cycle Arrest and p53-Dependent MDM2/p21 Expression in Human Hepatoma Cells. oxypeucadanin 34-47 H3 histone pseudogene 16 Homo sapiens 117-120 31941051-4 2020 The crystal of TCAD tetrahydrate is monoclinic, with space group P21/c with crystal parameters of a = 10.2935(2) A, b = 7.36760(10) A, c = 20.1447(4) A, V = 1500.27(5) A3, Z = 4, and F(000) = 688. thiazole-4-carboxamide adenine dinucleotide 15-32 H3 histone pseudogene 16 Homo sapiens 65-68 31922313-12 2020 Western blotting results revealed that the levels of p21, p27, cleaved caspase-3, Bax, TIMP-3, and E-cadherin were up-regulated while, the levels of CDK4, CDK6, pro-caspase-3, Bcl-2, MMP-2, MMP-9, N-cadherin, and Vimentin were down-regulated by euxanthone. euxanthone 245-255 H3 histone pseudogene 16 Homo sapiens 53-56 32071742-1 2020 Deuterated potassium orthophosphate hepta-hydrate, K3PO4 7D2O, crystallizes in the Sohnke space group P21, and its absolute structure was determined from 2017 Friedel pairs [Flack parameter 0.004 (16)]. potassium phosphate 51-61 H3 histone pseudogene 16 Homo sapiens 102-105 31796664-6 2020 The following clusters were found in the dendrogram: Nrf2 and p21 with ATP5B and GADPH in all the tissues and with NRF1 in all except the tumor tissues with metastasis; Bach1 with ATP5B and GAPDH in the tumor tissues; Keap1 with p62 in all the tissues, with LC3 in the tumor tissues and with NRF1 and HO1 in the tumor tissues with metastasis. gadph 81-86 H3 histone pseudogene 16 Homo sapiens 62-65 31605433-4 2020 Spalax fibroblasts undergo replicative senescence (RS) and etoposide-induced senescence (EIS), evidenced by an increased activity of senescence-associated beta-galactosidase (SA-beta-Gal), growth arrest, and overexpression of p21, p16, and p53 mRNAs. Etoposide 59-68 H3 histone pseudogene 16 Homo sapiens 226-229 31919338-9 2020 The expression of cyclin D1 and p21 proteins was significantly increased by 3,6-diazabicyclo[3.3.1]heptane in LNCaP and PC3 cells. triethylenediamine 76-92 H3 histone pseudogene 16 Homo sapiens 32-35 31919338-12 2020 The suppression of prostate cancer cell viability by 3,6-diazabicyclo[3.3.1]heptane involves apoptosis induction, cell cycle arrest and upregulation of p21 expression. triethylenediamine 53-69 H3 histone pseudogene 16 Homo sapiens 152-155 31948013-8 2020 Treatment with iPSC-CENVs significantly reduced the activity of senescence-associated-beta-galactosidase (SA-beta-Gal) in senescent HDFs, as well as suppressing the elevated expression of p53 and p21, key factors involved in cell cycle arrest, apoptosis, and cellular senescence signaling pathways. ipsc-cenvs 15-25 H3 histone pseudogene 16 Homo sapiens 196-199 31919305-3 2020 1-[(2,6-Dimethylphenoxy)ethyl]piperidin-4-ol, C15H23NO2, 1, and 1-[(2,3-dimethylphenoxy)ethyl]piperidin-4-ol, C15H23NO2, 2, crystallize in the orthorhombic system (space groups P212121 and Pbca, respectively), with one molecule in the asymmetric unit, whereas the N-oxide 1-[(2,3-dimethylphenoxy)ethyl]piperidin-4-ol N-oxide monohydrate, C15H23NO3 H2O, 3, crystallizes in the monoclinic space group P21/c, with one N-oxide molecule and one water molecule in the asymmetric unit. Mexiletine 0-44 H3 histone pseudogene 16 Homo sapiens 399-404 31919305-3 2020 1-[(2,6-Dimethylphenoxy)ethyl]piperidin-4-ol, C15H23NO2, 1, and 1-[(2,3-dimethylphenoxy)ethyl]piperidin-4-ol, C15H23NO2, 2, crystallize in the orthorhombic system (space groups P212121 and Pbca, respectively), with one molecule in the asymmetric unit, whereas the N-oxide 1-[(2,3-dimethylphenoxy)ethyl]piperidin-4-ol N-oxide monohydrate, C15H23NO3 H2O, 3, crystallizes in the monoclinic space group P21/c, with one N-oxide molecule and one water molecule in the asymmetric unit. Mexiletine 64-108 H3 histone pseudogene 16 Homo sapiens 399-404 32907364-6 2020 Accompanied with cell cycle disruption, cucurbitacin B altered the expression of proteins involved in the G2/M phase transition including downregulation of cyclin A, cyclin D1, and cdc25A, and upregulation of p21. cucurbitacin B 40-54 H3 histone pseudogene 16 Homo sapiens 209-212 31551201-1 2020 Peripheral blood leukocyte telomere length in omethoate-exposed workers is related to environmental exposure and single nucleotide polymorphisms (SNPs) in genes including p21, GSTM1, miR-145, etc. dimethoxon 46-55 H3 histone pseudogene 16 Homo sapiens 171-174 32907379-6 2020 ADAR1 and cyclin D1 protein levels were dramatically decreased, while p53 and p21 levels were increased after 8-Cl-Ado exposure. 8-chloroadenosine 110-118 H3 histone pseudogene 16 Homo sapiens 78-81 32907379-9 2020 Together, 8-Cl-Ado inhibits the cell proliferation, induces G1 phase arrest and apoptosis at least by targeting ADAR1/p53/p21 signaling pathway. 8-chloroadenosine 10-18 H3 histone pseudogene 16 Homo sapiens 122-125 31969092-12 2020 Lupeol also modulates the molecules involved in cell cycle regulation such as Cyclins, CDKs, P53, P21, and PCNA in different cancer types. lupeol 0-6 H3 histone pseudogene 16 Homo sapiens 98-101 31767563-7 2020 Ex vivo Nutlin-3 (MDM2 inhibitor) treatment of blood and BM increased p53 and p21 expression in CTCs and DTCs compared with DMSO controls. nutlin 3 8-16 H3 histone pseudogene 16 Homo sapiens 78-81 31520547-0 2020 Pyrroloquinoline quinone delays inflammaging induced by TNF-alpha through the p16/p21 and Jagged1 signalling pathways. PQQ Cofactor 0-24 H3 histone pseudogene 16 Homo sapiens 82-85 31957859-10 2020 In comparison with those in the IR group, ratios of p-AKT/AKT, p-mTOR/mTOR, and the level of PCNA were remarkably raised, while the level of P21 was remarkably reduced in IR+Gln group (p<0.05). arginyl-glutamine 174-177 H3 histone pseudogene 16 Homo sapiens 141-144 30913094-11 2020 The 9p21 locus mutation frequency was higher in the alcohol-smoking and leukoplakia groups. Alcohols 52-59 H3 histone pseudogene 16 Homo sapiens 5-8 31957859-17 2020 Gln can increase the PCNA level and reduce the P21 level, so as to enhance the proliferation ability of cardiomyocytes. arginyl-glutamine 0-3 H3 histone pseudogene 16 Homo sapiens 47-50 31908576-5 2020 In cultured VSMCs, hydrogen peroxide (H2O2) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated beta-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways. Hydrogen Peroxide 19-36 H3 histone pseudogene 16 Homo sapiens 238-241 31746354-6 2020 The present study demonstrated that Hnk was able to prevent Dox-induced senescence of H9c2 cardiomyocytes, indicated by decreased senescence-associated beta-galactosidase (SA-beta-gal) staining, as well as decreased expression of p16INK4A and p21. honokiol 36-39 H3 histone pseudogene 16 Homo sapiens 243-246 31746354-6 2020 The present study demonstrated that Hnk was able to prevent Dox-induced senescence of H9c2 cardiomyocytes, indicated by decreased senescence-associated beta-galactosidase (SA-beta-gal) staining, as well as decreased expression of p16INK4A and p21. Doxorubicin 60-63 H3 histone pseudogene 16 Homo sapiens 243-246 33302699-8 2020 The CcME-treated TNBC cells underwent apoptosis, associated with a concomitant increase of apoptosis-related protein expression, including cytochrome c, cleaved caspase-3, cyclin-dependent kinase inhibitor p21, and the anti-oxidant enzyme catalase, compared with the untreated cells. ccme 4-8 H3 histone pseudogene 16 Homo sapiens 206-209 33302699-9 2020 The CcME also enhanced the mitochondrial transition pore opening activity and induced G0/G1 cell growth arrest, which confirmed the cytochrome c release and the increase of the p21 expression detected in the CcME-treated TNBC cells. ccme 4-8 H3 histone pseudogene 16 Homo sapiens 177-180 33302699-9 2020 The CcME also enhanced the mitochondrial transition pore opening activity and induced G0/G1 cell growth arrest, which confirmed the cytochrome c release and the increase of the p21 expression detected in the CcME-treated TNBC cells. ccme 208-212 H3 histone pseudogene 16 Homo sapiens 177-180 32126555-14 2020 Resveratrol, an activator of sirtuin-1, postponed the IL-1beta-induced senescence through blocking the NF-kappaB/p53/p21 pathway and attenuated the osteoblastic transition and calcification in VSMCs. Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 117-120 31956358-0 2020 Dihydroartemisinin suppresses bladder cancer cell invasion and migration by regulating KDM3A and p21. artenimol 0-18 H3 histone pseudogene 16 Homo sapiens 97-100 31956358-5 2020 Further mechanism study showed that DHA performed its function via down-regulating the expression of histone demethylase KDM3A and inducing p21 expression. artenimol 36-39 H3 histone pseudogene 16 Homo sapiens 140-143 31908576-5 2020 In cultured VSMCs, hydrogen peroxide (H2O2) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated beta-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways. Water 38-42 H3 histone pseudogene 16 Homo sapiens 238-241 31934307-6 2019 Combined use of low-dose DAC and chidamide arrested the cell cycle at the G0/G1 phase by upregulating p21 expression, and the combination also suppressed PI3K/AKT/mTOR signaling pathway. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 33-42 H3 histone pseudogene 16 Homo sapiens 102-105 31905841-7 2019 siTNS3 treatment upregulated p16 and p21 levels and downregulated SOX2 expression and focal adhesion kinase, protein kinase B, and c-Jun N-terminal kinase phosphorylation. Nitrogen 3-4 H3 histone pseudogene 16 Homo sapiens 37-40 31842349-11 2019 Loss of p21 also leads to more palmitic acid-induced cell apoptosis in the HCT116 cell line compared with HCT116 p53+/+ and HCT116 p53-/-. Palmitic Acid 31-44 H3 histone pseudogene 16 Homo sapiens 8-11 30873870-4 2019 Shikonin caused G2/M phase arrest through upregulation of p21 and downregulation of cyclin B1. shikonin 0-8 H3 histone pseudogene 16 Homo sapiens 58-61 31885790-7 2019 Moreover, blocking AKT with the PI3K/AKT inhibitor LY294002 or knocking down AKT via RNA interference significantly decreased PBX1 expression, while increasing p16 and p21 expression and the number of SA-beta-gal-positive cells. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 51-59 H3 histone pseudogene 16 Homo sapiens 168-171 31890943-7 2019 Structurally, ethyl diclofenac reveals a P21/c monoclinic and the cocrystal between this ester with its parent drug is a P-1 triclinic system. Diclofenac 14-30 H3 histone pseudogene 16 Homo sapiens 41-46 31818017-6 2019 Coronarin D potently suppressed cell viability in glioblastoma U-251 cell line, and also induced G1 arrest by reducing p21 protein and histone H2AX phosphorylation, leading to DNA damage and apoptosis. coronarin D 0-11 H3 histone pseudogene 16 Homo sapiens 119-122 30880481-7 2019 We found that, salidroside remarkably reduced cell viability, colony formation and Cyclin D1 expression, but increased p21 expression and apoptosis in A549 cells. rhodioloside 15-26 H3 histone pseudogene 16 Homo sapiens 119-122 31220953-4 2019 NRF2 was examined as a mediating mechanism of salicin"s impact on cellular senescence and was found to account for salicin"s impact on SA-beta-Gal, p21, PAI-1 and p53. salicin 115-122 H3 histone pseudogene 16 Homo sapiens 148-151 31116036-5 2019 Specifically, this study confirmed that Ala induced G2/M phase arrest by upregulating p21, downregulating cyclin A1 and cyclin B1, and promoting cellular apoptosis by increasing the expression of cleaved caspase-3 and PARP. alantolactone 40-43 H3 histone pseudogene 16 Homo sapiens 86-89 31237151-6 2019 Mechanistically, we show that TC-G 1008 mitigates IL-1beta-induced cell cycle arrest at G1 phase by suppressing the expression of p53, p21, PAI-1, and K382 acetylation of p53. GPR39-C3 30-39 H3 histone pseudogene 16 Homo sapiens 135-138 31432697-7 2019 Salidroside inhibited GC cells proliferation, migration, invasion and promoted apoptosis, which coupled with the down-regulation of p21, Bcl-2, MMP2, RhoA, p-ROCK1, Vimentin and the up-regulations of CyclinD1, Bax, cleaved caspases. rhodioloside 0-11 H3 histone pseudogene 16 Homo sapiens 132-135 31404677-8 2019 RESULTS: mRNAs of PAI-1, HO-1, and p21 were upregulated after photoirradiation of HEK293, which was suppressed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger. Reactive Oxygen Species 137-160 H3 histone pseudogene 16 Homo sapiens 35-38 31432559-8 2019 Moreover, quinalizarin triggered G2/M phase cell arrest by modulating the protein expression levels of CDK 1/2, cyclin A, cyclin B, p21 and p27, and induced apoptosis by down-regulating the antiapoptotic protein Bcl-2 and upregulating the proapoptotic protein BAD, leading to the activation of caspase-3 and PARP in the caspase cascade in A375 cells. 1,2,5,8-tetrahydroxy anthraquinone 10-22 H3 histone pseudogene 16 Homo sapiens 132-135 31706015-8 2019 Anatomical studies show that the expression of Ki-67 was greater and ratio of p21-positive cells to the ratio of Ki-67-expressing cells was lower in animals in which the ethanol exposure included gastrulation. Ethanol 170-177 H3 histone pseudogene 16 Homo sapiens 78-81 31568920-0 2019 Regulation of p21 expression for anti-apoptotic activity of DDX3 against sanguinarine-induced cell death on intrinsic pathway. sanguinarine 73-85 H3 histone pseudogene 16 Homo sapiens 14-17 31404677-0 2019 Photoirradiation after aminolevulinic acid treatment suppresses cancer cell proliferation through the HO-1/p21 pathway. Aminolevulinic Acid 23-42 H3 histone pseudogene 16 Homo sapiens 107-110 31404677-8 2019 RESULTS: mRNAs of PAI-1, HO-1, and p21 were upregulated after photoirradiation of HEK293, which was suppressed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger. Acetylcysteine 114-133 H3 histone pseudogene 16 Homo sapiens 35-38 31404677-8 2019 RESULTS: mRNAs of PAI-1, HO-1, and p21 were upregulated after photoirradiation of HEK293, which was suppressed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger. Reactive Oxygen Species 162-165 H3 histone pseudogene 16 Homo sapiens 35-38 31404677-11 2019 CONCLUSION: ALA-PDD or ALA-PDT can result in rapid ROS-induced cell death and may decrease long-term recurrence rates through several pathways including the HO-1/p21 pathway. 5-amino levulinic acid 12-15 H3 histone pseudogene 16 Homo sapiens 162-165 31568920-11 2019 The results implied that p21 might be involved in the toxicity of sanguinarine to HeLa cells. sanguinarine 66-78 H3 histone pseudogene 16 Homo sapiens 25-28 31568920-12 2019 Overexpression and knockdown of DDX3 under sanguinarine-treated conditions showed that DDX3 inhibited p21 expression in sanguinarine-treated HeLa cells. sanguinarine 43-55 H3 histone pseudogene 16 Homo sapiens 102-105 31568920-12 2019 Overexpression and knockdown of DDX3 under sanguinarine-treated conditions showed that DDX3 inhibited p21 expression in sanguinarine-treated HeLa cells. sanguinarine 120-132 H3 histone pseudogene 16 Homo sapiens 102-105 31568920-14 2019 CONCLUSION: Taken together, the results suggest that the S90E residue is important for the regulation of p21 expression responsible for the anti-apoptotic activity of DDX3 in HeLa cells treated with sanguinarine. sanguinarine 199-211 H3 histone pseudogene 16 Homo sapiens 105-108 31404677-11 2019 CONCLUSION: ALA-PDD or ALA-PDT can result in rapid ROS-induced cell death and may decrease long-term recurrence rates through several pathways including the HO-1/p21 pathway. 5-amino levulinic acid 23-26 H3 histone pseudogene 16 Homo sapiens 162-165 31404677-11 2019 CONCLUSION: ALA-PDD or ALA-PDT can result in rapid ROS-induced cell death and may decrease long-term recurrence rates through several pathways including the HO-1/p21 pathway. Reactive Oxygen Species 51-54 H3 histone pseudogene 16 Homo sapiens 162-165 31438780-4 2019 Results: Cell senescence, characterized by senescence beta-galactosidase staining and senescence-related genes (p16, p21, and p53) expression, was attenuated by resveratrol. Resveratrol 161-172 H3 histone pseudogene 16 Homo sapiens 117-120 31885624-0 2019 Palmitic Acid Methyl Ester Induces G2/M Arrest in Human Bone Marrow-Derived Mesenchymal Stem Cells via the p53/p21 Pathway. methyl palmitate 0-26 H3 histone pseudogene 16 Homo sapiens 111-114 31885624-7 2019 Moreover, the level of Mdm2 protein decreased, while the levels of p21 and p53 protein increased in the PAME-treated hBM-MSCs. methyl palmitate 104-108 H3 histone pseudogene 16 Homo sapiens 67-70 31885624-13 2019 Taken together, these results suggest that PAME induced p53 stabilization, which in turn increased the levels of p53/p21 proteins and decreased the levels of Cdk1/cyclin B1 proteins, thereby preventing the activation of Cdk1, and eventually caused cell cycle arrest at the G2/M phase. methyl palmitate 43-47 H3 histone pseudogene 16 Homo sapiens 117-120 31738805-0 2019 Phosphorylation-dependent activity-based conformational changes in P21-activated kinase family members and screening of novel ATP competitive inhibitors. Adenosine Triphosphate 126-129 H3 histone pseudogene 16 Homo sapiens 67-70 31779710-7 2019 RESULTS: In vitro treatment of bone marrow-derived macrophages with APG-115 resulted in activation of p53 and p21, and a decrease in immunosuppressive M2 macrophage population through downregulation of c-Myc and c-Maf. AA-115 68-75 H3 histone pseudogene 16 Homo sapiens 110-113 31752013-11 2019 Simvastatin disrupted this senescence mechanism via the miR-155/SIRT1/FoxO-1/p21 pathway signaling. Simvastatin 0-11 H3 histone pseudogene 16 Homo sapiens 77-80 31752145-4 2019 In cancer cells, CN induced apoptosis and cell cycle arrest at G2/M phase through a p53-mediated mechanism, where p53 was activated, p21 and pro-apoptotic proteins Bid and Bak were upregulated, and PARP was cleaved. Curcumin 17-19 H3 histone pseudogene 16 Homo sapiens 133-136 31738805-1 2019 P21-activated kinases (PAKs) are serine/threonine protein kinases that are subdivided into two groups on the basis of their domain architecture: group-I (PAK1-3) and group-II (PAK4-6). cholecystokinin C-terminal flanking peptide 33-39 H3 histone pseudogene 16 Homo sapiens 0-3 31752145-5 2019 In non-transformed human mammary epithelial cells MCF10A, CN at 50 microM had no cytotoxicity and p53 was not activated, but curcumin at 12.5 microM activated p53 and p21 and inhibited MCF10A cell growth. Curcumin 125-133 H3 histone pseudogene 16 Homo sapiens 167-170 31738805-1 2019 P21-activated kinases (PAKs) are serine/threonine protein kinases that are subdivided into two groups on the basis of their domain architecture: group-I (PAK1-3) and group-II (PAK4-6). glycyl-threonine 40-49 H3 histone pseudogene 16 Homo sapiens 0-3 31613301-5 2019 Ca3(CH3COO)4(HCOO)2 4H2O crystallises in a primitive tetragonal unit cell with space group P41212 and lattice parameters of a = 6.8655(1) A and c = 45.5454(6) A, while Ca(CH3COO)(HCOO) H2O crystallises in a primitive monoclinic unit cell with space group P21/c and lattice parameters of a = 9.2729(1) A, b = 6.8002(1) A, c = 11.2219(2) A and beta = 121.232(1) . lead acetate 0-24 H3 histone pseudogene 16 Homo sapiens 255-260 31739520-9 2019 Furthermore, PL significantly increased p21 mRNA levels. piperlonguminine 13-15 H3 histone pseudogene 16 Homo sapiens 40-43 31686655-2 2019 It crystallizes from metacetamol-saturated 1:1 (v/v) water-ethanol solutions in a monoclinic structure (space group P21/n) and contains eight metacetamol and four water molecules per unit cell. 3-hydroxyacetanilide 21-32 H3 histone pseudogene 16 Homo sapiens 116-121 30521787-1 2019 Cabazitaxel as microtubule inhibitor and thymoquinone as HDAC inhibitor affects the important genes like p53, STAT3, Bax, BCL-2, p21 and down regulation of NF-kappaB are reported for potential activity against breast tumors. cabazitaxel 0-11 H3 histone pseudogene 16 Homo sapiens 129-132 30521787-1 2019 Cabazitaxel as microtubule inhibitor and thymoquinone as HDAC inhibitor affects the important genes like p53, STAT3, Bax, BCL-2, p21 and down regulation of NF-kappaB are reported for potential activity against breast tumors. thymoquinone 41-53 H3 histone pseudogene 16 Homo sapiens 129-132 31553341-5 2019 The Pt(ii) complexes could bind to and cleave DNA, while also inducing arrest of the cell cycle in S phase, leading to down-regulation of the levels of cyclin-dependent kinases and cyclin and up-regulation of the expression of p21. Platinum 4-10 H3 histone pseudogene 16 Homo sapiens 227-230 31446323-0 2019 Loading of some quinoxaline derivatives in poly (l-lactic) acid/Pluronic F-127 nanofibers enhances their anticancer efficiency and induces a p53 and p21 apoptotic-signaling pathway. Quinoxalines 16-27 H3 histone pseudogene 16 Homo sapiens 150-153 31446323-0 2019 Loading of some quinoxaline derivatives in poly (l-lactic) acid/Pluronic F-127 nanofibers enhances their anticancer efficiency and induces a p53 and p21 apoptotic-signaling pathway. poly(lactide) 43-63 H3 histone pseudogene 16 Homo sapiens 150-153 31446323-0 2019 Loading of some quinoxaline derivatives in poly (l-lactic) acid/Pluronic F-127 nanofibers enhances their anticancer efficiency and induces a p53 and p21 apoptotic-signaling pathway. Poloxamer 64-79 H3 histone pseudogene 16 Homo sapiens 150-153 31545472-10 2019 It was found that CdM downregulated H2O2-stimulated 8-hydroxydeoxyguanosine and gamma-H2AX levels and decreased the expression of the senescence-associated proteins p21 and p16. Water 36-40 H3 histone pseudogene 16 Homo sapiens 165-168 31001861-11 2019 The percentage of the S phase cells was evidently reduced by Nimotuzuma through regulating P21, Cyclin E1, and Cyclin D1. nimotuzuma 61-71 H3 histone pseudogene 16 Homo sapiens 91-94 31750234-7 2019 The present study highlighted the crucial role of RNase L in triggering apoptosis mechanism through the Caspase-3/ROCK-1/PARP/H2A.X+H2B/p21 axis during Act D treatment. Dactinomycin 152-157 H3 histone pseudogene 16 Homo sapiens 136-139 31339188-0 2019 CDK4/6 inhibitor protects chemerin-induced human granulosa-lutein cells from apoptosis by inhibiting the p53/p21 waf pathway. chemerin 26-34 H3 histone pseudogene 16 Homo sapiens 109-112 31339188-5 2019 Furthermore, we found that palbociclib suppressed chemerin-induced apoptotic protein expression, reversing the Bcl-2/Bax ratio and inhibiting the p53/p21 waf pathway. palbociclib 27-38 H3 histone pseudogene 16 Homo sapiens 150-153 31689825-0 2019 Polyphyllin I induces cell cycle arrest in prostate cancer cells via the upregulation of IL6 and P21 expression. polyphyllin I 0-13 H3 histone pseudogene 16 Homo sapiens 97-100 31689825-8 2019 Polyphyllin I induced cell cycle arrest by upregulating the expression of P21. polyphyllin I 0-13 H3 histone pseudogene 16 Homo sapiens 74-77 31689825-9 2019 Further studies showed that the upregulation of p21 expression induced by Polyphyllin I via the upregulation of IL6 expression. polyphyllin I 74-87 H3 histone pseudogene 16 Homo sapiens 48-51 31689825-10 2019 CONCLUSION: Polyphyllin I could induce cell cycle arrest in G0/G1 phase in prostate cancer cells by upregulating the expression of P21 and IL6. polyphyllin I 12-25 H3 histone pseudogene 16 Homo sapiens 131-134 31357283-4 2019 Herein, a functional nanosystem for in situ and real-time monitoring levels of p53 and p21 mRNA was constructed using reduced graphene oxide nanosheet assisted fluorescence probes. graphene oxide 126-140 H3 histone pseudogene 16 Homo sapiens 87-90 31671572-7 2019 These results indicate that ethanol-induced dysregulation of NRF2 coordinately regulates PCNA/CYCLIN-D1/p21 involving growth network, at least partially to set a stage for placental perturbations. Ethanol 28-35 H3 histone pseudogene 16 Homo sapiens 104-107 31565922-2 2019 In this paper, three conjugated quasilinear segments of 9,9-dimethyl-9H-fluorene, 9,9-dimethyl-2,7-diphenyl-9H-fluorene, and 2,6-diphenyldithieno[3,2-b:2",3"-d]thiophene are end-capped with two bis(4-methoxyphenyl)amino groups for structurally simple molecular semiconductors Z1, Z2, and Z3, which crystallize in the monoclinic P21/n, triclinic P1, and monoclinic C2/c space groups, respectively. Thiophenes 125-169 H3 histone pseudogene 16 Homo sapiens 328-347 31652983-7 2019 Finally, as oxidative stress-related signaling pathways can modulate the cell cycle through p53, we analyzed the expression of the p53 target gene p21 in BM cells, finding that it was significantly upregulated in patients with MDS and was significantly downregulated after DFX treatment. deferasirox 273-276 H3 histone pseudogene 16 Homo sapiens 147-150 31553596-2 2019 Here, a simple strategy of partial congener substitution is introduced to induce transformation of the known centrosymmetric K3Ga3Ge7Se20 (P21/c) to the new isostructural NCS species K3Ga3(Ge6.17Sn0.83)Se20 (1) and K3Ga3(Ge4.95Si2.05)Se20 (2) (Pc). gallium selenide 125-137 H3 histone pseudogene 16 Homo sapiens 139-144 31652494-4 2019 Copper sulfate also increased the levels of apoptosis, senescence, mitochondrial dysfunction, autophagy, ROS, and the expression of several stress proteins, including ATF3, c-Fos, DEC1 (differentiated embryonic chondrocyte gene 1), p21, p53, and HIF-1alpha (hypoxia-inducible factor 1 alpha). Copper Sulfate 0-14 H3 histone pseudogene 16 Homo sapiens 232-235 31637187-8 2019 Also, PTL increased Cyclin inhibition protein 1 (P21), Bcl-2-associated X protein (Bax), Cysteinyl aspartate specific proteinas-3 (Caspase-3) and Caspase-9 expression. parthenolide 6-9 H3 histone pseudogene 16 Homo sapiens 49-52 31559975-4 2019 (2,5-dmpz)0.5PbBr3 2((CH3)2SO) contained half a cation, which was completed by inversion symmetry, along with two dimethyl sulfoxide solvent molecules that crystallized in the monoclinic space group P21/c. methanesulfonamide 12-30 H3 histone pseudogene 16 Homo sapiens 199-204 31509399-4 2019 Zr(NaPO4)2 H2O crystallizes in the space group P21/c with cell parameters a = 8.7584(1) A, b = 5.3543(1) A, c = 18.1684(3) A, beta = 109.053 (1) , and Z = 4. Water 11-14 H3 histone pseudogene 16 Homo sapiens 47-50 31553596-2 2019 Here, a simple strategy of partial congener substitution is introduced to induce transformation of the known centrosymmetric K3Ga3Ge7Se20 (P21/c) to the new isostructural NCS species K3Ga3(Ge6.17Sn0.83)Se20 (1) and K3Ga3(Ge4.95Si2.05)Se20 (2) (Pc). Potassium 125-130 H3 histone pseudogene 16 Homo sapiens 139-144 31553596-2 2019 Here, a simple strategy of partial congener substitution is introduced to induce transformation of the known centrosymmetric K3Ga3Ge7Se20 (P21/c) to the new isostructural NCS species K3Ga3(Ge6.17Sn0.83)Se20 (1) and K3Ga3(Ge4.95Si2.05)Se20 (2) (Pc). Germanium 130-132 H3 histone pseudogene 16 Homo sapiens 139-144 31608167-11 2019 In addition, gene expression analysis revealed that MnIII complex exerts its antiproliferative effect via up-and down-regulation of p21 and cyclin D1, respectively, along with increased expression of Bax/Bcl-2 ratio, TNF-alpha, initiator caspase-8 and -10 and effector caspase-3 in MCF-7 and MDA-MB-231 cells. Manganese 52-57 H3 histone pseudogene 16 Homo sapiens 132-135 31553596-2 2019 Here, a simple strategy of partial congener substitution is introduced to induce transformation of the known centrosymmetric K3Ga3Ge7Se20 (P21/c) to the new isostructural NCS species K3Ga3(Ge6.17Sn0.83)Se20 (1) and K3Ga3(Ge4.95Si2.05)Se20 (2) (Pc). Tin 195-197 H3 histone pseudogene 16 Homo sapiens 139-144 31553596-2 2019 Here, a simple strategy of partial congener substitution is introduced to induce transformation of the known centrosymmetric K3Ga3Ge7Se20 (P21/c) to the new isostructural NCS species K3Ga3(Ge6.17Sn0.83)Se20 (1) and K3Ga3(Ge4.95Si2.05)Se20 (2) (Pc). Potassium 183-188 H3 histone pseudogene 16 Homo sapiens 139-144 31553596-2 2019 Here, a simple strategy of partial congener substitution is introduced to induce transformation of the known centrosymmetric K3Ga3Ge7Se20 (P21/c) to the new isostructural NCS species K3Ga3(Ge6.17Sn0.83)Se20 (1) and K3Ga3(Ge4.95Si2.05)Se20 (2) (Pc). Germanium 189-191 H3 histone pseudogene 16 Homo sapiens 139-144 31553596-2 2019 Here, a simple strategy of partial congener substitution is introduced to induce transformation of the known centrosymmetric K3Ga3Ge7Se20 (P21/c) to the new isostructural NCS species K3Ga3(Ge6.17Sn0.83)Se20 (1) and K3Ga3(Ge4.95Si2.05)Se20 (2) (Pc). Silicon 227-229 H3 histone pseudogene 16 Homo sapiens 139-144 31250942-4 2019 Doxorubicin (DXR) treatment induced senescence in 2 human breast cancer cell lines, MDA-MB-231 and BT-549, with the induction of gammaH2AX expression and increased expression of p21 or p16. Doxorubicin 0-11 H3 histone pseudogene 16 Homo sapiens 178-181 31284735-10 2019 Indeed, although WT MEF entered senescence accompanied by p21 increase, HMGB1 KO underwent apoptosis with p21 decrease by Dox treatment. Doxorubicin 122-125 H3 histone pseudogene 16 Homo sapiens 106-109 31607295-6 2019 Also, the treatment with 5 and 10 mumol/L of dehydrocostus lactone induced K562 cell apoptosis, the apoptotic rate of K562 cells was significantly higher than that the control group (P<0.05), and up-regulated the expression level of BAX and p21. dehydrocostus lactone 45-66 H3 histone pseudogene 16 Homo sapiens 241-244 31607295-8 2019 The study results also revealed that dehydrocostus lactone significantly inhibited the expression of BCR/ABL STAT3, STAT5, CyclinB1, CDK1 and BCL-2, and up-regulated the expression level of BAX and p21. dehydrocostus lactone 37-58 H3 histone pseudogene 16 Homo sapiens 198-201 31204039-5 2019 We also show the competence of the PCNA-Agarose column to purify non-PCNA binding proteins by fusing the PCNA-binding motif of human p21 as an affinity tag. Sepharose 40-47 H3 histone pseudogene 16 Homo sapiens 133-136 31478037-2 2019 The six newly discovered Si phases are in the space groups of Im3[combining macron]m, C2/c, I4/mcm, I4/mmm, P21/m, and P4/mbm, respectively. Silicon 25-27 H3 histone pseudogene 16 Homo sapiens 108-111 31288004-7 2019 beta-Cryptoxanthin treatment induced G0/G1 arrest, and reduced the expression of Cyclin E, Cyclin D1, cyclin-dependent kinases (CDK) of CDK4 and CDK6, and increased the expression of p53 and p21 in the two GC cells. Beta-Cryptoxanthin 0-18 H3 histone pseudogene 16 Homo sapiens 191-194 31460901-16 2019 Compared with matrine or acitretin group, the expression of p21 (P < 0.05, P < 0.05) and LC3II/I (P < 0.01, P < 0.05) in matrine plus acitretin group increased significantly and the expression of cyclin D1 (P < 0.01, P < 0.05) and p62 (P < 0.05, P < 0.05) was reduced significantly. matrine 14-21 H3 histone pseudogene 16 Homo sapiens 60-63 31460901-16 2019 Compared with matrine or acitretin group, the expression of p21 (P < 0.05, P < 0.05) and LC3II/I (P < 0.01, P < 0.05) in matrine plus acitretin group increased significantly and the expression of cyclin D1 (P < 0.01, P < 0.05) and p62 (P < 0.05, P < 0.05) was reduced significantly. Acitretin 25-34 H3 histone pseudogene 16 Homo sapiens 60-63 31460901-16 2019 Compared with matrine or acitretin group, the expression of p21 (P < 0.05, P < 0.05) and LC3II/I (P < 0.01, P < 0.05) in matrine plus acitretin group increased significantly and the expression of cyclin D1 (P < 0.01, P < 0.05) and p62 (P < 0.05, P < 0.05) was reduced significantly. matrine 121-128 H3 histone pseudogene 16 Homo sapiens 60-63 31460901-16 2019 Compared with matrine or acitretin group, the expression of p21 (P < 0.05, P < 0.05) and LC3II/I (P < 0.01, P < 0.05) in matrine plus acitretin group increased significantly and the expression of cyclin D1 (P < 0.01, P < 0.05) and p62 (P < 0.05, P < 0.05) was reduced significantly. Acitretin 134-143 H3 histone pseudogene 16 Homo sapiens 60-63 31325448-0 2019 The mTOR inhibitor everolimus overcomes CXCR4-mediated resistance to histone deacetylase inhibitor panobinostat through inhibition of p21 and mitotic regulators. Everolimus 19-29 H3 histone pseudogene 16 Homo sapiens 134-137 31325448-0 2019 The mTOR inhibitor everolimus overcomes CXCR4-mediated resistance to histone deacetylase inhibitor panobinostat through inhibition of p21 and mitotic regulators. Panobinostat 99-111 H3 histone pseudogene 16 Homo sapiens 134-137 31325448-9 2019 Whereas panobinostat increased the expression of the cell cycle inhibitor p21, co-treatment with everolimus abrogated the increase in p21 and synergistically downregulated the expression of DNA repair genes and mitotic checkpoint regulators. Everolimus 97-107 H3 histone pseudogene 16 Homo sapiens 134-137 31284735-7 2019 In senescent B16-F10, SK-MEL-24, and LS174T cells treated with Dox, p21 levels were increased by persistent HMGB1 expression. Doxorubicin 63-66 H3 histone pseudogene 16 Homo sapiens 68-71 31555380-7 2019 Compared with the NC group, the expression levels of PI3K, AKT, phosphorylated-AKT, P21 and MMP-2 and -9 were significantly altered in a dose dependent manner following treatment with GA (all P<0.05). gambogic acid 184-186 H3 histone pseudogene 16 Homo sapiens 84-87 31555380-8 2019 The results of the current study indicated that GA suppressed proliferation and dispersion of human colon cancer cells in a dose-dependent manner, possibly through a PI3K/AKT/P21/MMP-2/9-dependent pathway. gambogic acid 48-50 H3 histone pseudogene 16 Homo sapiens 175-184 31432844-4 2019 These are [Mn(IMHIm)2(MeOH)2]ClO4 H2O (1) and [Mn(IMHIm)2(MeOH)2]PF6 (2), which crystallize in the monoclinic P21/n and triclinic P1[combining macron] space groups, respectively. [mn(imhim)2(meoh)2]clo4 h2o 10-37 H3 histone pseudogene 16 Homo sapiens 110-113 31402371-2 2019 Our results show that these compounds crystallize in a three-dimensional perovskite-like monoclinic structure, space group P21/n, with two inequivalent TriBuMe+, one well-ordered and the second one showing distinct disorder. perovskite 73-83 H3 histone pseudogene 16 Homo sapiens 123-126 32123852-7 2019 Moreover, aspirin reduced p53 and p21 accumulation in DOX-treated human and mouse fibroblasts. Aspirin 10-17 H3 histone pseudogene 16 Homo sapiens 34-37 32123852-7 2019 Moreover, aspirin reduced p53 and p21 accumulation in DOX-treated human and mouse fibroblasts. Doxorubicin 54-57 H3 histone pseudogene 16 Homo sapiens 34-37 31250942-4 2019 Doxorubicin (DXR) treatment induced senescence in 2 human breast cancer cell lines, MDA-MB-231 and BT-549, with the induction of gammaH2AX expression and increased expression of p21 or p16. Doxorubicin 13-16 H3 histone pseudogene 16 Homo sapiens 178-181 31220525-10 2019 High glucose could induce VSMCs calcification/aging by increasing the expression of osteocalcin (OC) and p21 as well as the formation of mineralised nodules and SA-beta-gal positive cells. Glucose 5-12 H3 histone pseudogene 16 Homo sapiens 105-108 31495718-0 2019 Augmenting the therapeutic efficacy of adenosine against pancreatic cancer by switching the Akt/p21-dependent senescence to apoptosis. Adenosine 39-48 H3 histone pseudogene 16 Homo sapiens 96-99 31495718-5 2019 The Akt-p21 signalling axis was blocked by p21 silencing or by the Akt inhibitor GSK690693. GSK690693 81-90 H3 histone pseudogene 16 Homo sapiens 8-11 31495718-8 2019 Adenosine treatment in combination with the Akt inhibitor, GSK690693, or the silencing of p21 to interfere with the Akt-p21 axis can switch the senescence-to-apoptosis signal and alleviate drug resistance. Adenosine 0-9 H3 histone pseudogene 16 Homo sapiens 90-93 31495718-8 2019 Adenosine treatment in combination with the Akt inhibitor, GSK690693, or the silencing of p21 to interfere with the Akt-p21 axis can switch the senescence-to-apoptosis signal and alleviate drug resistance. Adenosine 0-9 H3 histone pseudogene 16 Homo sapiens 120-123 31322237-4 2019 Treatment with DP induced G2/M phase cell cycle arrest through upregulation of p21 and p27, and downregulation of cyclin B1 and Cdc2. dracorhodin 15-17 H3 histone pseudogene 16 Homo sapiens 79-82 31404297-8 2019 Further mechanistic studies, including western blotting and immunohistochemistry assays, revealed that combined MLN4924 and cisplatin treatment induced higher levels of DNA damage by increasing the accumulation of well-defined cullin-ring ligase substrates, such as chromatin licensing and DNA replication factor 1, origin recognition complex subunit 1, p21, p27 and phosphorylated IkappaBalpha. Cisplatin 124-133 H3 histone pseudogene 16 Homo sapiens 354-357 31470548-9 2019 Moreover, the BPA interaction with DOX on c-fos and p21 expression emphasize its cellular specificity and divergent effects. bisphenol A 14-17 H3 histone pseudogene 16 Homo sapiens 52-55 31894049-6 2019 S phase arrest induced by hispolon was associated with downregulation of cyclin B1, cyclin D1 and CDK4 while up-regulation of p21. hispolon 26-34 H3 histone pseudogene 16 Homo sapiens 126-129 31750822-13 2019 Conversely, the expression of P21 and P16 proteins in the TSA group were lower than those in the model group, and SIRT1 and p-eNOS/eNOS were higher in the TSA group than those in the model group. tanshinone 58-61 H3 histone pseudogene 16 Homo sapiens 30-33 31750822-13 2019 Conversely, the expression of P21 and P16 proteins in the TSA group were lower than those in the model group, and SIRT1 and p-eNOS/eNOS were higher in the TSA group than those in the model group. tanshinone 155-158 H3 histone pseudogene 16 Homo sapiens 30-33 31470629-8 2019 The effects of FUS were more potent than those of AFU, with FUS up-regulating p21 expression in a p53-dependent manner, as detected by Western blot analyses, likely the consequence of decreased ERK phosphorylation and increased p38 expression (both of which increase p21 stability). fusarubin 15-18 H3 histone pseudogene 16 Homo sapiens 78-81 31462222-9 2019 ARE induced cell death in G361 cells through the reactive oxygen species (ROS)-dependent regulation of p53 and p21 in G361 cells. Reactive Oxygen Species 49-72 H3 histone pseudogene 16 Homo sapiens 111-114 31462222-9 2019 ARE induced cell death in G361 cells through the reactive oxygen species (ROS)-dependent regulation of p53 and p21 in G361 cells. Reactive Oxygen Species 74-77 H3 histone pseudogene 16 Homo sapiens 111-114 31470548-9 2019 Moreover, the BPA interaction with DOX on c-fos and p21 expression emphasize its cellular specificity and divergent effects. Doxorubicin 35-38 H3 histone pseudogene 16 Homo sapiens 52-55 31470629-8 2019 The effects of FUS were more potent than those of AFU, with FUS up-regulating p21 expression in a p53-dependent manner, as detected by Western blot analyses, likely the consequence of decreased ERK phosphorylation and increased p38 expression (both of which increase p21 stability). fusarubin 15-18 H3 histone pseudogene 16 Homo sapiens 267-270 31304946-3 2019 The rubidium derivative crystallizes in an orthorhombic unit cell of the Pbcm space group in the structure which can be derived from ht-CrVO4, while CsSc(BH4)4 adopts a monoclinic (P21/c) unit cell which has monazite (CePO4) as a structural aristotype. Rubidium 4-12 H3 histone pseudogene 16 Homo sapiens 181-186 31470629-8 2019 The effects of FUS were more potent than those of AFU, with FUS up-regulating p21 expression in a p53-dependent manner, as detected by Western blot analyses, likely the consequence of decreased ERK phosphorylation and increased p38 expression (both of which increase p21 stability). anhydrofusarubin 50-53 H3 histone pseudogene 16 Homo sapiens 78-81 31470629-8 2019 The effects of FUS were more potent than those of AFU, with FUS up-regulating p21 expression in a p53-dependent manner, as detected by Western blot analyses, likely the consequence of decreased ERK phosphorylation and increased p38 expression (both of which increase p21 stability). fusarubin 60-63 H3 histone pseudogene 16 Homo sapiens 78-81 31470629-8 2019 The effects of FUS were more potent than those of AFU, with FUS up-regulating p21 expression in a p53-dependent manner, as detected by Western blot analyses, likely the consequence of decreased ERK phosphorylation and increased p38 expression (both of which increase p21 stability). fusarubin 60-63 H3 histone pseudogene 16 Homo sapiens 267-270 31299263-9 2019 Interestingly, anti-tumoral effects of CCL660 also in P53 mutant PDXs but with a functional p21 pathway were observed. ccl660 39-45 H3 histone pseudogene 16 Homo sapiens 92-95 31482012-6 2019 Interestingly, we also found that doxorubicin-induced p21 expression is activated by p53 in transcription-dependent manner, while camptothecin-induced p21 expression is p53-independent. Doxorubicin 34-45 H3 histone pseudogene 16 Homo sapiens 54-57 31482012-6 2019 Interestingly, we also found that doxorubicin-induced p21 expression is activated by p53 in transcription-dependent manner, while camptothecin-induced p21 expression is p53-independent. Camptothecin 130-142 H3 histone pseudogene 16 Homo sapiens 151-154 31393045-7 2019 We showed that CD enhanced the expression and nuclear translocation of Forkhead box O3 (FOXO3a) via upstream c-Jun N-terminal kinase, inducing the expression of FOXO3a and its target genes, including p21, p27, and Bim. cardamonin 15-17 H3 histone pseudogene 16 Homo sapiens 200-203 31355637-3 2019 A2Mg2TeB2O10 (A = Pb, Ba) can be regarded as the cosubstitution of Na2RE2TeB2O10 (RE = Y, Dy-Lu), which crystallize in a different space group, P21/c. na2re2teb2o10 67-80 H3 histone pseudogene 16 Homo sapiens 144-149 31365247-3 2019 In2(SO4)(TeO3)(OH)2(H2O) crystallized in centrosymmetric (CS) space group P21/n, while In3(SO4)(TeO3)2F3(H2O) formed a non-centrosymmetric (NCS) and chiral space group P212121. in2(so4)(teo3)(oh)2 0-19 H3 histone pseudogene 16 Homo sapiens 74-77 31365247-3 2019 In2(SO4)(TeO3)(OH)2(H2O) crystallized in centrosymmetric (CS) space group P21/n, while In3(SO4)(TeO3)2F3(H2O) formed a non-centrosymmetric (NCS) and chiral space group P212121. Water 20-23 H3 histone pseudogene 16 Homo sapiens 74-77 31406162-7 2019 Danazol also upregulated the cell cycle inhibitor p21 in MDR cancer cells. Danazol 0-7 H3 histone pseudogene 16 Homo sapiens 50-53 31380801-3 2019 However, DCV[3] and DCV[4] crystallized in the centrosymmetric space group P21/c which excludes their application as nonlinear optical materials in the crystalline state. daclatasvir 20-23 H3 histone pseudogene 16 Homo sapiens 75-78 31075264-0 2019 Aflatoxin B1 induces S phase arrest by upregulating the expression of p21 via MYC, PLK1 and PLD1. Aflatoxin B1 0-12 H3 histone pseudogene 16 Homo sapiens 70-73 31075264-10 2019 In summary, AFB1 markedly induces kidney damage and strongly induces S phase arrest by upregulating the expression of p21 via PLK1, PLD1 and MYC, which represents a noval mechanism of the renal toxicity of AFB1. Aflatoxin B1 12-16 H3 histone pseudogene 16 Homo sapiens 118-121 31075264-10 2019 In summary, AFB1 markedly induces kidney damage and strongly induces S phase arrest by upregulating the expression of p21 via PLK1, PLD1 and MYC, which represents a noval mechanism of the renal toxicity of AFB1. Aflatoxin B1 206-210 H3 histone pseudogene 16 Homo sapiens 118-121 31075264-6 2019 Upstream of p21, three negative regulators, PLK1, MYC, and PLD1, were significantly downregulated under AFB1 treatment. Aflatoxin B1 104-108 H3 histone pseudogene 16 Homo sapiens 12-15 31257531-5 2019 As determined by reverse transcription-quantitative PCR and western blotting, Survivin and p21 expression levels were significantly affected by SP treatment, suggesting that SP treatment suppressed cell proliferation in these lung cancer cell lines. sodium propionate 144-146 H3 histone pseudogene 16 Homo sapiens 91-94 31383247-6 2019 Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, gamma-H2AX, P53, and P21 involved in DNA damage response. artenimol 57-60 H3 histone pseudogene 16 Homo sapiens 179-182 30155717-10 2019 Importantly, the hexane partition derived from the crude extract presented cytotoxic effect both in vitro and in vivo, and initiates cell responses, such as DNA damage (H2AX activity), apoptosis via intrinsic pathway (cleavage of caspase-9, caspase-3, poly (ADP-ribose) polymerase (PARP) and mitochondrial membrane depolarization) and decreased p21 expression by ubiquitin proteasome pathway. Hexanes 17-23 H3 histone pseudogene 16 Homo sapiens 345-348 31257485-8 2019 Compared with the control group, the expression levels of p21 and p27 decreased under HG conditions, but were reversed by betaine. Betaine 122-129 H3 histone pseudogene 16 Homo sapiens 58-61 30940656-0 2019 Auranofin Protects Intestine against Radiation Injury by Modulating p53/p21 Pathway and Radiosensitizes Human Colon Tumor. Auranofin 0-9 H3 histone pseudogene 16 Homo sapiens 72-75 30940656-9 2019 RESULTS: Both in the mouse model of intestinal injury and in the human nonmalignant colon organoid culture, auranofin pretreatment prevented radiation toxicity and improved survival with the activation of p53/p21-mediated reversible cell-cycle arrest. Auranofin 108-117 H3 histone pseudogene 16 Homo sapiens 209-212 31257531-5 2019 As determined by reverse transcription-quantitative PCR and western blotting, Survivin and p21 expression levels were significantly affected by SP treatment, suggesting that SP treatment suppressed cell proliferation in these lung cancer cell lines. sodium propionate 174-176 H3 histone pseudogene 16 Homo sapiens 91-94 31257531-6 2019 Thus, it was proposed that the SP-mediated regulation of Survivin and p21 in lung cancer may be applicable to lung cancer therapy. sodium propionate 31-33 H3 histone pseudogene 16 Homo sapiens 70-73 31257544-11 2019 Cell cycle arrest in the G0/G1 phase was induced by siGCF2, which was accompanied by changes in the levels of cyclin E, CDK2 and p21. sigcf2 52-58 H3 histone pseudogene 16 Homo sapiens 129-132 31366086-10 2019 Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner. Doxorubicin 58-69 H3 histone pseudogene 16 Homo sapiens 128-131 31423185-8 2019 Consistent with the observed growth inhibitory effects, BPs also inhibited the cell cycle by promoting G1 phase arrest and the downregulation of cyclin D1 and upregulation of p21. Diphosphonates 56-59 H3 histone pseudogene 16 Homo sapiens 175-178 31423230-4 2019 The results of the present study indicate that pterostilbene significantly reduced cell viability and induced S phase arrest, and that treatment with pterostilbene was associated with the downregulation of cyclin A and cyclin E, as with the upregulation of p21 and p27 expression in H520 cells. pterostilbene 150-163 H3 histone pseudogene 16 Homo sapiens 257-260 31366086-10 2019 Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner. Fluorouracil 71-85 H3 histone pseudogene 16 Homo sapiens 128-131 31358785-5 2019 Ormeloxifene efficiently attenuated tumorigenic and metastatic properties of cervical cancer cells via arresting cell cycle at G1-S transition, inducing apoptosis, decreasing PI3K and Akt phosphorylation, mitochondrial membrane potential, and modulating G1-S transition related proteins (p21, cyclin E and Cdk2). ormeloxifene 0-12 H3 histone pseudogene 16 Homo sapiens 288-291 31336757-7 2019 Further investigation revealed that ailanthone promoted the expression of p21 and suppressed the expression of cyclin E in B16 cells or cyclin B in A375 cells through the PI3K-Akt signaling pathway. ailanthone 36-46 H3 histone pseudogene 16 Homo sapiens 74-77 31336690-11 2019 Flavopereirine also significantly repressed CRC cell xenograft growth in vivo by upregulating P53 and P21 and inducing apoptosis. flavopereirine 0-14 H3 histone pseudogene 16 Homo sapiens 102-105 31336690-12 2019 In conclusion, flavopereirine-mediated growth suppression in CRC cells depended on the P53-P21, but not the JAKs-STATs-c-Myc signaling pathway. flavopereirine 15-29 H3 histone pseudogene 16 Homo sapiens 91-94 31331008-2 2019 The current work investigated the influence of melatonin on the oncostatic activity of EGCG in two cancer cell lines, wherein melatonin induced an opposite response of p21. epigallocatechin gallate 87-91 H3 histone pseudogene 16 Homo sapiens 168-171 31331008-3 2019 In human tongue cancer TCA8113 cells, melatonin-induced p21 and EGCG-mediated formation of quinoproteins were positively associated with the oncostatic effects of melatonin and EGCG. Melatonin 38-47 H3 histone pseudogene 16 Homo sapiens 56-59 31331008-3 2019 In human tongue cancer TCA8113 cells, melatonin-induced p21 and EGCG-mediated formation of quinoproteins were positively associated with the oncostatic effects of melatonin and EGCG. Melatonin 163-172 H3 histone pseudogene 16 Homo sapiens 56-59 31331008-3 2019 In human tongue cancer TCA8113 cells, melatonin-induced p21 and EGCG-mediated formation of quinoproteins were positively associated with the oncostatic effects of melatonin and EGCG. epigallocatechin gallate 177-181 H3 histone pseudogene 16 Homo sapiens 56-59 31331008-4 2019 Melatonin-stimulated an increase in p21 which was correlated with a pronounced nuclear translocation of thioredoxin 1 and thioredoxin reductase 1, both of which are known to induce p21 via promoting p53 trans-activation. Melatonin 0-9 H3 histone pseudogene 16 Homo sapiens 36-39 31331008-4 2019 Melatonin-stimulated an increase in p21 which was correlated with a pronounced nuclear translocation of thioredoxin 1 and thioredoxin reductase 1, both of which are known to induce p21 via promoting p53 trans-activation. Melatonin 0-9 H3 histone pseudogene 16 Homo sapiens 181-184 31331008-8 2019 In human hepatocellular carcinoma HepG2 cells, melatonin suppressed p21 along with the induction of pro-survival proteins, PI3K and COX-2. Melatonin 47-56 H3 histone pseudogene 16 Homo sapiens 68-71 31331008-9 2019 However, EGCG prevented against melatonin-induced PI3K and COX-2, and melatonin probably sensitized HepG2 cells to EGCG cytotoxicity via down-regulating p21, Moreover, COX-2 and HO-1 were significantly reduced only by the co-treatment, and melatonin aided EGCG to achieve an increased inhibition on Bcl2 and NFkappaB. Melatonin 70-79 H3 histone pseudogene 16 Homo sapiens 153-156 31331008-9 2019 However, EGCG prevented against melatonin-induced PI3K and COX-2, and melatonin probably sensitized HepG2 cells to EGCG cytotoxicity via down-regulating p21, Moreover, COX-2 and HO-1 were significantly reduced only by the co-treatment, and melatonin aided EGCG to achieve an increased inhibition on Bcl2 and NFkappaB. Melatonin 70-79 H3 histone pseudogene 16 Homo sapiens 153-156 31331008-12 2019 Overall, the results gathered from these two cancer cell lines with a divergent p21 response to melatonin show that the various oncostatic activities of melatonin and EGCG together are more robust than each agent alone, suggesting that they may be useful partners in fighting cancer. Melatonin 96-105 H3 histone pseudogene 16 Homo sapiens 80-83 31331008-12 2019 Overall, the results gathered from these two cancer cell lines with a divergent p21 response to melatonin show that the various oncostatic activities of melatonin and EGCG together are more robust than each agent alone, suggesting that they may be useful partners in fighting cancer. Melatonin 153-162 H3 histone pseudogene 16 Homo sapiens 80-83 31331008-12 2019 Overall, the results gathered from these two cancer cell lines with a divergent p21 response to melatonin show that the various oncostatic activities of melatonin and EGCG together are more robust than each agent alone, suggesting that they may be useful partners in fighting cancer. epigallocatechin gallate 167-171 H3 histone pseudogene 16 Homo sapiens 80-83 31109646-7 2019 Furthermore, H2O2 triggers p53 activation and promotes p21 expression, indicating a role for the p53/p21 signaling pathway in oxidative stress-induced senescence in BCSCs. Hydrogen Peroxide 13-17 H3 histone pseudogene 16 Homo sapiens 55-58 31417778-1 2019 The title compound, 2-(methyl-amino)-cyclo-hepta-2,4,6-trien-1-one, C8H9NO, crystallizes in the monoclinic space group P21/c, with three independent mol-ecules in the asymmetric unit. 2-(methyl-amino)-cyclo-hepta-2,4,6-trien-1-one 20-66 H3 histone pseudogene 16 Homo sapiens 119-124 31417778-1 2019 The title compound, 2-(methyl-amino)-cyclo-hepta-2,4,6-trien-1-one, C8H9NO, crystallizes in the monoclinic space group P21/c, with three independent mol-ecules in the asymmetric unit. 2-methyl-3-phenyloxaziridine 68-74 H3 histone pseudogene 16 Homo sapiens 119-124 31292765-0 2019 A Tangeretin Derivative Inhibits the Growth of Human Prostate Cancer LNCaP Cells by Epigenetically Restoring p21 Gene Expression and Inhibiting Cancer Stem-like Cell Proliferation. tangeretin 2-12 H3 histone pseudogene 16 Homo sapiens 109-112 31109646-7 2019 Furthermore, H2O2 triggers p53 activation and promotes p21 expression, indicating a role for the p53/p21 signaling pathway in oxidative stress-induced senescence in BCSCs. Hydrogen Peroxide 13-17 H3 histone pseudogene 16 Homo sapiens 101-104 31308755-9 2019 Further, UC2288, an inhibitor of p21, was used to decrease the level of p21, and flow cytometry was used to detect cell cycle. UC2288 9-15 H3 histone pseudogene 16 Homo sapiens 33-36 31219114-1 2019 A new promising nonlinear optical crystal C25H25NO4S2 (HDB-T, P21 space group) exhibits significant macroscopic second-order optical nonlinearity about 1.5 times larger than that of the benchmark OH1 crystal benefiting from optimized orientated polar HDB cations. C25H25NO4S2 42-53 H3 histone pseudogene 16 Homo sapiens 62-65 31308755-9 2019 Further, UC2288, an inhibitor of p21, was used to decrease the level of p21, and flow cytometry was used to detect cell cycle. UC2288 9-15 H3 histone pseudogene 16 Homo sapiens 72-75 30508396-5 2019 Fetal ASM exposed to 40% O2 for 7 days exhibited elevated concentrations of senescence-associated markers, including beta-galactosidase; cell cycle checkpoint proteins p16, p21, and p-p53; and the DNA damage marker p-gammaH2A.X (phosphorylated gamma-histone family member X). Oxygen 25-27 H3 histone pseudogene 16 Homo sapiens 173-176 30508396-6 2019 The combination of dasatinib and quercetin, compounds known to eliminate senescent cells (senolytics), reduced the number of hyperoxia-exposed beta-galactosidase-, p21-, p16-, and p-gammaH2A.X-positive ASM cells. Dasatinib 19-28 H3 histone pseudogene 16 Homo sapiens 164-167 30508396-6 2019 The combination of dasatinib and quercetin, compounds known to eliminate senescent cells (senolytics), reduced the number of hyperoxia-exposed beta-galactosidase-, p21-, p16-, and p-gammaH2A.X-positive ASM cells. Quercetin 33-42 H3 histone pseudogene 16 Homo sapiens 164-167 30608861-6 2019 Exposing human lung fibroblasts to 150 muM hydrogen peroxide (H2O2) resulted in increased senescence-associated beta-galactosidase content and expression of p21 and IL-6, all of which are features of senescence. Hydrogen Peroxide 43-60 H3 histone pseudogene 16 Homo sapiens 157-160 30608861-6 2019 Exposing human lung fibroblasts to 150 muM hydrogen peroxide (H2O2) resulted in increased senescence-associated beta-galactosidase content and expression of p21 and IL-6, all of which are features of senescence. Hydrogen Peroxide 62-66 H3 histone pseudogene 16 Homo sapiens 157-160 30608861-9 2019 Targeting STAT3 activity using the small-molecule inhibitor STA-21 attenuated IL-6 production, reduced p21 levels, decreased senescence-associated beta-galactosidase accumulation, and restored normal mitochondrial function. STA-21 60-66 H3 histone pseudogene 16 Homo sapiens 103-106 31022596-6 2019 RESULTS: Sal-B (10 muM) treatment significantly ameliorated LPS injury to MH7 A cells, as cell viability was increased, expression of p53 and p21 was repressed, apoptosis was inhibited, and the release of MCP-1, IL-6 and TNF-alpha was reduced. salvianolic acid B 9-14 H3 histone pseudogene 16 Homo sapiens 142-145 30928633-5 2019 Mechanistically, 8-AHN induced p53 expression and enhanced transcriptional activity, subsequently elevating the expression of p53 target genes, including p21, FAS, and BAX, and then increased the level of activated caspase-3 and decreased the level of cyclin B and cyclin A. 8-acetonyldihydronitidine 17-22 H3 histone pseudogene 16 Homo sapiens 154-157 31078367-12 2019 TYL also decreased levels of p21 and p27 proteins, although at later time points than observed for cyclin D1. tylophorine 0-3 H3 histone pseudogene 16 Homo sapiens 29-32 30514066-8 2019 AZD6738 significantly increased apoptosis, G2/M arrest and p21, and decreased CDC2. ceralasertib 0-7 H3 histone pseudogene 16 Homo sapiens 59-62 31140859-0 2019 EZH2 Confers Sensitivity of Breast Cancer Cells to Taxol by Attenuating p21 Expression Epigenetically. Paclitaxel 51-56 H3 histone pseudogene 16 Homo sapiens 72-75 31140859-6 2019 Meanwhile, p21, the inhibitor of cell cycle entry, interference upregulated, while overexpression downregulated apoptosis induced by taxol. Paclitaxel 133-138 H3 histone pseudogene 16 Homo sapiens 11-14 31140859-8 2019 Collectively, EZH2 attenuates chemoresistance of breast cancer cells to taxol by dampening p21 epigenetically. Paclitaxel 72-77 H3 histone pseudogene 16 Homo sapiens 91-94 30478995-3 2019 Although the expression of p21 and growth arrest and DNA damage inducible alpha (GADD45a), which are important targets of p53, was downregulated in CtIP-deficient HCT116 cells, p53 deletion did not affect G2/M arrest after Eto treatment. Etoposide 223-226 H3 histone pseudogene 16 Homo sapiens 27-30 31004593-0 2019 Long non-coding RNA-p21 regulates MPP+-induced neuronal injury by targeting miR-625 and derepressing TRPM2 in SH-SY5Y cells. mangion-purified polysaccharide (Candida albicans) 34-38 H3 histone pseudogene 16 Homo sapiens 20-23 31004593-4 2019 Here, the results showed that lnc-p21 was highly expressed in human neuroblastoma SH-SY5Y cells treated with MPP+. mangion-purified polysaccharide (Candida albicans) 109-113 H3 histone pseudogene 16 Homo sapiens 34-37 31004593-6 2019 Furthermore, knockdown of lnc-p21 mitigated MPP+-induced oxidative stress and neuroinflammation, as evidenced by the decrease in ROS generation, increase in SOD activity and decline in TNF-alpha, IL-1beta and IL-6 levels. mangion-purified polysaccharide (Candida albicans) 44-48 H3 histone pseudogene 16 Homo sapiens 30-33 31004593-6 2019 Furthermore, knockdown of lnc-p21 mitigated MPP+-induced oxidative stress and neuroinflammation, as evidenced by the decrease in ROS generation, increase in SOD activity and decline in TNF-alpha, IL-1beta and IL-6 levels. ros 129-132 H3 histone pseudogene 16 Homo sapiens 30-33 31004593-9 2019 lnc-p21 overturned the inhibitory effect of miR-625 on MPP+-induced neuronal injury in SH-SY5Y cells. mangion-purified polysaccharide (Candida albicans) 55-59 H3 histone pseudogene 16 Homo sapiens 4-7 31004593-10 2019 Additionally, lnc-p21 positively regulated TRPM2 expression by targeting miR-625, and knockdown of TRPM2 inhibited MPP+-induced neuronal injury. mangion-purified polysaccharide (Candida albicans) 115-119 H3 histone pseudogene 16 Homo sapiens 18-21 31004593-11 2019 Overall, our study identified a new lnc-p21-miR-625-TRPM2 regulatory network that lnc-p21 regulated MPP + -induced neuronal injury by sponging miR-625 and upregulating TRPM2 in SH-SY5Y cells, which provide a better understanding for the pathogenesis of PD. mangion-purified polysaccharide (Candida albicans) 100-105 H3 histone pseudogene 16 Homo sapiens 40-43 31004593-11 2019 Overall, our study identified a new lnc-p21-miR-625-TRPM2 regulatory network that lnc-p21 regulated MPP + -induced neuronal injury by sponging miR-625 and upregulating TRPM2 in SH-SY5Y cells, which provide a better understanding for the pathogenesis of PD. mangion-purified polysaccharide (Candida albicans) 100-105 H3 histone pseudogene 16 Homo sapiens 86-89 31379409-8 2019 In addition, sublethal treatment with PAM induced phosphorylation of ATM kinase, accumulation of p53 protein, and expression of p21 and GADD45A, which are known p53 target genes, in a Zn2+-dependent manner. Zinc 184-188 H3 histone pseudogene 16 Homo sapiens 128-131 31680075-12 2019 Methadone hydrochloride induced apoptosis in HL-60 cells involved upregulation of Bid and caspase-8 expression and downregulation of Bcl-2, p21 and survivin expression. Methadone 0-23 H3 histone pseudogene 16 Homo sapiens 140-143 31078367-14 2019 Comparable time-dependent downregulation of cyclin D1, p21 and p27 in TYL- or CHX-treated cells, together with decreased protein synthesis observed in the Click-iT assay, suggests that TYL is a protein synthesis inhibitor. tylophorine 70-73 H3 histone pseudogene 16 Homo sapiens 55-58 31078367-14 2019 Comparable time-dependent downregulation of cyclin D1, p21 and p27 in TYL- or CHX-treated cells, together with decreased protein synthesis observed in the Click-iT assay, suggests that TYL is a protein synthesis inhibitor. tylophorine 185-188 H3 histone pseudogene 16 Homo sapiens 55-58 31181622-5 2019 The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins. Albendazole 68-79 H3 histone pseudogene 16 Homo sapiens 30-33 31189930-0 2019 LncRNA-p21 alters the antiandrogen enzalutamide-induced prostate cancer neuroendocrine differentiation via modulating the EZH2/STAT3 signaling. enzalutamide 35-47 H3 histone pseudogene 16 Homo sapiens 7-10 31117426-3 2019 The composition and structure of the oxide has been determined by powder X-ray diffraction, powder neutron diffraction, and transmission electron microscopy to be monoclinic with the space group P21/ n and with cationic ordering between the ions in the B and B" sites. Oxides 37-42 H3 histone pseudogene 16 Homo sapiens 195-198 31181622-5 2019 The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins. Albendazole 68-79 H3 histone pseudogene 16 Homo sapiens 131-134 31181622-5 2019 The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins. Fenbendazole 84-96 H3 histone pseudogene 16 Homo sapiens 30-33 31181622-5 2019 The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins. Fenbendazole 84-96 H3 histone pseudogene 16 Homo sapiens 131-134 31120902-8 2019 Exposure to G418 and mefloquine increased p53 phosphorylation at Ser15 and P21 transcript levels following DNA damage, indicating p53 produced via readthrough was functional. antibiotic G 418 12-16 H3 histone pseudogene 16 Homo sapiens 75-78 30927408-0 2019 Dexamethasone induces primary amnion epithelial cell senescence through telomere-P21 associated pathway . Dexamethasone 0-13 H3 histone pseudogene 16 Homo sapiens 81-84 30927408-7 2019 However, Dex caused dependent telomere length reduction and p38MAPK-independent but p21-dependent (confirmed by treatment with p21 inhibitor UC2288). Dexamethasone 9-12 H3 histone pseudogene 16 Homo sapiens 127-130 30927408-7 2019 However, Dex caused dependent telomere length reduction and p38MAPK-independent but p21-dependent (confirmed by treatment with p21 inhibitor UC2288). UC2288 141-147 H3 histone pseudogene 16 Homo sapiens 127-130 31089945-0 2019 Role of tea polyphenols in delaying hyperglycemia-induced senescence in human glomerular mesangial cells via miR-126/Akt-p53-p21 pathways. Polyphenols 12-23 H3 histone pseudogene 16 Homo sapiens 125-128 31004883-8 2019 Flow cytometry analysis revealed that PAB caused an obvious cell cycle arrest in G2/M phase and induced apoptosis with the induction of p21, Bax, cleaved-caspase-3, and cleaved-PARP in human HepG2 and SK-Hep-1 cells. pseudolaric acid B 38-41 H3 histone pseudogene 16 Homo sapiens 136-139 31391983-1 2019 The title binuclear CoIII complex, [Co2(C9H8BrNOS)2(C18H16Br2N2O2S2)] C3H7NO, with a Schiff base ligand formed in situ from cyste-amine (2-amino-ethane-thiol) and 5-bromo-salicyl-aldehyde crystallizes in the space group P21. co2(c9h8brnos)2(c18h16br2n2o2s2)] c3h7no 36-76 H3 histone pseudogene 16 Homo sapiens 220-223 31391983-1 2019 The title binuclear CoIII complex, [Co2(C9H8BrNOS)2(C18H16Br2N2O2S2)] C3H7NO, with a Schiff base ligand formed in situ from cyste-amine (2-amino-ethane-thiol) and 5-bromo-salicyl-aldehyde crystallizes in the space group P21. Schiff Bases 85-96 H3 histone pseudogene 16 Homo sapiens 220-223 31223423-7 2019 We found that MHY2233 increased the expression of SIRT1, and its deacetylase activity thereby decreased expression of the cellular senescence biomarkers, p53, p16, and p21. mhy2233 14-21 H3 histone pseudogene 16 Homo sapiens 168-171 31089945-4 2019 RESULTS: High glucose led to premature senescence of HGMCs, as evident from the increase in the percentage of SA-beta-gal-positive cells, decrease in telomere length, cell cycle arrest at G1 phase,decrease in the expression of miR-126 and p-Akt and increase in the expression of p53, p21 and Rb proteins in the HG group. Glucose 14-21 H3 histone pseudogene 16 Homo sapiens 284-287 31089945-6 2019 CONCLUSIONS: High glucose induces the senescence of HGMCs in vitro via the miR-126 and Akt-p53-p21 signaling pathways. Glucose 18-25 H3 histone pseudogene 16 Homo sapiens 95-98 31002342-9 2019 Mechanistically, MLN4924 enhanced the antitumor activity of sorafenib in HCC cells via upregulation of cullin-RING E3 ubiquitin ligase (CRL)/Skp1-Cullin1-F box (SCF) E3 ubiquitin ligase substrates p21, p27, Deptor and IkappaBalpha. Sorafenib 60-69 H3 histone pseudogene 16 Homo sapiens 197-200 31120902-8 2019 Exposure to G418 and mefloquine increased p53 phosphorylation at Ser15 and P21 transcript levels following DNA damage, indicating p53 produced via readthrough was functional. Mefloquine 21-31 H3 histone pseudogene 16 Homo sapiens 75-78 31360396-11 2019 Octaphyrin 15 crystallizes in the P21/c space group and exclusively isomer A was formed in the reaction. octaphyrin 15 0-13 H3 histone pseudogene 16 Homo sapiens 34-39 30991803-9 2019 For this reason, in the last set of calculations carried out for p21 N-ras Gln 61 mutants, only the active site structural conformations obtained through hybrid MD are considered. Glutamine 75-78 H3 histone pseudogene 16 Homo sapiens 65-68 31011729-2 2019 A symmetric di-Ni rotaxane crystallizes in the monoclinic P21/c space group with one rotaxane cation and four PF6- counterions in the asymmetric part of the unit cell. di-ni rotaxane 12-26 H3 histone pseudogene 16 Homo sapiens 58-63 31011729-2 2019 A symmetric di-Ni rotaxane crystallizes in the monoclinic P21/c space group with one rotaxane cation and four PF6- counterions in the asymmetric part of the unit cell. Rotaxanes 18-26 H3 histone pseudogene 16 Homo sapiens 58-63 31489252-9 2019 Of note, we found that metformin treatment of HeLa cells increased the levels of p21 and p27 (which are AMPK-dependent cell cycle inhibitors), leading to increased cell cycle arrest and apoptosis in HeLa cells compared to untreated cells. Metformin 23-32 H3 histone pseudogene 16 Homo sapiens 81-84 30724592-11 2019 Further, RG7112 restores p53 and p21 protein levels in IMR5 and LAN-5 in a dose-dependent manner. lan-5 64-69 H3 histone pseudogene 16 Homo sapiens 33-36 31062707-2 2019 The pseudo-hexagonal phase NaZnAl(PO4)2 crystallizes in the monoclinic space group P21/c. naznal(po4)2 27-39 H3 histone pseudogene 16 Homo sapiens 83-88 31062711-6 2019 While the tetrahydrate form of IVA-HCl crystallized in the orthorhombic space group P212121, the new form (hemihydrate) was solved in the monoclinic space group P21. iva-hcl 31-38 H3 histone pseudogene 16 Homo sapiens 84-87 30831390-6 2019 These results revealed that L-Ru exerted a strong inhibitory effect on the cells proliferation,G0/G1-arrest, accompanied with upregulation of p53, p21, p15, cleaved Poly (ADP-ribose) polymerase (PARP) protein and downregulation of cell cycle markers. l-ru 28-32 H3 histone pseudogene 16 Homo sapiens 147-150 31035650-5 2019 The citrate-induced increased levels of cyclin B1 and G2/M phase arrest were suppressed by the caspase-3 inhibitor Ac-DEVD-CMK and caspase-3 cleavage of mutant p21 (D112N). Citric Acid 4-11 H3 histone pseudogene 16 Homo sapiens 160-163 30742942-3 2019 In this study, we found that norcantharidin (NCTD) effectively induced cell senescence and cell cycle arrest in TNBC in vitro, which was accompanied by a decline in phosphorylated Akt and ERK1/2 and a rise in p21 and p16. norcantharidin 29-43 H3 histone pseudogene 16 Homo sapiens 209-212 31018506-11 2019 Activation of the key regulators p53 and p21 inhibited the cyclin-dependent kinases Cdk2 and Cdk4, suggesting that p53 and p21 activation in GO-PtNP-treated cells caused genotoxic stress and apoptosis. (4-toluoyl-3-nitro)piperazine 144-148 H3 histone pseudogene 16 Homo sapiens 41-44 31022952-2 2019 Here, the roles of RPL5 and RPL11 were investigated in association with p53/p21 signaling in the antitumor effect of puromycin mainly in HCT116 and H1299 cancer cells. Puromycin 117-126 H3 histone pseudogene 16 Homo sapiens 76-79 31018506-11 2019 Activation of the key regulators p53 and p21 inhibited the cyclin-dependent kinases Cdk2 and Cdk4, suggesting that p53 and p21 activation in GO-PtNP-treated cells caused genotoxic stress and apoptosis. (4-toluoyl-3-nitro)piperazine 144-148 H3 histone pseudogene 16 Homo sapiens 123-126 31097925-0 2019 Coelomic Fluid of Lumbricus rubellus Synergistically Enhances Cytotoxic Effect of 5-Fluorouracil through Modulation of Focal Adhesion Kinase and p21 in HT-29 Cancer Cell Line. Fluorouracil 82-96 H3 histone pseudogene 16 Homo sapiens 145-148 31003485-0 2019 Flexicaulin A, An ent-Kaurane Diterpenoid, Activates p21 and Inhibits the Proliferation of Colorectal Carcinoma Cells through a Non-Apoptotic Mechanism. Flexicaulin A 0-13 H3 histone pseudogene 16 Homo sapiens 53-56 31097925-3 2019 This study aims to investigate whether the combination of CFL and 5-fluorouracil could reduce FAK protein level and iCa2+ and enhance p21 level. Fluorouracil 66-80 H3 histone pseudogene 16 Homo sapiens 134-137 31097925-9 2019 Combination of CFL and 5-fluorouracil significantly decreased FAK expression (p<0.05), iCa2+ (p<0.05), and increased p21 expression (p<0.05) in HT-29 cells. Fluorouracil 23-37 H3 histone pseudogene 16 Homo sapiens 123-126 30939155-0 2019 Regulatory mechanisms of fluvastatin and lovastatin for the p21 induction in human cervical cancer HeLa cells. Fluvastatin 25-36 H3 histone pseudogene 16 Homo sapiens 60-63 30892319-3 2019 The compound [Pt(3-Me-5-(3,5-tBu2C6H3)-1,2-C3HTe(NO))4](BF4)2 crystallizes in the P21/C space group featuring a square planar complex in the lattice. pt(3-me-5-(3,5-tbu2c6h3)-1,2-c3hte 14-48 H3 histone pseudogene 16 Homo sapiens 82-87 30892319-3 2019 The compound [Pt(3-Me-5-(3,5-tBu2C6H3)-1,2-C3HTe(NO))4](BF4)2 crystallizes in the P21/C space group featuring a square planar complex in the lattice. no))4](bf4)2 49-61 H3 histone pseudogene 16 Homo sapiens 82-87 30890645-9 2019 In addition, dosing of TPPU to pregnant mothers from E5 to P21 could prevent cognitive deficits, and social interaction deficits and PV immunoreactivity in the medial prefrontal cortex of juvenile offspring after MIA. TPPU 23-27 H3 histone pseudogene 16 Homo sapiens 59-62 31183037-4 2019 The structure, which crystallizes in the monoclinic space group P21/m, consists of positively charged {Zn2Co(CN)6}+ DMC layers linked through acetate groups and presents a new layered structure to the family of double metal cyanides. zn2co(cn)6} 103-114 H3 histone pseudogene 16 Homo sapiens 64-67 31183037-4 2019 The structure, which crystallizes in the monoclinic space group P21/m, consists of positively charged {Zn2Co(CN)6}+ DMC layers linked through acetate groups and presents a new layered structure to the family of double metal cyanides. dmc 116-119 H3 histone pseudogene 16 Homo sapiens 64-67 30939155-0 2019 Regulatory mechanisms of fluvastatin and lovastatin for the p21 induction in human cervical cancer HeLa cells. Lovastatin 41-51 H3 histone pseudogene 16 Homo sapiens 60-63 30939155-5 2019 Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells. Fluvastatin 33-44 H3 histone pseudogene 16 Homo sapiens 302-305 30939155-5 2019 Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells. Lovastatin 49-59 H3 histone pseudogene 16 Homo sapiens 68-71 30939155-5 2019 Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells. Lovastatin 49-59 H3 histone pseudogene 16 Homo sapiens 302-305 30939155-6 2019 The curative effect repositioning of digoxin, a cardiovascular medication, was combined with fluvastatin and lovastatin, and the results further implied that p21 induction is involved in a p53-dependent and p53-independent manner. Digoxin 37-44 H3 histone pseudogene 16 Homo sapiens 158-161 30939155-6 2019 The curative effect repositioning of digoxin, a cardiovascular medication, was combined with fluvastatin and lovastatin, and the results further implied that p21 induction is involved in a p53-dependent and p53-independent manner. Fluvastatin 93-104 H3 histone pseudogene 16 Homo sapiens 158-161 30939155-6 2019 The curative effect repositioning of digoxin, a cardiovascular medication, was combined with fluvastatin and lovastatin, and the results further implied that p21 induction is involved in a p53-dependent and p53-independent manner. Lovastatin 109-119 H3 histone pseudogene 16 Homo sapiens 158-161 30939155-7 2019 Digoxin modified the effects of statins on ATF3, p21, p53, and cyclin D1 expression, while fluvastatin boosted its DNA damage effect and lovastatin impeded its DNA damage effect. Digoxin 0-7 H3 histone pseudogene 16 Homo sapiens 49-52 30793438-5 2019 Melatonin supplementation suppressed apoptosis (100 nM, p < 0.05) and enhanced G2/M phase (1 nM, 100 nM, p < 0.05) of cell cycle progression which was further corroborated by decrease in protein expression of caspase-3, p21, and p27 and increase in bcl2. Melatonin 0-9 H3 histone pseudogene 16 Homo sapiens 226-229 30943845-0 2019 p21 limits S phase DNA damage caused by the Wee1 inhibitor MK1775. adavosertib 59-65 H3 histone pseudogene 16 Homo sapiens 0-3 30987009-5 2019 Intriguingly, 25 muM luteolin reduced cell viability through apoptotic induction, which was intensified in p53-expressing cells while 1 muM oxaliplatin caused cell cycle arrest at G0/G1-phase via the p53/p21-dependent mechanism. Oxaliplatin 140-151 H3 histone pseudogene 16 Homo sapiens 204-207 30683654-3 2019 Here, we show TGFbeta induces p38-mediated FH phosphorylation at Thr 90, which leads to a FH/CSL (also known as RBP-Jkappa)/p53 complex formation and FH accumulation at p21 promoter under concomitant activation of Notch signaling; in turn, FH inhibits histone H3 Lys 36 demethylation and thereby promotes p21 transcription and cell growth arrest. Threonine 65-68 H3 histone pseudogene 16 Homo sapiens 169-172 30683654-3 2019 Here, we show TGFbeta induces p38-mediated FH phosphorylation at Thr 90, which leads to a FH/CSL (also known as RBP-Jkappa)/p53 complex formation and FH accumulation at p21 promoter under concomitant activation of Notch signaling; in turn, FH inhibits histone H3 Lys 36 demethylation and thereby promotes p21 transcription and cell growth arrest. Threonine 65-68 H3 histone pseudogene 16 Homo sapiens 305-308 30943845-2 2019 Here, we show that the p53 target and CDK inhibitor p21 protects against MK1775-induced DNA damage during S-phase. adavosertib 73-79 H3 histone pseudogene 16 Homo sapiens 52-55 30943845-4 2019 Furthermore, upon MK1775 treatment the levels of phospho-DNA PKcs S2056 and phospho-RPA S4/S8 were higher in the p21 deficient cells, consistent with increased DNA breakage. adavosertib 18-24 H3 histone pseudogene 16 Homo sapiens 113-116 30943845-7 2019 Moreover, p21 deficiency sensitized to combined treatment of MK1775 and the CHK1-inhibitor AZD6772, and to the combination of MK1775 with ionizing radiation. adavosertib 61-67 H3 histone pseudogene 16 Homo sapiens 10-13 30943845-7 2019 Moreover, p21 deficiency sensitized to combined treatment of MK1775 and the CHK1-inhibitor AZD6772, and to the combination of MK1775 with ionizing radiation. azd6772 91-98 H3 histone pseudogene 16 Homo sapiens 10-13 30943845-7 2019 Moreover, p21 deficiency sensitized to combined treatment of MK1775 and the CHK1-inhibitor AZD6772, and to the combination of MK1775 with ionizing radiation. adavosertib 126-132 H3 histone pseudogene 16 Homo sapiens 10-13 30720065-10 2019 Notably, TCDD treatment increased the levels of p53, retinoblastoma, p21 and regucalcin, which are depressors of carcinogenesis. Polychlorinated Dibenzodioxins 9-13 H3 histone pseudogene 16 Homo sapiens 69-72 30822424-9 2019 Meanwhile, down-regulation of Cyclin D1, MMP-2 and Vimentin, up-regulations of p53 and p21, as well as cleavage of caspase-3 and -9 were observed in Salidroside-treated cell. rhodioloside 149-160 H3 histone pseudogene 16 Homo sapiens 87-90 30649504-0 2019 Bromate-induced Changes in p21 DNA Methylation and Histone Acetylation in Renal Cells. Bromates 0-7 H3 histone pseudogene 16 Homo sapiens 27-30 30649504-2 2019 We recently showed that inhibitors of DNA methyltransferase 5-aza-2"-deoxycytidine (5-Aza) and histone deacetylase trichostatin A (TSA) increased BrO3- nephrotoxicity whereas altering the expression of the cyclin-dependent kinase inhibitor p21. Decitabine 84-89 H3 histone pseudogene 16 Homo sapiens 240-243 30649504-2 2019 We recently showed that inhibitors of DNA methyltransferase 5-aza-2"-deoxycytidine (5-Aza) and histone deacetylase trichostatin A (TSA) increased BrO3- nephrotoxicity whereas altering the expression of the cyclin-dependent kinase inhibitor p21. trichostatin A 115-129 H3 histone pseudogene 16 Homo sapiens 240-243 30649504-2 2019 We recently showed that inhibitors of DNA methyltransferase 5-aza-2"-deoxycytidine (5-Aza) and histone deacetylase trichostatin A (TSA) increased BrO3- nephrotoxicity whereas altering the expression of the cyclin-dependent kinase inhibitor p21. trichostatin A 131-134 H3 histone pseudogene 16 Homo sapiens 240-243 30649504-2 2019 We recently showed that inhibitors of DNA methyltransferase 5-aza-2"-deoxycytidine (5-Aza) and histone deacetylase trichostatin A (TSA) increased BrO3- nephrotoxicity whereas altering the expression of the cyclin-dependent kinase inhibitor p21. bro3 146-150 H3 histone pseudogene 16 Homo sapiens 240-243 30649504-7 2019 5-Aza also decreased methylation at the rat p21 promoter about 250 bp upstream of the p21 TSS. Decitabine 0-5 H3 histone pseudogene 16 Homo sapiens 86-89 30649504-9 2019 BrO3- exposure altered histone acetylation in NRK cells at the p21 TSS, but not in HEK293 cells. bro3 0-4 H3 histone pseudogene 16 Homo sapiens 63-66 30879017-7 2019 RESULTS Murrayanine treatment resulted in significant dose-dependent inhibition of the growth of A549 cells (p<0.05), with an IC50 of 9 microM, and arrested the cells at the G2/M phase of the cell cycle, reduced the expression of cyclin D and E, CDK2, 4, and 6, and increased the expression of p21 and p27. murrayanine 8-19 H3 histone pseudogene 16 Homo sapiens 297-300 30830756-1 2019 A new borosilicate, NaCa5BO3(SiO4)2, has been synthesized by a high-temperature solution method, which crystallizes in the centrosymmetric monoclinic space group P21/ c (No. borosilicate 6-18 H3 histone pseudogene 16 Homo sapiens 162-168 30830756-1 2019 A new borosilicate, NaCa5BO3(SiO4)2, has been synthesized by a high-temperature solution method, which crystallizes in the centrosymmetric monoclinic space group P21/ c (No. naca5bo3(sio4)2 20-35 H3 histone pseudogene 16 Homo sapiens 162-168 30803229-6 2019 WS-383 inhibits Cul3/1 neddylation selectively over other cullins and also induces accumulation of p21, p27, and NRF2. WS 383 hydrochloride 0-6 H3 histone pseudogene 16 Homo sapiens 99-102 30815646-1 2019 Mn2CoReO6, the fourth known magnetic transition-metal-only double perovskite oxide (space group P21/n) was synthesized at high pressure and temperature (8 GPa, 1350 C). mn2coreo6 0-9 H3 histone pseudogene 16 Homo sapiens 96-101 30915268-4 2019 At 300 K, barium guanidinate crystallizes in P21/c with a=6.26439(2) A, b=16.58527(5) A, c=6.25960(2) A, and a monoclinic angle of beta=90.000(1) . barium guanidinate 10-28 H3 histone pseudogene 16 Homo sapiens 45-48 30717973-7 2019 Moreover, we found that curcumin could regulate XIST/miR-106b-5p/P21 axis in RCC cells. Curcumin 24-32 H3 histone pseudogene 16 Homo sapiens 65-68 30678803-1 2019 The crystal structure of tetrazepam, a benzodiazepine derivative formerly used for its muscle relaxant properties, has been solved and found to be monoclinic, space group P21/c, with lattice parameters a=12.7386(7)A, b=11.3774(7)A, c=10.3084(7)A, beta=103.175(5) and Vunit-cell=1454.69(16) A3 at room temperature (293K) with Z=4 molecules in the unit-cell. tetrazepam 25-35 H3 histone pseudogene 16 Homo sapiens 171-176 30597146-0 2019 Kojic acid inhibits senescence of human corneal endothelial cells via NF-kappaB and p21 signaling pathways. kojic acid 0-10 H3 histone pseudogene 16 Homo sapiens 84-87 30476532-4 2019 Non-cytotoxic doses of carbon nanoparticles but not of bigger carbon particles led to an irreversible reduction of the proliferative capacity accompanied by the accumulation of the cell cycle blocking proteins p21 and p16 as well as a loss of both redox sensitive histone deacetylase SIRT1 and connexin-43. Carbon 23-29 H3 histone pseudogene 16 Homo sapiens 210-213 30248372-0 2019 Targeting the androgen receptor (AR) with AR degradation enhancer ASC-J9 led to increase docetaxel sensitivity via suppressing the p21 expression. Docetaxel 90-99 H3 histone pseudogene 16 Homo sapiens 132-135 30248372-6 2019 Preclinical studies with in vitro cells lines also demonstrated that targeting AR with ASC-J9 led to suppressing the AR-increased p21 expression to improve the docetaxel sensitivity in the CRPC cells that already developed docetaxel resistance. Docetaxel 161-170 H3 histone pseudogene 16 Homo sapiens 131-134 30597146-7 2019 The results showed that kojic acid could inhibit HCEC senescence, characterized by enhancing migration, decreasing the levels of SA-beta-Gal staining, galectin 8, laminin alpha1, laminin alpha2, laminin gamma1 and p21, and increasing that of p-NF-kappaB of senescent HCEC. kojic acid 24-34 H3 histone pseudogene 16 Homo sapiens 214-217 30597146-8 2019 The p-NF-kappaB inhibitor could reverse the anti-senescent effect of kojic acid, and p21 siRNA showed similar anti-senescence effect with kojic acid. kojic acid 138-148 H3 histone pseudogene 16 Homo sapiens 85-88 30597146-11 2019 These results indicated that kojic acid might inhibit HCEC senescence and following resulted angiogenesis via NF-kappaB and p21 signaling pathways, possibly through downregulation of galectin 8 and laminins. kojic acid 29-39 H3 histone pseudogene 16 Homo sapiens 124-127 30628640-10 2019 The EC cells treated with CP-31398 or siRNA against MDM2 exhibited an increased apoptosis and a suppressed migration and invasion, corresponding to an increased expression of p53, p21, Bad, Bax, Cyt-c and caspase-3, as well as to a decreased expression of Bcl-2, Cox-2, MMP-2 and MMP-9. CP 31398 26-34 H3 histone pseudogene 16 Homo sapiens 180-183 30783419-0 2019 miR-181b-5p promotes proliferation and inhibits apoptosis of hypertrophic scar fibroblasts through regulating the MEK/ERK/p21 pathway. mir-181b-5p 0-11 H3 histone pseudogene 16 Homo sapiens 122-125 30783419-11 2019 Taken together, increased expression of miR-181b-5p may serve important roles in the pathogenesis of HS through regulating the MEK/ERK/p21 pathway, suggesting that miR-181b-5p may be a therapeutic target for the treatment of HS. mir-181b-5p 40-51 H3 histone pseudogene 16 Homo sapiens 135-138 30783419-11 2019 Taken together, increased expression of miR-181b-5p may serve important roles in the pathogenesis of HS through regulating the MEK/ERK/p21 pathway, suggesting that miR-181b-5p may be a therapeutic target for the treatment of HS. mir-181b-5p 164-175 H3 histone pseudogene 16 Homo sapiens 135-138 29572098-0 2019 Ironing out the role of the cyclin-dependent kinase inhibitor, p21 in cancer: Novel iron chelating agents to target p21 expression and activity. ironing 0-7 H3 histone pseudogene 16 Homo sapiens 63-66 29572098-0 2019 Ironing out the role of the cyclin-dependent kinase inhibitor, p21 in cancer: Novel iron chelating agents to target p21 expression and activity. ironing 0-7 H3 histone pseudogene 16 Homo sapiens 116-119 29572098-0 2019 Ironing out the role of the cyclin-dependent kinase inhibitor, p21 in cancer: Novel iron chelating agents to target p21 expression and activity. Iron 84-88 H3 histone pseudogene 16 Homo sapiens 63-66 29572098-0 2019 Ironing out the role of the cyclin-dependent kinase inhibitor, p21 in cancer: Novel iron chelating agents to target p21 expression and activity. Iron 84-88 H3 histone pseudogene 16 Homo sapiens 116-119 30628639-0 2019 Long non-coding RNA UCA1 confers tamoxifen resistance in breast cancer endocrinotherapy through regulation of the EZH2/p21 axis and the PI3K/AKT signaling pathway. Tamoxifen 33-42 H3 histone pseudogene 16 Homo sapiens 119-122 30229997-5 2019 Further mechanism studies revealed that oridonin led cell cycle arrest in esophageal cancer cells via downregulating cell cycle-related proteins, such as cyclin B1 and CDK2, while upregulating p53 and p21. oridonin 40-48 H3 histone pseudogene 16 Homo sapiens 201-204 30664221-8 2019 It was also observed that quercetin increased the level of the p21 transcript and the pro-apoptotic Bax protein, which are two p53-downstream effectors. Quercetin 26-35 H3 histone pseudogene 16 Homo sapiens 63-66 30854080-6 2019 In addition, cell cycle distribution analysis revealed that G0/G1 phase arrest was induced following pristimerin treatment in CAL-27 and SCC-25 cells, which was strongly associated with upregulation of p21 and p27, coupled with downregulation of cyclin D1 and cyclin E. Meanwhile, pristimerin induced significant apoptosis of CAL-27 and SCC-25 cells, alongside decreased levels of caspase-3 and specific cleavage of poly (ADP-ribose) polymerase. pristimerin 101-112 H3 histone pseudogene 16 Homo sapiens 202-205 30633861-5 2019 We further revealed that the antiproliferative properties of miliusanes in carcinoma cells were highly associated with the p21-dependent induction of cellular senescence. miliusanes 61-71 H3 histone pseudogene 16 Homo sapiens 123-126 30729962-11 2019 The crystal structure of CuBMB is monoclinic, space group P21/n, with a = 11.9790(3) A, b = 14.0236(5) A, c = 12.1193(3) A, beta = 104.952(2) and Z = 4, and the copper ions are equatorially bonded to the benzoylthiourea and bipyridine ligands in a heavily distorted square pyramidal structure. cubmb 25-30 H3 histone pseudogene 16 Homo sapiens 58-61 30721035-3 2019 Various peculiar nitrogen polymerization forms composed of single/double nitrogen-nitrogen bonds were found at the nitrogen-rich condition, such as N -chains in P21/ m-SeN3, oligomeric N8-chains in P1-SeN4, and distorted N63- anion rings in P1-SeN5. Nitrogen 17-25 H3 histone pseudogene 16 Homo sapiens 161-164 30721035-3 2019 Various peculiar nitrogen polymerization forms composed of single/double nitrogen-nitrogen bonds were found at the nitrogen-rich condition, such as N -chains in P21/ m-SeN3, oligomeric N8-chains in P1-SeN4, and distorted N63- anion rings in P1-SeN5. Nitrogen 73-81 H3 histone pseudogene 16 Homo sapiens 161-164 30721035-3 2019 Various peculiar nitrogen polymerization forms composed of single/double nitrogen-nitrogen bonds were found at the nitrogen-rich condition, such as N -chains in P21/ m-SeN3, oligomeric N8-chains in P1-SeN4, and distorted N63- anion rings in P1-SeN5. Nitrogen 73-81 H3 histone pseudogene 16 Homo sapiens 161-164 30721035-3 2019 Various peculiar nitrogen polymerization forms composed of single/double nitrogen-nitrogen bonds were found at the nitrogen-rich condition, such as N -chains in P21/ m-SeN3, oligomeric N8-chains in P1-SeN4, and distorted N63- anion rings in P1-SeN5. Nitrogen 73-81 H3 histone pseudogene 16 Homo sapiens 161-164 29688163-0 2019 Human amniotic fluid stem cells (hAFSCs) expressing p21 and cyclin D1 genes retain excellent viability after freezing with (dimethyl sulfoxide) DMSO. Dimethyl Sulfoxide 144-148 H3 histone pseudogene 16 Homo sapiens 52-55 29688163-0 2019 Human amniotic fluid stem cells (hAFSCs) expressing p21 and cyclin D1 genes retain excellent viability after freezing with (dimethyl sulfoxide) DMSO. Dimethyl Sulfoxide 124-142 H3 histone pseudogene 16 Homo sapiens 52-55 30741995-5 2019 p21 and PAI-1, which are two p53 downstream targets critical for senescence, were significantly induced in SK-N-SH cells subjected to either PRMT1-KD or inhibitor treatment. sk-n 107-111 H3 histone pseudogene 16 Homo sapiens 0-3 30774659-0 2019 Metformin Counteracts HCC Progression and Metastasis Enhancing KLF6/p21 Expression and Downregulating the IGF Axis. Metformin 0-9 H3 histone pseudogene 16 Homo sapiens 68-71 30666499-8 2019 The reduction of CUL4A levels upon the knocking down of CREB or by U0126 treatment increases the protein levels of CUL4A substrates such as p21 and p27. U 0126 67-72 H3 histone pseudogene 16 Homo sapiens 140-143 30774764-12 2019 miR-194-5p induced p21 upregulation and G1 phase arrest in resistant cells by downregulating MDM2. mir-194-5p 0-10 H3 histone pseudogene 16 Homo sapiens 19-22 31933864-12 2019 CONCLUSION: Our study clarified that OGF inhibits cell migration and proliferation of HCC in animal experiments and that exogenous OGF enhances the anti-tumor activity of cisplatin on HCC by upregulating p21 and p53. Cisplatin 171-180 H3 histone pseudogene 16 Homo sapiens 204-207 30272249-7 2019 It suggested that reduction in stabilization of P53 induced by nicotine may be negative regulator for P53/P21 signaling pathway that acts to prevent the growth of cells. Nicotine 63-71 H3 histone pseudogene 16 Homo sapiens 106-109 30651718-0 2019 Rosiglitazone metformin adduct inhibits hepatocellular carcinoma proliferation via activation of AMPK/p21 pathway. rosiglitazone-metformin combination 0-23 H3 histone pseudogene 16 Homo sapiens 102-105 30634697-6 2019 Furthermore, molecular mechanisms of cytotoxicity of [4-NH2-2-Me(Q)H][VO(bcma)(H2O)]2H2O (T1) were dependent on antiproliterative activity, increased ROS generation, cell cycle arrest in G2/M phase with simultaneous triggering of the p53/p21 pathway, binucleation, and induction of autophagy. [4-nh2-2-me 53-64 H3 histone pseudogene 16 Homo sapiens 238-241 30655700-13 2019 HCEE promoted cell cycle arrest at G1 phase in HeLa cells by upregulating the levels of p53 and p21 and downregulating the levels of cyclin D1, CDK-4, and CDK-6. hcee 0-4 H3 histone pseudogene 16 Homo sapiens 96-99 30634697-6 2019 Furthermore, molecular mechanisms of cytotoxicity of [4-NH2-2-Me(Q)H][VO(bcma)(H2O)]2H2O (T1) were dependent on antiproliterative activity, increased ROS generation, cell cycle arrest in G2/M phase with simultaneous triggering of the p53/p21 pathway, binucleation, and induction of autophagy. (q)h][vo( 64-73 H3 histone pseudogene 16 Homo sapiens 238-241 30634697-6 2019 Furthermore, molecular mechanisms of cytotoxicity of [4-NH2-2-Me(Q)H][VO(bcma)(H2O)]2H2O (T1) were dependent on antiproliterative activity, increased ROS generation, cell cycle arrest in G2/M phase with simultaneous triggering of the p53/p21 pathway, binucleation, and induction of autophagy. bcma)(h2o)]2h2o 73-88 H3 histone pseudogene 16 Homo sapiens 238-241 30634697-6 2019 Furthermore, molecular mechanisms of cytotoxicity of [4-NH2-2-Me(Q)H][VO(bcma)(H2O)]2H2O (T1) were dependent on antiproliterative activity, increased ROS generation, cell cycle arrest in G2/M phase with simultaneous triggering of the p53/p21 pathway, binucleation, and induction of autophagy. titanium silicide 90-92 H3 histone pseudogene 16 Homo sapiens 238-241 30687637-5 2018 Furthermore, PDCD4 knockdown induced cellular senescence characterized by beta-galactosidase staining, and p21 knockdown rescued the senescence and cell death as well as the inhibition of Rb phosphorylation induced by PDCD4 knockdown. Rubidium 188-190 H3 histone pseudogene 16 Homo sapiens 107-110 30525531-2 2019 Specifically, we replaced one O2- in Ba3P3O10Cl by two Cl-, leading to the formation of a new compound of BaPO3Cl ( P21/ c). Oxygen 30-32 H3 histone pseudogene 16 Homo sapiens 116-119 30525531-2 2019 Specifically, we replaced one O2- in Ba3P3O10Cl by two Cl-, leading to the formation of a new compound of BaPO3Cl ( P21/ c). ba3p3o10cl 37-47 H3 histone pseudogene 16 Homo sapiens 116-119 30525531-2 2019 Specifically, we replaced one O2- in Ba3P3O10Cl by two Cl-, leading to the formation of a new compound of BaPO3Cl ( P21/ c). bapo3cl 106-113 H3 histone pseudogene 16 Homo sapiens 116-119 30713724-1 2019 A new polymorphic form of the title compound, C8H8O3, is described in the centrosymmetric monoclinic space group P21/c with Z" = 1 as compared to the first polymorph, which crystallizes with two conformers (Z" = 2) in the asymmetric unit in the same space group. 4-hydroxyphenylacetate 46-52 H3 histone pseudogene 16 Homo sapiens 113-116 30947677-9 2019 Compound TCH-5c inhibited proliferation, resulted in cell death, increased p21 protein expression to induce G0/G1 arrest and changed endothelial cell cytoskeleton organization and migration in EA.hy926 endothelial cells. tch-5c 9-15 H3 histone pseudogene 16 Homo sapiens 75-78 30398122-7 2019 Furthermore, western blot analysis showed that DMQ arrested cells at G2/M checkpoint by down-regulation of cyclin B1, cdc2 and cdc25c and up-regulation of p21, and induced cell apoptosis via affecting the ratio of Bax/Bcl-2, causing loss of the mitochondrial membrane potential and enhancing the expression of cleaved caspase-9 (C-caspase-9) and cleaved caspase-3 (C-caspase-3). 3,3'-di-O-methylquercetin 47-50 H3 histone pseudogene 16 Homo sapiens 155-158 30755813-6 2019 CP-31398 influenced expression of p53 and the downstream molecules in a cell-dependent manner, but constantly increased p21 expression at the transcriptional level with decreased YY1 expression. CP 31398 0-8 H3 histone pseudogene 16 Homo sapiens 120-123 30755813-8 2019 We also showed that CP-31398-induced cell cycle changes including increase of G2/M populations was attributable to the up-regulated p21. CP 31398 20-28 H3 histone pseudogene 16 Homo sapiens 132-135 30755813-9 2019 These data collectively indicated that CP-31398 augmented endogenous p21 levels and induced cell cycle changes through regulation of YY1, and that YY1 was a novel target of CP-31398 in p53 dysfunctional cells. CP 31398 39-47 H3 histone pseudogene 16 Homo sapiens 69-72 30482390-6 2019 Thus, the P/CAF-MDM2-p53-p21 axis enables the escape from mitotic cell death and confers resistance to nocodazole in HCT116(p53+/+) cells with SIRT2 suppression. Nocodazole 103-113 H3 histone pseudogene 16 Homo sapiens 25-28 30361254-5 2019 Temozolomide-induced senescence required functional p53 and was dependent on sustained p21 induction. Temozolomide 0-12 H3 histone pseudogene 16 Homo sapiens 87-90 30551478-10 2019 Finally, the co-treatment of p21 inhibitor increased the sensitivity of TALL-1 and HPB-ALL cells to prednisolone. Prednisolone 100-112 H3 histone pseudogene 16 Homo sapiens 29-32 31405322-8 2019 The prolongation of telomere length in omethoate-exposed workers was associated with genotypes (CA + AA) of p21 rs1801270, and interactions of (CA + AA) genotypes and smoking factor. dimethoxon 39-48 H3 histone pseudogene 16 Homo sapiens 108-111 30361254-0 2019 Temozolomide Induces Senescence and Repression of DNA Repair Pathways in Glioblastoma Cells via Activation of ATR-CHK1, p21, and NF-kappaB. Temozolomide 0-12 H3 histone pseudogene 16 Homo sapiens 120-123 30318011-0 2019 Combination Treatment of p53-Null HL-60 cells with Histone Deacetylase Inhibitors and Chlorambucil Augments Apoptosis and Increases BCL6 and p21 Gene Expression. Chlorambucil 86-98 H3 histone pseudogene 16 Homo sapiens 141-144 30318011-10 2019 CONCLUSION: The combination treatment of p53-null HL-60 cells with DNA-damaging agent CLB and HDACIs NaBu and TSA triggered additive to synergistic effects on apoptosis and upregulated BCL6 and p21 expression. sethoxydim 101-105 H3 histone pseudogene 16 Homo sapiens 194-197 30318011-10 2019 CONCLUSION: The combination treatment of p53-null HL-60 cells with DNA-damaging agent CLB and HDACIs NaBu and TSA triggered additive to synergistic effects on apoptosis and upregulated BCL6 and p21 expression. trichostatin A 110-113 H3 histone pseudogene 16 Homo sapiens 194-197 30339883-3 2019 We reported that ARPE-19 exposed to 25 mM glucose for 48 h did not induce apoptosis, but senescence validated by SA-beta-Gal staining, p21 expression and cell cycle distribution. Glucose 42-49 H3 histone pseudogene 16 Homo sapiens 135-138 30537571-6 2019 Moreover, cadmium suppressed astrocytic proliferation by inducing S and G2/M phase cell cycle arrest and promoting p53, p21, and p27 expression. Cadmium 10-17 H3 histone pseudogene 16 Homo sapiens 120-123 30242876-6 2019 Curcumin L6H4 can significantly inhibit the proliferation and induce the apoptosis of BGC-823 cells, thus enhancing the expression levels of p53, p21, Bax, and Bcl-2 noticeably in vivo and in vitro. curcumin l6h4 0-13 H3 histone pseudogene 16 Homo sapiens 146-149 30583560-12 2018 SAHA appears to induce cell necroptosis in a p21-dependent manner, and RG7388 seems to induce apoptosis in a p21-independent manner, outlining differential mechanisms of cell death induction. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 45-48 30145226-1 2019 We previously demonstrated that progesterone (P4) up-regulated p53 expression, which in turn increased p21 and p27 expression, and finally resulted in proliferation inhibition in human umbilical vein endothelial cells (HUVEC). Progesterone 32-44 H3 histone pseudogene 16 Homo sapiens 103-106 30613017-7 2018 Danu caused cell cycle arrest in G2/M phase in HepG2 cells and led to polyploidy accumulation via up-regulating the expressions of p53 and p21 and down-regulating the expressions of cyclin B1 and DC2. danusertib 0-4 H3 histone pseudogene 16 Homo sapiens 139-142 30583560-7 2018 Induction of cell cycle arrest by SAHA in cancer cells was evidenced by elevated p21 protein levels. Vorinostat 34-38 H3 histone pseudogene 16 Homo sapiens 81-84 31378763-7 2019 Furthermore, treatment of HCT116 cells with STA resulted in G0/G1 phase cell cycle arrest accompanied by decreased mRNA levels of cyclin-dependent kinase 4 (CDK4), p21 and c-myc. stephanthraniline A 44-47 H3 histone pseudogene 16 Homo sapiens 164-167 30783055-5 2019 Thus, we investigated crocetin"s effects on the PI3K/AKT, MAPK, and p53/p21 pathways in esophageal squamous carcinoma cell line KYSE-150 cells. crocetin 22-30 H3 histone pseudogene 16 Homo sapiens 72-75 30783055-11 2019 Furthermore, we have found that crocetin not only inhibited the activation of PI3K/AKT, extracellular signal-regulated kinase-1/2 (ERK1/2), and p38 but also upregulated the p53/p21 level. crocetin 32-40 H3 histone pseudogene 16 Homo sapiens 177-180 30286430-0 2018 EGR1 is essential for deoxynivalenol-induced G2/M cell cycle arrest in HepG2 cells via the ATF3DeltaZip2a/2b-EGR1-p21 pathway. deoxynivalenol 22-36 H3 histone pseudogene 16 Homo sapiens 114-117 30557404-3 2018 In the vitamin D plus calcium group relative to control, in the crypt differentiation zone (upper 40% of crypts), mib-1 expression decreased 24% (P = 0.28); p21 expression alone and relative to mib-1 expression increased 29% (P = 0.06) and 73% (P = 0.06), respectively; and bax expression relative to mib-1 expression increased 58% (P = 0.21). Vitamin D 7-16 H3 histone pseudogene 16 Homo sapiens 157-160 30557404-3 2018 In the vitamin D plus calcium group relative to control, in the crypt differentiation zone (upper 40% of crypts), mib-1 expression decreased 24% (P = 0.28); p21 expression alone and relative to mib-1 expression increased 29% (P = 0.06) and 73% (P = 0.06), respectively; and bax expression relative to mib-1 expression increased 58% (P = 0.21). Calcium 22-29 H3 histone pseudogene 16 Homo sapiens 157-160 30557404-6 2018 These pilot study results support further investigation of whether 1) vitamin D and calcium promote colorectal epithelial cell differentiation, reduce proliferation, and promote apoptosis in the normal-appearing human colorectal mucosa, 2) vitamin D and calcium act as chemopreventive agents against colorectal neoplasms, and 3) mib-1, p21, and bax are potential "treatable", pre-neoplastic, biomarkers of risk for colorectal neoplasms. Vitamin D 240-249 H3 histone pseudogene 16 Homo sapiens 336-339 30557404-6 2018 These pilot study results support further investigation of whether 1) vitamin D and calcium promote colorectal epithelial cell differentiation, reduce proliferation, and promote apoptosis in the normal-appearing human colorectal mucosa, 2) vitamin D and calcium act as chemopreventive agents against colorectal neoplasms, and 3) mib-1, p21, and bax are potential "treatable", pre-neoplastic, biomarkers of risk for colorectal neoplasms. Calcium 254-261 H3 histone pseudogene 16 Homo sapiens 336-339 30512924-2 2018 Another phase, P21/ c-ThH7, is found to be a superconductor with TC of 62 K. Analysis of the superconducting state was performed within Eliashberg formalism, and HC( T), Delta( T), and TC( P) functions with a jump in the specific heat at critical temperature were calculated. Technetium 65-67 H3 histone pseudogene 16 Homo sapiens 15-18 30286430-4 2018 In this study, we showed that DON induced strong G2/M cell cycle arrest in HepG2 cells, and the cell cycle-inhibitory protein p21 was highly upregulated by DON. deoxynivalenol 156-159 H3 histone pseudogene 16 Homo sapiens 126-129 30286430-11 2018 In summary, we found that DON induced G2/M cell cycle arrest by sequentially inducing the expression of ATF3DeltaZip2a/2b, EGR1 and p21, and EGR1 played an essential role in this process, which is a novel molecular mechanism of cell cycle arrest by DON and is important for understanding its toxicology. deoxynivalenol 26-29 H3 histone pseudogene 16 Homo sapiens 132-135 30524726-6 2018 R248W, but not R175H, can engage p21 and MDM2, which both function to limit oxidative stress and facilitate the switch to de novo serine synthesis. Serine 130-136 H3 histone pseudogene 16 Homo sapiens 33-36 29991711-7 2018 Knockdown of Rictor or treatment with the Akt inhibitor MK-2206 attenuated senescence-associated beta-galactosidase (beta-gal) staining and expression of p53 and p21 proteins in the senescent endothelial cells, suggesting that mTORC2/Akt facilitates endothelial senescence. MK 2206 56-63 H3 histone pseudogene 16 Homo sapiens 162-165 28374118-1 2018 In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0. Benzo(a)pyrene 87-101 H3 histone pseudogene 16 Homo sapiens 209-212 30339800-4 2018 The crystal structure of N-lauroyl tris (NLT), solved in monoclinic system in the P21/c space group, showed that owing to the bulky head group, NLT molecules pack in an interdigitated bilayer fashion. n-lauroyl tris 25-39 H3 histone pseudogene 16 Homo sapiens 82-87 28374118-1 2018 In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0. Benzo(a)pyrene 79-81 H3 histone pseudogene 16 Homo sapiens 209-212 28374118-1 2018 In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0. dibenzo(a,l)pyrene 58-76 H3 histone pseudogene 16 Homo sapiens 209-212 30118731-5 2018 The triethylammonium and the 1-methylpiperazinium salts solved in Pbca and P21/c, respectively. triethylammonium 4-20 H3 histone pseudogene 16 Homo sapiens 75-80 30671399-5 2018 Using immunoblot analysis, we assessed change of the activation of caspases, PARP, Akt, mitogen-activated protein kinases, and Skp2/p27/p21 pathway by imatinib and GNF5 in SK-HEP1 cells. Imatinib Mesylate 151-159 H3 histone pseudogene 16 Homo sapiens 136-139 30671399-8 2018 Treatment of imatinib and GNF5 decreased Skp2 expression and Akt phosphorylation, and increased the expression of p27, p21, and active-caspases in SK-HEP1 cells. Imatinib Mesylate 13-21 H3 histone pseudogene 16 Homo sapiens 119-122 30118731-5 2018 The triethylammonium and the 1-methylpiperazinium salts solved in Pbca and P21/c, respectively. 1-methylpiperazinium salts 29-55 H3 histone pseudogene 16 Homo sapiens 75-80 30717558-14 2018 L-TP could delay HGMCs senescence through regulating STAT3/miR-126 expressions and inhibiting the telomere-p53-p21-Rb signaling pathway activation. l-tp 0-4 H3 histone pseudogene 16 Homo sapiens 111-114 30274043-7 2018 Furthermore, doxorubicin released from biomaterials with cyclodextrin moderately induced the expression of tumor suppressor protein p53 whereas p21 expression was similar to control cells. Doxorubicin 13-24 H3 histone pseudogene 16 Homo sapiens 144-147 30272288-12 2018 MiR-451 inhibitor effectively inhibited the upregulatory effect of si-p21 on miR-451. Silicon 67-69 H3 histone pseudogene 16 Homo sapiens 70-73 30273694-2 2018 The trihydrate, isolated from a solution of 3 in moist methanol, recrystallizes in the orthorhombic space group, P212121, while that of the dihydrate, isolated from a 1:1 aqueous methanol solution, recrystallizes in the monoclinic space group, P21. trihydrate 4-14 H3 histone pseudogene 16 Homo sapiens 113-116 30400903-0 2018 Porcine reproductive and respiratory syndrome virus inhibits MARC-145 proliferation via inducing apoptosis and G2/M arrest by activation of Chk/Cdc25C and p53/p21 pathway. marc-145 61-69 H3 histone pseudogene 16 Homo sapiens 159-162 30555320-3 2018 Para-toluenesulfonamide (PTS) is a small molecule that inhibited cell proliferation of PC-3 and DU-145, two CRPC cell lines, through p21- and p27-independent G1 arrest of cell cycle in which cyclin D1 was down-regulated and Rb phosphorylation was inhibited. 4-toluenesulfonamide 0-23 H3 histone pseudogene 16 Homo sapiens 133-136 30555320-3 2018 Para-toluenesulfonamide (PTS) is a small molecule that inhibited cell proliferation of PC-3 and DU-145, two CRPC cell lines, through p21- and p27-independent G1 arrest of cell cycle in which cyclin D1 was down-regulated and Rb phosphorylation was inhibited. 4-toluenesulfonamide 25-28 H3 histone pseudogene 16 Homo sapiens 133-136 30358785-5 2018 Both [3]rotaxanes containing two DB24C8 macrocycles per molecule crystallise in P1[combining macron] and P21/n space groups. Rotaxanes 8-17 H3 histone pseudogene 16 Homo sapiens 105-108 30581715-4 2018 This high capacitive behavior in the P21/c crystal phase of fluorinated cHBC (F-cHBC) is caused mainly by the fluorine atoms at the end of each peripheral aromatic ring. Fluorine 110-118 H3 histone pseudogene 16 Homo sapiens 37-40 30396956-8 2018 In transforming growth factor-beta-treated cells, evodiamine attenuated variations in morphology, growth and migration, and increased p21 and p53 protein levels, and decreased beta-catenin, N-cadherin, vimentin, phospho-AKT, matrix metalloproteinase-2 and matrix metalloproteinase-9 protein levels. evodiamine 50-60 H3 histone pseudogene 16 Homo sapiens 134-137 30398206-1 2018 Tolnaftate, a classic antifungal compound, has been found to crystallize from 1:1 (v/v) acetone-water as large flat colorless needles in the centrosymmetric monoclinic space group P21/c. Tolnaftate 0-10 H3 histone pseudogene 16 Homo sapiens 180-185 30144329-7 2018 Isotretinoin enhanced FoxO1, p53 and p21 but inhibited p-FoxO1 and involucrin expression in HPKs. Isotretinoin 0-12 H3 histone pseudogene 16 Homo sapiens 37-40 30396923-5 2018 The mechanism of cytotoxic action indicated that 7h caused significant (p<0.05) MDA-MB-231 cells arrest in the S phase as well as moderate cells arrest in the G2/M phase; confirmed by up-regulation of cyclins A/B1, p21 and CDKs 4/6, and down-regulation of cyclin E2 and CDK2 regulatory proteins. 7,8-diacetoxy-3-(4-nitrophenyl)coumarin 49-51 H3 histone pseudogene 16 Homo sapiens 218-221 28884602-13 2018 Expression analysis by real-time PCR showed the significant up-regulation of two tumour suppressor genes, P53 and P21 in response to combination of silibinin and paclitaxel. Silybin 148-157 H3 histone pseudogene 16 Homo sapiens 114-117 28884602-13 2018 Expression analysis by real-time PCR showed the significant up-regulation of two tumour suppressor genes, P53 and P21 in response to combination of silibinin and paclitaxel. Paclitaxel 162-172 H3 histone pseudogene 16 Homo sapiens 114-117 30011042-5 2018 BPDE up-regulated the level of miR-194-3p, which further inhibited the phosphoinositide 3-kinase (PI3K)/AKT/ cell division cycle 42/ p21 (RAC1) activated kinase 1 signaling pathway and depressed the filophdia formation of Swan71 cells. 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 0-4 H3 histone pseudogene 16 Homo sapiens 133-136 30236600-3 2018 Treating Ishikawa cells with CS components resulted in increased cell growth and altered expression of cell cycle-related genes: the protein expression of cyclin D & E increased, while the levels of p21 & p27 were reduced following treatment of these five CS components. Cesium 29-31 H3 histone pseudogene 16 Homo sapiens 203-206 30405800-0 2018 Low dose dinaciclib enhances doxorubicin-induced senescence in myeloma RPMI8226 cells by transformation of the p21 and p16 pathways. dinaciclib 9-19 H3 histone pseudogene 16 Homo sapiens 111-114 30405800-0 2018 Low dose dinaciclib enhances doxorubicin-induced senescence in myeloma RPMI8226 cells by transformation of the p21 and p16 pathways. Doxorubicin 29-40 H3 histone pseudogene 16 Homo sapiens 111-114 30405800-7 2018 Furthermore, DOX resulted in increased alterations in DNA damage-related proteins such as p-ATM, p-Chk2, p-p53, p21 and gammaH2AX, but not p16. Doxorubicin 13-16 H3 histone pseudogene 16 Homo sapiens 112-115 30405800-8 2018 Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway. dinaciclib 28-38 H3 histone pseudogene 16 Homo sapiens 153-156 30405800-8 2018 Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway. Doxorubicin 43-46 H3 histone pseudogene 16 Homo sapiens 153-156 30405800-9 2018 Thus, low-dose dinaciclib enhanced anti-MM effects mediated by DOX via transformation of p21-p16 signaling pathways, leading to accelerated senescence, but not apoptosis. dinaciclib 15-25 H3 histone pseudogene 16 Homo sapiens 89-92 30266241-7 2018 Metformin could enhance the cytotoxicity of DOX by increasing DOX cellular uptake and cell cycle arrest at G1/S checkpoint which is associated with the enhancement of p21 protein expression. Metformin 0-9 H3 histone pseudogene 16 Homo sapiens 167-170 30266241-7 2018 Metformin could enhance the cytotoxicity of DOX by increasing DOX cellular uptake and cell cycle arrest at G1/S checkpoint which is associated with the enhancement of p21 protein expression. Doxorubicin 44-47 H3 histone pseudogene 16 Homo sapiens 167-170 30333875-5 2018 Damnacanthal treatment increased caspase-3/8 and 9 activity, and promoted B-cell lymphoma 2-associated X protein, tumor protein p53 (p53) and p21 protein expression levels in melanoma cells. damnacanthal 0-12 H3 histone pseudogene 16 Homo sapiens 142-145 30011042-5 2018 BPDE up-regulated the level of miR-194-3p, which further inhibited the phosphoinositide 3-kinase (PI3K)/AKT/ cell division cycle 42/ p21 (RAC1) activated kinase 1 signaling pathway and depressed the filophdia formation of Swan71 cells. mir-194-3p 31-41 H3 histone pseudogene 16 Homo sapiens 133-136 30410558-4 2018 We found that the combined use of A549/DDP cells with SFI and cisplatin enhanced cell cycle arrested in the G2/M phase, which was accompanied by upregulation of p53 and p21 protein expression and induced mitochondrial apoptosis in conjunction with the upregulation of Bax and the downregulation of Bcl-2 protein expression. Cisplatin 62-71 H3 histone pseudogene 16 Homo sapiens 169-172 30352966-7 2018 Idasanutlin strongly activates p53, as evidenced by the induction of p21 expression and potent cell cycle arrest in all the three cell lines tested, i.e., MCF-7, U-2 OS, and SJSA-1. RG7388 0-11 H3 histone pseudogene 16 Homo sapiens 69-72 30443188-3 2018 In our study, we evaluated effect of quisinostat alone and in combination with sorafenib in HCC cells via inducing G0/G1 phase arrest through PI3K/AKT/p21 pathway and apoptosis by JNK/c-Jun/caspase3 pathway in vitro and in vivo. quisinostat 37-48 H3 histone pseudogene 16 Homo sapiens 151-154 30443188-3 2018 In our study, we evaluated effect of quisinostat alone and in combination with sorafenib in HCC cells via inducing G0/G1 phase arrest through PI3K/AKT/p21 pathway and apoptosis by JNK/c-Jun/caspase3 pathway in vitro and in vivo. Sorafenib 79-88 H3 histone pseudogene 16 Homo sapiens 151-154 30443188-10 2018 Correspondingly quisinostat facilitated G0/G1 cycle arrest and apoptosis in HCC cells through PI3K/AKT/p21 pathways and JNK/c- jun/caspase3 pathways. quisinostat 16-27 H3 histone pseudogene 16 Homo sapiens 103-106 30443388-1 2018 The title compound, C13H16N2O4, crystallizes in the monoclinic centrosymmetric space group, P21/c, with four mol-ecules in the asymmetric unit, thus there is no crystallographically imposed symmetry and it is a racemic mixture. c13h16n2o4 20-30 H3 histone pseudogene 16 Homo sapiens 92-97 30533262-10 2018 However, RA treatment decreased the levels of p-ATM, p-p53, GADD45alpha, p21, MMP-3, -9, and -13 and increased the level of COL1A1 in a concentration-dependent manner. Radium 9-11 H3 histone pseudogene 16 Homo sapiens 73-76 30304835-0 2018 Cytoplasmic p21 Mediates 5-Fluorouracil Resistance by Inhibiting Pro-Apoptotic Chk2. Fluorouracil 25-39 H3 histone pseudogene 16 Homo sapiens 12-15 30304835-3 2018 Here, we show for the first time that cytoplasmic p21 mediates 5-Fluorouracil (5FU) resistance by shuttling p-Chk2 out of the nucleus to protect the tumor cells from its pro-apoptotic functions. Fluorouracil 63-77 H3 histone pseudogene 16 Homo sapiens 50-53 30304835-3 2018 Here, we show for the first time that cytoplasmic p21 mediates 5-Fluorouracil (5FU) resistance by shuttling p-Chk2 out of the nucleus to protect the tumor cells from its pro-apoptotic functions. Fluorouracil 79-82 H3 histone pseudogene 16 Homo sapiens 50-53 30125794-4 2018 In this report we found that three typical phthalates, diethylhexyl phthalate (DEHP), Butyl benzyl phthalate (BBP) and Dibutyl phthalate (DBP), up-regulated cyclinD1 and PCNA, down-regulated P21, inducing proliferation of prostate cancer cells. phthalic acid 43-53 H3 histone pseudogene 16 Homo sapiens 191-194 29923895-11 2018 Furthermore, western blot analysis showed that p27 and p21 were accumulated in the clones with Cif, compared with the colon cancer cell lines with GFP or with Cif. cif 95-98 H3 histone pseudogene 16 Homo sapiens 55-58 30341510-15 2018 High glucose led to high expression of p53, p21, Rb, p-stat1 and p-stat3 and premature senescence of HGMCs by activating the telomere-p53-p21-Rb and JAK/STAT signaling pathways. Glucose 5-12 H3 histone pseudogene 16 Homo sapiens 44-47 30341510-15 2018 High glucose led to high expression of p53, p21, Rb, p-stat1 and p-stat3 and premature senescence of HGMCs by activating the telomere-p53-p21-Rb and JAK/STAT signaling pathways. Glucose 5-12 H3 histone pseudogene 16 Homo sapiens 138-141 30047791-4 2018 METHODS: In the present study, we hypothesized that pioglitazone would decrease proliferation of human leukoplakia cells (MSK Leuk1) and transformed bronchial epithelial cells (BEAS-2B) through regulatory changes of G1 checkpoint protein regulators, p21 and cyclin-D1. Pioglitazone 52-64 H3 histone pseudogene 16 Homo sapiens 250-253 30047791-7 2018 We also observed p21 protein induction after treatment with pioglitazone, which was preceded by measurable increases in p21 mRNA induction. Pioglitazone 60-72 H3 histone pseudogene 16 Homo sapiens 17-20 30047791-7 2018 We also observed p21 protein induction after treatment with pioglitazone, which was preceded by measurable increases in p21 mRNA induction. Pioglitazone 60-72 H3 histone pseudogene 16 Homo sapiens 120-123 30047791-8 2018 CONCLUSIONS: We conclude the PPARgamma activator, pioglitazone, can activate p21, which is associated with decreased proliferation in 2 aerodigestive preneoplastic cell lines. Pioglitazone 50-62 H3 histone pseudogene 16 Homo sapiens 77-80 30047791-9 2018 In addition, the p21 gene may be a potential hypothesis-driven biomarker in translational studies of pioglitazone as a chemoprevention agent for aerodigestive cancer. Pioglitazone 101-113 H3 histone pseudogene 16 Homo sapiens 17-20 29933074-5 2018 Furthermore, increased intracellular reactive oxygen species, p-p53, and p21 (but not p38) levels were detected in MSCs from PGF patients. Prostaglandins F 125-128 H3 histone pseudogene 16 Homo sapiens 73-76 30125794-4 2018 In this report we found that three typical phthalates, diethylhexyl phthalate (DEHP), Butyl benzyl phthalate (BBP) and Dibutyl phthalate (DBP), up-regulated cyclinD1 and PCNA, down-regulated P21, inducing proliferation of prostate cancer cells. Diethylhexyl Phthalate 55-77 H3 histone pseudogene 16 Homo sapiens 191-194 30125794-4 2018 In this report we found that three typical phthalates, diethylhexyl phthalate (DEHP), Butyl benzyl phthalate (BBP) and Dibutyl phthalate (DBP), up-regulated cyclinD1 and PCNA, down-regulated P21, inducing proliferation of prostate cancer cells. Diethylhexyl Phthalate 79-83 H3 histone pseudogene 16 Homo sapiens 191-194 30125794-4 2018 In this report we found that three typical phthalates, diethylhexyl phthalate (DEHP), Butyl benzyl phthalate (BBP) and Dibutyl phthalate (DBP), up-regulated cyclinD1 and PCNA, down-regulated P21, inducing proliferation of prostate cancer cells. butylbenzyl phthalate 86-108 H3 histone pseudogene 16 Homo sapiens 191-194 29932882-10 2018 The expression of p21 was increased after Nutlin treatments in pterygium cells (2.49 folds in 20 muM Nutlin treated cells compared to control treated cells, p = 0.012). nutlin 42-48 H3 histone pseudogene 16 Homo sapiens 18-21 30125794-4 2018 In this report we found that three typical phthalates, diethylhexyl phthalate (DEHP), Butyl benzyl phthalate (BBP) and Dibutyl phthalate (DBP), up-regulated cyclinD1 and PCNA, down-regulated P21, inducing proliferation of prostate cancer cells. butylbenzyl phthalate 110-113 H3 histone pseudogene 16 Homo sapiens 191-194 30125794-4 2018 In this report we found that three typical phthalates, diethylhexyl phthalate (DEHP), Butyl benzyl phthalate (BBP) and Dibutyl phthalate (DBP), up-regulated cyclinD1 and PCNA, down-regulated P21, inducing proliferation of prostate cancer cells. Dibutyl Phthalate 119-136 H3 histone pseudogene 16 Homo sapiens 191-194 30125794-4 2018 In this report we found that three typical phthalates, diethylhexyl phthalate (DEHP), Butyl benzyl phthalate (BBP) and Dibutyl phthalate (DBP), up-regulated cyclinD1 and PCNA, down-regulated P21, inducing proliferation of prostate cancer cells. Dibutyl Phthalate 138-141 H3 histone pseudogene 16 Homo sapiens 191-194 30145367-6 2018 The stimulatory effect of NK1R inhibition on ATO cytotoxicity is probably mediated through up-regulation of p73, which can subsequently engage p21 and NF-kappaB pathway via transcriptional suppression of c-Myc. ato 45-48 H3 histone pseudogene 16 Homo sapiens 143-146 30233720-8 2018 In addition, propofol treatment significantly increased the levels of forkhead box (FOX)O1, FOXO3, Bim, pro-caspase-3, active caspase-3, p53 and p21. Propofol 13-21 H3 histone pseudogene 16 Homo sapiens 145-148 30026090-7 2018 Expressions of proapoptotic genes, such as cyclooxygenase (COX)-2, p21 and CDKN2, were induced by resveratrol in myoma cells. Resveratrol 98-109 H3 histone pseudogene 16 Homo sapiens 67-70 30066853-7 2018 Cerdulatinib induced cell cycle arrest in the G2/M phase, which was associated with a decreased cyclin-dependent kinase 1 and cyclin B1, and an increased p21 and p27 expression. 4-(cyclopropylamino)-2-((4-(4-(ethylsulfonyl)piperazin-1-yl)phenyl)amino)pyrimidine-5-carboxamide 0-12 H3 histone pseudogene 16 Homo sapiens 154-157 30015921-8 2018 Expression of p21 and p27 was upregulated, while cyclin E and CDK2 were downregulated in UPA-treated primary-cultured leiomyoma cells. ulipristal acetate 89-92 H3 histone pseudogene 16 Homo sapiens 14-17 30066859-8 2018 The results of western blot analysis revealed that TCDD increased the protein levels of p53, Rb, p21, and regucalcin, which are suppressors of the growth of tumor cells. Polychlorinated Dibenzodioxins 51-55 H3 histone pseudogene 16 Homo sapiens 97-100 30197676-6 2018 Consistent with previous studies, the present study demonstrated that cisplatin treatment and RBEL1A overexpression blocked the oligomerization of p53 in MCF-7 cells and led to a decrease of the transcriptional activity of p53 and its downstream target gene p21. Cisplatin 70-79 H3 histone pseudogene 16 Homo sapiens 258-261 29744857-4 2018 Accordingly, 10 microM NaHS significantly increased the percentage of cells undergoing DNA replication, elevated the mRNA and/or protein expression of Cyclin A2, Cyclin D1/3, Cyclin E2 and PCNA, and decreased p21 mRNA expression. sodium bisulfide 23-27 H3 histone pseudogene 16 Homo sapiens 209-212 30513211-14 2018 Further studies revealed that EGCG induced cell cycle arrest at G1 by downregulation of cyclin E and cyclin D1 and upregulation of p21. epigallocatechin gallate 30-34 H3 histone pseudogene 16 Homo sapiens 131-134 30214601-8 2018 Western blot and reverse transcription-quantitative polymerase chain reaction analyses suggested that chaetominine treatment facilitated the expression of p53, p21, checkpoint kinase 2 (Chk2) and phosphorylated ataxia telangiectasia mutated (p-ATM) and caused a reduction in the mRNA levels of cyclin E and cyclin-dependent kinases (CDKs) 2 and 4. chaetominine 102-114 H3 histone pseudogene 16 Homo sapiens 160-163 30214601-9 2018 These results suggest that chaetominine may be involved in the regulation of p53/p21 and ATM and Rad3-related (ATM)/Chk2 signaling in SW1116 cells. chaetominine 27-39 H3 histone pseudogene 16 Homo sapiens 81-84 29964052-11 2018 Silencing DLC1 markedly attenuated SA-beta-gal activity and p38MAPK, p27 and p21 protein levels, and increased Rb expression, indicating that resveratrol promoted senescence via targeting DLC1. Resveratrol 142-153 H3 histone pseudogene 16 Homo sapiens 77-80 29864457-5 2018 In this study, we showed that BBP induced proliferation of both ER(+) MCF-7 and ER(-) MDA-MB-231 breast cancer cells, proved by increased cell viability, transition of cell cycle from G1 to S phase, upregulation of proliferating cell nuclear antigen (PCNA) and Cyclin D1, and downregulation of p21. butylbenzyl phthalate 30-33 H3 histone pseudogene 16 Homo sapiens 294-297 29864457-6 2018 Meanwhile, the expression of oncogenic miR-19a/b and PTEN/AKT/p21 axis was also modulated by BBP. butylbenzyl phthalate 93-96 H3 histone pseudogene 16 Homo sapiens 62-65 30250579-7 2018 The apoptosis rate of SAOS2 and MG63 cells induced by cisplatin were increased in BAMBI-treated osteosarcoma SAOS2 and MG63 cells via downregulation of the anti-apoptosis genes P16, P21 and B-cell lymphoma 2. saos2 22-27 H3 histone pseudogene 16 Homo sapiens 182-185 30250579-7 2018 The apoptosis rate of SAOS2 and MG63 cells induced by cisplatin were increased in BAMBI-treated osteosarcoma SAOS2 and MG63 cells via downregulation of the anti-apoptosis genes P16, P21 and B-cell lymphoma 2. Cisplatin 54-63 H3 histone pseudogene 16 Homo sapiens 182-185 30211553-4 2018 Also, Kaempferol increased the PARP cleavages and activation of caspase-8, -9, and -3, phospho-p38 MAPK, p53, and p21 in HCT116 and HCT15 cells. kaempferol 6-16 H3 histone pseudogene 16 Homo sapiens 114-117 30141807-10 2018 Our data indicate that lipin1 overexpression may cause reduction of intracellular iron content, which could activate the p53-p21-p27 signaling pathways, leading to cell cycle arrest at the G0/G1 phase in the hepatic carcinoma cells. Iron 82-86 H3 histone pseudogene 16 Homo sapiens 125-128 29964052-6 2018 Our results showed that resveratrol inhibited proliferation of cancer cell lines (MCF-7, MDA-MB-231 and H1299) and induced senescence along with increase of SA-beta-gal activity and regulation of senescence-associated molecular markers p38MAPK, p-p38MAPK, p27, p21, Rb and p-Rb protein. Resveratrol 24-35 H3 histone pseudogene 16 Homo sapiens 261-264 30125085-7 2018 3D frameworks of NaK6Cl(UO2)3(Ge2O7)2 (space group Pnnm) and Na2Cs6Cl2(UO2)3(Ge2O7)2 ( P21/ c) can be constructed from the same SBUs [UGe4] pentamers. na2cs6cl2(uo2 61-74 H3 histone pseudogene 16 Homo sapiens 87-93 30124901-0 2018 Zinc oxide nanoparticles affect the expression of p53, Ras p21 and JNKs: an ex vivo/in vitro exposure study in respiratory disease patients. Zinc Oxide 0-10 H3 histone pseudogene 16 Homo sapiens 59-62 30141919-2 2018 ABa2MS4Cl (A = Rb, Cs; M = Ge, Sn) undergoes an interesting structural transition from P21/ c (alpha phase) to I4/ mcm (beta phase), which also leads to obvious disparities on the birefringence from 0.041 (alpha phase) to 0.094 (beta phase). aba2ms4cl 0-9 H3 histone pseudogene 16 Homo sapiens 87-130 30141919-2 2018 ABa2MS4Cl (A = Rb, Cs; M = Ge, Sn) undergoes an interesting structural transition from P21/ c (alpha phase) to I4/ mcm (beta phase), which also leads to obvious disparities on the birefringence from 0.041 (alpha phase) to 0.094 (beta phase). Cesium 19-21 H3 histone pseudogene 16 Homo sapiens 87-130 29901848-4 2018 [(COH)4 ][AsF6 ] crystallizes in the monoclinic space group P21 /n with two formula units per unit cell. [(coh)4 ][asf6 0-14 H3 histone pseudogene 16 Homo sapiens 60-63 29752478-4 2018 Western blot and real-time qPCR analysis revealed that bafilomycin C1 caused partial G0/G1 phase cell-cycle arrest, downregulated the expression of cyclin D3, cyclin E1, CDK2, CDK4, and CDK6 and upregulated the expression of p21. bafilomycin C1 55-69 H3 histone pseudogene 16 Homo sapiens 225-228 30221528-12 2018 Moreover, after 24 hours of exposure to hypericin with MDA- MB-231 IC50 concentration, the expression of P53 and P21 genes upregulated in MDA-MB-175-VII much more than MDA-MB-231 when both cell lines were treated with 24 hours IC50 dose of MDA-MB-231. hypericin 40-49 H3 histone pseudogene 16 Homo sapiens 113-116 30221528-13 2018 The ICC analysis on P21 confirmed that by treating both cell lines with MDA-MB-231 IC50 dose of hypericin for 24 hours, this protein is overexpressed much more in MDA-MB-175-VII cells. hypericin 96-105 H3 histone pseudogene 16 Homo sapiens 20-23 30091530-5 2018 SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 93-96 30091530-5 2018 SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 9-14 H3 histone pseudogene 16 Homo sapiens 93-96 30210693-8 2018 The cells were blocked in G0/G1 phase by chidamide, but when chidamide was combined with decitabine, the cell cycle was mainly blocked in G2/M phase, accompanied by the induction of p21 expression. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 61-70 H3 histone pseudogene 16 Homo sapiens 182-185 30302047-6 2018 Ammonia-induced senescence in astrocytes involves glutamine synthesis-dependent formation of reactive oxygen species (ROS), p53 activation and upregulation of cell cycle inhibitory factors p21 and GADD45alpha. Ammonia 0-7 H3 histone pseudogene 16 Homo sapiens 189-192 30225112-2 2018 Treatment of 1 with ZnCl2 results in the com-pound bis-[bis-(3,5-diiso-propyl-pyrazol-1-yl)acetato]-zinc(II), [Zn(C20H31N4O2)2] (2), whose structure has monoclinic (P21/c) symmetry. zinc chloride 20-25 H3 histone pseudogene 16 Homo sapiens 165-170 30225112-2 2018 Treatment of 1 with ZnCl2 results in the com-pound bis-[bis-(3,5-diiso-propyl-pyrazol-1-yl)acetato]-zinc(II), [Zn(C20H31N4O2)2] (2), whose structure has monoclinic (P21/c) symmetry. bis-[bis-(3,5-diiso-propyl-pyrazol-1-yl)acetato]-zinc 51-104 H3 histone pseudogene 16 Homo sapiens 165-170 30225112-2 2018 Treatment of 1 with ZnCl2 results in the com-pound bis-[bis-(3,5-diiso-propyl-pyrazol-1-yl)acetato]-zinc(II), [Zn(C20H31N4O2)2] (2), whose structure has monoclinic (P21/c) symmetry. [zn(c20h31n4o2)2 110-126 H3 histone pseudogene 16 Homo sapiens 165-170 29993185-6 2018 Taken together the in vitro, in vivo and ex vivo validation studies, it was proven that Gonearrestide could inhibit the growth of primary colon cancer cells and solid tumours by triggering cell cycle arrest in G1 phase through inhibition of cyclin-dependent kinases 4 (CDK4) and up-regulate the expression of cell cycle regulators/inhibitors-cyclin D3, p27, and p21. gonearrestide 88-101 H3 histone pseudogene 16 Homo sapiens 362-365 30210693-8 2018 The cells were blocked in G0/G1 phase by chidamide, but when chidamide was combined with decitabine, the cell cycle was mainly blocked in G2/M phase, accompanied by the induction of p21 expression. Decitabine 89-99 H3 histone pseudogene 16 Homo sapiens 182-185 29468525-11 2018 The implication of H19 EZH2 p21/PTEN pathway by VPA treatment suggests that we could repurpose an old drug, valproic acid, as an effective drug for treatment of ovarian cancer in the future. Valproic Acid 108-121 H3 histone pseudogene 16 Homo sapiens 28-31 30004684-1 2018 K2ZnGe3S8 belonging to the noncentrosymmetric space group P21 of the monoclinic system was discovered via a solid-state method. k2znge3s8 0-9 H3 histone pseudogene 16 Homo sapiens 58-61 30009594-4 2018 Remarkably, o-TolLi crystallizes in the noncentrosymmetric space group P212121 with two independent monomers, whereas the crystal structure of p-TolLi is described in spacegroup P21/ a. o-tolli 12-19 H3 histone pseudogene 16 Homo sapiens 71-74 29729264-9 2018 Similar to the effects of rapamycin, pretreatment with Dex also decreased the number of senescent tubular cells and weakened the protein expression of senescence-associated markers such as p53, p21, and p16. Dexmedetomidine 55-58 H3 histone pseudogene 16 Homo sapiens 194-197 30116377-7 2018 In conclusion, curcumin inhibited the proliferation of breast cancer cells and induced G2/M phase cell cycle arrest and apoptosis, which may be associated with the decrease of CDC25 and CDC2 and increase of P21 protein levels, as well as inhibition of the phosphorylation of Akt/mTOR and induction of the mitochondrial apoptotic pathway. Curcumin 15-23 H3 histone pseudogene 16 Homo sapiens 207-210 29381896-3 2018 RESULTS: Regardless of administration time, spermine supplementation significantly up-regulated cyclin A2 gene expression but down-regulated p21 and cyclin D3 mRNA levels in the thymus and spleen and reduced cyclin E2 gene expression in the thymus of piglets (p&lt; 0.05). Spermine 44-52 H3 histone pseudogene 16 Homo sapiens 141-144 29726704-9 2018 In contrast, zafirlukast showed a greater antiproliferative effect than montelukast and induced G0/G1 cell cycle arrest by upregulating p53 and p21 expression. zafirlukast 13-24 H3 histone pseudogene 16 Homo sapiens 144-147 28797827-0 2018 Interaction between mTOR pathway inhibition and autophagy induction attenuates adriamycin-induced vascular smooth muscle cell senescence through decreased expressions of p53/p21/p16. Doxorubicin 79-89 H3 histone pseudogene 16 Homo sapiens 174-177 28797827-7 2018 Results of further experiments showed that mTOR pathway inhibition regulates adriamycin-induced expression of senescence markers (p53/p21/p16), which plays an important role in different aspects of cellular aging. Doxorubicin 77-87 H3 histone pseudogene 16 Homo sapiens 134-137 30116377-5 2018 In-depth study of its mechanism of action revealed that curcumin induced cell cycle arrest at the G2/M phase and decreased the expression of the CDC25 and CDC2 proteins, while increasing the expression of P21. Curcumin 56-64 H3 histone pseudogene 16 Homo sapiens 205-208 29709426-7 2018 While knock-outing STIM1 by CRISPR-CAS9 in 16HBE or inhibiting STIM1 mediated SOCE activation ameliorated cell death caused by acute PQ treatment, which also leaded to alleviating the cell accumulation in S phase through the modulation the expression of cyclinD1, p21, cyclinA2 and CDK2. Paraquat 133-135 H3 histone pseudogene 16 Homo sapiens 264-267 29504068-0 2018 Histone deacetylase inhibitor chidamide induces growth inhibition and apoptosis in NK/T lymphoma cells through ATM-Chk2-p53-p21 signalling pathway. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 30-39 H3 histone pseudogene 16 Homo sapiens 124-127 29504068-6 2018 In addition, we found that chidamide suppressed the phosphorylation levels of proteins in the AKT/mTOR and MAPK signalling pathways and activated the DDR cell cycle checkpoint pathway, that is, the ATM-Chk2-p53-p21 pathway. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 27-36 H3 histone pseudogene 16 Homo sapiens 211-214 29504068-9 2018 Our results provide evidence that chidamide shows antitumour effects by inhibiting the AKT/mTOR and MAPK signalling pathways and activating the ATM-Chk2-p53-p21 signalling pathway in vitro. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 34-43 H3 histone pseudogene 16 Homo sapiens 157-160 29901174-9 2018 Furthermore, Bim and p21 were upregulated in OS cells following apcin treatment. apcin 64-69 H3 histone pseudogene 16 Homo sapiens 21-24 28679068-2 2018 In present study, berberine hydrochloride (BER) triggered proliferative inhibition and G2/M arrest in AGS cells, down-regulated protein expression of cyclin B1, Bcl-2, up-regulated expression of p21, p53 and cleaved caspase 3, but showed no effect on protein expression of CHOP, Bip, and caspase 4. berberine chloride 18-41 H3 histone pseudogene 16 Homo sapiens 195-198 28679068-2 2018 In present study, berberine hydrochloride (BER) triggered proliferative inhibition and G2/M arrest in AGS cells, down-regulated protein expression of cyclin B1, Bcl-2, up-regulated expression of p21, p53 and cleaved caspase 3, but showed no effect on protein expression of CHOP, Bip, and caspase 4. Berberine 43-46 H3 histone pseudogene 16 Homo sapiens 195-198 30008912-6 2018 Treatment of beta-elemene-paclitaxel arrested the cell cycle and decreased cyclin-dependent kinase, cyclin-B1, P21 and P27 expression levels and decreased resistant genes alterations of ATP binding cassette subfamily B member 1, LDL receptor related protein and TS in U-2OS cells. beta-elemene 13-25 H3 histone pseudogene 16 Homo sapiens 111-114 30008912-6 2018 Treatment of beta-elemene-paclitaxel arrested the cell cycle and decreased cyclin-dependent kinase, cyclin-B1, P21 and P27 expression levels and decreased resistant genes alterations of ATP binding cassette subfamily B member 1, LDL receptor related protein and TS in U-2OS cells. Paclitaxel 26-36 H3 histone pseudogene 16 Homo sapiens 111-114 30060617-6 2018 We verified that manzamine A induced cell cycle arrest at G0/G1 phase via inhibition of cyclin-dependent kinases by p53/p21/p27 and triggered a caspase-dependent apoptotic cell death through mitochondrial membrane potential depletion. manzamine A 17-28 H3 histone pseudogene 16 Homo sapiens 120-123 29778287-5 2018 One of the underlying mechanisms of the anti-cancer effect exerted by PGG, was owing to the induction p53 expression, a well-known tumor suppressor, and increased in P21, the representative target gene of p53. beta-penta-O-galloyl-glucose 70-73 H3 histone pseudogene 16 Homo sapiens 166-169 29998254-2 2018 The crystal structure of [Cr(C6H6)2][TDTD] belongs to the monoclinic P21/c space group, and involves a CdSO4-type network (or quartz dual net), which is formed by CHN hydrogen bonds between [Cr(C6H6)2]+ (S = 1/2) and [TDTD]- (S = 1/2). cr(c6h6)2 26-35 H3 histone pseudogene 16 Homo sapiens 69-74 29998254-2 2018 The crystal structure of [Cr(C6H6)2][TDTD] belongs to the monoclinic P21/c space group, and involves a CdSO4-type network (or quartz dual net), which is formed by CHN hydrogen bonds between [Cr(C6H6)2]+ (S = 1/2) and [TDTD]- (S = 1/2). [cr(c6h6)2 25-35 H3 histone pseudogene 16 Homo sapiens 69-74 29893564-5 2018 In contrast, alpha- and beta-Ba2[VO2F2(IO3)2]IO3 contain the cis-[VO2F2(IO3)2]3- Lambda-shaped polyanion and crystallize in the polar space groups Pna21 and P21, respectively. alpha- and beta-ba2[vo2f2(io3)2]io3 13-48 H3 histone pseudogene 16 Homo sapiens 157-160 29923573-5 2018 Mechanistically, PEITC induced ROS accumulation, nuclear translocation of p53 and p21 and G1/S cell cycle arrest in vitro; increased p53 and 8-oxo-dG levels; and decreased Ki-67 intense/mild staining ratios without TUNEL changes in vivo. phenethyl isothiocyanate 17-22 H3 histone pseudogene 16 Homo sapiens 82-85 29677534-6 2018 Senescence induced by punicalagin treatment was further confirmed by cell cycle arrest and upregulation of cyclin-dependent kinase inhibitor p21. punicalagin 22-33 H3 histone pseudogene 16 Homo sapiens 141-144 30093863-7 2018 Moreover, triptolide dose-dependently increased the protein expression levels of Fas, Bax, p53, p21, cyclin E, cleaved caspase-3, 8, and 9; and subsequent cleavage of poly (ADP-ribose) polymerase (PARP). triptolide 10-20 H3 histone pseudogene 16 Homo sapiens 96-99 29973425-4 2018 Salt 1s crystallizes in the space group P21/n with one cation and half an anion in the asymmetric unit across an inversion centre, while (2s) crystallizes in the space group P21 with four cations and two anions in the asymmetric unit. salt 1s 0-7 H3 histone pseudogene 16 Homo sapiens 40-43 29635125-6 2018 In the present study, NOB selectively suppressed the growth and proliferation of human SKOV3/TAX cells, inducing G0/G1 phase arrest and reducing G2/M phase, along with the increase of p53 and p21. nobiletin 22-25 H3 histone pseudogene 16 Homo sapiens 192-195 29988358-8 2018 Treatment of compound-1H could arrest cell cycle in S phase through up-regulating P21 and P53, and down-regulating cyclin A and E in a dose-dependent manner. Hydrogen 22-24 H3 histone pseudogene 16 Homo sapiens 82-85 29705383-8 2018 Flow cytometric analysis showed that endosulfan at 50 and 75 muM induced cell cycle G1 arrest, a response attributed to down-regulation of CDK6 and up-regulation of p21. Endosulfan 37-47 H3 histone pseudogene 16 Homo sapiens 165-168 29727601-3 2018 In these cell lines, trametinib treatment induced p21 expression and dephosphorylated RB1, leading to sustained suppression of survivin. trametinib 21-31 H3 histone pseudogene 16 Homo sapiens 50-53 30050935-5 2018 As anticipated, TMZ caused DNA damage mediated by the ATM/p53/p21 signaling pathway and induced significant G2 delay. Temozolomide 16-19 H3 histone pseudogene 16 Homo sapiens 62-65 30050935-7 2018 Mechanistic study showed that coadministration of caffeine and TMZ suppressed the phosphorylation of ATM and p53 and downregulated p21 expression, thus releasing DNA-damaged cells from G2 arrest into premature mitosis. Caffeine 50-58 H3 histone pseudogene 16 Homo sapiens 131-134 30050935-7 2018 Mechanistic study showed that coadministration of caffeine and TMZ suppressed the phosphorylation of ATM and p53 and downregulated p21 expression, thus releasing DNA-damaged cells from G2 arrest into premature mitosis. Temozolomide 63-66 H3 histone pseudogene 16 Homo sapiens 131-134 30050935-10 2018 In conclusion, our study demonstrated that caffeine enhanced the efficacy of TMZ through mitotic cell death by impeding ATM/p53/p21-mediated G2 arrest. Caffeine 43-51 H3 histone pseudogene 16 Homo sapiens 128-131 30050935-10 2018 In conclusion, our study demonstrated that caffeine enhanced the efficacy of TMZ through mitotic cell death by impeding ATM/p53/p21-mediated G2 arrest. Temozolomide 77-80 H3 histone pseudogene 16 Homo sapiens 128-131 29872820-6 2018 Furthermore, the reduction of the cellular iron content induced alterations of p53-p27-p21 signaling to arrest the cell cycle at S phase in SMMC7721 cells treated by chemerin. Iron 43-47 H3 histone pseudogene 16 Homo sapiens 87-90 29702091-5 2018 Significantly, MALAT1 deletion sensitized HepG2 cells to 5-FU-induced cell cycle arrest in G1 phase, as evidenced by the significant reduction in Cyclin D1 and CDK4 and increase in p53, p21 and p27 protein levels. Fluorouracil 57-61 H3 histone pseudogene 16 Homo sapiens 186-189 29997096-10 2018 PCa cells co-cultured with HMC-1 cells showed increased resistance to docetaxel, and silencing p21 partially reversed docetaxel resistance in PCa cells. Docetaxel 118-127 H3 histone pseudogene 16 Homo sapiens 95-98 29997096-11 2018 CONCLUSION: Infiltrating mast cells up-regulates p21 to promote NED and increase docetaxel resistance in PCa cells in vitro. Docetaxel 81-90 H3 histone pseudogene 16 Homo sapiens 49-52 29727601-4 2018 Knockdown of p21 or RB1 restored survivin expression in trametinib-treated cells, at least partially, which supports the contribution of these molecules to trametinib-mediated survivin suppression. trametinib 56-66 H3 histone pseudogene 16 Homo sapiens 13-16 29727601-4 2018 Knockdown of p21 or RB1 restored survivin expression in trametinib-treated cells, at least partially, which supports the contribution of these molecules to trametinib-mediated survivin suppression. trametinib 156-166 H3 histone pseudogene 16 Homo sapiens 13-16 29895782-2 2018 EtOH increased senescence activity, levels of reactive oxygen species (ROS) and the expression of cell cycle regulators (p53, p21 and p16) and senescence-associated secretory phenotype (SASP) genes (interleukin [IL]-1beta, IL-6, IL-8 and tumor necrosis factor-alpha) in HPDLCs and cementoblasts. Ethanol 0-4 H3 histone pseudogene 16 Homo sapiens 126-129 29695509-3 2018 In addition to the well-described tandem phosphorylation of Thr-52 and Ser-62 in the Myc transactivation domain linked to its degradation, P21 (RAC1)-activated kinase 2 (PAK2)-mediated phosphorylation of serine and threonine residues in the C-terminal basic helix-loop-helix leucine zipper (bHLH-LZ) region regulates Myc transcriptional activity. Threonine 215-224 H3 histone pseudogene 16 Homo sapiens 139-142 29695509-3 2018 In addition to the well-described tandem phosphorylation of Thr-52 and Ser-62 in the Myc transactivation domain linked to its degradation, P21 (RAC1)-activated kinase 2 (PAK2)-mediated phosphorylation of serine and threonine residues in the C-terminal basic helix-loop-helix leucine zipper (bHLH-LZ) region regulates Myc transcriptional activity. Threonine 60-63 H3 histone pseudogene 16 Homo sapiens 139-142 29695509-3 2018 In addition to the well-described tandem phosphorylation of Thr-52 and Ser-62 in the Myc transactivation domain linked to its degradation, P21 (RAC1)-activated kinase 2 (PAK2)-mediated phosphorylation of serine and threonine residues in the C-terminal basic helix-loop-helix leucine zipper (bHLH-LZ) region regulates Myc transcriptional activity. Serine 71-74 H3 histone pseudogene 16 Homo sapiens 139-142 29695509-3 2018 In addition to the well-described tandem phosphorylation of Thr-52 and Ser-62 in the Myc transactivation domain linked to its degradation, P21 (RAC1)-activated kinase 2 (PAK2)-mediated phosphorylation of serine and threonine residues in the C-terminal basic helix-loop-helix leucine zipper (bHLH-LZ) region regulates Myc transcriptional activity. Serine 204-210 H3 histone pseudogene 16 Homo sapiens 139-142 29927390-2 2018 Rietveld refinement of X-ray data for hydrothermal K2X2+Si5O12 (X = Fe2+, Co, Zn) samples shows that they crystallize in the monoclinic space group P21/c and have tetrahedral cations (Si and X) ordered onto distinct framework sites [cf. si5o12 56-62 H3 histone pseudogene 16 Homo sapiens 148-153 29770696-4 2018 In accordance with observed number of bands and group theoretical predictions, the most likely symmetry of all compounds in the Ba2Ln2/3TeO6 system was found to be monoclinic with P21 /n space group. ba2ln2 128-134 H3 histone pseudogene 16 Homo sapiens 180-183 29318697-8 2018 We found that oroxylin A inhibited ethanol-induced hepatocyte senescence by decreasing the number of SA-beta-gal-positive LO2 cells and reducing the expression of senescence markers p16, p21 and Hmga1 in vitro. 5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one 14-24 H3 histone pseudogene 16 Homo sapiens 187-190 29318697-8 2018 We found that oroxylin A inhibited ethanol-induced hepatocyte senescence by decreasing the number of SA-beta-gal-positive LO2 cells and reducing the expression of senescence markers p16, p21 and Hmga1 in vitro. Ethanol 35-42 H3 histone pseudogene 16 Homo sapiens 187-190 28926094-10 2018 Additionally, curcumin activated the P53 signaling pathway by up-regulating P53 and P21, which also inhibited PI3K pathway through down-regulating PI3K, p-Akt, and p-mTOR. Curcumin 14-22 H3 histone pseudogene 16 Homo sapiens 84-87 29512682-10 2018 Moreover, the p53-p21-retinoblastoma protein (Rb) pathway was activated by CMT to mediate the CMT-induced premature senescence of NP cells. cmt 75-78 H3 histone pseudogene 16 Homo sapiens 18-21 29658603-10 2018 Finally, we demonstrated that the marked changes in the A549/DDP cell response to NaHS may be triggered by the activation of p53, and overexpression of p21, caspase-3, Bax and MMP-2, as well as the downregulation of Bcl-xL. sodium bisulfide 82-86 H3 histone pseudogene 16 Homo sapiens 152-155 29741716-11 2018 Validation experiments also found that riboflavin depletion decreased p21 and p27 protein levels by ~20%, and increased cell cycle-related and expression-elevated protein in tumor (CREPT) protein expression >2-fold, resulting in cyclin D1 and CDK4 levels being increased ~1.5-fold, and cell cycle acceleration. Riboflavin 39-49 H3 histone pseudogene 16 Homo sapiens 70-73 28714320-6 2018 We also provide evidence that excessive ROS triggered by polyphyllin Iota could induce G2/M phase arrest via regulating cycle proteins expression of cell cycle regulators, such as p21 and cyclinB1. ros 40-43 H3 histone pseudogene 16 Homo sapiens 180-183 28714320-6 2018 We also provide evidence that excessive ROS triggered by polyphyllin Iota could induce G2/M phase arrest via regulating cycle proteins expression of cell cycle regulators, such as p21 and cyclinB1. polyphyllin iota 57-73 H3 histone pseudogene 16 Homo sapiens 180-183 29587241-5 2018 Results demonstrate that milimolar concentrations of butyrate has an anti-proliferative effect in all three colon cancer cell lines under study, leading to a decrease on cell viability, expression of P21, P53 and beta-catenin, being able to modulate P-glycoprotein activity and to induce apoptosis by modulation of BAX/BCL-2 ratio. Butyrates 53-61 H3 histone pseudogene 16 Homo sapiens 200-203 29458130-8 2018 Our previous studies demonstrated the importance of p21 in the antiviral activity of the HCMV kinase inhibitor, maribavir. maribavir 112-121 H3 histone pseudogene 16 Homo sapiens 52-55 29808802-9 2018 Further, cisplatin could induce apoptosis through increasing G0/G1 cell cycle arrest, p21 and cleaved-caspase-3 expression. Cisplatin 9-18 H3 histone pseudogene 16 Homo sapiens 86-89 29734760-5 2018 In the present study, we demonstrated that kaempferol induced G2/M cell cycle arrest via the Chk2/Cdc25C/Cdc2 pathway and Chk2/p21/Cdc2 pathway in human ovarian cancer A2780/CP70 cells. kaempferol 43-53 H3 histone pseudogene 16 Homo sapiens 127-130 29726462-4 2018 The second polymorph crystallized as a zwitterionic dihydrate in the space group P21 at 90 K, with Z" = 2. zwitterionic dihydrate 39-61 H3 histone pseudogene 16 Homo sapiens 81-84 29427610-2 2018 Here, we found that DTBP induces senescence in human gastric adenocarcinoma AGS cells as evidenced by upregulation of p21 and Rb and increased beta-galactosidase activity. 2,4-di-tert-butylphenol 20-24 H3 histone pseudogene 16 Homo sapiens 118-121 29743815-14 2018 Moreover, genistein, daidzein and ERB-041 treatment reduced p-FAK, p-PI3K, p-AKT, p-GSK3beta, p21 or cyclin D1 expression in ovarian cancer cells. Genistein 10-19 H3 histone pseudogene 16 Homo sapiens 94-97 29743815-14 2018 Moreover, genistein, daidzein and ERB-041 treatment reduced p-FAK, p-PI3K, p-AKT, p-GSK3beta, p21 or cyclin D1 expression in ovarian cancer cells. daidzein 21-29 H3 histone pseudogene 16 Homo sapiens 94-97 29743815-15 2018 Conclusion: Genistein, daidzein and ERB-041 decreased ovarian cancer cell migration, invasion, proliferation and sphere formation, and induced cell cycle arrest and apoptosis with altered FAK and PI3K/AKT/GSK signaling and p21/cyclin D1 expression, suggesting their roles on ovarian cancer cell metastasis, tumorigenesis and stem-like properties and their potential as alternative therapies for ovarian cancer patients. Genistein 12-21 H3 histone pseudogene 16 Homo sapiens 223-226 29928364-9 2018 Decreased chemosensitivity to cisplatin may be associated with increased expression of phosphorylated-protein kinase B and cyclin dependent kinase 2 and with decreased expression of p21 and the B cell lymphoma (Bcl)-2 associated X/Bcl-2 ratio. Cisplatin 30-39 H3 histone pseudogene 16 Homo sapiens 182-185 29843366-4 2018 The major causes of excessive DSBs in H1299 cells are as follows: First, defect of p53-p21 signal and phosphorylation of SMC1 increase S phase cells, where replication of DNA containing single-strand DNA break (SSB) produces more DSBs in H1299 cells. dsbs 30-34 H3 histone pseudogene 16 Homo sapiens 87-90 29762502-4 2018 Flow cytometric assay displayed that polyphyllin VI promoted the generation of reactive oxygen species (ROS), depolarized the mitochondrial membrane potential (MMP), and induced S phase cell cycle arrest by decreasing the expression of cyclin A2 and CDK2, while significantly increasing the expression of p21 protein. Polyphyllin VI 37-51 H3 histone pseudogene 16 Homo sapiens 305-308 29751524-8 2018 Additionally, beta-asarone modulated the cell cycle-related proteins p21, p27, Cdc25A, cyclin D, cyclin E, and CDK2. asarone 14-26 H3 histone pseudogene 16 Homo sapiens 69-72 29143360-0 2018 Identification of a pyridine derivative inducing senescence in ovarian cancer cell lines via P21 activation. pyridine 20-28 H3 histone pseudogene 16 Homo sapiens 93-96 29143360-11 2018 Furthermore, we found that p21 was up-regulated and DNA damage was accumulated in FPTHQ-treated ovarian cancer cells. fpthq 82-87 H3 histone pseudogene 16 Homo sapiens 27-30 29111607-5 2018 The perchlorate salt [FeL2 ][ClO4 ]2 Me2 CO also adopts phase 1 at room temperature but undergoes a different phase transition near 135 K to phase 3 (P21 /c, Z=8) without a change in spin state. perchlorate salt [fel2 ][clo4 ]2 me2 co 4-44 H3 histone pseudogene 16 Homo sapiens 151-154 29143360-12 2018 So far, our data suggest that FPTHQ can induce senescence in multiple ovarian cancer cell lines through activation of p21 signalling pathway by causing excessive DNA damage. fpthq 30-35 H3 histone pseudogene 16 Homo sapiens 118-121 29682649-4 2018 Its analogue 2 also crystallizes in P21/c at 293 K by changing the halogen atoms of both cations and anions of 1. Halogens 67-74 H3 histone pseudogene 16 Homo sapiens 36-39 29710846-8 2018 Certainly, our data illuminated that HPOB-mediated cell death occurs via transcriptional activation of p21, which was associated with an elevated level of global histone 3 acetylation (H3Ac) modification. h3ac 185-189 H3 histone pseudogene 16 Homo sapiens 103-106 29510199-8 2018 KEY FINDINGS: Linalool (0-2.5 mM) dose-dependently inhibited cell proliferation by inducing G0/G1 cell cycle arrest, through Cdk4 and cyclin A downregulation, p21 and p27 upregulation, and apoptosis, characterized by MMP loss, caspase-3 activation, PARP cleavage and DNA fragmentation. linalool 14-22 H3 histone pseudogene 16 Homo sapiens 159-162 29620022-2 2018 The 1:1 adduct of pyridine and urea, C5H5N CH4N2O, crystallizes in the P21/c space group with Z = 4. pyridine 18-26 H3 histone pseudogene 16 Homo sapiens 71-76 29620022-2 2018 The 1:1 adduct of pyridine and urea, C5H5N CH4N2O, crystallizes in the P21/c space group with Z = 4. Urea 31-35 H3 histone pseudogene 16 Homo sapiens 71-76 29620022-2 2018 The 1:1 adduct of pyridine and urea, C5H5N CH4N2O, crystallizes in the P21/c space group with Z = 4. c5h5n ch4n2o 37-49 H3 histone pseudogene 16 Homo sapiens 71-76 29620022-4 2018 The 1:1 adduct of pyridine and thiourea, C5H5N CH4N2S, crystallizes in the P21/n space group, with Z = 32 (Z" = 8). pyridine 18-26 H3 histone pseudogene 16 Homo sapiens 75-78 29620022-4 2018 The 1:1 adduct of pyridine and thiourea, C5H5N CH4N2S, crystallizes in the P21/n space group, with Z = 32 (Z" = 8). Thiourea 31-39 H3 histone pseudogene 16 Homo sapiens 75-78 29620022-4 2018 The 1:1 adduct of pyridine and thiourea, C5H5N CH4N2S, crystallizes in the P21/n space group, with Z = 32 (Z" = 8). c5h5n ch4n2s 41-53 H3 histone pseudogene 16 Homo sapiens 75-78 29290529-8 2018 RESULTS: Treatment with SAHA inhibited the proliferation of SK-Mel-5 cells, enhanced the phosphorylation of R-Smad, and up-regulated p21 protein. Vorinostat 24-28 H3 histone pseudogene 16 Homo sapiens 133-136 29432993-6 2018 Oridonin also induced G2/M phase arrest in OSCC cells via down-regulating the G2/M transition-related proteins such as cyclin B1 or up-regulating cyclin D1, cyclin D3, P21, p-CDK1 and cyclin A2. oridonin 0-8 H3 histone pseudogene 16 Homo sapiens 168-171 29332828-9 2018 Using the UPLC-MS/MS data, peaks P14, P19, P21, and P30 were respectively identified as chlorogenic acid, quercetin, kaempferol, and isorhamnetin, and then the results were confirmed through comparison with the standards and other references. Quercetin 106-115 H3 histone pseudogene 16 Homo sapiens 43-46 29543494-8 2018 In addition, piperlongumine was reported to interfere with the expression of p21, p27, cleaved caspases-3, Bax, Bcl-2, and p-Jun N-terminal kinase (JNK), which are typical regulators associated with cell proliferation, intrinsic apoptosis, and JNKs pathway. piperlonguminine 13-27 H3 histone pseudogene 16 Homo sapiens 77-80 29436653-6 2018 Mechanistically, 4-AP upregulated the phosphatase and tensin homolog (PTEN) and modulated the phosphoinositide 3-kinase/protein kinase B signaling pathway and its downstream cell cycle factors, including cyclin D1, cyclin-dependent kinase 4 and p21, as well as apoptosis-associated proteins B-cell lymphoma 2, pro-caspase 9, pro-caspase 3, cleaved caspase 9 and cleaved caspase 3. 4-Aminopyridine 17-21 H3 histone pseudogene 16 Homo sapiens 245-248 29332828-9 2018 Using the UPLC-MS/MS data, peaks P14, P19, P21, and P30 were respectively identified as chlorogenic acid, quercetin, kaempferol, and isorhamnetin, and then the results were confirmed through comparison with the standards and other references. Chlorogenic Acid 88-104 H3 histone pseudogene 16 Homo sapiens 43-46 29332828-9 2018 Using the UPLC-MS/MS data, peaks P14, P19, P21, and P30 were respectively identified as chlorogenic acid, quercetin, kaempferol, and isorhamnetin, and then the results were confirmed through comparison with the standards and other references. kaempferol 117-127 H3 histone pseudogene 16 Homo sapiens 43-46 29332828-9 2018 Using the UPLC-MS/MS data, peaks P14, P19, P21, and P30 were respectively identified as chlorogenic acid, quercetin, kaempferol, and isorhamnetin, and then the results were confirmed through comparison with the standards and other references. 3-methylquercetin 133-145 H3 histone pseudogene 16 Homo sapiens 43-46 30023857-3 2018 The Rietveld-refined X-ray diffraction patterns shows all compounds to exist in the layered monoclinic LiV3O8 phase belonging to the space group of P21/m. liv3o8 103-109 H3 histone pseudogene 16 Homo sapiens 148-151 29544306-6 2018 We further uncover new tetragonal and monoclinic structures of PbS with space group P21/c and I41/amd, respectively. Lead 63-66 H3 histone pseudogene 16 Homo sapiens 84-97 29309885-6 2018 Upregulation of p53 and p21 upon etoposide treatment is attenuated in HBXIP knock-down cells. Etoposide 33-42 H3 histone pseudogene 16 Homo sapiens 24-27 29568320-3 2018 The enzymes responsible for arginine methylation, protein arginine methyltransferases (PRMTs), have been shown to methylate or associate with important regulatory proteins of the cell cycle and DNA damage repair pathways, such as cyclin D1, p53, p21 and the retinoblastoma protein. Arginine 28-36 H3 histone pseudogene 16 Homo sapiens 246-249 29504556-9 2018 Bis(3,4-dimethylpyridine-3,4-dimethylpyridinium) diiodidoaurate(I) iodide, [(3,4-lut)2H+]2 [AuI2]- I-, (2), crystallizes as two polymorphs, each forming pseudosymmetric inversion twins, in the space groups P21 and Pc (but resembling P21/m and P2/c), respectively. bis(3,4-dimethylpyridine-3,4-dimethylpyridinium) diiodidoaurate 0-63 H3 histone pseudogene 16 Homo sapiens 206-216 29523159-10 2018 Two miRNA clusters, miR-17-92 and miR-106b-25, were significantly suppressed by triptolide, which resulted in the upregulation of their common target genes, including BIM, PTEN, and p21. triptolide 80-90 H3 histone pseudogene 16 Homo sapiens 182-185 29513749-10 2018 Also, CQ increased the p21 level but reduced that of cyclin B1. Chloroquine 6-8 H3 histone pseudogene 16 Homo sapiens 23-26 31458563-5 2018 The complex 2 crystallizes in the monoclinic symmetry with the P21/c space group in which the N-O unit of the radical coordinates with the Co ion through hydrogen bonding of a water molecule. Water 176-181 H3 histone pseudogene 16 Homo sapiens 63-68 29331588-9 2018 Notably, montelukast reduced expression of the senescence markers p53, p21 and PAI-1. montelukast 9-20 H3 histone pseudogene 16 Homo sapiens 71-74 29779106-0 2018 Modular Nanotransporter with P21 Fragment Inhibits DNA Repair after Bleomycin Treatment. Bleomycin 68-77 H3 histone pseudogene 16 Homo sapiens 29-32 29779106-2 2018 This p21 fragment in MNT can significantly inhibit DNA repair in A431 human carcinoma cells after bleomycin treatment. Bleomycin 98-107 H3 histone pseudogene 16 Homo sapiens 5-8 29444596-5 2018 Importantly, our results display interleukin-1betatreatment significantly increased the expressions of senescence genes (caveolin-1, PAI-1 and p21), which were prevented by agonist arachidonyl-2-chloroethylamide treatment. arachidonyl-2-chloroethylamide 181-211 H3 histone pseudogene 16 Homo sapiens 143-146 29223572-8 2018 Our results confirmed the induction of p53/p21 axis and G0/G1 cell cycle arrest in anticancer activities of both drugs, an effect more pronounced for the CFZ-curcumin tested combinations. carfilzomib 154-157 H3 histone pseudogene 16 Homo sapiens 43-46 29363886-3 2018 Treatment of two OSCC cell lines with honokiol resulted in reducing the cell proliferation and arresting the cell cycle at G1 stage which was correlated with the down-regulation of Cdk2 and Cdk4 and the up-regulation of cell cycle suppressors, p21 and p27. honokiol 38-46 H3 histone pseudogene 16 Homo sapiens 244-247 31938221-8 2018 We found that 125I significantly induced cell apoptosis through mitochondrial pathway, triggered S phase arrest via regulating cyclinA2, p21 and CDK6 expressions. 2-iodotyrosine 14-18 H3 histone pseudogene 16 Homo sapiens 137-140 29235378-13 2018 In conclusion, these data suggest that the BM"s hexane fraction inhibited proliferation of cell lines mainly by a p21-dependent, p53-independent mechanism and promoted apoptosis through activation of caspase-3, but not caspase-8 or -9. Hexanes 48-54 H3 histone pseudogene 16 Homo sapiens 114-117 29629344-10 2018 The induced expression of cytochrome c, p53, p21 and p27, and down-regulated CDK2 and CDK4 may be the underlying molecular mechanisms of esculetin effect. esculetin 137-146 H3 histone pseudogene 16 Homo sapiens 45-48 29346597-5 2018 Exenatide treatment also suppressed Keap-1 protein (P < 0.05) and increased messenger RNA expression of NQO-1, glutathione S-transferase PI, heme oxygenase-1, and p21 and increased NAD(P)H dehydrogenase [quinone] 1 protein (P < 0.05) in mononuclear cells. Exenatide 0-9 H3 histone pseudogene 16 Homo sapiens 166-169 29467390-10 2018 Etoposide induced p21 expression as expected, but p21 protein levels were even increased in the presence of FGF1. Etoposide 0-9 H3 histone pseudogene 16 Homo sapiens 18-21 29411966-1 2018 In the search for superconductivity in a BaAu2Sb2-type monoclinic structure, we have successfully synthesized the new compound BaPt2Bi2, which crystallizes in the space group P21/m (No. bapt2bi2 127-135 H3 histone pseudogene 16 Homo sapiens 175-180 29765714-1 2018 The title compound, C16H16BrNO3, which shows enol-imine tautomerism, crystallizes in the monoclinic P21/c space group. c16h16brno3 20-31 H3 histone pseudogene 16 Homo sapiens 100-105 29511449-4 2018 Valproic acid (VPA) as a HDAC inhibitor was found to suppress SCLC cell growth and cell cycle arrest at phase G1, and observed to decrease HDAC4 and increase acetylation of histone H4 (AcH4) while activating Notch signalling with an increase of Notch1, Notch target gene HES1 and p21. Valproic Acid 0-13 H3 histone pseudogene 16 Homo sapiens 280-283 29511449-4 2018 Valproic acid (VPA) as a HDAC inhibitor was found to suppress SCLC cell growth and cell cycle arrest at phase G1, and observed to decrease HDAC4 and increase acetylation of histone H4 (AcH4) while activating Notch signalling with an increase of Notch1, Notch target gene HES1 and p21. Valproic Acid 15-18 H3 histone pseudogene 16 Homo sapiens 280-283 29643975-4 2018 In this study, we found that physiological hypoxia (10% O2) enhanced the stemness properties and promoted the proliferation ability of iHepSCs by accelerating G1/S transition via p53-p21 signaling pathway. Oxygen 56-58 H3 histone pseudogene 16 Homo sapiens 183-186 29456503-8 2017 Moreover, GDC-0449 partially reduced cell proliferation, which was associated with upregulation of p21 and downregulation of CycD1. HhAntag691 10-18 H3 histone pseudogene 16 Homo sapiens 99-102 29410485-0 2018 Quinacrine upregulates p21/p27 independent of p53 through autophagy-mediated downregulation of p62-Skp2 axis in ovarian cancer. Quinacrine 0-10 H3 histone pseudogene 16 Homo sapiens 23-26 29400323-1 2018 Pentachloropyridine N-oxide, C5Cl5NO, crystallizes in the monoclinic space group P21/c. pentachloropyridine n-oxide 0-27 H3 histone pseudogene 16 Homo sapiens 81-86 29472861-8 2018 We further demonstrated that PGG decreased MYC expression in protein and mRNA levels and reversed the mRNA expression of MYC target genes such as p21, p27, and cyclin D2. pgg 29-32 H3 histone pseudogene 16 Homo sapiens 146-149 29400323-1 2018 Pentachloropyridine N-oxide, C5Cl5NO, crystallizes in the monoclinic space group P21/c. c5cl5no 29-36 H3 histone pseudogene 16 Homo sapiens 81-86 28947337-5 2018 The anhydrous form of tasimelteon, C15H19NO2, crystallizes in the monoclinic P21 space group, with a = 11.130(4), b = 4.907(2), c = 12.230(6) A, beta = 91.03(3) , V = 667.8(5) A3; Z = 2. c15h19no2 35-44 H3 histone pseudogene 16 Homo sapiens 77-80 29063134-8 2018 In addition, PFOS exposure increased CDK4 and decreased p27, p21, and p53 levels in the cells. perfluorooctane sulfonic acid 13-17 H3 histone pseudogene 16 Homo sapiens 61-64 29285650-10 2018 Furthermore, gemigliptin augments the inhibitory effect of metformin on proliferation and migration through involvement of matrix metalloproteinase-2, matrix metalloproteinase-9, p53, p21, VCAM-1, and ERK in thyroid carcinoma cells. LC15-0444 13-24 H3 histone pseudogene 16 Homo sapiens 184-187 29285650-10 2018 Furthermore, gemigliptin augments the inhibitory effect of metformin on proliferation and migration through involvement of matrix metalloproteinase-2, matrix metalloproteinase-9, p53, p21, VCAM-1, and ERK in thyroid carcinoma cells. Metformin 59-68 H3 histone pseudogene 16 Homo sapiens 184-187 29105282-8 2018 The experimental results revealed that escitalopram oxalate significantly inhibits the proliferation and invasive ability of U-87MG cells and significantly reduced the expressions of cell cycle inhibitors such as Skp2, P57, P21 and P27. Citalopram 39-59 H3 histone pseudogene 16 Homo sapiens 224-227 28915362-7 2018 Real-time RT-PCR studies revealed significant (p < 0.01) up-regulation of P21 in the cells pretreated with auraptene after heat shock, whereas no significant change was observed in HSP27 expression. aurapten 110-119 H3 histone pseudogene 16 Homo sapiens 77-80 29434929-2 2018 The present study demonstrated that vernodalol, an active compound isolated from Centratherum anthelminticum, suppresses APL cell proliferation and induces cell cycle arrest in the G2/M phase through the upregulation of p21 and cell division cycle 25. vernodalol 36-46 H3 histone pseudogene 16 Homo sapiens 220-223 29207090-0 2018 Long intergenic non-coding RNA-p21 mediates cardiac senescence via the Wnt/beta-catenin signaling pathway in doxorubicin-induced cardiotoxicity. Doxorubicin 109-120 H3 histone pseudogene 16 Homo sapiens 31-34 29434841-8 2018 In addition, A172 cells treated with SB exhibited positivity for senescence-associated (SA) beta-galactosidase (gal) staining and elevated protein expression of p53 and p21 in a time- and dose-dependent manner, whereas the expression of p21 mRNA decreased. Butyric Acid 37-39 H3 histone pseudogene 16 Homo sapiens 169-172 29378575-6 2018 DHA, Omegaven and oxaliplatin were associated with significant downregulation of VEGF and p53 protein, and upregulation of p21 protein. dehydroacetic acid 0-3 H3 histone pseudogene 16 Homo sapiens 124-127 29434841-8 2018 In addition, A172 cells treated with SB exhibited positivity for senescence-associated (SA) beta-galactosidase (gal) staining and elevated protein expression of p53 and p21 in a time- and dose-dependent manner, whereas the expression of p21 mRNA decreased. Butyric Acid 37-39 H3 histone pseudogene 16 Homo sapiens 237-240 29303911-5 2018 RESULTS: Treatment of PANC-1 cells over 4 days with 0.5 muM TSA restored cellular differentiation, inhibited proliferation, and enhanced p21 protein expression. trichostatin A 60-63 H3 histone pseudogene 16 Homo sapiens 137-140 29600625-9 2018 Moreover, notoginsenoside R1 decreased the mRNA expressions of miRNA-34a and p53 and the protein expression of p53, p21 and p16.At the same time, notoginsenoside R1 increased the protein and mRNA expressions of SIRT1. notoginsenoside 10-25 H3 histone pseudogene 16 Homo sapiens 116-119 29600625-9 2018 Moreover, notoginsenoside R1 decreased the mRNA expressions of miRNA-34a and p53 and the protein expression of p53, p21 and p16.At the same time, notoginsenoside R1 increased the protein and mRNA expressions of SIRT1. notoginsenoside 146-161 H3 histone pseudogene 16 Homo sapiens 116-119 29323682-1 2018 A mononuclear complex [Co(neo)(PhCOO)2,], neo = neocuproine, PhCOO- = the benzoate anion, was prepared in two polymorph forms crystallizing in the C2/c, (1) and P21/c, (2) space groups. co(neo)(phcoo)2 23-38 H3 histone pseudogene 16 Homo sapiens 161-166 29378575-6 2018 DHA, Omegaven and oxaliplatin were associated with significant downregulation of VEGF and p53 protein, and upregulation of p21 protein. fish oil triglycerides 5-13 H3 histone pseudogene 16 Homo sapiens 124-127 29378575-6 2018 DHA, Omegaven and oxaliplatin were associated with significant downregulation of VEGF and p53 protein, and upregulation of p21 protein. Oxaliplatin 19-30 H3 histone pseudogene 16 Homo sapiens 124-127 28684297-13 2018 RT-qPCR and Western blot data showed that curcumol enhanced the expression of GSK3beta, P27, p21 and P16, and decreased the levels of PI3K, phosphorylated Akt (p-Akt), cyclin D1, CDK4, cyclin E and CDK2. curcumol 42-50 H3 histone pseudogene 16 Homo sapiens 93-96 29348392-4 2018 The senescence-associated beta-galactosidase activity, the protein expression of P16 and P21, and inflammatory-related marker gene levels IL-1beta, IL-6, and TNF-alpha were increased in bleomycin-treated AFSCs in a dose-dependent manner. Bleomycin 186-195 H3 histone pseudogene 16 Homo sapiens 89-92 29348392-5 2018 Rapamycin treatment decreased the gene expression of MMP-3, MMP-13, IL-1beta, IL-6, TNF-alpha, and protein levels of P16 and P21 in bleomycin-treated AFSCs. Sirolimus 0-9 H3 histone pseudogene 16 Homo sapiens 125-128 29348392-5 2018 Rapamycin treatment decreased the gene expression of MMP-3, MMP-13, IL-1beta, IL-6, TNF-alpha, and protein levels of P16 and P21 in bleomycin-treated AFSCs. Bleomycin 132-141 H3 histone pseudogene 16 Homo sapiens 125-128 29850051-1 2018 The title compound, C6H4BrNS, crystallizes in the space group P21/n with one complete mol-ecule in the asymmetric unit. c6h4brns 20-28 H3 histone pseudogene 16 Homo sapiens 62-65 29232132-4 2018 The [PPN]4[1] 2MeCN salt was also structurally characterized, crystallizing in the monoclinic P21/c space group. [ppn]4[1] 2mecn salt 4-24 H3 histone pseudogene 16 Homo sapiens 94-111 29850034-2 2018 It crystallizes in the alpha-Na2CuP2O7 structure type in space group P21/n. alpha-na2cup2o7 23-38 H3 histone pseudogene 16 Homo sapiens 69-72 29303497-3 2018 Three stereoisomers of the diamine cocrystallize in the centrosymmetric space group P21/c with Z" = 1.5. Diamines 27-34 H3 histone pseudogene 16 Homo sapiens 84-87 29053388-7 2018 The cells treated with 5-FU or IRINO exhibited several hallmarks of SIPS: growth arrest, increased size and granularity, polyploidization, augmented activity of the SA-beta-galactosidase, accumulation of P21 and CYCLIN D1 proteins, and the senescence-associated secretory phenotype. Fluorouracil 23-27 H3 histone pseudogene 16 Homo sapiens 204-207 29399562-5 2018 In addition, mRNA expression of pro-apoptotic genes, p21 and Bax, was decreased and of anti-apoptotic genes, Bcl-2 and Bcl-xl, was increased with metformin treatment compared to QUIN-induced cells. Metformin 146-155 H3 histone pseudogene 16 Homo sapiens 53-56 28901264-0 2018 Inhibition of Proliferation and Induction of Apoptosis by Thymoquinone via Modulation of TGF Family, p53, p21 and Bcl-2alpha in Leukemic Cells. thymoquinone 58-70 H3 histone pseudogene 16 Homo sapiens 106-109 28901264-14 2018 TQ mediated its anti-proliferative effect and apoptosis induction by an up-regulation of TGFbeta1, p53 and p21 and a down-regulation of TGF-alpha and Bcl-2alpha. N-(6-methoxy-8-quinolyl)-4-toluenesulfonamide 0-2 H3 histone pseudogene 16 Homo sapiens 107-110 29793319-6 2018 The results indicated that oroxyloside significantly suppressed the proliferation of human glioma cells through inducing cell cycle arrest at G0/G1 phase through reducing Cyclin D1 and cyclin-dependent kinase 2 (CDK2) while enhancing p53 and p21 expressions. oroxylin A-7-O-glucuronide 27-38 H3 histone pseudogene 16 Homo sapiens 242-245 29793319-9 2018 In vivo, oroxyloside administration significantly inhibited the glioma cell xenograft tumorigenesis through various signaling pathways, including suppression of Cyclin D1/CDK2 and ECM pathways, as well as potentiation of p53/p21 and Caspases pathways. oroxylin A-7-O-glucuronide 9-20 H3 histone pseudogene 16 Homo sapiens 225-228 28745237-9 2018 Further, anethole induced G2/M phase arrest, downregulation of cyclins D1, CDK-4 and c-Myc proteins and upregulation of p21 and p27. anethole 9-17 H3 histone pseudogene 16 Homo sapiens 120-123 28676953-3 2018 Gallotannin suppressed viability and colony formation, increased subG1 portion and also induced senescence via upregulation of p21, G0/G1 arrest and higher SA-beta-gal activity in HepG2 and SK-Hep1 cells. Hydrolyzable Tannins 0-11 H3 histone pseudogene 16 Homo sapiens 127-130 29203243-8 2018 Notably, we found that rottlerin upregulated DDX3 expression and subsequently downregulated Cyclin D1 expression and increased p21 level. rottlerin 23-32 H3 histone pseudogene 16 Homo sapiens 127-130 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. NVP-CGM097 30-36 H3 histone pseudogene 16 Homo sapiens 129-132 27871087-0 2018 The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1. Fluorouracil 103-117 H3 histone pseudogene 16 Homo sapiens 129-132 29312515-5 2017 The combination increased the acetylation levels of histone H3 and decreased HDAC activity in MDS cells.A low concentration (25 and 50 nM) of chidamide combined with low-dose cytarabine (50 nM) inhibited cell proliferation and arrested the cell cycle in the G0/G1 phasevia down-regulating CDK2 and up-regulating p21. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 142-151 H3 histone pseudogene 16 Homo sapiens 312-315 27871087-10 2018 NVP-CGM097 and 5-fluorouracil increased p53 and p21 expression in an additive manner. Fluorouracil 15-29 H3 histone pseudogene 16 Homo sapiens 48-51 29953997-7 2018 The suppression of STAT3 activation by CDDO-me in W4P-LHB-NIH3T3 cells was further confirmed by decreased cyclin D1 protein levels and increased p21 and p53 mRNA synthesis. bardoxolone methyl 39-46 H3 histone pseudogene 16 Homo sapiens 145-148 30465624-3 2018 Our results show that N6-isopentenyladenosine induced a significant reduction of cell viability, upregulated p21 and promoted caspase-3 cleavage in a dose dependent manner leading to apoptotic cell death as detected by FACS analysis. Isopentenyladenosine 22-45 H3 histone pseudogene 16 Homo sapiens 109-112 29317830-5 2018 The combination of irradiation and quercetin treatment aggravated DNA damages and caused typical apoptotic cell death; as well the expression of Bax and p21 elevated and the expression of Bcl-2 decreased. Quercetin 35-44 H3 histone pseudogene 16 Homo sapiens 153-156 29383186-3 2017 Our data showed that BPA induces the down regulation of cyclin D1 expression and the upregulation of the cell cycle inhibitors p21 and p27, leading to cell cycle arrest. bisphenol A 21-24 H3 histone pseudogene 16 Homo sapiens 127-130 29312515-5 2017 The combination increased the acetylation levels of histone H3 and decreased HDAC activity in MDS cells.A low concentration (25 and 50 nM) of chidamide combined with low-dose cytarabine (50 nM) inhibited cell proliferation and arrested the cell cycle in the G0/G1 phasevia down-regulating CDK2 and up-regulating p21. Cytarabine 175-185 H3 histone pseudogene 16 Homo sapiens 312-315 28838761-5 2017 A 3-fold higher induction of apoptosis and stronger activation of Bax and p21 was also measured in the P53WT MES-SA cells, compared to the P53mut SK-LMS-1 cells. mes-sa 109-115 H3 histone pseudogene 16 Homo sapiens 74-77 29416744-7 2018 Western blotting showed that PDOX caused much higher expressions of P53, P21, Aparf-1, pro- and cleaved-caspase 3, compared with DOX. Doxorubicin 30-33 H3 histone pseudogene 16 Homo sapiens 73-113 29416632-6 2018 Mechanically, PAC-320 induced cell cycle arrest is associated with an increase of p21 and decrease of cyclin A and cyclin B1, while PAC-320 induced apoptosis is mediated through mitochondria apoptotic pathway and is closely associated with increase of BH3-only proteins Noxa and Hrk. pac-320 14-21 H3 histone pseudogene 16 Homo sapiens 82-85 29187454-0 2017 P-gp Inhibition by XL019, a JAK2 Inhibitor, Increases Apoptosis of Vincristine-treated Resistant KBV20C Cells with Increased p21 and pH2AX Expression. Vincristine 67-78 H3 histone pseudogene 16 Homo sapiens 125-128 29187454-8 2017 Moreover, G2 phase arrest and apoptosis of cells co-treated with vincristine and XL019 resulted from the up-regulation of phosphorylated retinoblastoma protein (pRb), p21, and the DNA-damage protein, phosphorylated H2A histone family, member X (pH2AX). Vincristine 65-76 H3 histone pseudogene 16 Homo sapiens 167-170 29143344-4 2017 5-Aza-dC inhibited E6 and E7 expression and up-regulated p53, p21, and Rb expression. Decitabine 0-8 H3 histone pseudogene 16 Homo sapiens 62-65 29187454-0 2017 P-gp Inhibition by XL019, a JAK2 Inhibitor, Increases Apoptosis of Vincristine-treated Resistant KBV20C Cells with Increased p21 and pH2AX Expression. XL019 19-24 H3 histone pseudogene 16 Homo sapiens 125-128 29143344-5 2017 Cells transfected with siRNAs targeting p16 and MGMT as well as cells stimulated with 5-Aza-dC were arrested in S phase, and the expression of p53, p21, and Rb was up-regulated more significantly. Azacitidine 86-91 H3 histone pseudogene 16 Homo sapiens 148-151 28540540-10 2017 The qRT-PCR and western blot analysis indicated that the mRNA and protein expressions of Bax and P21 were significantly up-regulated whereas that of Bc1-2 was down-regulated after treatment with BBE for 24 h. Our results revealed a correlation between gene regulation and BBE-induced apoptosis, which might indicate the potential of BBE in cancer therapy. CHEMBL145735 195-198 H3 histone pseudogene 16 Homo sapiens 97-100 28540540-10 2017 The qRT-PCR and western blot analysis indicated that the mRNA and protein expressions of Bax and P21 were significantly up-regulated whereas that of Bc1-2 was down-regulated after treatment with BBE for 24 h. Our results revealed a correlation between gene regulation and BBE-induced apoptosis, which might indicate the potential of BBE in cancer therapy. CHEMBL145735 272-275 H3 histone pseudogene 16 Homo sapiens 97-100 28540540-10 2017 The qRT-PCR and western blot analysis indicated that the mRNA and protein expressions of Bax and P21 were significantly up-regulated whereas that of Bc1-2 was down-regulated after treatment with BBE for 24 h. Our results revealed a correlation between gene regulation and BBE-induced apoptosis, which might indicate the potential of BBE in cancer therapy. CHEMBL145735 272-275 H3 histone pseudogene 16 Homo sapiens 97-100 28804952-6 2017 In GBM 8401 cells, propofol induced G2/M phase cell arrest, which affected the CDK1, cyclin B1, p53, and p21 protein expression levels. Propofol 19-27 H3 histone pseudogene 16 Homo sapiens 105-108 28485543-6 2017 In the present study, we showed that Andro-induced G2/M cell cycle arrest of chondrosarcoma by fine-tuning the expressions of several cell cycle regulators such as p21, p27, and Cyclins, and that prolonged treatment of cells with Andro caused pronounced cell apoptosis. andrographolide 37-42 H3 histone pseudogene 16 Homo sapiens 164-167 29157814-13 2017 The levels of several cell cycle regulator, p21 and apoptosis related protein, X-linked inhibitor of apoptosis, was found to be induced and reduced by VAE treatment, respectively. 3-{[(E)-1-Carboxy-2-Phenylethenyl]oxy}-2-Hydroxybenzoic Acid 151-154 H3 histone pseudogene 16 Homo sapiens 44-47 29218097-0 2017 Histone deacetylase inhibitor NaBut suppresses cell proliferation and induces apoptosis by targeting p21 in multiple myeloma. nabut 30-35 H3 histone pseudogene 16 Homo sapiens 101-104 29024179-1 2017 The reaction of Ca(CO3 ) with H3 BO3 in oleum (20 % SO3 ) yielded colorless single-crystals of CaB2 S4 O16 (monoclinic, P21 /c, a=5.5188(2), b=15.1288(6), c=13.2660(6) A, beta=92.88(1) , V=1106.22(8) A3 ). Calcium Carbonate 16-24 H3 histone pseudogene 16 Homo sapiens 120-123 29024179-1 2017 The reaction of Ca(CO3 ) with H3 BO3 in oleum (20 % SO3 ) yielded colorless single-crystals of CaB2 S4 O16 (monoclinic, P21 /c, a=5.5188(2), b=15.1288(6), c=13.2660(6) A, beta=92.88(1) , V=1106.22(8) A3 ). boric acid 30-36 H3 histone pseudogene 16 Homo sapiens 120-123 28982980-5 2017 We found that carbofuran increases TGF-beta signaling (i.e. increased phosphorylated SMAD-2/3 and reduced SMAD-7 expression) in the hippocampus, which reduced NSC proliferation because of increased p21 levels and reduced cyclin D1 levels. Carbofuran 14-24 H3 histone pseudogene 16 Homo sapiens 198-201 29169370-12 2017 Activation of PI3K/AKT signalling drives SP"s into an undifferentiated, anti-apoptotic stage through upregulating P21, P27,cFLIP expression. sp 41-43 H3 histone pseudogene 16 Homo sapiens 114-117 29250410-1 2017 The title compound, C10H13NOS, is a second monoclinic polymorph (space group P21/c, Z" = 2) of the previously reported C2/c (Z = 1) polymorph [Tadbuppa & Tiekink (2005 ). c10h13nos 20-29 H3 histone pseudogene 16 Homo sapiens 77-82 29177004-14 2017 Conclusions: The active fraction HS7 from n-hexane extract of T. camphoratus exerts multi-targeting activity on the suppression of AKT-mTOR, ERK and STAT3 pathways and induction of p15, p21 and p27 in EGFR wild-type NSCLC cells. n-hexane 42-50 H3 histone pseudogene 16 Homo sapiens 186-189 29200826-6 2017 Results: At 3, 6, 12, and 24 microg/mL exposure, DEN and DEN-HPbetaCD complex significantly affected apoptosis in HT-29 cells through the down-regulation of Bcl-2 and cyclin A in turn, and up-regulation of Bax, p53, p21, cytochrome c at both protein and mRNA levels. dentatin 49-52 H3 histone pseudogene 16 Homo sapiens 216-219 29200826-6 2017 Results: At 3, 6, 12, and 24 microg/mL exposure, DEN and DEN-HPbetaCD complex significantly affected apoptosis in HT-29 cells through the down-regulation of Bcl-2 and cyclin A in turn, and up-regulation of Bax, p53, p21, cytochrome c at both protein and mRNA levels. den-hpbetacd 57-69 H3 histone pseudogene 16 Homo sapiens 216-219 29218097-8 2017 Moreover, NaBut induced MM cell apoptosis via transcriptional activation of p21. nabut 10-15 H3 histone pseudogene 16 Homo sapiens 76-79 29200992-10 2017 On the other hand, O-TFDG induced HCT116 cells apoptosis mainly by increasing the expression of p53, p21, and cleaved caspase-3. o-tfdg 19-25 H3 histone pseudogene 16 Homo sapiens 101-104 28970011-10 2017 Crocetin induced G1 arrest, reduced PCNA protein expression and increased the p21 and p53 accumulation in ARPE-19 cells. crocetin 0-8 H3 histone pseudogene 16 Homo sapiens 78-81 29043340-2 2017 The copper-containing MOF crystallizes in the monoclinic crystal system within the space group P21/n (no. Copper 4-10 H3 histone pseudogene 16 Homo sapiens 95-100 28911263-9 2017 In the presence of RA, we observed a decrease of OCT4 expression, associated with a loss of clonogenic and proliferation capacities, cell cycle arrest, and upregulation of p21, in HL60, NB4, KASUMI, and Me-1 cell lines. Tretinoin 19-21 H3 histone pseudogene 16 Homo sapiens 172-175 29061795-7 2017 RESULTS: Compared to berberine or evodiamine treatments alone, the combination treatment of berberine (25 muM) and evodiamine (15 muM) synergistically inhibited the proliferation of MCF-7 cells in a time-dependent manner and resulted in the G0/G1 phase accumulation of cells that exhibited increased expression levels of the CDK inhibitors p21 and p27 with a concomitant reduction in the expression levels of cell-cycle checkpoint proteins cyclin D1, cyclin E, CDK4, and CDK6. Berberine 92-101 H3 histone pseudogene 16 Homo sapiens 340-343 28913568-8 2017 Increased p21 via the p53-independent pathway in PL-treated CCA cells led to G2/M phase arrest and cell apoptosis. piperlonguminine 49-51 H3 histone pseudogene 16 Homo sapiens 10-13 28938245-0 2017 Gallic acid induces G1 phase arrest and apoptosis of triple-negative breast cancer cell MDA-MB-231 via p38 mitogen-activated protein kinase/p21/p27 axis. Gallic Acid 0-11 H3 histone pseudogene 16 Homo sapiens 140-143 29061795-7 2017 RESULTS: Compared to berberine or evodiamine treatments alone, the combination treatment of berberine (25 muM) and evodiamine (15 muM) synergistically inhibited the proliferation of MCF-7 cells in a time-dependent manner and resulted in the G0/G1 phase accumulation of cells that exhibited increased expression levels of the CDK inhibitors p21 and p27 with a concomitant reduction in the expression levels of cell-cycle checkpoint proteins cyclin D1, cyclin E, CDK4, and CDK6. evodiamine 115-125 H3 histone pseudogene 16 Homo sapiens 340-343 28960945-9 2017 These results suggest that afuresertib-induced p21 expression promotes G1 phase arrest by inducing FOXO activity. afuresertib 27-38 H3 histone pseudogene 16 Homo sapiens 47-50 28946186-4 2017 Mechanistic study revealed that Cryptotanshinone suppressed the expression of p-STAT3, Bcl-2, CDK2, Snail and MMP2, and induced the expression of E-cadherin, P53, P21 and beta-catenin. cryptotanshinone 32-48 H3 histone pseudogene 16 Homo sapiens 163-166 28801242-8 2017 H2O2 contributed to T/B-mediated ERK1/2 activation that mediated p53 phosphorylation at serine 15 (Ser15) and increased p21 expression. Hydrogen Peroxide 0-4 H3 histone pseudogene 16 Homo sapiens 120-123 28938245-8 2017 Collectively, our findings indicate that GA inhibits the cell viability of TNBC cells, which may attribute to the G1 phase arrest and cellular apoptosis via p38 mitogen-activated protein kinase/p21/p27 axis. Gallic Acid 41-43 H3 histone pseudogene 16 Homo sapiens 194-197 28994324-4 2017 Hyaluronic acid (HA) was introduced to shield the PEI/dsRNA-p21 binary complexes (BC-dsRNA-p21) for reducing the cytotoxicity of PEI and for increasing the tumor-targeted intracellular uptake by cancer cells through HA-CD44 mediated endocytosis. Hyaluronic Acid 0-15 H3 histone pseudogene 16 Homo sapiens 60-63 28994324-4 2017 Hyaluronic acid (HA) was introduced to shield the PEI/dsRNA-p21 binary complexes (BC-dsRNA-p21) for reducing the cytotoxicity of PEI and for increasing the tumor-targeted intracellular uptake by cancer cells through HA-CD44 mediated endocytosis. Hyaluronic Acid 0-15 H3 histone pseudogene 16 Homo sapiens 91-94 28994324-4 2017 Hyaluronic acid (HA) was introduced to shield the PEI/dsRNA-p21 binary complexes (BC-dsRNA-p21) for reducing the cytotoxicity of PEI and for increasing the tumor-targeted intracellular uptake by cancer cells through HA-CD44 mediated endocytosis. Hyaluronic Acid 17-19 H3 histone pseudogene 16 Homo sapiens 60-63 28994324-4 2017 Hyaluronic acid (HA) was introduced to shield the PEI/dsRNA-p21 binary complexes (BC-dsRNA-p21) for reducing the cytotoxicity of PEI and for increasing the tumor-targeted intracellular uptake by cancer cells through HA-CD44 mediated endocytosis. Hyaluronic Acid 17-19 H3 histone pseudogene 16 Homo sapiens 91-94 28901484-6 2017 These DOX-resistant cells also showed increases in p21, Bcl-2 and MDR-1 expression. Doxorubicin 6-9 H3 histone pseudogene 16 Homo sapiens 51-54 28982057-5 2017 BIX-01294 upregulates cell cycle inhibitor P21 expression and induces cell cycle arrest in the phase G0/G1. BIX 01294 0-9 H3 histone pseudogene 16 Homo sapiens 43-46 28892096-8 2017 Cholangioids exposed to hydrogen peroxide exhibited cellular senescence and the senescence-associated secretory phenotype (SASP; increased IL-6, p21, SA-beta-Gal, yH2A.x and p16 expression). Hydrogen Peroxide 24-41 H3 histone pseudogene 16 Homo sapiens 145-148 29113274-10 2017 Additionally, simvastatin in combination with doxorubicin significantly induced expression of the cyclin-dependent kinase inhibitor p21, increased cytochrome c and caspase 3 expression and reduced cyclin D1 expression. Simvastatin 14-25 H3 histone pseudogene 16 Homo sapiens 132-135 29113274-10 2017 Additionally, simvastatin in combination with doxorubicin significantly induced expression of the cyclin-dependent kinase inhibitor p21, increased cytochrome c and caspase 3 expression and reduced cyclin D1 expression. Doxorubicin 46-57 H3 histone pseudogene 16 Homo sapiens 132-135 29416718-8 2018 A specific p300 HAT inhibitor C646 impaired ING5-increased acetylation of H3K18 and p53K382, and subsequent expression of p21 and Bax. C646 30-34 H3 histone pseudogene 16 Homo sapiens 122-125 29094813-9 2017 P21 was up-regulated and cyclin D1 was down-regulated at both mRNA and protein levels under sodium valproate (2.0 mmol/L, 48h)(P<0.05), although cyclin E and cyclin A remained changed. Valproic Acid 92-108 H3 histone pseudogene 16 Homo sapiens 0-3 29093644-0 2017 Synergistic anticancer effect of combined crocetin and cisplatin on KYSE-150 cells via p53/p21 pathway. crocetin 42-50 H3 histone pseudogene 16 Homo sapiens 91-94 29093644-0 2017 Synergistic anticancer effect of combined crocetin and cisplatin on KYSE-150 cells via p53/p21 pathway. Cisplatin 55-64 H3 histone pseudogene 16 Homo sapiens 91-94 29093644-14 2017 The wild-type p53 inhibitor, PFT-alpha suppressed the overexpression of p53/p21 and the synergistic effect induced by the combination of crocetin and cisplatin. crocetin 137-145 H3 histone pseudogene 16 Homo sapiens 76-79 29093644-15 2017 Conclusions: We concluded that crocetin combined with cisplatin exerts a synergistic anticancer effect by up-regulating the p53/p21 pathway. crocetin 31-39 H3 histone pseudogene 16 Homo sapiens 128-131 29093644-15 2017 Conclusions: We concluded that crocetin combined with cisplatin exerts a synergistic anticancer effect by up-regulating the p53/p21 pathway. Cisplatin 54-63 H3 histone pseudogene 16 Homo sapiens 128-131 29051574-7 2017 Furthermore, FLO also induces G0/G1 cell cycle arrest via increase of p21 levels through activating ROS/p53/p21 pathway. florfenicol 13-16 H3 histone pseudogene 16 Homo sapiens 70-73 29051574-7 2017 Furthermore, FLO also induces G0/G1 cell cycle arrest via increase of p21 levels through activating ROS/p53/p21 pathway. florfenicol 13-16 H3 histone pseudogene 16 Homo sapiens 108-111 29051574-7 2017 Furthermore, FLO also induces G0/G1 cell cycle arrest via increase of p21 levels through activating ROS/p53/p21 pathway. Reactive Oxygen Species 100-103 H3 histone pseudogene 16 Homo sapiens 70-73 29051574-7 2017 Furthermore, FLO also induces G0/G1 cell cycle arrest via increase of p21 levels through activating ROS/p53/p21 pathway. Reactive Oxygen Species 100-103 H3 histone pseudogene 16 Homo sapiens 108-111 28649131-10 2017 In p53 wild-type A549 cells, PAB (20 mumol/L) caused senescence, and time-dependently increased glucose utilization; knockdown of p53 or p21 significantly decreased the uptake and metabolism of glucose but elevated PAB-induced apoptosis. pseudolaric acid B 215-218 H3 histone pseudogene 16 Homo sapiens 137-140 28991260-7 2017 We demonstrate that TIS Cal51 cells treated with 75 nM PTX for 7 days became senescent (senescence-associated beta-galactosidase (SA-beta-Gal) positive, Ki67-negative, increased p21 and p16, G2/M cell cycle arrest) and released significantly more EVs (P=0.0002) and exosomes (P=0.0007) than non-senescent control cells. Paclitaxel 55-58 H3 histone pseudogene 16 Homo sapiens 178-181 28670762-8 2017 TRIB2 was involved in the induction of a cisplatin-dependent cell cycle arrest and apoptosis by influencing p21 and survivin expression. Cisplatin 41-50 H3 histone pseudogene 16 Homo sapiens 108-111 28766629-1 2017 The isomeric compounds, 4-bromo-2-chloro benzoic acid (4Br) and 2-bromo-4-chlorobenzoic acid (2Br), crystallize in entirely different space groups, P21/n and P1[combining macron] respectively. 4-Bromo-2-chlorobenzoic acid 24-53 H3 histone pseudogene 16 Homo sapiens 148-151 28766629-1 2017 The isomeric compounds, 4-bromo-2-chloro benzoic acid (4Br) and 2-bromo-4-chlorobenzoic acid (2Br), crystallize in entirely different space groups, P21/n and P1[combining macron] respectively. 4BR 55-58 H3 histone pseudogene 16 Homo sapiens 148-151 28766629-1 2017 The isomeric compounds, 4-bromo-2-chloro benzoic acid (4Br) and 2-bromo-4-chlorobenzoic acid (2Br), crystallize in entirely different space groups, P21/n and P1[combining macron] respectively. 2-Bromo-4-chlorobenzoic acid 64-92 H3 histone pseudogene 16 Homo sapiens 148-151 28766629-1 2017 The isomeric compounds, 4-bromo-2-chloro benzoic acid (4Br) and 2-bromo-4-chlorobenzoic acid (2Br), crystallize in entirely different space groups, P21/n and P1[combining macron] respectively. 2-bromophenol 94-97 H3 histone pseudogene 16 Homo sapiens 148-151 28649131-2 2017 Our previous study showed that PAB mainly induced senescence via p53-p21 activation rather than apoptosis in suppression of the growth of human lung cancer A549 cells (p53 wild-type). pseudolaric acid B 31-34 H3 histone pseudogene 16 Homo sapiens 69-72 28649131-10 2017 In p53 wild-type A549 cells, PAB (20 mumol/L) caused senescence, and time-dependently increased glucose utilization; knockdown of p53 or p21 significantly decreased the uptake and metabolism of glucose but elevated PAB-induced apoptosis. Glucose 194-201 H3 histone pseudogene 16 Homo sapiens 137-140 28981000-1 2017 Crystals of cis-Re[(PNPCH2-iPr)(CO)2Cl] (1) are made up of two geometrically non-equivalent polytypes with respective symmetries of P21/c and I2/a. cis-re[(pnpch2-ipr) 12-31 H3 histone pseudogene 16 Homo sapiens 132-144 28691365-8 2017 Additionally, p21 and Akt separately controlled cell cycle arrest and ROS levels, respectively, during H-Ras-induced senescence in human normal fibroblasts. Reactive Oxygen Species 70-73 H3 histone pseudogene 16 Homo sapiens 14-17 27887857-10 2017 In vitro studies demonstrated that the inhibition of DPP-4 promoted PMA-induced monocytic cells differentiation, with increased CD68 and p21 expression, regulated by extracellular signal-regulated protein kinase 1/2 activation. Tetradecanoylphorbol Acetate 68-71 H3 histone pseudogene 16 Homo sapiens 137-140 28300289-3 2017 Dehydrocostus lactone suppresses the expression of cyclin B1, cyclin A, cyclin E, cyclin-dependent kinase 2 (CDK2), and cyclin-dependent kinase 1 (CDK1) and increases p21 expression, resulting in S-G2/M phase arrest in K562 cells. Lactones 14-21 H3 histone pseudogene 16 Homo sapiens 167-170 28757460-0 2017 Critical role of p21 on olaquindox-induced mitochondrial apoptosis and S-phase arrest involves activation of PI3K/AKT and inhibition of Nrf2/HO-1pathway. olaquindox 24-34 H3 histone pseudogene 16 Homo sapiens 17-20 28757460-3 2017 The present study aims to explore the molecular mechanism of p21 on olaquindox-induced mitochondrial apoptosis and S-phase arrest in human hepatoma G2 cells (HepG2). olaquindox 68-78 H3 histone pseudogene 16 Homo sapiens 61-64 28757460-4 2017 As a result, olaquindox promoted production of ROS, suppressed the protein expression p21 in p53-independent way and phosphorylated p21. olaquindox 13-23 H3 histone pseudogene 16 Homo sapiens 86-89 28757460-4 2017 As a result, olaquindox promoted production of ROS, suppressed the protein expression p21 in p53-independent way and phosphorylated p21. olaquindox 13-23 H3 histone pseudogene 16 Homo sapiens 132-135 28757460-7 2017 Furthermore, knockdown of p21 decreased cell viability, enhanced oxidative stress, aggravated olaquindox-induced mitochondrial apoptosis and S-phase arrest involvement of activating PI3K/AKT and inhibiting Nrf2/HO-1 pathway. olaquindox 94-104 H3 histone pseudogene 16 Homo sapiens 26-29 28757460-9 2017 In conclusion, knockdown of p21 increased olaquindox-induced mitochondrial apoptosis and S-phase arrest through further activating PI3K/AKT and inhibiting Nrf2/HO-1pathway. olaquindox 42-52 H3 histone pseudogene 16 Homo sapiens 28-31 28741869-0 2017 Increased baseline RUNX2, caspase 3 and p21 gene expressions in the peripheral blood of disease-modifying anti-rheumatic drug-naive rheumatoid arthritis patients are associated with improved clinical response to methotrexate therapy. Methotrexate 212-224 H3 histone pseudogene 16 Homo sapiens 40-43 28741869-11 2017 Increased baseline gene expressions of RUNX2, p21 and caspase 3 in the peripheral blood might predict better responses to MTX therapy. Methotrexate 122-125 H3 histone pseudogene 16 Homo sapiens 46-49 29441880-9 2017 We concluded that, in the absence of a guest, solvent channels are lost during transformation to the monoclinic crystal system and space group P21/c (Form I) so that water cannot enter after desolvation. Water 166-171 H3 histone pseudogene 16 Homo sapiens 143-148 28888100-5 2017 In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed. MK-8776 83-92 H3 histone pseudogene 16 Homo sapiens 50-53 28888100-5 2017 In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed. Cisplatin 97-106 H3 histone pseudogene 16 Homo sapiens 50-53 28888100-5 2017 In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed. UNII-37WM0V5E17 110-115 H3 histone pseudogene 16 Homo sapiens 50-53 28849226-7 2017 Cell cycle was arrested at G1 phase and expression of cyclin D1, c-myc, PCNA was reduced while p21 was upregulated during daidzein treatment. daidzein 122-130 H3 histone pseudogene 16 Homo sapiens 95-98 28928376-5 2017 Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells. oligo-fucoidan 29-43 H3 histone pseudogene 16 Homo sapiens 98-101 28627468-0 2017 A novel chalcone derivative, LQFM064, induces breast cancer cells death via p53, p21, KIT and PDGFRA. Chalcone 8-16 H3 histone pseudogene 16 Homo sapiens 81-84 28906520-3 2017 Both compounds 1 and 2 crystallize in the monoclinic space group P21/c as two-dimensional coordination polymers (2D-CPs). Polymers 103-111 H3 histone pseudogene 16 Homo sapiens 65-70 28993733-0 2017 LncRNA-uc002mbe.2 Interacting with hnRNPA2B1 Mediates AKT Deactivation and p21 Up-Regulation Induced by Trichostatin in Liver Cancer Cells. trichostatin A 104-116 H3 histone pseudogene 16 Homo sapiens 75-78 28993733-5 2017 Knockdown of uc002mbe.2 prohibited TSA-induced G2/M cell cycle arrest, p21 induction, and apoptosis of Huh7 cells and reversed the TSA-mediated decrease in p-AKT. trichostatin A 35-38 H3 histone pseudogene 16 Homo sapiens 71-74 28993733-9 2017 In addition, the ability of TSA to reduce hnRNPA2B1 and p-AKT levels and induce p21 in the xenograft tumors was prevented by uc002mbe.2 knockdown. trichostatin A 28-31 H3 histone pseudogene 16 Homo sapiens 80-83 28993733-10 2017 Therefore, the interaction of uc002mbe.2 and hnRNPA2B1 in mediating AKT deactivation and p21 induction is involved in the cytostatic effect of trichostatin in liver cancer cells. trichostatin A 143-155 H3 histone pseudogene 16 Homo sapiens 89-92 28928376-5 2017 Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells. Etoposide 47-56 H3 histone pseudogene 16 Homo sapiens 98-101 28894133-8 2017 Rapamycin abrogated 5-MTP-mediated suppression of p16, p21, SA-beta-Gal and IL-6 and rise of BrdU incorporation. Sirolimus 0-9 H3 histone pseudogene 16 Homo sapiens 55-58 28777576-3 2017 Two molecules in the unit cell of the monoclinic P21 crystal form a net of NH OS and C*H OS hydrogen bonds. Hydrogen 96-104 H3 histone pseudogene 16 Homo sapiens 49-52 29250352-1 2017 The title compounds, C16H14O2S2 and C16H14O3S, which are monomeric models (models D and E) for a polythio-noester and a poly(ester-co-thio-noester), respectively, crystallize in the space group P21/c and are isostructural with each other. Phenylacetyl disulfide 21-31 H3 histone pseudogene 16 Homo sapiens 194-199 29250352-1 2017 The title compounds, C16H14O2S2 and C16H14O3S, which are monomeric models (models D and E) for a polythio-noester and a poly(ester-co-thio-noester), respectively, crystallize in the space group P21/c and are isostructural with each other. SMR000011762 36-45 H3 histone pseudogene 16 Homo sapiens 194-199 27458249-6 2017 The results of this study suggest that FKB induced cell death through p21-mediated cell cycle arrest and activation of p38. flavokawain B 39-42 H3 histone pseudogene 16 Homo sapiens 70-73 28872062-1 2017 After reporting the structure of a new polymorph of 1,3,5-trifluoro-2,4,6-triiodobenzene (denoted BzF3I3), C6F3I3, (I), which crystallized in the space group P21/c, we perform a comparative analysis with the already reported P21/n polymorph, (II) [Reddy et al. 1,3,5-trifluoro-2,4,6-triiodobenzene 52-88 H3 histone pseudogene 16 Homo sapiens 158-163 28872062-1 2017 After reporting the structure of a new polymorph of 1,3,5-trifluoro-2,4,6-triiodobenzene (denoted BzF3I3), C6F3I3, (I), which crystallized in the space group P21/c, we perform a comparative analysis with the already reported P21/n polymorph, (II) [Reddy et al. 1,3,5-trifluoro-2,4,6-triiodobenzene 52-88 H3 histone pseudogene 16 Homo sapiens 225-246 28639950-7 2017 We found that AZD1152-HQPA treatment induced defective cell survival, polyploidy, micronuclei formation, cell enlargement, and cell death by significant overexpression of p73, p21 and downregulation of cell cycle-regulatory genes in a drug concentration-dependent manner. AZD 1152-HQPA 14-26 H3 histone pseudogene 16 Homo sapiens 176-179 29024968-9 2017 Quantitative analysis of immunohistochemical staining revealed that human ovarian tissue sections with positive Prussian blue staining had lower levels of proliferating cell nuclear antigen expression, but higher levels of p21, p53, and CDC25C expression than those with negative Prussian blue staining. prussian 112-120 H3 histone pseudogene 16 Homo sapiens 223-226 28700975-6 2017 Detailed study shows that astilbin leads to S phase arrest of the cell cycle by induction of p53 and p21 and activated-AMPK. astilbin 26-34 H3 histone pseudogene 16 Homo sapiens 101-104 28872062-1 2017 After reporting the structure of a new polymorph of 1,3,5-trifluoro-2,4,6-triiodobenzene (denoted BzF3I3), C6F3I3, (I), which crystallized in the space group P21/c, we perform a comparative analysis with the already reported P21/n polymorph, (II) [Reddy et al. bzf3i3 98-104 H3 histone pseudogene 16 Homo sapiens 158-163 28872062-1 2017 After reporting the structure of a new polymorph of 1,3,5-trifluoro-2,4,6-triiodobenzene (denoted BzF3I3), C6F3I3, (I), which crystallized in the space group P21/c, we perform a comparative analysis with the already reported P21/n polymorph, (II) [Reddy et al. bzf3i3 98-104 H3 histone pseudogene 16 Homo sapiens 225-246 28816773-5 2017 In our study, combined 3-BP and 5-FU treatment upregulated p53 and p21, whereas cyclin-dependent kinase CDK4 and CDK2 were downregulated, which led to G0/G1 phase arrest. bromopyruvate 23-27 H3 histone pseudogene 16 Homo sapiens 67-70 28816773-5 2017 In our study, combined 3-BP and 5-FU treatment upregulated p53 and p21, whereas cyclin-dependent kinase CDK4 and CDK2 were downregulated, which led to G0/G1 phase arrest. Fluorouracil 32-36 H3 histone pseudogene 16 Homo sapiens 67-70 28780382-9 2017 Mechanistically GO and MGO induce senescence by increasing the ROS production, the expression of p21, the accumulation of AGEs and the arrest of HVECs in the G2 cell cycle phase. Pyruvaldehyde 23-26 H3 histone pseudogene 16 Homo sapiens 97-100 28927780-9 2017 The combination of specific inhibitors of ERK1/2, JNK or PI3K/Akt pathway and metformin further promoted cell apoptosis and the up-regulation of p21, Bax, Bad, cleaved caspase-3 and -9 as well as the down-regulation of Bcl-2 mediated by metformin alone, but inhibition of p38 pathway exhibited the opposite results. Metformin 78-87 H3 histone pseudogene 16 Homo sapiens 145-148 28818808-6 2017 Levels of cell cycle-DNA repair regulator p21, CHK1 and FANCD2 levels were markedly affected by givinostat treatment. givinostat 96-106 H3 histone pseudogene 16 Homo sapiens 42-45 28797070-4 2017 We find that methyl pyruvate protects irinotecan-treated normal lung fibroblast cell line (MRC-5) probably by turning off the p53/p21 axis of the apoptotic pathways. methyl pyruvate 13-28 H3 histone pseudogene 16 Homo sapiens 130-133 27644130-8 2017 The transcriptional activation of p21 was shown to be dependent on p53, as it can be blocked by PFT-alpha, and correlated with the increased phosphorylation of p53 at Serine 15. Serine 167-173 H3 histone pseudogene 16 Homo sapiens 34-37 27644130-9 2017 Our results suggest that in FAD lymphocytes, the p53-mediated increase in p21 transcription, together with a shift in the nucleocytoplasmic localization of p21, confers a survival advantage against 2dRib-induced apoptosis. 2drib 198-203 H3 histone pseudogene 16 Homo sapiens 74-77 27644130-9 2017 Our results suggest that in FAD lymphocytes, the p53-mediated increase in p21 transcription, together with a shift in the nucleocytoplasmic localization of p21, confers a survival advantage against 2dRib-induced apoptosis. 2drib 198-203 H3 histone pseudogene 16 Homo sapiens 156-159 28675489-8 2017 Moreover, real-time reverse transcription polymerase chain reaction analysis indicated significant (p < 0.01) overexpression of p21, but not GATA6, in auraptene pretreated cells after radiotherapy, and also significant (p < 0.01) down regulation of CD44 and ALDH1 by auraptene. aurapten 154-163 H3 histone pseudogene 16 Homo sapiens 131-134 28675489-8 2017 Moreover, real-time reverse transcription polymerase chain reaction analysis indicated significant (p < 0.01) overexpression of p21, but not GATA6, in auraptene pretreated cells after radiotherapy, and also significant (p < 0.01) down regulation of CD44 and ALDH1 by auraptene. aurapten 273-282 H3 histone pseudogene 16 Homo sapiens 131-134 28711224-7 2017 RESULTS: In vitro pTyr pre-treatment showed no radioprotection on Y79 cells, but led to p53 stabilisation in unirradiated Y79 cells and to a facilitation of radiation-induced p21 up-regulation, confirming a modulation of p53 activity by pTyr. Phosphotyrosine 18-22 H3 histone pseudogene 16 Homo sapiens 175-178 28851980-7 2017 Surprisingly, these effects did not involve changes in p21 expression, indicating that other hypoxia-activated factors may induce p21 in CPCs. cpcs 137-141 H3 histone pseudogene 16 Homo sapiens 130-133 28837147-12 2017 In keeping, p21 mRNA, that is induced by p53 and inhibited by ZEB1, is induced by DOXO treatment and is decreased by SDF1 administration. Doxorubicin 82-86 H3 histone pseudogene 16 Homo sapiens 12-15 28777561-2 2017 Increasing the calcium concentration to form YSr0.5Ca1.5Mn2O7 leads to a change in the cooperative tilting on the MnO6 units to a novel a-b-c-/b-a-c- arrangement described in space group P21/n11. Calcium 15-22 H3 histone pseudogene 16 Homo sapiens 187-190 28777561-2 2017 Increasing the calcium concentration to form YSr0.5Ca1.5Mn2O7 leads to a change in the cooperative tilting on the MnO6 units to a novel a-b-c-/b-a-c- arrangement described in space group P21/n11. mno6 114-118 H3 histone pseudogene 16 Homo sapiens 187-190 28819136-9 2017 In addition, BPA caused DNA damage through the p53-p21 signaling pathway. bisphenol A 13-16 H3 histone pseudogene 16 Homo sapiens 51-54 28471807-10 2017 Deguelin induced differentiation by downregulating the Mt-NPM1 protein levels, which was accompanied by a decrease in SIRT1, p21, and HDAC1 and an increase in CEBPbeta and granulocyte colony-stimulating factor receptor protein expression levels. deguelin 0-8 H3 histone pseudogene 16 Homo sapiens 125-128 28737380-2 2017 The structure of TcO2 between 25 and 1000 C has been determined in situ using X-ray powder diffraction methods and is found to remain monoclinic in space group P21/c. dioxotechnetium 17-21 H3 histone pseudogene 16 Homo sapiens 161-166 28583901-8 2017 In addition, encapsulating BA-TPQ in the hydrogels amplifies the potency of the drug via down-regulation of MDM2 oncogenic protein and upregulation of p53 (a tumor suppressor) and p21 (cell proliferation suppressor) expression in HepG2 liver cancer cells. 7-(benzylamino)-1,3,4,8-tetrahydropyrrolo(4,3,2-de)quinolin-8(1H)-one 27-33 H3 histone pseudogene 16 Homo sapiens 180-183 28823263-5 2017 RESULTS: Phenelzine inhibited proliferation and promoted apoptosis of Jeko-1 cells in a dose-dependent way by increasing the expression of apoptosis related protein BAX, Caspase-3 and p21, while decreasing anti-apoptotic protein BCL-2. Phenelzine 9-19 H3 histone pseudogene 16 Homo sapiens 184-187 28341289-5 2017 Furthermore, high dose LPS (>=10mug/ml) induced cell death involving mitochondrial pathways, death receptors as well as p21-dependent DNA damage response activation mediated by ROS generation and TNF-alpha release. ros 180-183 H3 histone pseudogene 16 Homo sapiens 123-126 28705212-13 2017 Finally, MAC was found to trigger apoptotic death pathway (based on expression levels of cleaved-caspase 3, Bax/Bcl-2 balance, p53 and p21). mac 9-12 H3 histone pseudogene 16 Homo sapiens 135-138 28702644-3 2017 The noteworthy order-disorder transition of the phosphonium cation and the motions of anions contribute to the phase transition, leading to the space group P21/c at a low temperature phase to C2/c at a high temperature phase. Phosphoranes 48-59 H3 histone pseudogene 16 Homo sapiens 156-161 28728544-14 2017 The figure shows that Cladosporol A induced apoptosis through ROS mediated mitochondrial pathway and increased p21 protein expression in MCF-7 cells in vitro. cladosporol A 22-35 H3 histone pseudogene 16 Homo sapiens 111-114 28702525-1 2017 Hafnium oxide (HfO2) can exist in different crystalline structures such as monoclinic at room temperature, tetragonal at 1700 C and cubic at 2600 C. In the present study, nanocrystalline powders of HfO2 synthesized by a Pechini type sol-gel technique show a monoclinic phase, P21/c, at room temperature. hafnium oxide 0-13 H3 histone pseudogene 16 Homo sapiens 278-283 28702525-1 2017 Hafnium oxide (HfO2) can exist in different crystalline structures such as monoclinic at room temperature, tetragonal at 1700 C and cubic at 2600 C. In the present study, nanocrystalline powders of HfO2 synthesized by a Pechini type sol-gel technique show a monoclinic phase, P21/c, at room temperature. hafnium oxide 15-19 H3 histone pseudogene 16 Homo sapiens 278-283 28702525-2 2017 By incorporating Dy into the HfO2 lattice, the intensity of all diffraction peaks corresponding to P21/c decreases and at a concentration of 11 at% of Dy, the monoclinic phase transforms completely to the cubic phase, Fm3[combining macron]m, showing a mixed phase of monoclinic and cubic at intermediate concentrations (5-9 at%) of Dy. hafnium oxide 29-33 H3 histone pseudogene 16 Homo sapiens 99-104 28696369-4 2017 It was discovered that DHAP downregulated the expression of oncogenic gene products like Bcl-xl, Bcl-2, Mcl-1, Survivin, Cyclin D1, IAP-1, Cyclin E, COX-2, and MMP-9, and upregulated the expression of Bax and p21 proteins, consistent with the induction of G2/M phase cell cycle arrest and apoptosis in U266 cells. Dihydroxyacetone Phosphate 23-27 H3 histone pseudogene 16 Homo sapiens 209-212 28243656-5 2017 The second charge consisted of the imido carbonate (tBu3SiO)(Me3SiO)C[double bond, length as m-dash]N-SitBu3 (monoclinic, space group P21/n). tbu3sio 52-59 H3 histone pseudogene 16 Homo sapiens 134-137 28243656-5 2017 The second charge consisted of the imido carbonate (tBu3SiO)(Me3SiO)C[double bond, length as m-dash]N-SitBu3 (monoclinic, space group P21/n). me3sio 61-67 H3 histone pseudogene 16 Homo sapiens 134-137 28190316-4 2017 When HaCaT cells were pretreated with 4-O-methylhonokiol, TGF-beta1-induced G1/G0 phase arrest and TGF-beta1-induced p21 expression were decreased. 4-O-methylhonokiol 38-56 H3 histone pseudogene 16 Homo sapiens 117-120 28245170-10 2017 CFEZO treatments induced upregulation of p53 and p21 expression and downregulation of cyclin D1 and cyclin-dependent kinase-4 expression, which were accompanied by G2/M phase arrest. cfezo 0-5 H3 histone pseudogene 16 Homo sapiens 49-52 28598608-5 2017 Furthermore, a high-pressure phase of SrO2 with P21/c symmetries containing two layers of peroxide ions with different orientations is uncovered at pressures higher than 36 GPa. sro2 38-42 H3 histone pseudogene 16 Homo sapiens 48-51 28718371-11 2017 These results demonstrated that the messenger RNA expression levels of p53 and p21 may have a relationship with the changes in telomere length induced by omethoate and provided strong evidence for the mechanism of canceration induced by poison. dimethoxon 154-163 H3 histone pseudogene 16 Homo sapiens 79-82 28251795-4 2017 Quercetin-induced G0 /G1 -phase arrest occurred when expressions of cyclin-dependent kinase (CDK)2/4 were inhibited and the CDK inhibitors, p16 and p21, were induced. Quercetin 0-9 H3 histone pseudogene 16 Homo sapiens 148-151 28672399-10 2017 HCECs cultured without SB203580 showed high positive SA-beta-gal staining, a low nuclear/cytoplasm ratio, and expression of p16 and p21. SB 203580 23-31 H3 histone pseudogene 16 Homo sapiens 132-135 28808400-0 2017 Induction of Apoptosis and Cell Cycle Arrest by Flavokawain C on HT-29 Human Colon Adenocarcinoma via Enhancement of Reactive Oxygen Species Generation, Upregulation of p21, p27, and GADD153, and Inactivation of Inhibitor of Apoptosis Proteins. flavokawain C 48-61 H3 histone pseudogene 16 Homo sapiens 169-172 28463795-8 2017 Western blot analysis indicated remarkable concentration dependent alterations in the expression of proliferation and survival proteins CD1, E2F, CE1, p53, p21, BAX, BCL-2, cytochrome C and cleaved PARP in cisatracurium-treated groups as compared with the untreated group. cisatracurium 206-219 H3 histone pseudogene 16 Homo sapiens 156-159 28318508-7 2017 Unlike TBMEHP, TBPH caused early apoptosis after G2/M phase arrest only at 10mug/mL via up-regulation of p21 and down-regulation of CDK2 and CDK4. bis(2-ethylhexyl) 2,3,4,5-tetrabromophthalate 15-19 H3 histone pseudogene 16 Homo sapiens 105-108 28757172-0 2017 Polyphyllin VII increases sensitivity to gefitinib by modulating the elevation of P21 in acquired gefitinib resistant non-small cell lung cancer. polyphyllin VII 0-15 H3 histone pseudogene 16 Homo sapiens 82-85 28757172-0 2017 Polyphyllin VII increases sensitivity to gefitinib by modulating the elevation of P21 in acquired gefitinib resistant non-small cell lung cancer. Gefitinib 41-50 H3 histone pseudogene 16 Homo sapiens 82-85 28757172-0 2017 Polyphyllin VII increases sensitivity to gefitinib by modulating the elevation of P21 in acquired gefitinib resistant non-small cell lung cancer. Gefitinib 98-107 H3 histone pseudogene 16 Homo sapiens 82-85 28757172-5 2017 In the present study, we aim to examined the sensitizing effect of Polyphyllin VII to gefitinib by modulating P21 signaling pathway in gefitinib acquired resistant NSCLC in vitro and in vivo. polyphyllin VII 67-82 H3 histone pseudogene 16 Homo sapiens 110-113 28757172-5 2017 In the present study, we aim to examined the sensitizing effect of Polyphyllin VII to gefitinib by modulating P21 signaling pathway in gefitinib acquired resistant NSCLC in vitro and in vivo. Gefitinib 86-95 H3 histone pseudogene 16 Homo sapiens 110-113 28757172-5 2017 In the present study, we aim to examined the sensitizing effect of Polyphyllin VII to gefitinib by modulating P21 signaling pathway in gefitinib acquired resistant NSCLC in vitro and in vivo. Gefitinib 135-144 H3 histone pseudogene 16 Homo sapiens 110-113 28757172-8 2017 Polyphyllin VII enhanced the anti-proliferative effects of gefitinib and gefitinib-induced G1 phase arrest by modulation of P21 signaling pathway in acquired gefitinib resistant cells in vitro and in vivo. polyphyllin VII 0-15 H3 histone pseudogene 16 Homo sapiens 124-127 28757172-8 2017 Polyphyllin VII enhanced the anti-proliferative effects of gefitinib and gefitinib-induced G1 phase arrest by modulation of P21 signaling pathway in acquired gefitinib resistant cells in vitro and in vivo. Gefitinib 59-68 H3 histone pseudogene 16 Homo sapiens 124-127 28757172-8 2017 Polyphyllin VII enhanced the anti-proliferative effects of gefitinib and gefitinib-induced G1 phase arrest by modulation of P21 signaling pathway in acquired gefitinib resistant cells in vitro and in vivo. Gefitinib 73-82 H3 histone pseudogene 16 Homo sapiens 124-127 28757172-8 2017 Polyphyllin VII enhanced the anti-proliferative effects of gefitinib and gefitinib-induced G1 phase arrest by modulation of P21 signaling pathway in acquired gefitinib resistant cells in vitro and in vivo. Gefitinib 73-82 H3 histone pseudogene 16 Homo sapiens 124-127 28757172-9 2017 Polyphyllin VII elevated sensitization of gefitinib acquired resistant NSCLC cells to gefitinib through G1 phase arrest and modulation of P21 signaling pathway. polyphyllin VII 0-15 H3 histone pseudogene 16 Homo sapiens 138-141 28757172-9 2017 Polyphyllin VII elevated sensitization of gefitinib acquired resistant NSCLC cells to gefitinib through G1 phase arrest and modulation of P21 signaling pathway. Gefitinib 42-51 H3 histone pseudogene 16 Homo sapiens 138-141 28757172-9 2017 Polyphyllin VII elevated sensitization of gefitinib acquired resistant NSCLC cells to gefitinib through G1 phase arrest and modulation of P21 signaling pathway. Gefitinib 86-95 H3 histone pseudogene 16 Homo sapiens 138-141 28808400-12 2017 FKC induced cell cycle arrest at the G1 and G2/M phases via upregulation of p21 and p27 in a p53-independent manner. flavokawain C 0-3 H3 histone pseudogene 16 Homo sapiens 76-79 28465245-0 2017 1,25-Dihydroxyvitamin D3 suppresses gastric cancer cell growth through VDR- and mutant p53-mediated induction of p21. Calcitriol 0-24 H3 histone pseudogene 16 Homo sapiens 113-116 28881801-0 2017 A screen for inducers of bHLH activity identifies pitavastatin as a regulator of p21, Rb phosphorylation and E2F target gene expression in pancreatic cancer. pitavastatin 50-62 H3 histone pseudogene 16 Homo sapiens 81-84 28881801-8 2017 At the molecular level, pitavastatin induced expression of the cyclin dependent kinase (CDK) inhibitor p21 in a cholesterol independent manner, blocked repressive phosphorylation of the Retinoblastoma tumor suppressor protein at CDK targeted sites, and reduced expression of E2F target genes required for progression through the G1/S boundary. pitavastatin 24-36 H3 histone pseudogene 16 Homo sapiens 103-106 28881801-8 2017 At the molecular level, pitavastatin induced expression of the cyclin dependent kinase (CDK) inhibitor p21 in a cholesterol independent manner, blocked repressive phosphorylation of the Retinoblastoma tumor suppressor protein at CDK targeted sites, and reduced expression of E2F target genes required for progression through the G1/S boundary. Cholesterol 112-123 H3 histone pseudogene 16 Homo sapiens 103-106 28661480-5 2017 The reason for this may be an increase in the level of cellular ROS after knockdown of Prdx2, which may subsequently lead to an increase in the expression of phosphorylated p53 (p-p53) and p38-MAPK/p21. Reactive Oxygen Species 64-67 H3 histone pseudogene 16 Homo sapiens 198-201 28465245-7 2017 Furthermore, 1,25(OH)2D3 stimulated p21 expression and suppressed cyclin-dependent kinase 2 (CDK2) expression in TMK1 in a VDR-dependent manner. Calcitriol 13-24 H3 histone pseudogene 16 Homo sapiens 36-39 28465245-9 2017 Besides, mutp53 but not wild type p53 was essential for 1,25(OH)2D3-stimulated upregulation of p21 in gastric cancer cells. (oh)2d3 60-67 H3 histone pseudogene 16 Homo sapiens 95-98 28465245-11 2017 SIGNIFICANCE: Our results suggest that 1,25(OH)2D3 inhibits gastric cancer cell growth through VDR and mutp53 interaction followed by the modulation of p21/CDK2. Calcitriol 39-50 H3 histone pseudogene 16 Homo sapiens 152-155 28594934-10 2017 GW6471 treatment was associated with a marked decrease of CDK4, cyclin D3 and cyclin B1 protein expression, along with an increased expression of p21 in HNPGL cells. GW 6471 0-6 H3 histone pseudogene 16 Homo sapiens 146-149 28620223-2 2017 The produced crystalline AlCl3.6H2O and Al(NO3)3.9H2O in the first stage of the preparation method were characterized by single-crystal XRD, giving two crystal structures, a trigonal (R-3c) and monoclinic (P21/c) structure, respectively. Aluminum Chloride 25-35 H3 histone pseudogene 16 Homo sapiens 206-211 28620223-2 2017 The produced crystalline AlCl3.6H2O and Al(NO3)3.9H2O in the first stage of the preparation method were characterized by single-crystal XRD, giving two crystal structures, a trigonal (R-3c) and monoclinic (P21/c) structure, respectively. al(no3)3.9h2o 40-53 H3 histone pseudogene 16 Homo sapiens 206-211 28492321-1 2017 Crystals of a Vanthoffite mineral, Na6Mn(SO4)4, grown from an aqueous solution, belong to a monoclinic system, P21/c, Z = 2, at ambient temperature. vanthoffite 14-25 H3 histone pseudogene 16 Homo sapiens 111-123 28492321-1 2017 Crystals of a Vanthoffite mineral, Na6Mn(SO4)4, grown from an aqueous solution, belong to a monoclinic system, P21/c, Z = 2, at ambient temperature. na6mn 35-40 H3 histone pseudogene 16 Homo sapiens 111-123 27859531-7 2017 Rolipram (10 muM) and DC-TA-46 (0.5 muM) produced a decrease of cyclin expression, in particular of cyclin A, as well as an increase in p21, p27 and p53, as evaluated by Western blot analysis. Rolipram 0-8 H3 histone pseudogene 16 Homo sapiens 136-139 28572552-4 2017 Whereas pure CaCuGe2O6 exhibits P21/c symmetry with a strong distortion of the M1 octahedra and two different Ge sites, one of them with an unusual fivefold coordination, the replacement of Cu2+ by Zn2+ induces a chemically driven phase change to the C2/c symmetry. cacuge2o6 13-22 H3 histone pseudogene 16 Homo sapiens 32-37 28213701-5 2017 Triterpenotids (5-10 microM) caused G0/G1 cell cycle arrest, an increase in p21 levels and SA-beta-galactosidase staining that was accompanied by oxidative stress and DNA damage. triterpenotids 0-14 H3 histone pseudogene 16 Homo sapiens 76-79 27530507-11 2017 Teneligliptin improves proliferation rates in human umbilical vein endothelial cells exposed to high glucose, regulating the expression of cell-cycle inhibitors markers (P53, P21 and P27), and reducing proapoptotic genes (BAX and CASP3), while promotes BCL2 expression. 3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine 0-13 H3 histone pseudogene 16 Homo sapiens 175-178 28588670-11 2017 beta-elemene with hyperthermia treatment significantly promoted P21 and Bax mRNA expression (P<0.01) and significantly decreased caspase-9, Bcl-2 and survivin mRNA expression (P<0.01) in A549 cells. beta-elemene 0-12 H3 histone pseudogene 16 Homo sapiens 64-67 27859531-7 2017 Rolipram (10 muM) and DC-TA-46 (0.5 muM) produced a decrease of cyclin expression, in particular of cyclin A, as well as an increase in p21, p27 and p53, as evaluated by Western blot analysis. 7-benzylamino-6-chloro-2-piperazino-4-pyrrolidinopteridine 22-30 H3 histone pseudogene 16 Homo sapiens 136-139 28558682-9 2017 Meanwhile, the expression of several regulators that contribute to G1/S phased transition, such as Cyclin D1, CDK4 and CDK6, were significantly down-regulated with the up-regulation of cell cycle inhibitors, p21 and p53, after treatment with glucosamine. Glucosamine 242-253 H3 histone pseudogene 16 Homo sapiens 208-211 28572741-2 2017 TLBZT effectively induces cell senescence in colorectal carcinoma, accompanied by p21 upregulation. tlbzt 0-5 H3 histone pseudogene 16 Homo sapiens 82-85 28530706-6 2017 Interestingly, the p21 deceleration was rescued by incubating the cells with 3-AWA in the presence of an ER stress inhibitor, Salubrinal. 3-awa 77-82 H3 histone pseudogene 16 Homo sapiens 19-22 28530706-6 2017 Interestingly, the p21 deceleration was rescued by incubating the cells with 3-AWA in the presence of an ER stress inhibitor, Salubrinal. salubrinal 126-136 H3 histone pseudogene 16 Homo sapiens 19-22 28719347-0 2017 Regulatory effects of the novel synthesized Indole-3-carbaldehyde on expression of cell cycle genes: A study on Cyclin D and P21 expression by acute promylocytic leukemia cell line (NB4) This article has been withdrawn. indole-3-carbaldehyde 44-65 H3 histone pseudogene 16 Homo sapiens 125-128 28572741-4 2017 Specific knockdown of p21 expression by small interfering RNA significantly attenuated TLBZT-induced cell senescence in human colorectal carcinoma LS174T cells. tlbzt 87-92 H3 histone pseudogene 16 Homo sapiens 22-25 28572741-8 2017 These data suggested that TLBZT induces cell senescence in LS174T cells through a mechanism involving p21 upregulation via histone H3 and H4 acetylation. tlbzt 26-31 H3 histone pseudogene 16 Homo sapiens 102-105 28572741-3 2017 In this study, we further explored the role of p21 in TLBZT-induced cell senescence, as well as the mechanism by which TLBZT upregulates p21. tlbzt 119-124 H3 histone pseudogene 16 Homo sapiens 137-140 28735518-9 2017 The short OS group exhibits a decrease in Smad 7 expression and also low levels of p21 immunostaining, which represents a common target of the two pathways. Osmium 10-12 H3 histone pseudogene 16 Homo sapiens 83-86 28496336-0 2017 Curcumin exerts its antitumor activity through regulation of miR-7/Skp2/p21 in nasopharyngeal carcinoma cells. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 72-75 28560001-5 2017 Mechanistically, ICA II induced apoptosis and cell cycle arrest, and this cytotoxic effect was dependent on the reduction of Forkhead box O3a(FOXO3a) phosphorylation mediated by Akt and the enrichment of nuclear FOXO3a, which initiated the transcription of p21/p27. isocyanic acid 17-20 H3 histone pseudogene 16 Homo sapiens 257-260 28522974-11 2017 Up-regulation of p53 and p21 in colorectal carcinoma cells treated with low-dose PTX also contributed to inhibition of tumor cell growth. Paclitaxel 81-84 H3 histone pseudogene 16 Homo sapiens 25-28 28494020-9 2017 5-Aminoimidazole-4-carboxamide-ribonucleoside (AICAR), an activator of AMPK, reduced mDP cell proliferation and induced p21 expression. acadesine 0-45 H3 histone pseudogene 16 Homo sapiens 120-123 28494020-9 2017 5-Aminoimidazole-4-carboxamide-ribonucleoside (AICAR), an activator of AMPK, reduced mDP cell proliferation and induced p21 expression. acadesine 47-52 H3 histone pseudogene 16 Homo sapiens 120-123 28494020-11 2017 Taken together, our results suggest that Panx3 modulates intracellular ATP levels, resulting in the inhibition of odontoblast proliferation through the AMPK/p21 signaling pathway and promotion of cell differentiation by the BMP/Smad signaling pathway. Adenosine Triphosphate 71-74 H3 histone pseudogene 16 Homo sapiens 157-160 28375611-2 2017 We report that this [(CH3)2NH2]PbI3 compound with 2H-perovskite structure experiences a first-order transition at 250 K from hexagonal symmetry P63/mmc (HT phase) to monoclinic symmetry P21/c (LT phase), which involves two cooperative processes: an off-center shift of the Pb2+ cations and an order-disorder process of the N atoms of the DMA cations. [(ch3)2nh2]pbi3 20-35 H3 histone pseudogene 16 Homo sapiens 187-192 28915591-7 2017 Furthermore eugenol for external (1 mg) markedly decreased the protein expressions of HER2 (62.9%), AKT (58.6%), PDK1 (56.4%), p85 (54.3%), Bcl2 (59.3%), NF-kappaB (65.7%), Bad (64.0%), Cyclin D1 (43.0%), while p21, p27 and Bax protein expressions were respectively increased 1.83-, 2.52- and 2.51-fold. Eugenol 12-19 H3 histone pseudogene 16 Homo sapiens 211-214 27633574-8 2017 Carbon ions caused larger increase in the quantity of p53 and p21 compared to therapeutic protons. Carbon 0-6 H3 histone pseudogene 16 Homo sapiens 62-65 28375611-2 2017 We report that this [(CH3)2NH2]PbI3 compound with 2H-perovskite structure experiences a first-order transition at 250 K from hexagonal symmetry P63/mmc (HT phase) to monoclinic symmetry P21/c (LT phase), which involves two cooperative processes: an off-center shift of the Pb2+ cations and an order-disorder process of the N atoms of the DMA cations. 2h-perovskite 50-63 H3 histone pseudogene 16 Homo sapiens 187-192 28459194-6 2017 Therapy-induced senescence by 3-deazaneplanocin A was mediated through p53-p21 pathway and triggered by enhanced ataxia-telangiectasia mutated activation related to chromatin changes. 3-deazaneplanocin 30-49 H3 histone pseudogene 16 Homo sapiens 75-78 28447756-8 2017 The mRNA expression levels of p53 and p21 in the group treated with 240 mg/l matrine were significantly higher compared with the control group. matrine 77-84 H3 histone pseudogene 16 Homo sapiens 38-41 28447756-10 2017 The protein expression levels of p53 and p21 were significantly higher in the 240 mg/l matrine group compared with the control group. matrine 87-94 H3 histone pseudogene 16 Homo sapiens 41-44 28521485-6 2017 Celecoxib treatment led to G1 arrest via the upregulation of p21 and p27 expression in GBC-SD and NOZ cells, whereas PD184161 did not affect cell cycle distribution. Celecoxib 0-9 H3 histone pseudogene 16 Homo sapiens 61-64 28140474-13 2017 PL significantly reduced the p53 (-80%), p21 (-84%), and Ki-67 (-48%) positive cells. pl 0-2 H3 histone pseudogene 16 Homo sapiens 41-44 28004224-10 2017 Moreover, TBBE and TBWE treated MCF-7, HeLa and U87 cells showed upregulation of p53 and p21 proteins. tbbe 10-14 H3 histone pseudogene 16 Homo sapiens 89-92 27982581-6 2017 Etoposide caused rapid accumulation of 53bp1-GFP in DNA damage foci, which was later followed by the concentration dependent nuclear accumulation of p53-GFP and subsequent induction of p21-GFP. Etoposide 0-9 H3 histone pseudogene 16 Homo sapiens 185-188 28428754-6 2017 In particular, the JNK-specific inhibitor SP600125 restored the induction of P-JNK, P-p53 (Ser15), p21, CyclinD1 and CyclinE by Pu-erh tea extract. pyrazolanthrone 42-50 H3 histone pseudogene 16 Homo sapiens 99-102 28428754-6 2017 In particular, the JNK-specific inhibitor SP600125 restored the induction of P-JNK, P-p53 (Ser15), p21, CyclinD1 and CyclinE by Pu-erh tea extract. pu-erh 128-134 H3 histone pseudogene 16 Homo sapiens 99-102 28216618-5 2017 The signaling pathways involved in DAG-caused cell cycle arrest was further analyzed in LN229 cells, which revealed that DAG dose-dependently activated two parallel signaling cascades, ie, the p53-p21 cascade and the CDC25C-CDK1 cascade. Dianhydrogalactitol 35-38 H3 histone pseudogene 16 Homo sapiens 197-200 28216618-5 2017 The signaling pathways involved in DAG-caused cell cycle arrest was further analyzed in LN229 cells, which revealed that DAG dose-dependently activated two parallel signaling cascades, ie, the p53-p21 cascade and the CDC25C-CDK1 cascade. Dianhydrogalactitol 121-124 H3 histone pseudogene 16 Homo sapiens 197-200 28427193-3 2017 Importantly, with the lower IC50 and stronger anti-tumor effect than selective inhibitors, SNS-314, the pan-inhibitor of Aurora kinases, which induced YAP (Yes-associated protein) reduction and resulted in P21 accumulation, significantly promoted the polyploidy (> 4N) formation and apoptosis in HCC. SNS 314 91-98 H3 histone pseudogene 16 Homo sapiens 206-209 28427193-5 2017 Moreover, silencing YAP also induced P21 accumulation, and knockdown P21, which enhanced YAP accumulation and weakened the SNS-314-induced YAP reduction, impaired SNS-314-induced apoptosis. SNS 314 123-130 H3 histone pseudogene 16 Homo sapiens 69-72 28427193-5 2017 Moreover, silencing YAP also induced P21 accumulation, and knockdown P21, which enhanced YAP accumulation and weakened the SNS-314-induced YAP reduction, impaired SNS-314-induced apoptosis. SNS 314 163-170 H3 histone pseudogene 16 Homo sapiens 69-72 28427193-6 2017 Therefore, P21 enhanced the apoptotic effect of SNS-314 in HCC. SNS 314 48-55 H3 histone pseudogene 16 Homo sapiens 11-14 28465635-10 2017 In KYSE-70 cells treated with 50 mumol/L berberine for 48 h, the number of cells in G2/M phase (25.94% +- 5.01%) was significantly higher than that in the control group (9.77% +- 1.28%, P < 0.01), and berberine treatment resulted in p21 up-regulation in KYSE-70 cells. Berberine 41-50 H3 histone pseudogene 16 Homo sapiens 236-239 28369097-10 2017 Moderate to high concentrations of alcohol (0.1-0.8% v/v) induced p53 activation, as indicated by increased p53 phosphorylation, reporter gene activity, and p21/Bax gene expression, which led to G0/G1 cell cycle arrest. Alcohols 35-42 H3 histone pseudogene 16 Homo sapiens 157-160 28369097-11 2017 Importantly, compared to MCF-7/Con cells, alcohol-induced DNA damage was significantly enhanced, while alcohol-induced p21/Bax expression and cell cycle arrest were attenuated in MCF-7/sip53 cells. Alcohols 103-110 H3 histone pseudogene 16 Homo sapiens 119-122 28161489-9 2017 Consistent with FOXO1 dephosphorylation/activation, p21 mRNA expression is increased by Bortezomib in a MKP-3-dependent way. Bortezomib 88-98 H3 histone pseudogene 16 Homo sapiens 52-55 28161489-11 2017 It is concluded that in vGPCR cells, Bortezomib decreases ERK1/2 and FOXO1 phosphorylation through MKP-3 accumulation, leading ERK1/2 deactivation and FOXO1 activation respectively and, consequently, to cell proliferation inhibition, p21 induction and VEGF repression. Bortezomib 37-47 H3 histone pseudogene 16 Homo sapiens 234-237 28004224-10 2017 Moreover, TBBE and TBWE treated MCF-7, HeLa and U87 cells showed upregulation of p53 and p21 proteins. tbwe 19-23 H3 histone pseudogene 16 Homo sapiens 89-92 27539251-7 2017 Moreover, the protein level of p21 and E-cadherin decreased in response to treatment with fludioxonil, but remained at the control level when co-treated with ICI 182,780. fludioxonil 90-101 H3 histone pseudogene 16 Homo sapiens 31-34 27463516-7 2017 Western blot analysis indicated that PCB77 increased the expression of cyclin E, CDK2, p21, and caspase-9, while PCB40 decreased the expression of these proteins (except CDK2 and p21). 3,4,3',4'-tetrachlorobiphenyl 37-42 H3 histone pseudogene 16 Homo sapiens 87-90 28454475-5 2017 Detailed signaling pathway analysis by western blotting demonstrated that the expression levels of p53 and p21 were upregulated, whereas the expression of cyclin-dependent kinase 1 was downregulated following oridonin treatment, which led to cell cycle arrest in the G2/M phase. oridonin 209-217 H3 histone pseudogene 16 Homo sapiens 107-110 28126652-2 2017 The protein encoded by this gene forms an activated complex with GTP-bound RAS-like (P21), CDC2 and RAC1 proteins which then mediates a variety of cellular processes. Guanosine Triphosphate 65-68 H3 histone pseudogene 16 Homo sapiens 85-88 28254430-5 2017 Intriguingly, we found that Idelalisib-induced apoptosis in NB4, as the most sensitive cell line with the lowest expression level of the aforementioned genes, is executed probably via alteration in the transcriptional level of apoptosis-related genes coupled with p21-mediated caspase-3 activation. idelalisib 28-38 H3 histone pseudogene 16 Homo sapiens 264-267 27995497-6 2017 Mechanically, salinomycin-induced cell growth inhibition against human glioma was mainly achieved by induction of G1-phase arrest via triggering reactive oxide species (ROS)-mediated DNA damage, as convinced by the activation of histone, p53, p21 and p27. salinomycin 14-25 H3 histone pseudogene 16 Homo sapiens 243-246 28454438-5 2017 In addition, western blot analyses revealed that valproic acid induced tumor suppressor protein (p)53 and p21 expression, and activated checkpoint kinase 2 (CHK2) in MCF7 cells and primary mouse embryonic fibroblasts. Valproic Acid 49-62 H3 histone pseudogene 16 Homo sapiens 106-109 28120534-6 2017 Sulforaphane induced G2/M cell-cycle arrest with the induction of p21 in KF112 cells. sulforaphane 0-12 H3 histone pseudogene 16 Homo sapiens 66-69 28454438-6 2017 Notably, treatment with valproic acid also induced increases in the level of p21 protein levels and CHK2 activity in p53-null colon cancer HCT116 cells. Valproic Acid 24-37 H3 histone pseudogene 16 Homo sapiens 77-80 28341848-8 2017 In addition, we found that Nrf2 knockdown prevented gAcrp-induced p62 expression, and p21 knockdown prevented Nrf2 induction, suggesting the role of p21/Nrf2 axis in gAcrp-induced p62 expression. gacrp 166-171 H3 histone pseudogene 16 Homo sapiens 86-89 28341848-8 2017 In addition, we found that Nrf2 knockdown prevented gAcrp-induced p62 expression, and p21 knockdown prevented Nrf2 induction, suggesting the role of p21/Nrf2 axis in gAcrp-induced p62 expression. gacrp 166-171 H3 histone pseudogene 16 Homo sapiens 149-152 28356713-7 2017 Gene and protein expression studies revealed significant upregulation of cytochrome c, Bax, caspases 7 and 9, and p21 in Artonin E-treated MCF-7 cells, while MAPK and cyclin D were downregulated. artonin E 121-130 H3 histone pseudogene 16 Homo sapiens 114-117 28386336-8 2017 A combination of celecoxib and irradiation treatment induced much more gamma-H2AX foci formation, higher levels of radiation injury-related proteins phosphorylation, G2/M arrest, apoptosis, and p53 and p21 expression, and lower levels of Cyclin B1 in HCT116 cells than those in cells treated with irradiation alone. Celecoxib 17-26 H3 histone pseudogene 16 Homo sapiens 202-205 28386336-11 2017 Celecoxib affects the functions of p53 and inhibits the recovery from the irradiation-induced injury by up-regulating the expression of BCCIP, and subsequently regulates the expressions of genes such as p21 and Cyclin B1 to enhance the radiosensitivity of HCT116 cells in a COX-2 independent manner. Celecoxib 0-9 H3 histone pseudogene 16 Homo sapiens 203-206 28098861-8 2017 Triptolide treatment of HepG2 cells caused a significant increase in the expression of p21, Bax and DR5 genes in HepG2 cells. triptolide 0-10 H3 histone pseudogene 16 Homo sapiens 87-90 28092770-8 2017 RESULTS: Magnolin inhibited the proliferation and viability of the tumor cells by triggering cell cycle arrest via P53/P21 activation and inducing apoptosis in vitro and in vivo. magnolin 9-17 H3 histone pseudogene 16 Homo sapiens 119-122 28081982-4 2017 RESULTS: The results showed that prolonged HG induced senescence in fibroblasts through activation of p21 and p16 in a reactive oxygen species (ROS)-dependent manner, further delayed the viability and migration in fibroblasts and also depressed fibroblast differentiation through the TGF-beta/Smad signaling pathway. Reactive Oxygen Species 119-142 H3 histone pseudogene 16 Homo sapiens 102-105 28081982-4 2017 RESULTS: The results showed that prolonged HG induced senescence in fibroblasts through activation of p21 and p16 in a reactive oxygen species (ROS)-dependent manner, further delayed the viability and migration in fibroblasts and also depressed fibroblast differentiation through the TGF-beta/Smad signaling pathway. Reactive Oxygen Species 144-147 H3 histone pseudogene 16 Homo sapiens 102-105 28107195-5 2017 Furthermore, CA-PZ markedly increased the protein expression levels of acetyl-H3, acetyl-H4 and p21 in HT-29 cells and MIA PaCa-2 cells. cinnamoylphenazine 13-18 H3 histone pseudogene 16 Homo sapiens 96-99 28382091-11 2017 RESULTS: FK866 treatment was able to increase p53 levels and acetylation, upregulate BAX and p21 expression, and induce apoptosis in MCF-7 cells. N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide 9-14 H3 histone pseudogene 16 Homo sapiens 93-96 28280414-5 2017 Moreover, quercetin increased FasL mRNA expression and p51, p21 and GADD45 signaling activities. Quercetin 10-19 H3 histone pseudogene 16 Homo sapiens 60-63 28280414-9 2017 Knockdown of Foxo3a and inhibition of JNK activity reduced the signaling activities of p53, p21 and GADD45, triggered by quercetin. Quercetin 121-130 H3 histone pseudogene 16 Homo sapiens 92-95 28184921-8 2017 Moreover, the expression levels of Ki-67, PCAN, MMP-2, MMP-9 and FOXM1 were decreased, and P21 was increased in the TSN-treated SGC-7901 cells (p<0.01). tanshinone 116-119 H3 histone pseudogene 16 Homo sapiens 91-94 29027433-6 2017 Combined use of JNK inhibitor SP600125 and p38 inhibitor SB203580 could decrease p21 and increase beta-Catenin protein expressions. pyrazolanthrone 30-38 H3 histone pseudogene 16 Homo sapiens 81-84 29027433-6 2017 Combined use of JNK inhibitor SP600125 and p38 inhibitor SB203580 could decrease p21 and increase beta-Catenin protein expressions. SB 203580 57-65 H3 histone pseudogene 16 Homo sapiens 81-84 27677740-4 2017 Reverse-phase protein array, mass-cytometry and Western analyses revealed that BETi treatment attenuated the protein expressions of c-MYC, p-STAT5, Bcl-xL, CDK4/6, PIM1 and IL-7R, whereas it concomitantly induced the levels of HEXIM1, p21 and BIM in the sAML cells. beti 79-83 H3 histone pseudogene 16 Homo sapiens 235-238 28351316-9 2017 In addition, cyclopentaquinoline derivatives induced expression of cyclin-dependent kinase 2 inhibitor, p21; however, tetrahydroacridine derivatives had no significant effect on p21. Cyclopentaquinoline 13-32 H3 histone pseudogene 16 Homo sapiens 104-107 28382142-7 2017 Results: Ectopic expression of PRC1 significantly increased the chemoresistance, promoted the tumor growth and abrogated 5-FU-induced G2/M phase arrest via p21/p27-pRBs pathway. Fluorouracil 121-125 H3 histone pseudogene 16 Homo sapiens 156-159 28055975-7 2017 BTZ stabilized p21, CDC2, and cyclin B in RRCL and in primary tumor cells. Bortezomib 0-3 H3 histone pseudogene 16 Homo sapiens 15-18 28230855-0 2017 Simvastatin-induced cell cycle arrest through inhibition of STAT3/SKP2 axis and activation of AMPK to promote p27 and p21 accumulation in hepatocellular carcinoma cells. Simvastatin 0-11 H3 histone pseudogene 16 Homo sapiens 118-121 28230855-5 2017 In this study, we demonstrated simvastatin-induced G0/G1 arrest by inducing p21 and p27 accumulation in HepG2 and Hep3B cells. Simvastatin 31-42 H3 histone pseudogene 16 Homo sapiens 76-79 28230855-6 2017 Simvastatin also promoted AMP-activated protein kinase (AMPK) activation, which induced p21 upregulation by increasing its transcription. Simvastatin 0-11 H3 histone pseudogene 16 Homo sapiens 88-91 28230855-10 2017 Mevalonate decreased simvastatin-induced AMPK activation and rescued phospho-STAT3 and Skp2 expression in HCC cells, which resulted in the prevention of G0/G1 arrest through inhibition of p21 and p27 accumulation. Mevalonic Acid 0-10 H3 histone pseudogene 16 Homo sapiens 188-191 28230855-10 2017 Mevalonate decreased simvastatin-induced AMPK activation and rescued phospho-STAT3 and Skp2 expression in HCC cells, which resulted in the prevention of G0/G1 arrest through inhibition of p21 and p27 accumulation. Simvastatin 21-32 H3 histone pseudogene 16 Homo sapiens 188-191 28230855-12 2017 Consistently, we found that simvastatin also increased p21 and p27 expression in tumor sections by reducing Skp2 expression and inducing AMPK activation and STAT3 suppression in the same tumor tissues. Simvastatin 28-39 H3 histone pseudogene 16 Homo sapiens 55-58 28230855-13 2017 Taken together, these findings are demonstrative of the existence of a novel pathway in which simvastatin induces G0/G1 arrest by upregulating p21 and p27 by activating AMPK and inhibiting the STAT3-Skp2 axis, respectively. Simvastatin 94-105 H3 histone pseudogene 16 Homo sapiens 143-146 28367100-6 2017 The recruitment of PADI4 and histone H3 arginine modifications to p21 promoter was measured by chromatin immunoprecipitation. Arginine 40-48 H3 histone pseudogene 16 Homo sapiens 66-69 28367100-12 2017 PADI4 suppresses p21 transcription through altering histone H3 arginine modifications on p21 promoter region. Arginine 63-71 H3 histone pseudogene 16 Homo sapiens 17-20 28367100-12 2017 PADI4 suppresses p21 transcription through altering histone H3 arginine modifications on p21 promoter region. Arginine 63-71 H3 histone pseudogene 16 Homo sapiens 89-92 28055975-8 2017 Transient p21 knockdown alleviates BTZ-induced senescence inhibition, G2-M cell cycle blockade, and mitotic catastrophe. Bortezomib 35-38 H3 histone pseudogene 16 Homo sapiens 10-13 28055975-9 2017 Our data suggest that BTZ can induce apoptosis or mitotic catastrophe and that p21 has a pivotal role in BTZ activity against RRCL. Bortezomib 105-108 H3 histone pseudogene 16 Homo sapiens 79-82 27908660-6 2017 Mechanistic studies showed that triptonide induced senescence followed by apoptosis mainly by suppressing transcription of TERT and oncogenic c-Myc, while concomitantly promoting transcription of senescence-promoting genes p16 and p21 and the pro-apoptotic gene encoding DNA damage-inducible transcript 3. triptonide 32-42 H3 histone pseudogene 16 Homo sapiens 231-234 28067494-3 2017 These new thiophosphates crystallize in four different structure types, with the space groups Fdd2, P1, P21, and P21/c, respectively. thiophosphoric acid 10-24 H3 histone pseudogene 16 Homo sapiens 104-107 28112302-2 2017 It appears that the structure of beta-CdTeO3 (Pnma, Z = 16, a = 7.45850(3) A, b = 14.52185(6) A, c = 11.04584(5) A) is closely related to that of alpha-CdTeO3 (P21/c, Z = 8, a = 7.790(1) A, b = 11.253(2) A, c = 7.418(1) A, beta = 113.5(1) ) previously reported. beta-cdteo3 33-44 H3 histone pseudogene 16 Homo sapiens 160-172 28124696-8 2017 Clonidine crystallizes in the monoclinic space group P21/c as a twinned crystal. Clonidine 0-9 H3 histone pseudogene 16 Homo sapiens 53-58 27894814-10 2017 Finally, the apoptotic molecules such as Bax/Bcl2, cleavage caspase 3 and the cell cycle regulation factors including p21, cyclin D1, and CDK6 were changed by Tanshinone IIA. tanshinone 159-169 H3 histone pseudogene 16 Homo sapiens 118-121 28067494-3 2017 These new thiophosphates crystallize in four different structure types, with the space groups Fdd2, P1, P21, and P21/c, respectively. thiophosphoric acid 10-24 H3 histone pseudogene 16 Homo sapiens 113-118 28143426-13 2017 Induction of apoptosis by frondoside A was associated with the regulation of several pro-apoptotic factors, like caspase-3, -8, and -9, PARP, Bax, p21, DNA fragmentation, and externalization of phosphatidylserine. frondoside A 26-38 H3 histone pseudogene 16 Homo sapiens 147-150 27307158-0 2017 Hydroquinone-induced FOXP3-ADAM17-Lyn-Akt-p21 signaling axis promotes malignant progression of human leukemia U937 cells. hydroquinone 0-12 H3 histone pseudogene 16 Homo sapiens 42-45 28157129-3 2017 3-(4-Fluorophenyl)-1-(naphthalen-2-yl)prop-2-en-1-one, C19H13FO, (I), crystallizes with Z" = 2 in the space group P-1 and the four molecules in the unit cell adopt an arrangement which resembles that in the space group P21/a. 3-(4-fluorophenyl)-1-(naphthalen-2-yl)prop-2-en-1-one 0-53 H3 histone pseudogene 16 Homo sapiens 219-222 28157129-3 2017 3-(4-Fluorophenyl)-1-(naphthalen-2-yl)prop-2-en-1-one, C19H13FO, (I), crystallizes with Z" = 2 in the space group P-1 and the four molecules in the unit cell adopt an arrangement which resembles that in the space group P21/a. c19h13fo 55-63 H3 histone pseudogene 16 Homo sapiens 219-222 27939630-3 2017 We also found that endosulfan can damage microfilaments, microtubules, and nuclei; arrest mitosis; remarkably increase the expressions of Dll4, Notch1, Cleaved-Notch1, Jagged1, Notch4, Hes1, and p21; and significantly induce ROS and malondialdehyde production in HUVECs. Endosulfan 19-29 H3 histone pseudogene 16 Homo sapiens 195-198 27939630-4 2017 The presence of DAPT antagonized the above changes of cycle arrest, proliferation inhibition, and expressions of Dll4, Notch1, Cleaved-Notch1, Hes1, and p21 caused by endosulfan; however, NAC could attenuate LDH release; ROS and malondialdehyde production; apoptosis; and the expression levels of Dll4, Notch1, Cleaved-Notch1, Notch4, and Hes1 induced by endosulfan. dapt 16-20 H3 histone pseudogene 16 Homo sapiens 153-156 28101580-12 2017 MeOH fraction arrested HepG2 cells at the G0/G1 phase in a concentration-dependent manner, and resulted in decreased expression of cyclin D1, cyclin E, cyclin-dependent kinase (CDK)2, CDK4, CDK6, p21, and p27. Methanol 0-4 H3 histone pseudogene 16 Homo sapiens 196-199 28272690-0 2017 Licorice and its active compound glycyrrhizic acid ameliorates cisplatin-induced nephrotoxicity through inactivation of p53 by scavenging ROS and overexpression of p21 in human renal proximal tubular epithelial cells. Glycyrrhizic Acid 33-50 H3 histone pseudogene 16 Homo sapiens 164-167 28272690-0 2017 Licorice and its active compound glycyrrhizic acid ameliorates cisplatin-induced nephrotoxicity through inactivation of p53 by scavenging ROS and overexpression of p21 in human renal proximal tubular epithelial cells. Cisplatin 63-72 H3 histone pseudogene 16 Homo sapiens 164-167 28272690-13 2017 Meanwhile, LE and GA enhanced cisplatin-induced p21 expression, which then led to S-phase arrest in cell cycle and limited cell growth. Cisplatin 30-39 H3 histone pseudogene 16 Homo sapiens 48-51 28272690-14 2017 Presumably, increased p21 expression may contribute to cellular prevention from cisplatin-induced apoptosis, because p21 is the key molecule to cytoprotection during cisplatin-induced nephrotoxicity. Cisplatin 80-89 H3 histone pseudogene 16 Homo sapiens 22-25 28272690-14 2017 Presumably, increased p21 expression may contribute to cellular prevention from cisplatin-induced apoptosis, because p21 is the key molecule to cytoprotection during cisplatin-induced nephrotoxicity. Cisplatin 80-89 H3 histone pseudogene 16 Homo sapiens 117-120 28272690-14 2017 Presumably, increased p21 expression may contribute to cellular prevention from cisplatin-induced apoptosis, because p21 is the key molecule to cytoprotection during cisplatin-induced nephrotoxicity. Cisplatin 166-175 H3 histone pseudogene 16 Homo sapiens 22-25 28272690-14 2017 Presumably, increased p21 expression may contribute to cellular prevention from cisplatin-induced apoptosis, because p21 is the key molecule to cytoprotection during cisplatin-induced nephrotoxicity. Cisplatin 166-175 H3 histone pseudogene 16 Homo sapiens 117-120 28035361-6 2017 An increase in the total apoptotic cells and G2/M cell cycle arrest with decreased protein expression of CDC25C, CDK1, cyclin B1 and p21 were observed in Hep3B cells treated with flavonoids of C. platymamma. Flavonoids 179-189 H3 histone pseudogene 16 Homo sapiens 133-136 27793694-8 2017 In addition, BI 6727 treatment caused a marked induction of p53 and p21 in vitro as well as in vivo. BI 6727 13-20 H3 histone pseudogene 16 Homo sapiens 68-71 26755751-4 2017 In the present study, norcantharidin suppressed the proliferation and cloning ability of SK-N-SH cells in a dose-dependent manner, apparently by reducing the mitochondrial membrane potential and arresting SK-N-SH cells at the G2/M stage, accompanied by elevated expressions of p21 and decreased expressions of cyclin B1 and cell division control 2. norcantharidin 22-36 H3 histone pseudogene 16 Homo sapiens 277-280 27592355-3 2017 RESULTS: Cellular viability revealed that high doses of hydroxytyrosol reduced cancer cells viability concomitantly with a reduction of cyclin D1 expression and an up-regulation of cell cycle key modulator p21 levels. 3,4-dihydroxyphenylethanol 56-70 H3 histone pseudogene 16 Homo sapiens 206-209 27842004-2 2017 The compound is synthesized by nitrate route and is found to crystallize in monoclinic P21/n space group. Nitrates 31-38 H3 histone pseudogene 16 Homo sapiens 87-90 28103869-6 2017 In addition, our results suggested that sinularin triggered DNA damage and subsequently induced cell cycle G2/M arrest associated with up-regulation of p-ATM (Ser(1981)), p-Chk2 (Tyr(68)), p-cdc2 (Tyr(15)), and p53 coupled with increased expression of downstream proteins p21 and down-regulation of p-cdc25 (Ser(216)). sinularin 40-49 H3 histone pseudogene 16 Homo sapiens 272-275 27238838-7 2017 Furthermore, the elevated ROS levels that accompanied Foxp3 overexpression were paralleled by an increase in p21 expression. Reactive Oxygen Species 26-29 H3 histone pseudogene 16 Homo sapiens 109-112 28011195-3 2017 In this study, using direct co-culture model with LPS-activated and Dox-induced senescent THP-1 monocytes, we reported for the first time ROS-induced DNA damage, reduced metabolic activity, proliferation inhibition and cell cycle arrest followed by p16-, p21- and p27-mediated DNA damage response pathways activation, premature senescence and apoptosis induction in HeLa cells. Doxorubicin 68-71 H3 histone pseudogene 16 Homo sapiens 255-258 28011195-3 2017 In this study, using direct co-culture model with LPS-activated and Dox-induced senescent THP-1 monocytes, we reported for the first time ROS-induced DNA damage, reduced metabolic activity, proliferation inhibition and cell cycle arrest followed by p16-, p21- and p27-mediated DNA damage response pathways activation, premature senescence and apoptosis induction in HeLa cells. ros 138-141 H3 histone pseudogene 16 Homo sapiens 255-258 27238838-8 2017 Knockdown of p21 in Foxp3-expressing MEFs abrogated the Foxp3-dependent increase in ROS levels, indicating that Foxp3 acts through the induction of p21 and the subsequent ROS elevation to trigger senescence. Reactive Oxygen Species 84-87 H3 histone pseudogene 16 Homo sapiens 13-16 27238838-8 2017 Knockdown of p21 in Foxp3-expressing MEFs abrogated the Foxp3-dependent increase in ROS levels, indicating that Foxp3 acts through the induction of p21 and the subsequent ROS elevation to trigger senescence. Reactive Oxygen Species 84-87 H3 histone pseudogene 16 Homo sapiens 148-151 27238838-8 2017 Knockdown of p21 in Foxp3-expressing MEFs abrogated the Foxp3-dependent increase in ROS levels, indicating that Foxp3 acts through the induction of p21 and the subsequent ROS elevation to trigger senescence. Reactive Oxygen Species 171-174 H3 histone pseudogene 16 Homo sapiens 13-16 27911270-3 2017 The treatment with SAHA increased the expression of acetyl-histones 3 and 4, which were recruited to the promoters of p21, p27, Cyclin D1, c-myc and Nanog to down-regulate their transcriptional levels. Vorinostat 19-23 H3 histone pseudogene 16 Homo sapiens 118-121 28068431-0 2017 CIL-102-Induced Cell Cycle Arrest and Apoptosis in Colorectal Cancer Cells via Upregulation of p21 and GADD45. 1-(4-(furo(2,3-b)quinolin-4-ylamino)phenyl)ethanone 0-7 H3 histone pseudogene 16 Homo sapiens 95-98 27901471-6 2017 Furthermore, the levels of p27 and p21, two key regulators of the cell cycle, were up-regulated by the esculetin-mediated down-regulation of Sp1; the level of a third cell-cycle regulator, survivin, was decreased, resulting in caspase-dependent apoptosis. esculetin 103-112 H3 histone pseudogene 16 Homo sapiens 35-38 27890807-4 2017 Diosmin caused G2/M cell cycle arrest, elevation in p53, p21 and p27 levels and stress-induced premature senescence when used at lower concentrations (5 and 10muM). Diosmin 0-7 H3 histone pseudogene 16 Homo sapiens 57-60 28068431-8 2017 Collectively, our results demonstrated that CIL-102 induced cell cycle arrest and apoptosis of colon cancer cells by upregulating p21 and GADD45 expression and by activating JNK1/2, NFkappaB p50 and p300 to provide a new mechanism for CIL-102 treatment. 1-(4-(furo(2,3-b)quinolin-4-ylamino)phenyl)ethanone 44-51 H3 histone pseudogene 16 Homo sapiens 130-133 27816443-4 2017 Correspondingly, lucidone promoted the cell-cycle by increasing PCNA/CDK4 and decreasing p21/p27 expressions. lucidone 17-25 H3 histone pseudogene 16 Homo sapiens 89-92 29050481-6 2017 CONCLUSION: MiR-497 can activate P21 expression by inhibiting the expression of MAPK/Erk signaling pathway, thus promoting the apoptosis of osteosarcoma cells (Fig. mir-497 12-19 H3 histone pseudogene 16 Homo sapiens 33-36 27913286-6 2017 Coumestrol treatment induced ROS generation coupled to DNA fragmentation, up-regulation of p53/p21, cell cycle arrest at G1/S phase, mitochondrial membrane depolarization and caspases 9/3 activation. Coumestrol 0-10 H3 histone pseudogene 16 Homo sapiens 95-98 27913286-6 2017 Coumestrol treatment induced ROS generation coupled to DNA fragmentation, up-regulation of p53/p21, cell cycle arrest at G1/S phase, mitochondrial membrane depolarization and caspases 9/3 activation. ros 29-32 H3 histone pseudogene 16 Homo sapiens 95-98 27853777-4 2016 K3La(BH4)6 crystallizes in the monoclinic crystal system with unit cell parameters a = 7.938(2), b = 8.352(2), c = 11.571(3) A, beta = 90.19(6) and space group P21/n with a double-perovskite type structure. k3la 0-4 H3 histone pseudogene 16 Homo sapiens 161-164 28043143-9 2017 Annexin V-FITC/PI staining showed a significant dose-dependent induction of apoptosis by ALA-PDT in H8 cells, associated with accumulation of the tumor suppressor protein p53 and the cyclin-dependent kinase inhibitor p21. Alanine 89-92 H3 histone pseudogene 16 Homo sapiens 217-220 28004113-3 2017 Interesting, suberoyl bis-hydroxamic acid (SBHA) administration could induce Notch1 intracellular domain levels in a dose-dependent manner, coupled with the increase of p53 and p21. suberoyl bis-hydroxamic acid 13-41 H3 histone pseudogene 16 Homo sapiens 177-180 28004113-3 2017 Interesting, suberoyl bis-hydroxamic acid (SBHA) administration could induce Notch1 intracellular domain levels in a dose-dependent manner, coupled with the increase of p53 and p21. suberoyl bis-hydroxamic acid 43-47 H3 histone pseudogene 16 Homo sapiens 177-180 28045428-7 2017 Although butyrate increased H3 histone deacetylation and p21 tumor suppressor expression in both cell types, p21 protein level was greater with intense expression around the nuclei in HCT116 cells when compared with that in NCM460 cells. Butyrates 9-17 H3 histone pseudogene 16 Homo sapiens 57-60 28203649-3 2016 We observed increased expression of heme and iron-regulated genes, previously shown to inhibit HIV-1, including ferroportin, IKBalpha, HO-1, p21, and SAM domain and HD domain-containing protein 1 (SAMHD1). Heme 36-40 H3 histone pseudogene 16 Homo sapiens 141-144 28203649-3 2016 We observed increased expression of heme and iron-regulated genes, previously shown to inhibit HIV-1, including ferroportin, IKBalpha, HO-1, p21, and SAM domain and HD domain-containing protein 1 (SAMHD1). Iron 45-49 H3 histone pseudogene 16 Homo sapiens 141-144 27853777-4 2016 K3La(BH4)6 crystallizes in the monoclinic crystal system with unit cell parameters a = 7.938(2), b = 8.352(2), c = 11.571(3) A, beta = 90.19(6) and space group P21/n with a double-perovskite type structure. sapropterin 5-8 H3 histone pseudogene 16 Homo sapiens 161-164 28003970-0 2016 Effects of resveratrol on ARPE-19 cell proliferation and migration via regulating the expression of proliferating cell nuclear antigen, P21, P27 and p38MAPK/MMP-9. Resveratrol 11-22 H3 histone pseudogene 16 Homo sapiens 136-139 27958228-14 2016 The mRNA and protein expression levels of the p21 and p27 in the K562/A02 cells were also significantly higher in the Wog-MNPs-Fe3O4group compared with those of the wogonin group (all P< 0.001). fe3o4group 127-137 H3 histone pseudogene 16 Homo sapiens 46-49 27912880-11 2016 Combination treatment of BA and HCPT induced BGC823 cells apoptosis mainly via intrinsic rather than extrinsic pathways, and preferentially arresting cell cycle in G1 and G2 phases with the aid of p21. baicalein 25-27 H3 histone pseudogene 16 Homo sapiens 197-200 27912880-11 2016 Combination treatment of BA and HCPT induced BGC823 cells apoptosis mainly via intrinsic rather than extrinsic pathways, and preferentially arresting cell cycle in G1 and G2 phases with the aid of p21. 10-hydroxycamptothecin 32-36 H3 histone pseudogene 16 Homo sapiens 197-200 27941214-6 2016 Particularly, loading with BAPTA attenuated phosphorylation of the main DNA damage response members, including ATM, 53BP1 and H2A.X and reduced activation of the p53/p21/Rb pathway in H2O2-stimulated cells. 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid 27-32 H3 histone pseudogene 16 Homo sapiens 166-169 27676608-5 2016 Specifically, (-)-bassianolide induced G0/G1 arrest associated with a decrease of cyclin A, D1 and an increase of p53, MDM2, and p21 expression in MDA-MB 231 cells. bassianolide 14-30 H3 histone pseudogene 16 Homo sapiens 129-132 27771218-5 2016 The crystal structures of N-lauroyl-beta-alanine (NLBA) and N-myristoyl-beta-alanine (NMBA) were solved in monoclinic system in the P21/c space group. N-lauroyl-beta-alanine 26-48 H3 histone pseudogene 16 Homo sapiens 132-137 27981533-3 2016 We wished to ascertain if TA induces toxicity by causing oxidative stress and alters expression of P21, growth differentiation factor (GDF)15, and cFos. Triamcinolone Acetonide 26-28 H3 histone pseudogene 16 Homo sapiens 99-102 27354472-9 2016 Ganetespib with radiation also dose-dependently upregulated p21 and downregulated pRb levels that were not apparent with either drug or radiation alone. STA 9090 0-10 H3 histone pseudogene 16 Homo sapiens 60-63 27824003-12 2016 Moreover, IKKbeta inhibitor SC-514 totally reversed the upregulation of IKKbeta and downregulation of p53 and p21 by LPS in SiHa cells. SC 514 28-34 H3 histone pseudogene 16 Homo sapiens 110-113 28053903-10 2016 Also, immunoblotting analysis indicated that p53 and p21 were detected only in YD-8 and YD-9 cell lines after cisplatin treatment. Cisplatin 110-119 H3 histone pseudogene 16 Homo sapiens 53-56 27818231-20 2016 In addition, 5muM PEITC significantly enhanced p21, caspase-3, 7 and Bax levels and reduced Cyclin B1 expression compared with the control group. phenethyl isothiocyanate 18-23 H3 histone pseudogene 16 Homo sapiens 47-50 27882937-0 2016 EZH2 mediates lidamycin-induced cellular senescence through regulating p21 expression in human colon cancer cells. C 1027 14-23 H3 histone pseudogene 16 Homo sapiens 71-74 27534652-9 2016 Our data also demonstrated that miR-181a inhibitor arrested cell cycle progression of HeLa and CaSKi cells by up-regulation of p21 and p27 expressions. mir-181a 32-40 H3 histone pseudogene 16 Homo sapiens 127-130 27588384-9 2016 Exposure to p-coumaric acid increased p53 and p21 expression but decreased CDK4 levels in both cell types, which could result in the observed G0/G1 arrest. p-coumaric acid 12-27 H3 histone pseudogene 16 Homo sapiens 46-49 27432063-8 2016 These results indicated that over expression of miR-200c might enhance the sensitivity of A549 cells to methotrexate through the P53/P21 pathway. Methotrexate 104-116 H3 histone pseudogene 16 Homo sapiens 133-136 27934318-2 2016 Cd3(MoO4)(TeO3)2 is a monoclinic crystal system, and it exhibits the polar space group P21 (No. cd3(moo4)(teo3)2 0-16 H3 histone pseudogene 16 Homo sapiens 87-90 27736799-7 2016 TM5441 exerts its inhibitory effect on Doxorubicin-induced cellular senescence by decreasing reactive oxygen species generation, induction of antioxidants like catalase and suppression of stress-induced senescence cadre p53, p21, p16, PAI-1 and IGFBP3. TM5441 0-6 H3 histone pseudogene 16 Homo sapiens 225-228 27904675-4 2016 Real-time quantitative PCR showed that HOTAIR, p21 and p53 mRNA expressions in doxorubicin (DOX)-treated or gamma-ray-irradiated Tca8113 cells were up-regulated. Doxorubicin 79-90 H3 histone pseudogene 16 Homo sapiens 47-50 27904675-4 2016 Real-time quantitative PCR showed that HOTAIR, p21 and p53 mRNA expressions in doxorubicin (DOX)-treated or gamma-ray-irradiated Tca8113 cells were up-regulated. Doxorubicin 92-95 H3 histone pseudogene 16 Homo sapiens 47-50 27980829-1 2016 The structure of the title compound, {(NH4)2[Cu(C2O4)2]} n , at 100 K has monoclinic (P21/c) symmetry with the CuII atom on an inversion center. {(nh4)2[cu(c2o4)2]} n 37-58 H3 histone pseudogene 16 Homo sapiens 86-91 27736799-7 2016 TM5441 exerts its inhibitory effect on Doxorubicin-induced cellular senescence by decreasing reactive oxygen species generation, induction of antioxidants like catalase and suppression of stress-induced senescence cadre p53, p21, p16, PAI-1 and IGFBP3. Doxorubicin 39-50 H3 histone pseudogene 16 Homo sapiens 225-228 27608273-2 2016 Conjugate addition of phenethylamine to an achiral aroyl acrylamide under homogeneous conditions gave the alpha-amino amides in quantitative yields, which crystallized as a conglomerate of a P21 crystal system. phenethylamine 22-36 H3 histone pseudogene 16 Homo sapiens 191-194 27608273-2 2016 Conjugate addition of phenethylamine to an achiral aroyl acrylamide under homogeneous conditions gave the alpha-amino amides in quantitative yields, which crystallized as a conglomerate of a P21 crystal system. aroyl acrylamide 51-67 H3 histone pseudogene 16 Homo sapiens 191-194 27608273-2 2016 Conjugate addition of phenethylamine to an achiral aroyl acrylamide under homogeneous conditions gave the alpha-amino amides in quantitative yields, which crystallized as a conglomerate of a P21 crystal system. alpha-amino amides 106-124 H3 histone pseudogene 16 Homo sapiens 191-194 27726305-6 2016 Solanine regulates the protein levels of cell cycle proteins, including Cyclin D1, Cyclin E1, CDK2, CDK4, CDK6, and P21 in vivo and in vitro. Solanine 0-8 H3 histone pseudogene 16 Homo sapiens 116-119 27824155-5 2016 Cucurbitacin D treatment of cervical cancer cells arrested the cell cycle in G1/S phase, inhibited constitutive expression of E6, Cyclin D1, CDK4, pRb, and Rb and induced the protein levels of p21 and p27. cucurbitacin D 0-14 H3 histone pseudogene 16 Homo sapiens 193-196 27593857-9 2016 The results of flow cytometric assays suggested that knockdown of PKM2 or docetaxel treatment, whether used singly or in combination, blocked the cells in the G2/M phase, which is in consistent with the effect of the two on the expression of p21. Docetaxel 74-83 H3 histone pseudogene 16 Homo sapiens 242-245 27687545-4 2016 Compared with PC3, PC3-PR exhibited some unique phenotypes that might be associated with PTX resistance, including decreased expression of acetylated alpha-tubulin and the cell cycle regulator p21, and increased expression of betaIII tubulin, histone deacetylase 6 (HDAC6), and the anti-apoptotic protein Bcl2. Paclitaxel 89-92 H3 histone pseudogene 16 Homo sapiens 193-196 27687545-8 2016 The pan-HDAC inhibitors trichostatin A and suberanilohydroxamic acid and the HDAC6-specific inhibitor tubacin inhibited PC3-PR proliferation and increased expression of p21 and acetylated alpha-tubulin in a manner similar to CTX. trichostatin A 24-38 H3 histone pseudogene 16 Homo sapiens 169-172 27687545-8 2016 The pan-HDAC inhibitors trichostatin A and suberanilohydroxamic acid and the HDAC6-specific inhibitor tubacin inhibited PC3-PR proliferation and increased expression of p21 and acetylated alpha-tubulin in a manner similar to CTX. tubacin 102-109 H3 histone pseudogene 16 Homo sapiens 169-172 27826196-5 2016 An immunofluorescence assay and a Western blotting assay showed that AC-MFB delayed the abrogation of gamma-H2AX, upregulated p21 expression, and attenuated the radiation-induced phosphorylation of ataxia telangiectasia-mutated kinase and checkpoint kinase 2. ac-mfb 69-75 H3 histone pseudogene 16 Homo sapiens 126-129 30108691-6 2017 At the molecular level, the pharmacological effect of DLC-carboranes is exerted through activation of the p53/p21 axis. carboranes 58-68 H3 histone pseudogene 16 Homo sapiens 110-113 27732642-4 2016 The reduced production of H2S falls within the same time-frame that the hallmarks of replicative senescence appear including accumulation of SA-beta-Gal, enhanced expression of p16, p21, and RRM2B while the expression of RRM2, hTERT, SIRT1, NAMPT, and NAD/NADH ratio all fall. Hydrogen Sulfide 26-29 H3 histone pseudogene 16 Homo sapiens 182-185 27840723-5 2016 The title salt is a second monoclinic polymorph of the l-dopa HCl structure reported earlier in the monoclinic space group P21 [Jandacek & Earle (1971 ). Salts 10-14 H3 histone pseudogene 16 Homo sapiens 123-126 27840723-5 2016 The title salt is a second monoclinic polymorph of the l-dopa HCl structure reported earlier in the monoclinic space group P21 [Jandacek & Earle (1971 ). l-dopa hcl 55-65 H3 histone pseudogene 16 Homo sapiens 123-126 29871161-9 2016 After interference by 5-azacytidine, p21 gene is activated. Azacitidine 22-35 H3 histone pseudogene 16 Homo sapiens 37-40 29871161-12 2016 After 5-azacytidine intervention, the degree of methylation was obviously decreased and even showed unmethylation.Conclusion:There was p21 gene promoter CpG island hypermethylation in laryngeal cancer and laryngeal cancer cell line Hep-2, which was a molecular event distinguished laryngeal cancer from normal laryngeal tissue. Azacitidine 6-19 H3 histone pseudogene 16 Homo sapiens 135-138 29871161-14 2016 Demethylation of drug 5-azacytidine can induce p21 gene promoter CpG island demethylation modification, change the regulation of tumor cell cycle genes in cells and promote tumor cell apoptosis. Azacitidine 22-35 H3 histone pseudogene 16 Homo sapiens 47-50 27280688-5 2016 At the molecular and cellular level, curcumin can blunt epithelial-to-mesenchymal transition and affect many targets that are involved in melanoma initiation and progression (e.g., BCl2, MAPKS, p21 and some microRNAs). Curcumin 37-45 H3 histone pseudogene 16 Homo sapiens 194-197 27568863-4 2016 In order to better understand the multiple interconnected pathways of gentamicin-induced apoptosis and ensuing renal cell toxicity, we investigated the effect of gentamicin on p53 and p21 levels. Gentamicins 162-172 H3 histone pseudogene 16 Homo sapiens 184-187 27543423-9 2016 The effect of 5-Aza and TSA on DNA methyltransferase and histone deacetylase activity, respectively, was confirmed by assessing the methylation and acetylation of the CDK inhibitor p21. Decitabine 14-19 H3 histone pseudogene 16 Homo sapiens 181-184 27543423-9 2016 The effect of 5-Aza and TSA on DNA methyltransferase and histone deacetylase activity, respectively, was confirmed by assessing the methylation and acetylation of the CDK inhibitor p21. trichostatin A 24-27 H3 histone pseudogene 16 Homo sapiens 181-184 27712032-3 2016 Electrochemical performance depends on impurities such as MnO as well as crystallite size, surface area, and non-stoichiometric phases, which lead to the formation of additional polymorphs such as Pmnb and P21 /n of Li2 MnSiO4 at low calcination temperatures. li2 mnsio4 216-226 H3 histone pseudogene 16 Homo sapiens 206-209 27777210-8 2016 Both RITA and TMZ, especially the latter, significantly increased the expressions of p53, p21, puma, and other apoptosis-associated genes to accelerate apoptosis and inhibit the growth and colony formation of U87 cells, and the effect was more obvious with a combined treatment. RITA 5-9 H3 histone pseudogene 16 Homo sapiens 90-93 27777210-8 2016 Both RITA and TMZ, especially the latter, significantly increased the expressions of p53, p21, puma, and other apoptosis-associated genes to accelerate apoptosis and inhibit the growth and colony formation of U87 cells, and the effect was more obvious with a combined treatment. Temozolomide 14-17 H3 histone pseudogene 16 Homo sapiens 90-93 27477352-9 2016 In addition, radotinib induced G0/G1 phase arrest by inducing CDKIs p21 and p27 and by inhibiting CDK2, CDK4, and CDK6. 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide 13-22 H3 histone pseudogene 16 Homo sapiens 68-71 27477352-11 2016 Moreover, these results indicate that radotinib inhibits AML cell proliferation by inducing mitochondria-dependent apoptosis and CDKIs p21 and p27. 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide 38-47 H3 histone pseudogene 16 Homo sapiens 135-138 27556514-8 2016 The anti-apoptotic activity of Y-27632 correlated with a reduction in p53 serine 15 phosphorylation and the consequent reduction in the expression of downstream target genes p21 and DAPK1, two genes involved in the induction of cell death. Y 27632 31-38 H3 histone pseudogene 16 Homo sapiens 174-177 27529569-0 2016 Hypertonic Saline Primes Activation of the p53-p21 Signaling Axis in Human Small Airway Epithelial Cells That Prevents Inflammation Induced by Pro-inflammatory Cytokines. Sodium Chloride 11-17 H3 histone pseudogene 16 Homo sapiens 47-50 27760664-10 2016 The expression of p53, Bax, Mdm2 and p21 was up-regulated by doxorubicin and further increased in response to combination. Doxorubicin 61-72 H3 histone pseudogene 16 Homo sapiens 37-40 27427852-7 2016 Moreover, induced p21, subsequent G1 cell cycle arrest and transcriptional suppression of survivin-mediated c-Myc and hTERT expression may contribute in the enhanced growth suppressive effect of ATO-plus-melatonin. Melatonin 204-213 H3 histone pseudogene 16 Homo sapiens 18-21 27716272-0 2016 The histone deacetylase inhibitor trichostatin a decreases lymphangiogenesis by inducing apoptosis and cell cycle arrest via p21-dependent pathways. trichostatin A 34-48 H3 histone pseudogene 16 Homo sapiens 125-128 27498709-6 2016 The H2O2-exposed hMSCs showed cellular senescence with significantly increased protein levels of acetyl-p53 and p21 in comparison with the untreated hMSCs, and these effects were prevented by pre-treatment with EGCG. Hydrogen Peroxide 4-8 H3 histone pseudogene 16 Homo sapiens 112-115 27498709-6 2016 The H2O2-exposed hMSCs showed cellular senescence with significantly increased protein levels of acetyl-p53 and p21 in comparison with the untreated hMSCs, and these effects were prevented by pre-treatment with EGCG. epigallocatechin gallate 211-215 H3 histone pseudogene 16 Homo sapiens 112-115 27498709-7 2016 By contrast, in Nrf2-knockdown hMSCs, EGCG lost its antioxidant effect, exhibiting high levels of acetyl-p53 and p21 following EGCG pre-treatment and H2O2 exposure. epigallocatechin gallate 38-42 H3 histone pseudogene 16 Homo sapiens 113-116 27498709-8 2016 This indicates that Nrf2 and p53/p21 may be involved in the anti-senescent effect of EGCG in hMSCs. epigallocatechin gallate 85-89 H3 histone pseudogene 16 Homo sapiens 33-36 26885564-4 2016 Butyrate induced apoptosis of lymphoma tumor cells and significantly up-regulated histone 3 acetylation (H3ac) level and target genes such as Fas, P21, P27. Butyrates 0-8 H3 histone pseudogene 16 Homo sapiens 147-150 27509880-0 2016 Combination of the histone deacetylase inhibitor depsipeptide and 5-fluorouracil upregulates major histocompatibility complex class II and p21 genes and activates caspase-3/7 in human colon cancer HCT-116 cells. Depsipeptides 49-61 H3 histone pseudogene 16 Homo sapiens 139-142 27165055-8 2016 Keratinocytes treated with erlotinib in vitro showed a significant down-modulation of hyaluronan synthases (HAS2 and HAS3), whereas senescence-associated genes (p21, p53, IL-6, maspin) were upregulated, along with a G1 cell cycle arrest and stronger SA beta-Gal activity. Erlotinib Hydrochloride 27-36 H3 histone pseudogene 16 Homo sapiens 161-164 27468725-0 2016 Dimethylfumarate inhibits melanoma cell proliferation via p21 and p53 induction and bcl-2 and cyclin B1 downregulation. Dimethyl Fumarate 0-16 H3 histone pseudogene 16 Homo sapiens 58-61 27468725-11 2016 Interestingly, DMF induced p53 and p21 yet inhibited cyclin B1 expression in a concentration-dependent manner. Dimethyl Fumarate 15-18 H3 histone pseudogene 16 Homo sapiens 35-38 27427852-7 2016 Moreover, induced p21, subsequent G1 cell cycle arrest and transcriptional suppression of survivin-mediated c-Myc and hTERT expression may contribute in the enhanced growth suppressive effect of ATO-plus-melatonin. ato-plus 195-203 H3 histone pseudogene 16 Homo sapiens 18-21 27541047-3 2016 In vitro, at low concentration (<250nM) of Chidamide inhibited cell proliferation and delayed G0/G1 cell cycle progression by down-regulating CDK2 and regulating p-P53 and P21 protein expression. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 46-55 H3 histone pseudogene 16 Homo sapiens 175-178 27673450-8 2016 When ASPL-TFE3 was expressed in human bone marrow-derived mesenchymal stem cells in a tetracycline-inducible manner, we observed the up-regulation of p21 expression and the induction of senescence-associated beta-galactosidase activity. Tetracycline 86-98 H3 histone pseudogene 16 Homo sapiens 150-153 27509880-0 2016 Combination of the histone deacetylase inhibitor depsipeptide and 5-fluorouracil upregulates major histocompatibility complex class II and p21 genes and activates caspase-3/7 in human colon cancer HCT-116 cells. Fluorouracil 66-80 H3 histone pseudogene 16 Homo sapiens 139-142 27716272-12 2016 Furthermore, siRNA assays were performed to analyse the role of p21 and p53 on TSA-mediated anti-lymphangiogenic effects. trichostatin A 79-82 H3 histone pseudogene 16 Homo sapiens 64-67 27716272-15 2016 Additionally, we observed that p21 protein accumulated in cellular nuclei after treatment with TSA. trichostatin A 95-98 H3 histone pseudogene 16 Homo sapiens 31-34 27716272-20 2016 Interestingly, siRNA-mediated p21 depletion almost completely reversed the anti-proliferative effects of TSA in LEC. trichostatin A 105-108 H3 histone pseudogene 16 Homo sapiens 30-33 27564099-9 2016 Moreover, pretreatment with U0126 suppressed curcumin and cisplatin-induced upregulation of p53, p21, and p-STAT3 and downregulation of survival proteins in both cells. U 0126 28-33 H3 histone pseudogene 16 Homo sapiens 97-100 27564099-9 2016 Moreover, pretreatment with U0126 suppressed curcumin and cisplatin-induced upregulation of p53, p21, and p-STAT3 and downregulation of survival proteins in both cells. Curcumin 45-53 H3 histone pseudogene 16 Homo sapiens 97-100 27564099-7 2016 In addition, when 253J-Bv cells were co-treated with curcumin and cisplatin, p53 and p21 expression levels were markedly increased when compared to controls. Curcumin 53-61 H3 histone pseudogene 16 Homo sapiens 85-88 27564099-7 2016 In addition, when 253J-Bv cells were co-treated with curcumin and cisplatin, p53 and p21 expression levels were markedly increased when compared to controls. Cisplatin 66-75 H3 histone pseudogene 16 Homo sapiens 85-88 27564099-9 2016 Moreover, pretreatment with U0126 suppressed curcumin and cisplatin-induced upregulation of p53, p21, and p-STAT3 and downregulation of survival proteins in both cells. Cisplatin 58-67 H3 histone pseudogene 16 Homo sapiens 97-100 27357535-6 2016 Specific inhibitors of p38 (SB203580), ERK (PD98059), and JNK (SP600125) inhibited MK1-EPS-induced HUVEC proliferation, tube formation, and cell migration, and partially attenuated MKI-EPS-induced expression of p21 and ICAM1, and STAT3 phosphorylation. eps 87-90 H3 histone pseudogene 16 Homo sapiens 211-214 27725901-7 2016 The molecular basis of curcumin-mediated cell growth inhibition we identified is that curcumin significantly suppressed Skp2 expression and subsequently induced p21 expression. Curcumin 23-31 H3 histone pseudogene 16 Homo sapiens 161-164 27725901-7 2016 The molecular basis of curcumin-mediated cell growth inhibition we identified is that curcumin significantly suppressed Skp2 expression and subsequently induced p21 expression. Curcumin 86-94 H3 histone pseudogene 16 Homo sapiens 161-164 27093475-7 2016 Moreover, CS extract induced cellular senescence in cultured human airway epithelial cells, represented by induced senescence-associated beta-galactosidase activity, inhibited cell proliferation, increased p21 expression, and increased release of high-mobility group box 1 and IL-6. Cesium 10-12 H3 histone pseudogene 16 Homo sapiens 206-209 27673332-12 2016 CDDP increased the expression of p53 and p21 indicating cell cycle arrest. Cisplatin 0-4 H3 histone pseudogene 16 Homo sapiens 41-44 27500422-1 2016 A mononuclear cobalt(II) complex [Co(3,5-dnb)2(py)2(H2O)2] {3,5-Hdnb = 3,5-dinitrobenzoic acid; py = pyridine} was isolated in two polymorphs, in space groups C2/c (1) and P21/c (2). Cobalt(2+) 14-24 H3 histone pseudogene 16 Homo sapiens 172-177 27500422-1 2016 A mononuclear cobalt(II) complex [Co(3,5-dnb)2(py)2(H2O)2] {3,5-Hdnb = 3,5-dinitrobenzoic acid; py = pyridine} was isolated in two polymorphs, in space groups C2/c (1) and P21/c (2). co(3,5-dnb)2(py)2(h2o)2] 34-58 H3 histone pseudogene 16 Homo sapiens 172-177 27432642-6 2016 The present study also demonstrated that combinational treatment is more effective in inducing G1 phase arrest and activating apoptosis compared tamoxifen alone, which may be due to upregulation of P21 expression and downregulation of the B-cell CLL/lymphoma 2(Bcl-2)/Bcl-2 associated X protein ratio. Tamoxifen 145-154 H3 histone pseudogene 16 Homo sapiens 198-201 27403577-8 2016 Results revealed that doxorubicin induced senescence and increased p21 expression in MCF-7 cells. Doxorubicin 22-33 H3 histone pseudogene 16 Homo sapiens 67-70 27403577-10 2016 Moreover, p21 expression was decreased in combination studies compared to doxorubicin group. Doxorubicin 74-85 H3 histone pseudogene 16 Homo sapiens 10-13 27747012-8 2016 CONCLUSIONS: The main finding of this study is that cytoplasmic p21 expression negatively influences the outcome of malignant TETs and correlates with metastatic activity. tetramethylenedisulfotetramine 126-130 H3 histone pseudogene 16 Homo sapiens 64-67 27403577-12 2016 Our findings demonstrate that low-dose doxorubicin induced senescence via the activation of ATM, -chk2, and -p21 pathways, while inhibition of ATM and chk2 cannot consider as a new target for sensitization of MCF-7 cells to doxorubicin. Doxorubicin 39-50 H3 histone pseudogene 16 Homo sapiens 109-112 27432244-5 2016 Curcumin induced G1 phase arrest through downregulating the expression of cyclin D3 and cyclin-dependent kinase (CDK)2/6 and upregulating the expression of CDK inhibitor proteins p21 and p27. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 179-182 27078502-5 2016 Costunolide induced apoptosis of Eca-109 cells as well as cell cycle arrest in G1/S phase by upregulation of P53 and P21. costunolide 0-11 H3 histone pseudogene 16 Homo sapiens 117-120 27640744-5 2016 In ZR-75-1 cells, cytochalasin B triggered G2/M phase arrest through the modulation of CDK1, cyclin B1, p53, p27 and p21 expressions. Cytochalasin B 18-32 H3 histone pseudogene 16 Homo sapiens 117-120 27474499-6 2016 We also detected the expression and activities of cell-cycle positive regulators (cyclin D1, cyclin E, CDK2, CDK4 and CDK6) and negative regulators (p21 and p27) in human PASMCs by western blots and co-immuoprecipitation (IP). pasmcs 171-177 H3 histone pseudogene 16 Homo sapiens 149-152 27470351-0 2016 Histone deacetylase inhibitor, Romidepsin (FK228) inhibits endometrial cancer cell growth through augmentation of p53-p21 pathway. romidepsin 43-48 H3 histone pseudogene 16 Homo sapiens 118-121 27447743-3 2016 SAHA induced the overexpression of acetyl histone 3 and 4, which were recruited to p21, p27, Cyclin D1, c-myc and nanog promoters to transcriptionally up-regulate the former two and down-regulate the latter three. acetyl histone 35-49 H3 histone pseudogene 16 Homo sapiens 83-86 27470351-9 2016 Moreover, FK228 treatment significantly increased the mRNA and protein expressions of p53, p21, cleaved caspases such as 3, 7 and 8 and PARP. romidepsin 10-15 H3 histone pseudogene 16 Homo sapiens 91-94 27470351-11 2016 CONCLUSION: In conclusion, FK228 inhibits EC tumor cell proliferation and induces apoptosis by activation caspase/PARP via the induction of p53/p21 signaling cascades, suggesting that FK228 is a potential therapeutic agent for EC. romidepsin 27-32 H3 histone pseudogene 16 Homo sapiens 144-147 27470351-11 2016 CONCLUSION: In conclusion, FK228 inhibits EC tumor cell proliferation and induces apoptosis by activation caspase/PARP via the induction of p53/p21 signaling cascades, suggesting that FK228 is a potential therapeutic agent for EC. romidepsin 184-189 H3 histone pseudogene 16 Homo sapiens 144-147 27333051-10 2016 These findings demonstrate that the CRL4-CDT2-SET8/p21 degradation axis is the primary target of inhibition by pevonedistat in melanoma and suggest that a broad patient population may benefit from pevonedistat therapy. pevonedistat 197-209 H3 histone pseudogene 16 Homo sapiens 51-54 27094504-9 2016 Also, treatment with honokiol and rosiglitazone induced cell cycle arrest in the G0/G1 phase; increased p21; and decreased cyclin D1, cyclin E1, and Rb expression in SK-Hep1 hepatoma cells. honokiol 21-29 H3 histone pseudogene 16 Homo sapiens 104-107 27333051-10 2016 These findings demonstrate that the CRL4-CDT2-SET8/p21 degradation axis is the primary target of inhibition by pevonedistat in melanoma and suggest that a broad patient population may benefit from pevonedistat therapy. pevonedistat 111-123 H3 histone pseudogene 16 Homo sapiens 51-54 27233942-5 2016 Stronger intracellular TrxR inhibition and higher accumulation of ROS (O2( -) and H2O2) are responsible for more effective S-phase arrest and mitochondria-mediated apoptotic induction of A549 cells by PL-CL than PLvia p53-p21-cyclinA/CDK2 and ASK1-JNK/p38 signaling cascade pathways, respectively. Reactive Oxygen Species 66-69 H3 histone pseudogene 16 Homo sapiens 222-225 27233942-5 2016 Stronger intracellular TrxR inhibition and higher accumulation of ROS (O2( -) and H2O2) are responsible for more effective S-phase arrest and mitochondria-mediated apoptotic induction of A549 cells by PL-CL than PLvia p53-p21-cyclinA/CDK2 and ASK1-JNK/p38 signaling cascade pathways, respectively. pl-cl 201-206 H3 histone pseudogene 16 Homo sapiens 222-225 27062045-5 2016 Here, we found that the melatonin treatment markedly inhibited the senescent characteristics of CPCs after exposed to sublethal concentration of H2 O2 , including the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive CPCs, senescence-associated heterochromatin loci (SAHF), secretory IL-6 level, and the upregulation of p53 and p21 proteins. Melatonin 24-33 H3 histone pseudogene 16 Homo sapiens 354-357 27295412-3 2016 The structure of 5-nitro-(2-phenyl amino) benzoic acid (4) was confirmed by X-ray crystallography and was found to crystallize in P21/c space group. 5-nitro-(2-phenyl amino) benzoic acid 17-54 H3 histone pseudogene 16 Homo sapiens 130-135 27094504-9 2016 Also, treatment with honokiol and rosiglitazone induced cell cycle arrest in the G0/G1 phase; increased p21; and decreased cyclin D1, cyclin E1, and Rb expression in SK-Hep1 hepatoma cells. Rosiglitazone 34-47 H3 histone pseudogene 16 Homo sapiens 104-107 27094504-10 2016 CONCLUSION: Honokiol combined with rosiglitazone showed more effective growth inhibition in hepatoma cells mediated through the regulation of G0/G1 phase-related proteins p21, cyclin D1, cyclin E1, and Rb and cell cycle progression. honokiol 12-20 H3 histone pseudogene 16 Homo sapiens 171-174 27094504-10 2016 CONCLUSION: Honokiol combined with rosiglitazone showed more effective growth inhibition in hepatoma cells mediated through the regulation of G0/G1 phase-related proteins p21, cyclin D1, cyclin E1, and Rb and cell cycle progression. Rosiglitazone 35-48 H3 histone pseudogene 16 Homo sapiens 171-174 26886286-9 2016 Our findings suggest a possible association between p21 Ser31tabArg polymorphism and susceptibility to the development of cervical lesions in women from Pernambuco. ser31tabarg 56-67 H3 histone pseudogene 16 Homo sapiens 52-55 27329589-6 2016 Western blot showed that quercetin downregulated c-myc expression and upregulated p21 expression. Quercetin 25-34 H3 histone pseudogene 16 Homo sapiens 82-85 27231022-0 2016 Vitamin C promotes the proliferation of human adipose-derived stem cells via p53-p21 pathway. Ascorbic Acid 0-9 H3 histone pseudogene 16 Homo sapiens 81-84 27421652-8 2016 The inhibitory effect of everolimus was due to G1 arrest as a result of downregulation of cyclin D1 and p21. Everolimus 25-35 H3 histone pseudogene 16 Homo sapiens 104-107 27411103-4 2016 Molecularly, Glc exposure increased oxidative stress and activated Forkhead box O3a (FOXO3a), promoting increased expression and activity of the ROS-removal enzymes superoxide dismutase and catalase and the cell-cycle inhibitors p21(cip1) and p27(kip1). Glucose 13-16 H3 histone pseudogene 16 Homo sapiens 229-232 27411103-5 2016 Diabetic Glc also promoted beta-catenin nuclear localization and the formation of a complex with FOXO3a that localized to the promoters of Sod2, p21(cip1), and potentially p27(kip1). Glucose 9-12 H3 histone pseudogene 16 Homo sapiens 145-148 27231022-9 2016 Western blot analysis indicated that vitamin C treatment up-regulated the expression levels of cyclin E1 and CDK2, but down-regulated p53 and p21 proteins expression, which contributed to cell proliferation and cell cycle progression. Ascorbic Acid 37-46 H3 histone pseudogene 16 Homo sapiens 142-145 27231022-11 2016 These findings suggest that vitamin C can promote the proliferation and cell cycle progression in the ADSCs possibly through regulation of p53-p21 signal pathway. Ascorbic Acid 28-37 H3 histone pseudogene 16 Homo sapiens 143-146 27109893-10 2016 Pre-mature senescence induced due to limited glucose availability was found to be regulated by nuclear translocated p53 which, in turn, induced p21, pAkt and pERK. Glucose 45-52 H3 histone pseudogene 16 Homo sapiens 144-147 27482284-7 2016 All of the studies indicated that curcumin decreased glioblastoma cell viability through various pathways (i.e. decrease in prosurvival proteins such as nuclear factor kappaB, activator protein 1, and phosphoinositide 3 kinase, and upregulation of apoptotic pathways like p21, p53, and executor caspase 3). Curcumin 34-42 H3 histone pseudogene 16 Homo sapiens 272-275 27131434-14 2016 The cell cycle arrest in DCM-DS-treated MDA-MB-231 cells is possibly via p53-independent but p21-dependent pathway. Methylene Chloride 25-28 H3 histone pseudogene 16 Homo sapiens 93-96 27131434-14 2016 The cell cycle arrest in DCM-DS-treated MDA-MB-231 cells is possibly via p53-independent but p21-dependent pathway. Deuterium 29-31 H3 histone pseudogene 16 Homo sapiens 93-96 27364904-4 2016 The sensitivity of ARID1A-deficient cells to dasatinib was associated with G1-S cell-cycle arrest and was dependent upon both p21 and Rb. Dasatinib 45-54 H3 histone pseudogene 16 Homo sapiens 126-129 27347927-7 2016 Cyanidin-3-O-glucoside chloride decreased mutant p21 expression, and increased the ratio of Bax/Bcl-2 and the activation of caspase-3 to induce apoptosis. asterin 0-31 H3 histone pseudogene 16 Homo sapiens 49-52 27351203-0 2016 miR-24-3p Suppresses Malignant Behavior of Lacrimal Adenoid Cystic Carcinoma by Targeting PRKCH to Regulate p53/p21 Pathway. mir-24-3p 0-9 H3 histone pseudogene 16 Homo sapiens 112-115 27351203-8 2016 These results suggest that miR-24-3p promotes the p53/p21 pathway by down-regulating PRKCH expression in lacrimal adenoid cystic carcinoma cells. mir-24-3p 27-36 H3 histone pseudogene 16 Homo sapiens 54-57 26763252-9 2016 Cisplatin-resistant ovarian cancer cell lines have reduced MSX1 expression, and MSX1 overexpression leads to cisplatin sensitization, increased apoptosis, and increased cisplatin-induced p21 expression. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 187-190 26763252-9 2016 Cisplatin-resistant ovarian cancer cell lines have reduced MSX1 expression, and MSX1 overexpression leads to cisplatin sensitization, increased apoptosis, and increased cisplatin-induced p21 expression. Cisplatin 169-178 H3 histone pseudogene 16 Homo sapiens 187-190 27255182-10 2016 Breast cancer cell lines MCF10A and MDA-MB-231 grown in methionine-restricted cysteine-depleted media for 24 h also up-regulated P21 and P27 gene expression, and MDA-MB-231 cells had decreased proliferation. Methionine 56-66 H3 histone pseudogene 16 Homo sapiens 129-132 27235710-14 2016 Furthermore, the results of qRT-PCR showed that lupeol pre-treatment significantly (p<0.05) decreased mancozeb-induced expression of DNA damage (p53, MDM2, COX-2, GADD45alpha and p21) and increased expression of DNA repair responsive genes (hOGG1 and XRCC1) in CHLs. mancozeb 105-113 H3 histone pseudogene 16 Homo sapiens 182-185 27255182-10 2016 Breast cancer cell lines MCF10A and MDA-MB-231 grown in methionine-restricted cysteine-depleted media for 24 h also up-regulated P21 and P27 gene expression, and MDA-MB-231 cells had decreased proliferation. Cysteine 78-86 H3 histone pseudogene 16 Homo sapiens 129-132 27091351-8 2016 AZD1152 treatment induced activation of G2/M checkpoint which in turn led to transient G2/M arrest in a p21-independent manner. 2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate 0-7 H3 histone pseudogene 16 Homo sapiens 104-107 27253379-2 2016 Based on our recent finding that the host factor p21 regulates HIV transcription during antiretroviral therapy (ART), and published data demonstrating that the human carbohydrate-binding immunomodulatory protein galectin-9 regulates p21, we hypothesized that galectin-9 modulates HIV transcription. Carbohydrates 166-178 H3 histone pseudogene 16 Homo sapiens 49-52 27253379-2 2016 Based on our recent finding that the host factor p21 regulates HIV transcription during antiretroviral therapy (ART), and published data demonstrating that the human carbohydrate-binding immunomodulatory protein galectin-9 regulates p21, we hypothesized that galectin-9 modulates HIV transcription. Carbohydrates 166-178 H3 histone pseudogene 16 Homo sapiens 233-236 27035641-0 2016 The effect of sulforaphane on the cell cycle, apoptosis and expression of cyclin D1 and p21 in the A549 non-small cell lung cancer cell line. sulforaphane 14-26 H3 histone pseudogene 16 Homo sapiens 88-91 27221738-0 2016 miR-30c and miR-181a synergistically modulate p53-p21 pathway in diabetes induced cardiac hypertrophy. mir-181a 12-20 H3 histone pseudogene 16 Homo sapiens 50-53 26905466-3 2016 Here, we report the first structure (at a 2.34A resolution) of a complex of human HINT1 with a non-hydrolyzable analog of an Ap4A dinucleotide, containing bis-phosphorothioated glycerol mimicking a polyphosphate chain, obtained from a primitive monoclinic space group P21 crystal. Glycerol 177-185 H3 histone pseudogene 16 Homo sapiens 268-271 26905466-3 2016 Here, we report the first structure (at a 2.34A resolution) of a complex of human HINT1 with a non-hydrolyzable analog of an Ap4A dinucleotide, containing bis-phosphorothioated glycerol mimicking a polyphosphate chain, obtained from a primitive monoclinic space group P21 crystal. ap4a dinucleotide 125-142 H3 histone pseudogene 16 Homo sapiens 268-271 26905466-3 2016 Here, we report the first structure (at a 2.34A resolution) of a complex of human HINT1 with a non-hydrolyzable analog of an Ap4A dinucleotide, containing bis-phosphorothioated glycerol mimicking a polyphosphate chain, obtained from a primitive monoclinic space group P21 crystal. bis-phosphorothioated 155-176 H3 histone pseudogene 16 Homo sapiens 268-271 27221738-2 2016 We investigated role of microRNAs in regulating p53-p21 pathway in high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis. Glucose 72-79 H3 histone pseudogene 16 Homo sapiens 52-55 26876863-2 2016 The beta-CD-CA complex crystallizes in the monoclinic P21 space group, whereas the beta-CD-EC complex crystallizes in both the monoclinic P21 and triclinic P1 space groups. beta-cd-ec 83-93 H3 histone pseudogene 16 Homo sapiens 138-141 26687645-5 2016 Co-treatment with OMT and 5-Fu caused G0/G1 phase arrest by upregulating P21 and P27 and downregulating cyclin D, and induced apoptosis through increasing the production of reactive oxygen species (ROS) and decreasing the levels of p-ERK. oxymatrine 18-21 H3 histone pseudogene 16 Homo sapiens 73-76 26687645-5 2016 Co-treatment with OMT and 5-Fu caused G0/G1 phase arrest by upregulating P21 and P27 and downregulating cyclin D, and induced apoptosis through increasing the production of reactive oxygen species (ROS) and decreasing the levels of p-ERK. Fluorouracil 26-30 H3 histone pseudogene 16 Homo sapiens 73-76 27219337-5 2016 Interestingly, UA at low concentrations (10-15 muM) enhanced the antitumoral effects of DXR by up to 2-fold, while in parallel inhibiting DXR-induced AKT activation and p21 expression, two proteins implicated in antitumoral drug resistance and cell survival. ursolic acid 15-17 H3 histone pseudogene 16 Homo sapiens 169-172 27098189-11 2016 Simvastatin enhanced the release of cytochrome c, caspase 3, and increased p21 levels, especially for the KKU-100 cells. Simvastatin 0-11 H3 histone pseudogene 16 Homo sapiens 75-78 27104737-4 2016 Based on density function theory with the ultrasoft pseudopotential scheme in the frame of the local density approximation and the generalized gradient approximation, we have systematically studied the structural stability, absorption spectra, electronic, optical and mechanical properties and minimum thermal conductivity of two novel silicon phases, Cm-32 silicon and P21/m silicon. Silicon 336-343 H3 histone pseudogene 16 Homo sapiens 370-373 27104737-6 2016 The absorption spectra of Cm-32 silicon and P21/m silicon exhibit significant overlap with the solar spectrum and thus, excellent photovoltaic efficiency with great improvements over Fd3[combining macron]m Si. Silicon 206-208 H3 histone pseudogene 16 Homo sapiens 44-47 27168162-11 2016 The cisplatin-induced expression of pAkt was not affected by LCN2; however, the expression of p53 and p21 was increased by LCN2-silencing. Cisplatin 4-13 H3 histone pseudogene 16 Homo sapiens 102-105 26596838-6 2016 In both cell lines, aspirin induced p21(CIP1). Aspirin 20-27 H3 histone pseudogene 16 Homo sapiens 36-39 27128904-6 2016 Moreover, AdoMet increased p53 and p21 expression, while Tyrosol reduced p21 expression and enhanced the expression of uncleaved caspase 3 and 9, suggesting that its protective effect may be related to the inhibition of the apoptotic machinery. 4-hydroxyphenylethanol 57-64 H3 histone pseudogene 16 Homo sapiens 73-76 26678889-5 2016 Our results showed that the level of either Hes1 or p21 was lower in LSCs or LPs than in HSCs whereas the level of miR-9 was highest in LPs and lowest in HSCs. lps 77-80 H3 histone pseudogene 16 Homo sapiens 52-55 27491234-10 2016 ICT and DOX could cause either early or late stage apoptosis, down-regulate Bcl-2 gene expression, and up-regulate gene expressions of Caspase-3 and p21 respectively (P < 0.05). Doxorubicin 8-11 H3 histone pseudogene 16 Homo sapiens 149-152 27491234-12 2016 CONCLUSION: CT combined DOX had additive or synergistic inhibition effect for the proliferation of osteosarcoma MG-63 cells, which might be related with regulating gene expressions of bcl-2, caspase-3, and p21. Doxorubicin 24-27 H3 histone pseudogene 16 Homo sapiens 206-209 27219337-4 2016 UA treatment (6-9 h) strongly blocked the survival AKT/GSK3beta/beta-catenin signalling pathway, which led to a concomitant reduction of the anti-apoptotic proteins c-Myc and p21, altogether resulting in the activation of intrinsic apoptosis. ursolic acid 0-2 H3 histone pseudogene 16 Homo sapiens 175-178 27064011-9 2016 Treatment of U87 MG cells with honokiol increased p53 phosphorylation and p21 levels. honokiol 31-39 H3 histone pseudogene 16 Homo sapiens 74-77 27064011-11 2016 Pretreatment of U87 MG cells with PFN-alpha significantly reversed honokiol-induced p53 phosphorylation and p21 augmentation. honokiol 67-75 H3 histone pseudogene 16 Homo sapiens 108-111 27064011-14 2016 In our in vivo model, administration of honokiol prolonged the survival rate of nude mice implanted with U87 MG cells and induced caspase-3 activation and chronological changes in p53, p21, CDK6, CDK4, cyclin D1, p-RB, and E2F1. honokiol 40-48 H3 histone pseudogene 16 Homo sapiens 185-188 27041463-11 2016 Furthermore, co-treatment with lidocaine and hyaluronan significantly decreased the levels of p53 and its transcription targets Bax and p21 in SW1353 cells, although treatment with lidocaine alone did not significantly change these proteins. Lidocaine 31-40 H3 histone pseudogene 16 Homo sapiens 136-139 27041463-11 2016 Furthermore, co-treatment with lidocaine and hyaluronan significantly decreased the levels of p53 and its transcription targets Bax and p21 in SW1353 cells, although treatment with lidocaine alone did not significantly change these proteins. Hyaluronic Acid 45-55 H3 histone pseudogene 16 Homo sapiens 136-139 26210997-6 2016 RG108-treated ALS-MSCs exhibit increased expression of the anti-senescence genes TERT, VEGF, and ANG, and decreased expression of the senescence-related genes ATM and p21. RG108 0-5 H3 histone pseudogene 16 Homo sapiens 167-170 27006469-4 2016 Iso-3 induced growth arrest of cancer cells in G0/G1 concomitant with increased p21 and p27 expression and reduced cyclin E1, PCNA and c-myc levels. isofistularin-3 0-5 H3 histone pseudogene 16 Homo sapiens 80-83 26847145-5 2016 Lico B caused cell cycle arrest at G1 phase along with downregulation of cyclin D1 and upregulation of p21 and p27 proteins. licochalcone B 0-6 H3 histone pseudogene 16 Homo sapiens 103-106 27048725-2 2016 Diethylaminoalane crystallizes in the monoclinic space group P21/c with a = 7.4020 (2), b = 12.9663 (3), c = 7.2878 (2) A and beta = 90.660 (2) at 293 K. The crystal structure was confirmed by DFT calculations and Raman spectroscopy. diethylaminoalane 0-17 H3 histone pseudogene 16 Homo sapiens 61-64 26776764-5 2016 In our study, we found that benzidine increased the proliferation of human bladder cancer T24 cells, triggered transition of the cells from G1 to S phase, elevated the expression of cyclin D1 and proliferating cell nuclear antigen (PCNA) and decreased p21 expression. benzidine 28-37 H3 histone pseudogene 16 Homo sapiens 252-255 27143925-4 2016 Our results demonstrated that the molecular mechanisms of the effect of carvacrol in Tca-8113 induces G1/S cell cycle arrest through downregulation of CDK regulator CCND1 and CDK4, and upregulation of CDK inhibitor P21. carvacrol 72-81 H3 histone pseudogene 16 Homo sapiens 215-218 27143925-4 2016 Our results demonstrated that the molecular mechanisms of the effect of carvacrol in Tca-8113 induces G1/S cell cycle arrest through downregulation of CDK regulator CCND1 and CDK4, and upregulation of CDK inhibitor P21. tca-8113 85-93 H3 histone pseudogene 16 Homo sapiens 215-218 26979598-3 2016 At 293 K, PEA-ZnCl4 crystallizes in a monoclinic unit-cell in the P21/c space group a = 7.449(2) A, b = 24.670(3) A, c = 11.187(2) A and beta = 91.762(5) , V = 2054.8(2) A(3) and Z = 4. zncl4 14-19 H3 histone pseudogene 16 Homo sapiens 66-71 27011117-2 2016 The homobimetallic Ru(II) and Os(II) complexes were found to crystallize in monoclinic form with space group P21/n. ru(ii) 19-25 H3 histone pseudogene 16 Homo sapiens 109-112 27011117-2 2016 The homobimetallic Ru(II) and Os(II) complexes were found to crystallize in monoclinic form with space group P21/n. os(ii) 30-36 H3 histone pseudogene 16 Homo sapiens 109-112 26846469-7 2016 The results indicated that Dp treatment significantly inhibited cell proliferation in a dose- and time-dependent manner, and blocked cell cycle progression at the G1/S phase in the U87MG and T98G cells via the upregulation of p53 and p21 protein expression, and simultaneous downregulation of Cdc25A, Cdc2 and P-Cdc2 protein expression. dracorhodin 27-29 H3 histone pseudogene 16 Homo sapiens 234-237 26785286-10 2016 CONCLUSION: These data reveal that 5-FU-induced cellular apoptosis in corneal epithelial cells may be mediated through caspase-8, caspase-9, and mitochondria-regulated pathways, as well as by upregulation of p21 and downregulation of Bcl-2-dependent signal transduction pathways. Fluorouracil 35-39 H3 histone pseudogene 16 Homo sapiens 208-211 26898539-0 2016 Retinoid N-(1H-benzo[d]imidazol-2-yl)-5,5,8,8-tetramethyl-5,6,7,8-tetrahydronaphthalene-2-carboxamide induces p21-dependent senescence in breast cancer cells. Retinoids 0-8 H3 histone pseudogene 16 Homo sapiens 110-113 26898539-0 2016 Retinoid N-(1H-benzo[d]imidazol-2-yl)-5,5,8,8-tetramethyl-5,6,7,8-tetrahydronaphthalene-2-carboxamide induces p21-dependent senescence in breast cancer cells. n-(1h-benzo[d]imidazol-2-yl)-5,5,8,8-tetramethyl-5,6,7,8-tetrahydronaphthalene-2-carboxamide 9-101 H3 histone pseudogene 16 Homo sapiens 110-113 26898539-5 2016 The breast cancer selective growth inhibitory action by retinoid 17 was defined as p21-dependent cell death, reminiscent of senescence, which is an indicator of targeted receptor mediated bioactivity. Retinoids 56-64 H3 histone pseudogene 16 Homo sapiens 83-86 26508031-10 2016 Moreover, esculetin increased the percentage of cells in G2/M phase and regulated the expressions of p53, p21, CDK1, and cyclin B1. esculetin 10-19 H3 histone pseudogene 16 Homo sapiens 106-109 26959833-3 2016 ICC adopts monoclinic space groups C2/c and P21/c in phase (I) and (III), respectively. inecalcitol 0-3 H3 histone pseudogene 16 Homo sapiens 44-49 26934645-5 2016 Furthermore, SKi or ABC294640 or fenretinide increase the expression of the senescence markers, p53 and p21 in LNCaP-AI prostate cancer cells. Fenretinide 33-44 H3 histone pseudogene 16 Homo sapiens 104-107 26934320-6 2016 Mechanistically, treatment with carfilzomib and CUDC-101 increased p21 expression and poly (ADP-ribose) polymerase protein cleavage. carfilzomib 32-43 H3 histone pseudogene 16 Homo sapiens 67-70 26934645-7 2016 Moreover, N-acetylcysteine (reactive oxygen species scavenger) blocked the SK inhibitor-induced increase in p21 and p53 expression but had no effect on the proteasomal degradation of SK1a. Acetylcysteine 10-26 H3 histone pseudogene 16 Homo sapiens 108-111 26934320-6 2016 Mechanistically, treatment with carfilzomib and CUDC-101 increased p21 expression and poly (ADP-ribose) polymerase protein cleavage. 7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide 48-56 H3 histone pseudogene 16 Homo sapiens 67-70 26934645-7 2016 Moreover, N-acetylcysteine (reactive oxygen species scavenger) blocked the SK inhibitor-induced increase in p21 and p53 expression but had no effect on the proteasomal degradation of SK1a. Reactive Oxygen Species 28-51 H3 histone pseudogene 16 Homo sapiens 108-111 26883108-6 2016 Over time cells treated with GSK2830371 accumulated in G1 and G2 phases of the cell cycle in a p21-dependent manner and were prone to induction of senescence by a low dose of MDM2 antagonist nutlin-3. GSK2830371 29-39 H3 histone pseudogene 16 Homo sapiens 95-98 27036461-2 2016 A high pressure monoclinic phase is predicted to exist above 1.3 GPa accompanied with a coordination change of aluminium resulting from a transformation from the ambient pressure 4-coordinated primitive monoclinic phase with space group P21/c to the monoclinic 6-coordinated structure with space group C2/m. Aluminum 111-120 H3 histone pseudogene 16 Homo sapiens 237-242 26982218-7 2016 We experimentally verify that prolonged exposure to low doses of BPA results in a delayed response to UV-C-induced DNA damage, due to impairment of p21-Tp53 axis, with the BPA-treated cells more prone to cell death and DNA damage accumulation. bisphenol A 65-68 H3 histone pseudogene 16 Homo sapiens 148-151 26982218-7 2016 We experimentally verify that prolonged exposure to low doses of BPA results in a delayed response to UV-C-induced DNA damage, due to impairment of p21-Tp53 axis, with the BPA-treated cells more prone to cell death and DNA damage accumulation. bisphenol A 172-175 H3 histone pseudogene 16 Homo sapiens 148-151 26898117-5 2016 A critical temperature of Tc 125 K for the magnetostructural phase transition between the two stable structures I4/m and P21/c is predicted. Technetium 26-28 H3 histone pseudogene 16 Homo sapiens 122-127 26940882-9 2016 Treatment of PLC/PRF/5 cells with siRNA-ERRgamma or GSK5182 inhibited proliferation through G1 arrest, increased expression of p21 and p27 and decreased expression of phosphorylated retinoblastoma protein. GSK5182 52-59 H3 histone pseudogene 16 Homo sapiens 127-130 26924930-0 2016 Agmatine Ameliorates High Glucose-Induced Neuronal Cell Senescence by Regulating the p21 and p53 Signaling. Agmatine 0-8 H3 histone pseudogene 16 Homo sapiens 85-88 26621097-12 2016 In contrast, the G2-to-M inhibitor p21 was increased in JA-treated cells. jasmonic acid 56-58 H3 histone pseudogene 16 Homo sapiens 35-38 26807478-0 2016 Prevention of vascular smooth muscle cell proliferation and injury-induced neointimal hyperplasia by CREB-mediated p21 induction: An insight from a plant polyphenol. Polyphenols 154-164 H3 histone pseudogene 16 Homo sapiens 115-118 26807478-5 2016 The SAA-induced upregulation of p21 involves the cAMP/PKA signaling pathway; a cAMP analog mimicked the effects of SAA and a specific cAMP/PKA inhibitor opposed these effects. Cyclic AMP 49-53 H3 histone pseudogene 16 Homo sapiens 32-35 26807478-5 2016 The SAA-induced upregulation of p21 involves the cAMP/PKA signaling pathway; a cAMP analog mimicked the effects of SAA and a specific cAMP/PKA inhibitor opposed these effects. Cyclic AMP 79-83 H3 histone pseudogene 16 Homo sapiens 32-35 26807478-5 2016 The SAA-induced upregulation of p21 involves the cAMP/PKA signaling pathway; a cAMP analog mimicked the effects of SAA and a specific cAMP/PKA inhibitor opposed these effects. Cyclic AMP 79-83 H3 histone pseudogene 16 Homo sapiens 32-35 26807478-10 2016 Our results indicate that SAA promotes p21 expression in SMCs through the cAMP/PKA/CREB signaling cascade in vitro and prevents injury-induced neointimal hyperplasia. Cyclic AMP 74-78 H3 histone pseudogene 16 Homo sapiens 39-42 25727911-10 2016 Furthermore, simvastatin effectively reduced the expression of p53 and p21. Simvastatin 13-24 H3 histone pseudogene 16 Homo sapiens 71-74 26718100-0 2016 [Corrigendum] Brassinin induces G1 phase arrest through increase of p21 and p27 by inhibition of the phosphatidylinositol 3-kinase signaling pathway in human colon cancer cells. brassinin 14-23 H3 histone pseudogene 16 Homo sapiens 68-71 26758421-2 2016 Here, we show that Bufalin can inhibit cervical cancer cell proliferation, block cell cycle in G2/M phase, induce cellular apoptosis and reduce cell metastasis through stimulation of p21(waf/cip1), p27(cip/kip), Bax and E-cadherin, and suppression of cyclin A, cyclin B1, CDK2, Bcl-2, Bcl-xl, MMP9 and SNAIL1. bufalin 19-26 H3 histone pseudogene 16 Homo sapiens 183-186 26848703-11 2016 Both drugs induced apoptosis through a p53-independent mechanism, whereas the expression of p21 was only seen in thymoquinone treatment. thymoquinone 113-125 H3 histone pseudogene 16 Homo sapiens 92-95 26985469-0 2016 Retraction notice to "Curcumin induces the degradation of cyclin E expression through ubiquitin-dependent pathway and up-regulates cyclin-dependent kinase inhibitors p21 and p27 in multiple human tumor cell lines" [Biochem. Curcumin 22-30 H3 histone pseudogene 16 Homo sapiens 166-169 26924930-6 2016 Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Glucose 38-45 H3 histone pseudogene 16 Homo sapiens 10-13 26924930-6 2016 Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Agmatine 80-88 H3 histone pseudogene 16 Homo sapiens 10-13 26924930-7 2016 Ultimately, agmatine inhibits the neuronal cell senescence through the activation of p53 and the inhibition of p21. Agmatine 12-20 H3 histone pseudogene 16 Homo sapiens 111-114 26314218-13 2016 In addition, in vitro exposure of RRCL to vorinostat resulted in an increase in p21 and acetylation of histone H3 leading to G1 cell cycle arrest. rrcl 34-38 H3 histone pseudogene 16 Homo sapiens 80-83 26648284-0 2016 MiR-512-5p induces apoptosis and inhibits glycolysis by targeting p21 in non-small cell lung cancer cells. mir-512-5p 0-10 H3 histone pseudogene 16 Homo sapiens 66-69 26648284-7 2016 Overexpression of miR-512-5p led to the decrease of p21 protein and mRNA level. mir-512-5p 18-28 H3 histone pseudogene 16 Homo sapiens 52-55 26314218-13 2016 In addition, in vitro exposure of RRCL to vorinostat resulted in an increase in p21 and acetylation of histone H3 leading to G1 cell cycle arrest. Vorinostat 42-52 H3 histone pseudogene 16 Homo sapiens 80-83 27014985-8 2016 (4) Phenelzine could upregulate the expression of Bax, caspase-3, p21, and downregulate Bcl-2 expression. Phenelzine 4-14 H3 histone pseudogene 16 Homo sapiens 66-69 26398108-8 2016 Selinexor induced p53, p21, and cleaved PARP in several solid tumor models. selinexor 0-9 H3 histone pseudogene 16 Homo sapiens 23-26 26408176-5 2016 We also observed that fangchinoline inhibits tumor cell proliferation and invasiveness and induces apoptosis through suppressing the Akt-mediated signaling cascades, including Akt/p21, Akt/Bad, and Akt/matrix metalloproteinases (MMPs). fangchinoline 22-35 H3 histone pseudogene 16 Homo sapiens 180-183 27014985-11 2016 CONCLUSIONS: Phenelzine increased the methylation of histone H3K4me1, H3K4me2, acetylation of histone H3 and p21, and decreased the expression of DNMT1 and p15, and ultimately inhibited the proliferation and apoptosis of Molt-4 cells. Phenelzine 13-23 H3 histone pseudogene 16 Homo sapiens 109-112 26958402-1 2016 The title compounds, C19H16ClNO5, (I), and C19H15Cl2NO5, (II), both crystallize in the monoclinic space group P21/n. c19h15cl2no5 43-55 H3 histone pseudogene 16 Homo sapiens 110-113 27268647-7 2016 Silibinin upregulated PTEN in MCF-7 and caused slightly increased P21 mRNA expression in T47D cells and slightly increased PTEN and P21 expression in MCF-10A cells. Silybin 0-9 H3 histone pseudogene 16 Homo sapiens 66-69 26713361-0 2016 Evodiamine selectively targets cancer stem-like cells through the p53-p21-Rb pathway. evodiamine 0-10 H3 histone pseudogene 16 Homo sapiens 70-73 26713361-7 2016 Surprisingly, evodiamine selectively activated p53 and p21 and decreased inactive Rb, the master molecules in G1/S checkpoint. evodiamine 14-24 H3 histone pseudogene 16 Homo sapiens 55-58 26794658-5 2016 Furthermore, we observed that overexpression of HDAC1 was associated with the downregulation of p21, a known HDAC target, in advanced NSCLC patients with paclitaxel treatment, and predicted chemotherapy resistance and bad outcome. Paclitaxel 154-164 H3 histone pseudogene 16 Homo sapiens 96-99 27109154-7 2016 The induced G2/M phase arrest indicated by the Western blotting assay showed that casticin promoted the expression of p53, p21 and CHK-1 proteins and inhibited the protein levels of Cdc25c, CDK-1, Cyclin A and B. casticin 82-90 H3 histone pseudogene 16 Homo sapiens 123-126 26623721-8 2016 Moreover, dasatinib-induced senescence was dependent on Chk1 and p21, proteins known to mediate DNA damage-induced senescence. Dasatinib 10-19 H3 histone pseudogene 16 Homo sapiens 65-68 27039820-7 2016 The fact that bromodeoxyuridine had the strongest effects on growth inhibition and senescence induction implies that senescence in cholangiocarcinoma cells is likely controlled by DNA damage response pathways relating to the p53/p21 signaling. Bromodeoxyuridine 14-31 H3 histone pseudogene 16 Homo sapiens 229-232 27268647-7 2016 Silibinin upregulated PTEN in MCF-7 and caused slightly increased P21 mRNA expression in T47D cells and slightly increased PTEN and P21 expression in MCF-10A cells. Silybin 0-9 H3 histone pseudogene 16 Homo sapiens 132-135 27997894-12 2016 CONCLUSION: Zedoarondiol inhibits PDGF-BB-induced VSMCs proliferation via AMPK-mediated down-regulation of the mTOR/p70S6K pathway and up-regulation of the p53/p21 pathway. zedoarondiol 12-24 H3 histone pseudogene 16 Homo sapiens 160-163 27725445-8 2016 The compounds vaticanol B, hemsleyanol D, and resveratrol significantly increased the expression of p21, suggesting that they are able to block cell cycle progression. Vaticanol B 14-25 H3 histone pseudogene 16 Homo sapiens 100-103 27725445-8 2016 The compounds vaticanol B, hemsleyanol D, and resveratrol significantly increased the expression of p21, suggesting that they are able to block cell cycle progression. hemsleyanol 27-38 H3 histone pseudogene 16 Homo sapiens 100-103 27725445-8 2016 The compounds vaticanol B, hemsleyanol D, and resveratrol significantly increased the expression of p21, suggesting that they are able to block cell cycle progression. Resveratrol 46-57 H3 histone pseudogene 16 Homo sapiens 100-103 26636375-5 2016 ATM inhibition allowed H(2)O(2)-stimulated hMESCs to escape the permanent cell cycle arrest due to loss of the functional ATM/p53/p21/Rb pathway, and induced bypass of mitosis and re-entry into S phase, resulting in tetraploid cells. Hydrogen Peroxide 23-31 H3 histone pseudogene 16 Homo sapiens 130-133 26918580-6 2016 Our results showed that EDH exerted anti-proliferative effects in SCC-9 cells by stabilizing the cell cycle at G1 phase in association with reduced intracellular levels of cyclins D and E and increased level of p21. EDH 24-27 H3 histone pseudogene 16 Homo sapiens 211-214 27997894-11 2016 In addition, zedoarondiol activated AMPK and ACC, inhibited the phosphorylation of mTOR and p70S6K, increased the expression of p53 and p21, and decreased the expression of CDK2 and cyclin E. Compound C (an AMPK inhibitor) abrogated, whereas 5-aminoimidazole-4-carboxamide 1-beta-ribofuranoside (AICAR, an AMPK activator) enhanced zedoarondiol-mediated inhibition of VSMCs proliferation and DNA synthesis. zedoarondiol 13-25 H3 histone pseudogene 16 Homo sapiens 136-139 26590797-9 2016 Moreover, IAZP augmented the doxorubicin-induced degradation of p21, activation of p53, CDK2, caspase 3/7 and phosphorylation of Rb protein. Doxorubicin 29-40 H3 histone pseudogene 16 Homo sapiens 64-67 26938985-11 2016 Moreover, DHT-dependent activation of AR involves regulation in the cell cycle related genes, including p73, p21 and Cyclin D1. Dihydrotestosterone 10-13 H3 histone pseudogene 16 Homo sapiens 109-112 26625870-8 2016 Moreover, PLK2 inhibition combined with cisplatin treatment in osteosarcoma Saos2 cells up-regulated p21 and puma mRNA expression to a greater extent than cisplatin treatment alone. Cisplatin 40-49 H3 histone pseudogene 16 Homo sapiens 101-104 26091707-7 2016 Additionally, after treatment of cell lines with DHT, protein levels of TGF-beta1 receptors (TGFBR1-TGFBR2) showed a decrease (p < 0.05) that might cause a potential disorder in TGF-beta1 response, represented by the significant decrease in p21 protein levels in the presence of DHT (p < 0.001). Dihydrotestosterone 49-52 H3 histone pseudogene 16 Homo sapiens 244-247 26575528-14 2016 Single agents or combination did not affect p53 expression, however, combination of cisplatin and HDACIs increased the expression of p21 in KKU-M214 cells. Cisplatin 84-93 H3 histone pseudogene 16 Homo sapiens 133-136 26276860-0 2016 Control of Trx1 redox state modulates protection against methyl methanesulfonate-induced DNA damage via stabilization of p21. Methyl Methanesulfonate 57-80 H3 histone pseudogene 16 Homo sapiens 121-124 26276860-6 2016 Trx1 overexpression and small interfering RNA knockdown in cells revealed that reduced Trx1 after exposure to lower doses of MMS attenuated DNA damage, assessed by comet assay, and level of the DNA-damage marker histone gamma-H2AX, possibly through scavenging intracellular ROS and an increase in p21 protein level via enhancing its stability. Methyl Methanesulfonate 125-128 H3 histone pseudogene 16 Homo sapiens 297-300 27232977-4 2016 TBZA and its Co(II) complex crystallize in the triclinic P-1 space group, while the Cu(II) complex crystallizes in the monoclinic P21/c space group. cu(ii) 84-90 H3 histone pseudogene 16 Homo sapiens 130-147 26585176-8 2016 DHMA significantly increased the expression of anti-apoptotic protein such as p53, p21, Bax, and caspase-3 but downregulated the expression of NF-kappaB in NCI-H460 cell line. dhma 0-4 H3 histone pseudogene 16 Homo sapiens 83-86 26531053-0 2016 Curcumin improves the efficacy of cisplatin by targeting cancer stem-like cells through p21 and cyclin D1-mediated tumour cell inhibition in non-small cell lung cancer cell lines. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 88-91 26774139-8 2016 In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 13-22 H3 histone pseudogene 16 Homo sapiens 104-107 26774139-8 2016 In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells. Fluorouracil 52-56 H3 histone pseudogene 16 Homo sapiens 104-107 26531053-0 2016 Curcumin improves the efficacy of cisplatin by targeting cancer stem-like cells through p21 and cyclin D1-mediated tumour cell inhibition in non-small cell lung cancer cell lines. Cisplatin 34-43 H3 histone pseudogene 16 Homo sapiens 88-91 26828437-3 2016 We studied the kinetics of intrinsic GTP hydrolysis reaction in the absence and presence of a biologically active peptide derivative of a p21-activated kinase effector (PBD46) for wt Cdc42 and compared it to the Switch 1 variant Cdc42(T35A). Guanosine Triphosphate 37-40 H3 histone pseudogene 16 Homo sapiens 138-141 27131314-9 2016 Further studies suggested that the cell cycle inhibitor p21 was aberrantly downregulated in CRC cells, whereas this inhibition was reversed by miR-92a inhibitor. mir-92a 143-150 H3 histone pseudogene 16 Homo sapiens 56-59 26549417-0 2016 Harmine Hydrochloride Triggers G2 Phase Arrest and Apoptosis in MGC-803 Cells and SMMC-7721 Cells by Upregulating p21, Activating Caspase-8/Bid, and Downregulating ERK/Bad Pathway. Harmine Hydrochloride 0-21 H3 histone pseudogene 16 Homo sapiens 114-117 26549524-8 2016 A549 cells exposed to the chemotherapeutic drug cisplatin (10 muM, 24 h) reveal signs of apoptosis, i.e. 25% reduction in cell viability as well as 1.3-, 1.5- and 3.3-fold increase in the expression of LRRC8A, Bax (regulator of apoptosis) and p21 (regulator of cell cycle progression), respectively. Cisplatin 48-57 H3 histone pseudogene 16 Homo sapiens 243-246 26432358-5 2015 The involvement of estrogen induced ROS in the p38 MAPK mediated p21 expression and cell growth arrest was established by observing that scavenging of ROS by NAC abrogated p38 MAPK activation and p21 expression during hypoxia. ros 36-39 H3 histone pseudogene 16 Homo sapiens 65-68 26694420-8 2015 Experiments using the specific MEK inhibitor U0126 showed that MytiLec-induced phosphorylation of the MEK-ERK pathway up-regulated expression of the cyclin-dependent kinase inhibitor p21, leading to cell cycle arrest and TNF-alpha production. U 0126 45-50 H3 histone pseudogene 16 Homo sapiens 183-186 26677335-5 2015 Consequently, Echinacoside treatment induced an immediate and dramatic increase in DNA damage markers and upregulation of the G1/S-CDK inhibitor p21, which were followed by marked apoptotic cell death and cell cycle arrest in cancer but not in noncancer cells. echinacoside 14-26 H3 histone pseudogene 16 Homo sapiens 145-148 26600068-4 2015 Yellow Na2TeS3 crystallizes in the space group P21/c. na2tes3 7-14 H3 histone pseudogene 16 Homo sapiens 47-52 26432358-5 2015 The involvement of estrogen induced ROS in the p38 MAPK mediated p21 expression and cell growth arrest was established by observing that scavenging of ROS by NAC abrogated p38 MAPK activation and p21 expression during hypoxia. ros 36-39 H3 histone pseudogene 16 Homo sapiens 196-199 26432358-5 2015 The involvement of estrogen induced ROS in the p38 MAPK mediated p21 expression and cell growth arrest was established by observing that scavenging of ROS by NAC abrogated p38 MAPK activation and p21 expression during hypoxia. ros 151-154 H3 histone pseudogene 16 Homo sapiens 65-68 26432358-5 2015 The involvement of estrogen induced ROS in the p38 MAPK mediated p21 expression and cell growth arrest was established by observing that scavenging of ROS by NAC abrogated p38 MAPK activation and p21 expression during hypoxia. ros 151-154 H3 histone pseudogene 16 Homo sapiens 196-199 26629991-0 2015 Metformin and Resveratrol Inhibited High Glucose-Induced Metabolic Memory of Endothelial Senescence through SIRT1/p300/p53/p21 Pathway. Metformin 0-9 H3 histone pseudogene 16 Homo sapiens 123-126 26629991-0 2015 Metformin and Resveratrol Inhibited High Glucose-Induced Metabolic Memory of Endothelial Senescence through SIRT1/p300/p53/p21 Pathway. Resveratrol 14-25 H3 histone pseudogene 16 Homo sapiens 123-126 26629991-9 2015 Furthermore, we found that RSV or MET treatment prevented senescent "memory" by modulating SIRT1/p300/p53/p21 pathway. Resveratrol 27-30 H3 histone pseudogene 16 Homo sapiens 106-109 26629991-11 2015 In conclusion, short-term high glucose stimulation could induce sustained endothelial senescence via SIRT1/p300/p53/p21 pathway. Glucose 31-38 H3 histone pseudogene 16 Homo sapiens 116-119 26788188-4 2015 Additional investigations revealed that NVP-BEZ235 attenuated PI3K/Akt/mTOR signaling and upregulated the levels of the cell cycle inhibitors p21 and p27. dactolisib 44-50 H3 histone pseudogene 16 Homo sapiens 142-145 26884857-6 2015 And we found that halofuginone inhibits tumor cell cycle possibly by up-regulating p15 and p21 of expression. halofuginone 18-30 H3 histone pseudogene 16 Homo sapiens 91-94 27093815-5 2015 RESULT: The results showed that PTX could increase the apoptosis and the expression of Caspase3, PARP, CytC, AIF and Bax and reduce the proliferation, membrane potential and the expression of PI3K, p-AKT, p53, p21, Cleavage-PARP, Cleavage-Caspase3 and Bcl-2 in CNE2 cell in a concentration-dependent manner. ptx 32-35 H3 histone pseudogene 16 Homo sapiens 210-213 26404525-6 2015 Interestingly, inhibition of p53 or knockdown of p21, abolished LMP-induced caspase-3 activity and cell death. (2~{s},3~{r},4~{s})-2-[(2~{s},3~{r})-1,3-Bis(Oxidanyl)-1-Oxidanylidene-Butan-2-Yl]-4-[(3~{s},5~{s})-5-(Dimethylcarbamoyl)pyrrolidin-3-Yl]sulfanyl-3-Methyl-3,4-Dihydro-2~{h}-Pyrrole-5-Carboxylic Acid 64-67 H3 histone pseudogene 16 Homo sapiens 49-52 26404525-7 2015 Blocking oxidized phospholipid-rich LMPs with a specific antibody significantly prevented LMP-induced Rb apoptosis and reversed the expression patterns of SYK, p53, p21. Phospholipids 18-30 H3 histone pseudogene 16 Homo sapiens 165-168 26520903-8 2015 Corroborating the involvement of alpha1beta1 integrin, the pretreatment of VSMC with obtustatin impaired Ang II-induced FAK phosphorylation, AKT activation, p21 degradation and the increase of ILK expression. vsmc 75-79 H3 histone pseudogene 16 Homo sapiens 157-160 26520903-8 2015 Corroborating the involvement of alpha1beta1 integrin, the pretreatment of VSMC with obtustatin impaired Ang II-induced FAK phosphorylation, AKT activation, p21 degradation and the increase of ILK expression. obtustatin 85-95 H3 histone pseudogene 16 Homo sapiens 157-160 26041389-5 2015 The expressions of p53 and p21 were decreased in H2O2-treated RTEF-1 o/e human umbilical vein endothelial cells. Hydrogen Peroxide 49-53 H3 histone pseudogene 16 Homo sapiens 27-30 26498137-9 2015 In addition, curcumin was found to cause the induction of p21, a cyclin-dependent kinase inhibitor, and reduction of X-linked inhibitor of apoptosis protein (XIAP), an anti-apoptotic molecule, in parental H460 cells as well as chemoresistant cells, H460/CisR and H460/TR. Curcumin 13-21 H3 histone pseudogene 16 Homo sapiens 58-61 26375402-3 2015 p21-activated kinases are serine-threonine kinases that serve as targets for the small GTP binding proteins Cdc42 and Rac1 and have been implicated in different morphogenetic processes through remodeling of the actin cytoskeleton such as synapse formation and neuritogenesis. Serine 26-32 H3 histone pseudogene 16 Homo sapiens 0-3 26375402-3 2015 p21-activated kinases are serine-threonine kinases that serve as targets for the small GTP binding proteins Cdc42 and Rac1 and have been implicated in different morphogenetic processes through remodeling of the actin cytoskeleton such as synapse formation and neuritogenesis. Guanosine Triphosphate 87-90 H3 histone pseudogene 16 Homo sapiens 0-3 26467393-4 2015 Human aortic smooth muscle cells treated with beta-Glycerophosphate (BGP, 10mM) suffered cellular senescence by increasing p53, p21 and p16 expression and the senescence associated beta-galactosidase activity. beta-glycerophosphoric acid 46-67 H3 histone pseudogene 16 Homo sapiens 128-131 26486083-7 2015 Cisplatin also activated p53 and phosphorylated activator protein (AP-1) component, c-Jun at serine (63, 73) residue simultaneously leading to cell cycle arrest through stimulation of p21 and down regulation of cyclins and cyclin dependent kinases in APL cell lines. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 184-187 26320837-6 2015 Transcriptional analysis of several cancer-associated genes (c-fos, AURKA, p21, bcl-xl and CLU) shows that BPA exposure induces slight up-regulation exclusively of bcl-xl without affecting cell viability. bisphenol A 107-110 H3 histone pseudogene 16 Homo sapiens 75-78 26320837-8 2015 Conversely, DOX at a therapeutic concentration (4 muM) results in distinct and very severe transcriptional alterations of c-fos, AURKA, p21 and CLU that are counteracted by co-exposure with BPA resulting in transcript levels similar to those of control. Doxorubicin 12-15 H3 histone pseudogene 16 Homo sapiens 136-139 26343756-5 2015 Moreover, Bis-GMA induced a depletion of mitochondrial membrane potential, an increase in the Bax/Bcl-2 ratio, an activation of caspase-3 and altered expressions of cell cycle-related proteins (p21, PCNA, cyclinD1). Bisphenol A-Glycidyl Methacrylate 10-17 H3 histone pseudogene 16 Homo sapiens 194-197 26320837-8 2015 Conversely, DOX at a therapeutic concentration (4 muM) results in distinct and very severe transcriptional alterations of c-fos, AURKA, p21 and CLU that are counteracted by co-exposure with BPA resulting in transcript levels similar to those of control. bisphenol A 190-193 H3 histone pseudogene 16 Homo sapiens 136-139 26474283-2 2015 However, no evidence are presently available on a direct cytotoxic anti-tumor activity of axitinib in RCC.Herein we reported by western blot analysis that axitinib treatment induces a DNA damage response (DDR) initially characterized by gamma-H2AX phosphorylation and Chk1 kinase activation and at later time points by p21 overexpression in A-498 and Caki-2 RCC cells although with a different potency. Axitinib 155-163 H3 histone pseudogene 16 Homo sapiens 319-322 26708876-7 2015 The mRNA expression of P21 and P27 was significantly increased after indomethacin treatment in U266 and K562 cell lines except for the P27 mRNA expression of U937. Indomethacin 69-81 H3 histone pseudogene 16 Homo sapiens 23-26 26501364-2 2015 X-ray diffraction measurements determined the crystal structure of CdDLHis at 100 and 298 K. CdDLHis crystallizes in the monoclinic space group P21/c with two cadmium complexes per asymmetric unit. cddlhis 93-100 H3 histone pseudogene 16 Homo sapiens 144-147 26415552-2 2015 Treating prostate cancer cells with physapubescin B resulted in the accumulation of cells in the G2/M phase, which was associated with reduced Cdc25C levels and increased levels of CyclinB1, P21 as well as p-Cdk1 (Tyr15). physapubescin B 36-51 H3 histone pseudogene 16 Homo sapiens 191-194 26559563-8 2015 These results indicate that butyrate is able to modify colon cancer-relevant miRNAs like miR-106b and miR-135a which are involved in the regulation of cell cycle-relevant genes like p21 and might influence inhibition of adenoma cell proliferation. Butyrates 28-36 H3 histone pseudogene 16 Homo sapiens 182-185 26525771-4 2015 Mechanistic studies showed that ailanthone induced G0/G1-phase cell cycle arrest, as indicated by decreased expression of cyclins and CDKs and increased expression of p21 and p27. ailanthone 32-42 H3 histone pseudogene 16 Homo sapiens 167-170 26276715-8 2015 Experimental evidence postulates multiple potential mechanisms by which calcitriol analogues may exert their anti-cancer effect, the most common being by action on cyclin-dependent kinases p21 and p27. Calcitriol 72-82 H3 histone pseudogene 16 Homo sapiens 189-192 26559563-0 2015 Influence of miRNA-106b and miRNA-135a on butyrate-regulated expression of p21 and Cyclin D2 in human colon adenoma cells. Butyrates 42-50 H3 histone pseudogene 16 Homo sapiens 75-78 26559563-3 2015 The impact of distinct miRNAs (miR-106b, miR-135a) on butyrate-mediated regulation of p21 and Cyclin D2 gene and protein expression as well as the effect on LT97 cell proliferation (non-transfected, miR-106b and miR-135a mimic transfected) was analyzed. Butyrates 54-62 H3 histone pseudogene 16 Homo sapiens 86-89 26559563-5 2015 Levels of p21 mRNA and protein were significantly increased by butyrate and TSA (~threefold and 4.5-fold, respectively, 24 h) in non-transfected but not in miR-106b transfected LT97 cells. Butyrates 63-71 H3 histone pseudogene 16 Homo sapiens 10-13 26722252-0 2015 Cantharidin modulates the E2F1/MCM7-miR-106b-93/p21-PTEN signaling axis in MCF-7 breast cancer cells. Cantharidin 0-11 H3 histone pseudogene 16 Homo sapiens 48-51 26559563-5 2015 Levels of p21 mRNA and protein were significantly increased by butyrate and TSA (~threefold and 4.5-fold, respectively, 24 h) in non-transfected but not in miR-106b transfected LT97 cells. trichostatin A 76-79 H3 histone pseudogene 16 Homo sapiens 10-13 26492346-6 2015 PNAP-6h led to cell arrest at the S phase, most likely due to increasing levels of p21 and p27 and decreasing levels of cyclin D1, CDK4, cyclin E, and CDK2. 6H 5-7 H3 histone pseudogene 16 Homo sapiens 83-86 26491966-6 2015 In addition, quercetin effectively suppressed the expression of CyclinD1, p21, Twist and phospho p38MAPK, which was not observed in MDA-MB-231 cells. Quercetin 13-22 H3 histone pseudogene 16 Homo sapiens 74-77 26352101-12 2015 Treatment with doxorubicin alone significantly induced the cell cycle-dependent kinase inhibitor protein p21, whereas ferritin reduced p21 expression. Doxorubicin 15-26 H3 histone pseudogene 16 Homo sapiens 105-108 26345349-2 2015 A novel structure, with SiC2O6 stoichiometry and the P21/c space group is calculated to be stable against decomposition within a wide pressure window from 7.2 to 41 GPa, and metastable under ambient conditions. sic2o6 24-30 H3 histone pseudogene 16 Homo sapiens 53-58 26491966-8 2015 Quercetin effectively regulated the expression of Twist, in turn p16 and p21 which induced apoptosis in MCF-7 cells. Quercetin 0-9 H3 histone pseudogene 16 Homo sapiens 73-76 26594373-1 2015 A new monoclinic polymorph, form II (P21/c, Z = 4), has been isolated for 3,4-dimethoxycinnamic acid (DMCA). 3-(3,4-dimethoxyphenyl)propenoic acid 74-100 H3 histone pseudogene 16 Homo sapiens 37-49 26594373-1 2015 A new monoclinic polymorph, form II (P21/c, Z = 4), has been isolated for 3,4-dimethoxycinnamic acid (DMCA). 3-(3,4-dimethoxyphenyl)propenoic acid 102-106 H3 histone pseudogene 16 Homo sapiens 37-49 26187313-0 2015 Distinct roles of transforming growth factor-beta signaling and transforming growth factor-beta receptor inhibitor SB431542 in the regulation of p21 expression. 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide 115-123 H3 histone pseudogene 16 Homo sapiens 145-148 26465338-3 2015 Fibroblasts cultured on commercial tissue culture polystyrene (TCPS) entered senescence after 55-60 population doublings (PDs), and were accompanied by larger cell shape, higher senescence-associated beta-galactosidase (SA beta-gal) activity, lower proliferation capacity, and upregulation of senescence-associated molecular markers p21, p53, retinoblastoma (pRB), and p16. tcps 63-67 H3 histone pseudogene 16 Homo sapiens 333-336 26187313-10 2015 On the other hand, treatment with SB431542 up-regulated p21 expression while inhibiting cell growth. 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide 34-42 H3 histone pseudogene 16 Homo sapiens 56-59 26187313-13 2015 These findings suggest that downregulation of Sp1 expression is responsible for SB43154-induced p21 expression. 2-(4-Methylpiperidin-1-yl)-5-nitroaniline 80-87 H3 histone pseudogene 16 Homo sapiens 96-99 25716429-4 2015 Among them, compound 4 (quercetagetin 3,4"-dimethyl ether) showed inhibitory activity against cellular senescence, which was confirmed by senescence-associated beta-galactosidase (SA-beta-gal) activity, p53 and p21 protein levels, and intracellular ROS levels. quercetagetin 3,4'-dimethyl ether 24-57 H3 histone pseudogene 16 Homo sapiens 211-214 25965512-2 2015 This complex is structurally characterized by single crystal X-ray diffraction, revealing a three-dimensional structure crystallized in the monoclinic space-group P21/n, where thorium cation is nine coordinated by four SO4(2-) oxygen atoms, four bridging F(-), and one H2O molecule. Thorium 176-183 H3 histone pseudogene 16 Homo sapiens 163-166 25965512-2 2015 This complex is structurally characterized by single crystal X-ray diffraction, revealing a three-dimensional structure crystallized in the monoclinic space-group P21/n, where thorium cation is nine coordinated by four SO4(2-) oxygen atoms, four bridging F(-), and one H2O molecule. sulfuric acid 219-222 H3 histone pseudogene 16 Homo sapiens 163-166 26181229-0 2015 Cell cycle arrest and apoptosis induced by aspidin PB through the p53/p21 and mitochondria-dependent pathways in human osteosarcoma cells. aspidin PB 43-53 H3 histone pseudogene 16 Homo sapiens 70-73 26181229-2 2015 We reported that aspidin PB induced cell cycle arrest and apoptosis through the p53/p21 and mitochondria-dependent pathways in human osteosarcoma cells. aspidin PB 17-27 H3 histone pseudogene 16 Homo sapiens 84-87 26181229-4 2015 Aspidin PB induced changes in the cell cycle regulators (cyclin A, pRb, CDK2, p53, and p21), which caused cell cycle arrest in the S phase. aspidin PB 0-10 H3 histone pseudogene 16 Homo sapiens 87-90 26181229-6 2015 Moreover, after treatment with aspidin PB, the p21-silenced cells decreased significantly at the S phase. aspidin PB 31-41 H3 histone pseudogene 16 Homo sapiens 47-50 26422222-1 2015 The crystal structure of 5-iodouracil, C4H3IN2O2, has been determined in the noncentrosymmetric space group P21 on a nonmerohedrally twinned crystal. 5-iodouracil 25-37 H3 histone pseudogene 16 Homo sapiens 108-111 26422222-1 2015 The crystal structure of 5-iodouracil, C4H3IN2O2, has been determined in the noncentrosymmetric space group P21 on a nonmerohedrally twinned crystal. c4h3in2o2 39-48 H3 histone pseudogene 16 Homo sapiens 108-111 26410576-6 2015 Furthermore, vorinostat-NPs have similar effectiveness in the suppression or expression of histone deacetylase, mutant type p53, p21, and PARP/cleaved caspase-3. Vorinostat 13-23 H3 histone pseudogene 16 Homo sapiens 129-132 26217035-6 2015 Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression. Doxorubicin 189-199 H3 histone pseudogene 16 Homo sapiens 208-211 26217035-9 2015 Recruitment of JunB to the p21 promoter was promoted by Adriamycin stimulation and was further enhanced by co-treatment with the c-Abl inhibitor imatinib. Doxorubicin 56-66 H3 histone pseudogene 16 Homo sapiens 27-30 26217035-9 2015 Recruitment of JunB to the p21 promoter was promoted by Adriamycin stimulation and was further enhanced by co-treatment with the c-Abl inhibitor imatinib. Imatinib Mesylate 145-153 H3 histone pseudogene 16 Homo sapiens 27-30 26217035-11 2015 Taken together, these results suggest that, although JunB represses p21 promoter activity, c-Abl phosphorylates JunB and conversely inhibits its suppressive role on p21 promoter activity upon Adriamycin stimulation. Doxorubicin 192-202 H3 histone pseudogene 16 Homo sapiens 165-168 26217035-12 2015 Therefore JunB is likely to be a key target of c-Abl in expression of p21 in Adriamycin-induced DDR. Doxorubicin 77-87 H3 histone pseudogene 16 Homo sapiens 70-73 26314270-4 2015 First, PA dose-dependently induced cell cycle arrest at G2/M phase, as shown by accumulation of the mitosis-related proteins, p21, survivin and Aurora B. podophyllotoxin acetate 7-9 H3 histone pseudogene 16 Homo sapiens 126-129 26206334-8 2015 Furthermore, GTPase inhibition by R-ketorolac reduces downstream p21-activated kinases (PAK1/PAK2) effector activation by >80%. (R)-Ketorolac 34-45 H3 histone pseudogene 16 Homo sapiens 65-68 26217035-0 2015 c-Abl-mediated tyrosine phosphorylation of JunB is required for Adriamycin-induced expression of p21. Tyrosine 15-23 H3 histone pseudogene 16 Homo sapiens 97-100 26217035-0 2015 c-Abl-mediated tyrosine phosphorylation of JunB is required for Adriamycin-induced expression of p21. Doxorubicin 64-74 H3 histone pseudogene 16 Homo sapiens 97-100 26217035-6 2015 Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression. Doxorubicin 124-134 H3 histone pseudogene 16 Homo sapiens 75-78 26217035-6 2015 Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression. Doxorubicin 136-147 H3 histone pseudogene 16 Homo sapiens 75-78 25808410-3 2015 According to our observation, treatment with TDF and ABC affects the ability of the cells to produce calcium deposits with a reduced expression of type I collagen gene and p21 mRNA, also increasing the activity of Wnt3a related pathway. Calcium 101-108 H3 histone pseudogene 16 Homo sapiens 172-175 26166196-8 2015 The findings revealed that curcumin significantly decreased cell proliferation, which was associated with increased expression of the p21/CIP1 and p27/KIP1 cyclin-dependent kinase inhibitors, and inhibited expression of cyclin D1. Curcumin 27-35 H3 histone pseudogene 16 Homo sapiens 134-137 24645745-7 2015 Despite the limitations, the results of the present meta-analysis suggested that, in the p21 Ser31Arg polymorphism, Ser-allele and Ser/Ser genotype might be risk factors for gastrointestinal tract tumor in Asian populations. Serine 93-96 H3 histone pseudogene 16 Homo sapiens 89-92 26420673-3 2015 Here we show that arginine methylation of KLF4 by PRMT5 inhibits KLF4 ubiquitylation by VHL and thereby reduces KLF4 turnover, resulting in the elevation of KLF4 protein levels concomitant with increased transcription of KLF4-dependent p21 and reduced expression of KLF4-repressed Bax. Arginine 18-26 H3 histone pseudogene 16 Homo sapiens 236-239 26317649-10 2015 Thus, we observed for the first time a differential effect of cancer versus non-cancer cells after treatment with SAHA and SBE13, which might be due to the dual role of p21. SBE13 123-128 H3 histone pseudogene 16 Homo sapiens 169-172 26378933-7 2015 Corroborating the clinical outcome of the patients, our data provides a potential explanation regarding the poor response of MM patients with del(8)(p21) to bortezomib treatment. Bortezomib 157-167 H3 histone pseudogene 16 Homo sapiens 149-152 26378933-2 2015 In this study, we aimed to identify the immunological and molecular consequences of del(8)(p21) with regards to treatment response and bortezomib resistance. Bortezomib 135-145 H3 histone pseudogene 16 Homo sapiens 91-94 26378933-8 2015 Furthermore, our clinical analysis suggests that including immunomodulatory agents such as Lenalidomide in the treatment regimen may help to overcome this negative effect, providing an alternative consideration in treatment planning of MM patients with del(8)(p21). Lenalidomide 91-103 H3 histone pseudogene 16 Homo sapiens 260-263 26378933-3 2015 In patients receiving bortezomib as a single first line agent without any high-dose therapy, we have observed that patients with del(8)(p21) responded poorly to bortezomib with 50% showing no response while patients without the deletion had a response rate of 90%. Bortezomib 22-32 H3 histone pseudogene 16 Homo sapiens 136-139 26378933-3 2015 In patients receiving bortezomib as a single first line agent without any high-dose therapy, we have observed that patients with del(8)(p21) responded poorly to bortezomib with 50% showing no response while patients without the deletion had a response rate of 90%. Bortezomib 161-171 H3 histone pseudogene 16 Homo sapiens 136-139 26299825-0 2015 Synthesis of 1,2-benzisoxazole tethered 1,2,3-triazoles that exhibit anticancer activity in acute myeloid leukemia cell lines by inhibiting histone deacetylases, and inducing p21 and tubulin acetylation. 1,2-benzisoxazole 13-30 H3 histone pseudogene 16 Homo sapiens 175-178 26378933-4 2015 In vitro analysis revealed a higher resistance to bortezomib possibly due to an altered gene expression profile caused by del(8)(p21) including genes such as TRAIL-R4, CCDC25, RHOBTB2, PTK2B, SCARA3, MYC, BCL2 and TP53. Bortezomib 50-60 H3 histone pseudogene 16 Homo sapiens 129-132 26299825-0 2015 Synthesis of 1,2-benzisoxazole tethered 1,2,3-triazoles that exhibit anticancer activity in acute myeloid leukemia cell lines by inhibiting histone deacetylases, and inducing p21 and tubulin acetylation. 1,2,3-triazoles 40-55 H3 histone pseudogene 16 Homo sapiens 175-178 26225749-5 2015 Treatment of MCF-7 cells with metformin or phenformin induced increase in p53 protein levels and the transcription of its downstream target genes, Bax and p21, in a dose-dependent manner. Metformin 30-39 H3 histone pseudogene 16 Homo sapiens 155-158 26091798-6 2015 The present study has examined activity and expression of 53 and its downstream target protein p21 upon acute or chronic exposure of BEAS-2B cells to arsenic and Cr(VI). Arsenic 150-157 H3 histone pseudogene 16 Homo sapiens 95-98 26091798-6 2015 The present study has examined activity and expression of 53 and its downstream target protein p21 upon acute or chronic exposure of BEAS-2B cells to arsenic and Cr(VI). Chromium 162-164 H3 histone pseudogene 16 Homo sapiens 95-98 26091798-7 2015 The results show that short-term exposure of BEAS-2B cells to arsenic or Cr(VI) was able to activate both p53 and p21. Arsenic 62-69 H3 histone pseudogene 16 Homo sapiens 114-117 26091798-7 2015 The results show that short-term exposure of BEAS-2B cells to arsenic or Cr(VI) was able to activate both p53 and p21. chromium hexavalent ion 73-79 H3 histone pseudogene 16 Homo sapiens 114-117 26225749-5 2015 Treatment of MCF-7 cells with metformin or phenformin induced increase in p53 protein levels and the transcription of its downstream target genes, Bax and p21, in a dose-dependent manner. Phenformin 43-53 H3 histone pseudogene 16 Homo sapiens 155-158 26405550-6 2015 Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Arginine 247-255 H3 histone pseudogene 16 Homo sapiens 48-51 26405550-6 2015 Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Arginine 257-260 H3 histone pseudogene 16 Homo sapiens 48-51 26405550-6 2015 Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Proline 271-274 H3 histone pseudogene 16 Homo sapiens 48-51 26405550-6 2015 Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Proline 262-269 H3 histone pseudogene 16 Homo sapiens 48-51 26405550-6 2015 Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Proline 276-279 H3 histone pseudogene 16 Homo sapiens 48-51 24665044-9 2015 A significantly higher number of senescent cells, over-expression of p53 and p21 were observed in the As-exposed individuals when compared to unexposed. Arsenic 102-104 H3 histone pseudogene 16 Homo sapiens 77-80 26405550-6 2015 Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Proline 276-279 H3 histone pseudogene 16 Homo sapiens 48-51 26405550-6 2015 Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Arginine 368-371 H3 histone pseudogene 16 Homo sapiens 48-51 26405550-6 2015 Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P<0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC. Arginine 368-371 H3 histone pseudogene 16 Homo sapiens 48-51 26194899-4 2015 In further experiments, p53 protein expression was increased, and H2AX phosphorylation and p21 protein expression were induced after treatment with 3EZ, 20Ac-ingenol. 3EZ 148-151 H3 histone pseudogene 16 Homo sapiens 91-94 26194899-4 2015 In further experiments, p53 protein expression was increased, and H2AX phosphorylation and p21 protein expression were induced after treatment with 3EZ, 20Ac-ingenol. 20ac-ingenol 153-165 H3 histone pseudogene 16 Homo sapiens 91-94 26713523-4 2015 The expression of cleaved poly-ADP-ribose polymerase(cleaved-PARP) and p21 protein was analyzed by Western-blotting when A549 cells were challenged with 2.5mumol/L SAHA and 5mumol/L lovastatin. Vorinostat 164-168 H3 histone pseudogene 16 Homo sapiens 71-74 26287184-4 2015 Methyl sartortuoate treatment led to reduced expression of cdc2 and up-regulated p21 and p53, suggesting that Methyl sartortuoate induced G2-M arrest through modulation of p53/p21/cdc2 pathways. methyl sartortuoate 0-19 H3 histone pseudogene 16 Homo sapiens 81-84 26713523-7 2015 Treatment with 2.5mumol/L SAHA significantly up-regulated the expression of p21 protein in 48 h, while the protein expression was reduced in combined treatment with 5mumol/L lovastatin. Vorinostat 26-30 H3 histone pseudogene 16 Homo sapiens 76-79 26713523-7 2015 Treatment with 2.5mumol/L SAHA significantly up-regulated the expression of p21 protein in 48 h, while the protein expression was reduced in combined treatment with 5mumol/L lovastatin. Lovastatin 174-184 H3 histone pseudogene 16 Homo sapiens 76-79 26713523-8 2015 CONCLUSION: Statins can synergize the anti-tumor effect of SAHA in human NSCLC cells through a p21-dependent way. Vorinostat 59-63 H3 histone pseudogene 16 Homo sapiens 95-98 26224795-10 2015 JQ1 treatment in PAH-PASMCs increased p21 expression, thus triggering cell cycle arrest. pasmcs 21-27 H3 histone pseudogene 16 Homo sapiens 38-41 26287184-4 2015 Methyl sartortuoate treatment led to reduced expression of cdc2 and up-regulated p21 and p53, suggesting that Methyl sartortuoate induced G2-M arrest through modulation of p53/p21/cdc2 pathways. methyl sartortuoate 0-19 H3 histone pseudogene 16 Homo sapiens 176-179 26287184-4 2015 Methyl sartortuoate treatment led to reduced expression of cdc2 and up-regulated p21 and p53, suggesting that Methyl sartortuoate induced G2-M arrest through modulation of p53/p21/cdc2 pathways. methyl sartortuoate 110-129 H3 histone pseudogene 16 Homo sapiens 81-84 26287184-4 2015 Methyl sartortuoate treatment led to reduced expression of cdc2 and up-regulated p21 and p53, suggesting that Methyl sartortuoate induced G2-M arrest through modulation of p53/p21/cdc2 pathways. methyl sartortuoate 110-129 H3 histone pseudogene 16 Homo sapiens 176-179 26148683-2 2015 The progressive substitution of the paramagnetic Co(2+) high spin ion by the diamagnetic Mg(2+), of about the same size, induces changes in the room temperature crystal structure, from a distorted P2(1)/n phase for the undoped Sr(2)CoTeO(6) oxide to the I4/m of the end member (Sr(2)MgTeO(6)). Cobalt(2+) 49-55 H3 histone pseudogene 16 Homo sapiens 197-202 26148683-2 2015 The progressive substitution of the paramagnetic Co(2+) high spin ion by the diamagnetic Mg(2+), of about the same size, induces changes in the room temperature crystal structure, from a distorted P2(1)/n phase for the undoped Sr(2)CoTeO(6) oxide to the I4/m of the end member (Sr(2)MgTeO(6)). magnesium ion 89-95 H3 histone pseudogene 16 Homo sapiens 197-202 26162681-7 2015 Downstream events, measured by time-series reverse-phase protein microarrays, high-content imaging, and flow cytometry, showed a dramatic increase in mitochondrially produced reactive oxygen species (ROS) and subsequent DNA damage with up-regulation of ATM, p53, and p21 proteins. Reactive Oxygen Species 175-198 H3 histone pseudogene 16 Homo sapiens 267-270 25441423-5 2015 The protein expressions of p21 were significantly increased by the co-treatment of EGCG and curcumin, whereas it was not changed by the treatment with each individual compound. epigallocatechin gallate 83-87 H3 histone pseudogene 16 Homo sapiens 27-30 25441423-5 2015 The protein expressions of p21 were significantly increased by the co-treatment of EGCG and curcumin, whereas it was not changed by the treatment with each individual compound. Curcumin 92-100 H3 histone pseudogene 16 Homo sapiens 27-30 25441423-7 2015 These results suggest that the enhanced inhibitory effect of EGCG on PC3 cell proliferation by curcumin was mediated by the synergic up-regulation of p21-induced growth arrest and followed cell growth arrest. epigallocatechin gallate 61-65 H3 histone pseudogene 16 Homo sapiens 150-153 25441423-7 2015 These results suggest that the enhanced inhibitory effect of EGCG on PC3 cell proliferation by curcumin was mediated by the synergic up-regulation of p21-induced growth arrest and followed cell growth arrest. Curcumin 95-103 H3 histone pseudogene 16 Homo sapiens 150-153 26043725-15 2015 Butyrate increased levels of cyclin D1, p21 and PARP p86, but decreased Bcl-XL and survivin levels. Butyrates 0-8 H3 histone pseudogene 16 Homo sapiens 40-43 26043725-18 2015 ALCAR independently induced a 20% decrease in p21. Acetylcarnitine 0-5 H3 histone pseudogene 16 Homo sapiens 46-49 25979648-6 2015 The anticancer effect of delta-T3 was achieved by its up-regulation of cyclin-dependent kinase inhibitors (p21 and p27), the activation of caspases and the suppression of phosphorylation of protein kinase B (Akt) at Thr(308) and Ser(473). delta-t3 25-33 H3 histone pseudogene 16 Homo sapiens 107-110 26154989-3 2015 The structure of Ba2V(VO4)2(OH) is monoclinic in space group P21/m, a = 7.8783(2) A, b = 6.1369(1) A, c = 9.1836(2) A, beta = 113.07(3) , V = 408.51(2) A(3). ba2v 17-21 H3 histone pseudogene 16 Homo sapiens 61-64 26162681-7 2015 Downstream events, measured by time-series reverse-phase protein microarrays, high-content imaging, and flow cytometry, showed a dramatic increase in mitochondrially produced reactive oxygen species (ROS) and subsequent DNA damage with up-regulation of ATM, p53, and p21 proteins. Reactive Oxygen Species 200-203 H3 histone pseudogene 16 Homo sapiens 267-270 26062558-8 2015 Moreover, inhibition of miR-92a could significantly suppress HCC growth in vitro and in vivo by upregulating p21. mir-92a 24-31 H3 histone pseudogene 16 Homo sapiens 109-112 25813178-1 2015 beta-Alaninium tetrafluoroborate crystallizes in the monoclinic system (space group P21/n, Z=4). beta-alaninium tetrafluoroborate 0-32 H3 histone pseudogene 16 Homo sapiens 84-87 25232917-9 2015 P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004). Serine 125-128 H3 histone pseudogene 16 Homo sapiens 4-7 25860284-2 2015 We have previously reported that the combination of the EGFR-TKI erlotinib and epigallocatechin-3-gallate (EGCG) exhibited synergistic chemopreventive effects in head and neck cancers by inducing the expression of Bim, p21, p27, and by inhibiting the phosphorylation of ERK and AKT and expression of Bcl-2. epigallocatechin gallate 107-111 H3 histone pseudogene 16 Homo sapiens 219-222 25860284-2 2015 We have previously reported that the combination of the EGFR-TKI erlotinib and epigallocatechin-3-gallate (EGCG) exhibited synergistic chemopreventive effects in head and neck cancers by inducing the expression of Bim, p21, p27, and by inhibiting the phosphorylation of ERK and AKT and expression of Bcl-2. Erlotinib Hydrochloride 65-74 H3 histone pseudogene 16 Homo sapiens 219-222 25860284-2 2015 We have previously reported that the combination of the EGFR-TKI erlotinib and epigallocatechin-3-gallate (EGCG) exhibited synergistic chemopreventive effects in head and neck cancers by inducing the expression of Bim, p21, p27, and by inhibiting the phosphorylation of ERK and AKT and expression of Bcl-2. epigallocatechin gallate 79-105 H3 histone pseudogene 16 Homo sapiens 219-222 25232917-9 2015 P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004). Serine 129-132 H3 histone pseudogene 16 Homo sapiens 4-7 26003431-2 2015 SUMMARY ANSWER: Neddylation inhibition by a selective NEDD8-activating enzyme inhibitor, MLN4924, significantly impairs human endometrial stromal cell (HESC) proliferation and decidualization and facilitates cell senescence, via p21 accumulation. pevonedistat 89-96 H3 histone pseudogene 16 Homo sapiens 229-232 25232917-9 2015 P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004). Serine 204-207 H3 histone pseudogene 16 Homo sapiens 4-7 25232917-9 2015 P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004). Arginine 208-211 H3 histone pseudogene 16 Homo sapiens 4-7 25232917-9 2015 P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004). Arginine 289-292 H3 histone pseudogene 16 Homo sapiens 4-7 25232917-9 2015 P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004). Arginine 289-292 H3 histone pseudogene 16 Homo sapiens 4-7 25382668-5 2015 In addition, TCDD altered the expression of senescence marker proteins, such as p16, p21 and GFAP, which together have been reported to be upregulated in aging astrocytes, in both dose- and time-dependent manners. Polychlorinated Dibenzodioxins 13-17 H3 histone pseudogene 16 Homo sapiens 85-88 26100134-9 2015 Furthermore, EGCG reduced the mRNA levels of various cell cycle-related genes, while increasing the expression of the cell cycle inhibitor p21 and the apoptosis-related death receptor 5 (p < 0.05). epigallocatechin gallate 13-17 H3 histone pseudogene 16 Homo sapiens 139-142 26132569-4 2015 Treatment of the human SW480 cancer cells with Echinacoside resulted in marked apoptosis and cell cycle arrest, together with a significant increase in active caspase 3 and cleaved PARP, and upregulation of the G1/S-CDK blocker CDKN1B (p21). echinacoside 47-59 H3 histone pseudogene 16 Homo sapiens 236-239 25623228-1 2015 The perovskite polymorph of Mn(2)CrSbO(6) compound has been synthesized at 8 GPa and 1473 K. It crystallizes in the monoclinic P21/n space group with cell parameters a = 5.2180 (2) A, b = 5.3710(2) A, c = 7.5874(1) A and beta = 90.36(1) . mn(2)crsbo 28-38 H3 histone pseudogene 16 Homo sapiens 127-130 26096298-3 2015 The superconducting critical temperature Tc values of I4/mmm, Cmma, and P21/m are 47-193 mK, 5.99-8.16 K and 10.62-12.8 K at 1 atm, 180 and 260 GPa, respectively. Technetium 41-43 H3 histone pseudogene 16 Homo sapiens 72-75 25623228-1 2015 The perovskite polymorph of Mn(2)CrSbO(6) compound has been synthesized at 8 GPa and 1473 K. It crystallizes in the monoclinic P21/n space group with cell parameters a = 5.2180 (2) A, b = 5.3710(2) A, c = 7.5874(1) A and beta = 90.36(1) . perovskite 4-14 H3 histone pseudogene 16 Homo sapiens 127-130 25714087-5 2015 Results show that chabamide inhibited the growth of K562/ADR cells in a dose-dependent and time-dependent manner, and significantly inhibited cell proliferation by cell cycle arrest in the G0/G1 phase, which was associated with an obvious increase in p21 and decrease in cyclin D1 and CDK2/4/6 protein expression. chabamide 18-27 H3 histone pseudogene 16 Homo sapiens 251-254 25972089-5 2015 As p21 is one of the few PIP-box sequences to contain a tyrosine rather than a phenylalanine in the eighth conserved position, we probed the significance of the hydroxyl group at this position using a mutational approach. Tyrosine 56-64 H3 histone pseudogene 16 Homo sapiens 3-6 25972089-5 2015 As p21 is one of the few PIP-box sequences to contain a tyrosine rather than a phenylalanine in the eighth conserved position, we probed the significance of the hydroxyl group at this position using a mutational approach. Phenylalanine 79-92 H3 histone pseudogene 16 Homo sapiens 3-6 26047480-9 2015 EADs is postulated to induce cell cycle arrest that is p53- and p21-dependent based on the upregulated expression of p53 and p21 (P<0.05). eads 0-4 H3 histone pseudogene 16 Homo sapiens 64-67 26047480-9 2015 EADs is postulated to induce cell cycle arrest that is p53- and p21-dependent based on the upregulated expression of p53 and p21 (P<0.05). eads 0-4 H3 histone pseudogene 16 Homo sapiens 125-128 26279892-1 2015 A new polymorph of the title compound 2-(eta-C5H5)-2,1,7-closo-CoC2B9H11, [Co(C5H5)(C2H11B9)], in the space group P21/n has been characterized, including the unambiguous location of both cage C atoms. 2-(eta-c5h5)- 38-51 H3 histone pseudogene 16 Homo sapiens 114-117 26279892-1 2015 A new polymorph of the title compound 2-(eta-C5H5)-2,1,7-closo-CoC2B9H11, [Co(C5H5)(C2H11B9)], in the space group P21/n has been characterized, including the unambiguous location of both cage C atoms. 2,1,7-closo-coc2b9h11 51-72 H3 histone pseudogene 16 Homo sapiens 114-117 26011150-3 2015 The reaction of Na2PdCl6 with neat SO3 afforded yellow crystals of Na2Pd(S4O13)2 (monoclinic, P21/c, a = 6.9953(4) A, b = 15.9420(9) A, c = 9.2299(5) A, beta = 100.235(2) , V = 1012.45(1) A3). na2pdcl6 16-24 H3 histone pseudogene 16 Homo sapiens 94-99 26011150-3 2015 The reaction of Na2PdCl6 with neat SO3 afforded yellow crystals of Na2Pd(S4O13)2 (monoclinic, P21/c, a = 6.9953(4) A, b = 15.9420(9) A, c = 9.2299(5) A, beta = 100.235(2) , V = 1012.45(1) A3). sulfur trioxide 35-38 H3 histone pseudogene 16 Homo sapiens 94-99 26011150-3 2015 The reaction of Na2PdCl6 with neat SO3 afforded yellow crystals of Na2Pd(S4O13)2 (monoclinic, P21/c, a = 6.9953(4) A, b = 15.9420(9) A, c = 9.2299(5) A, beta = 100.235(2) , V = 1012.45(1) A3). na2pd(s4o13)2 67-80 H3 histone pseudogene 16 Homo sapiens 94-99 26166660-0 2015 Apigenin inhibits indoxyl sulfate-induced endoplasmic reticulum stress and anti-proliferative pathways, CHOP and IL-6/p21, in human renal proximal tubular cells. Indican 18-33 H3 histone pseudogene 16 Homo sapiens 118-121 26166660-11 2015 CONCLUSIONS: These results suggest that apigenin may inhibit IS-induced ER stress and expression of IL-6 and p21 proteins in HK-2 cells. Apigenin 40-48 H3 histone pseudogene 16 Homo sapiens 109-112 26166660-11 2015 CONCLUSIONS: These results suggest that apigenin may inhibit IS-induced ER stress and expression of IL-6 and p21 proteins in HK-2 cells. Indican 61-63 H3 histone pseudogene 16 Homo sapiens 109-112 26166660-1 2015 OBJECTIVE: Indoxyl sulfate (IS) has been reported to induce endoplasmic reticulum (ER) stress in tubular cells and to inhibit the cell proliferation via ER stress and ERK/IL-6/p21 pathways. Indican 11-26 H3 histone pseudogene 16 Homo sapiens 176-179 26166660-1 2015 OBJECTIVE: Indoxyl sulfate (IS) has been reported to induce endoplasmic reticulum (ER) stress in tubular cells and to inhibit the cell proliferation via ER stress and ERK/IL-6/p21 pathways. Indican 28-30 H3 histone pseudogene 16 Homo sapiens 176-179 26059034-9 2015 Our main finding was that compared to CONTROL, arousal latency to hypoxia is increased in ETOH pups at P15 and P21, and the concentration of brainstem GABA is elevated at P21. gamma-Aminobutyric Acid 151-155 H3 histone pseudogene 16 Homo sapiens 171-174 26151043-6 2015 Notably, esculetin modulated Sp1 downstream target genes including p27, p21 and cyclin D1, resulted in activation of apoptosis signaling molecules such as caspase-3 and PARP in G361 HMM cells. esculetin 9-18 H3 histone pseudogene 16 Homo sapiens 72-75 26117010-8 2015 Also, the expression of BCL-2 and survivin significantly decreased, while the expression of BAX, P21 and P27 was significantly upregulated in HL-60 cells after being treated with 5.0 micromol/L As2O3. Arsenic Trioxide 194-199 H3 histone pseudogene 16 Homo sapiens 97-100 25917058-3 2015 Synthesized silver sulfide nanopowders have a monoclinic (space group P21/c) acanthite-type structure but the occupancy of the metal sublattice sites by Ag atoms is smaller than 1. silver sulfide 12-26 H3 histone pseudogene 16 Homo sapiens 70-75 26025442-7 2015 RESULTS: We report that Bz-surviving MM cells in vitro and in vivo enter quiescence characterized by p21(CIP1) upregulation. Bortezomib 24-26 H3 histone pseudogene 16 Homo sapiens 101-104 26025442-14 2015 CONCLUSIONS: We conclude that Bz-surviving MM cells display a GRP78(HIGH)/p21(HIGH)/CDK6(LOW)/P-Rb(LOW) profile, and these markers may identify quiescent MM cells capable of fueling recurrences. Bortezomib 30-32 H3 histone pseudogene 16 Homo sapiens 74-77 26038719-12 2015 SAHA alone showed increased expression of p21, while ATO alone and in combination with SAHA showed no significant change. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 42-45 25797115-0 2015 Induction of cell cycle arrest and apoptosis by betulinic acid-rich fraction from Dillenia suffruticosa root in MCF-7 cells involved p53/p21 and mitochondrial signalling pathway. betulinic acid 48-62 H3 histone pseudogene 16 Homo sapiens 137-140 26090138-4 2015 CsCrAs2O7 is isotypic with the monoclinic A (I) M (III) X 2O7 (A (I) = alkali metal; M (III) = Al, Cr, Fe; X = As, P) type I family of compounds crystallizing in the space group P21/c. Chromium 2-4 H3 histone pseudogene 16 Homo sapiens 178-183 26090138-4 2015 CsCrAs2O7 is isotypic with the monoclinic A (I) M (III) X 2O7 (A (I) = alkali metal; M (III) = Al, Cr, Fe; X = As, P) type I family of compounds crystallizing in the space group P21/c. Arsenic 4-6 H3 histone pseudogene 16 Homo sapiens 178-183 26221255-10 2015 Moreover, p53, p21 and Bax/Bcl-2 were significantly upregulated by honokiol treatment. honokiol 67-75 H3 histone pseudogene 16 Homo sapiens 15-18 28962410-0 2015 Occupational health hazards of trichloroethylene among workers in relation to altered mRNA expression of cell cycle regulating genes (p53, p21, bax and bcl-2) and PPARA. Trichloroethylene 31-48 H3 histone pseudogene 16 Homo sapiens 139-142 25521075-0 2015 Synergistic anti-tumour effects of tetrandrine and chloroquine combination therapy in human cancer: a potential antagonistic role for p21. tetrandrine 35-46 H3 histone pseudogene 16 Homo sapiens 134-137 25710892-2 2015 l-Methioninium picrate crystallizes in the monoclinic system (space group P21, Z=2). l-methioninium picrate 0-22 H3 histone pseudogene 16 Homo sapiens 74-77 25748550-4 2015 Treatment with TVX caused cell cycle arrest, enhanced expression of p21 and impaired proliferation, but cell death only occurred after cotreatment with TVX and TNF. trovafloxacin 15-18 H3 histone pseudogene 16 Homo sapiens 68-71 25521075-10 2015 Lack of p21 protein (p21(-/-) HCT116 cells) increased sensitivity to the apoptotic effects of the combination of tetrandrine and chloroquine. tetrandrine 113-124 H3 histone pseudogene 16 Homo sapiens 8-11 25521075-10 2015 Lack of p21 protein (p21(-/-) HCT116 cells) increased sensitivity to the apoptotic effects of the combination of tetrandrine and chloroquine. tetrandrine 113-124 H3 histone pseudogene 16 Homo sapiens 21-24 25521075-10 2015 Lack of p21 protein (p21(-/-) HCT116 cells) increased sensitivity to the apoptotic effects of the combination of tetrandrine and chloroquine. Chloroquine 129-140 H3 histone pseudogene 16 Homo sapiens 8-11 25521075-10 2015 Lack of p21 protein (p21(-/-) HCT116 cells) increased sensitivity to the apoptotic effects of the combination of tetrandrine and chloroquine. Chloroquine 129-140 H3 histone pseudogene 16 Homo sapiens 21-24 25906041-5 2015 EA caused a slight, but significant cell cycle arrest at the G1 phase, and urolithins caused cell cycle arrest at the G2/M phase and upregulated p21 expression. urolithins 75-85 H3 histone pseudogene 16 Homo sapiens 145-148 25683911-2 2015 Treatment of p53 wild-type melanoma cells with the genotoxic agent doxorubicin induces G2-M arrest, inhibitory phosphorylation of cell cycle kinase Cdc2 (CDK1) and enhanced expression of p53/p21. Doxorubicin 67-78 H3 histone pseudogene 16 Homo sapiens 191-194 25683911-10 2015 Moreover, knockdown of p21 dramatically reduces stress-induced G0-G1 arrest under doxorubicin and Chk1 inhibitor treatment accompanied by massive DNA damage and apoptosis induction. Doxorubicin 82-93 H3 histone pseudogene 16 Homo sapiens 23-26 25652782-2 2015 The structure analysis reveals that the copper(II) complex crystallizes in the monoclinic space group P21 /c, and the copper(II) ion has a distorted square pyramidal coordination geometry. cupric ion 40-50 H3 histone pseudogene 16 Homo sapiens 102-105 25583641-7 2015 Further, the expression of two important cell cycle inhibitory proteins, p21 and p53, in the curcumin- and culture medium-treated cells without curcumin was evaluated by intracellular flow cytometry. Curcumin 93-101 H3 histone pseudogene 16 Homo sapiens 73-76 25583641-10 2015 Flow cytometry analysis showed a twofold increase in the expression of both p21 and p53 in curcumin-treated cells as compared to the medium-treated cells, suggesting that curcumin inhibits EPC growth by mainly inhibiting the G1 to S phase transition in the cell cycle. Curcumin 91-99 H3 histone pseudogene 16 Homo sapiens 76-79 25583641-10 2015 Flow cytometry analysis showed a twofold increase in the expression of both p21 and p53 in curcumin-treated cells as compared to the medium-treated cells, suggesting that curcumin inhibits EPC growth by mainly inhibiting the G1 to S phase transition in the cell cycle. Curcumin 171-179 H3 histone pseudogene 16 Homo sapiens 76-79 25776829-7 2015 In addition, quercetin aglycone and PAC DP-9 deactivated MAPK-ERK pathway, induced downregulation of cyclin D1, DNA-PK, phospho-histone H3 and upregulation of p21, and arrested cell cycle progression. quercetin aglycone 13-31 H3 histone pseudogene 16 Homo sapiens 159-162 25652782-2 2015 The structure analysis reveals that the copper(II) complex crystallizes in the monoclinic space group P21 /c, and the copper(II) ion has a distorted square pyramidal coordination geometry. cupric ion 118-128 H3 histone pseudogene 16 Homo sapiens 102-105 26109778-0 2015 Anti-lung cancer potential of pure esteric-glycoside condurangogenin A against nonsmall-cell lung cancer cells in vitro via p21/p53 mediated cell cycle modulation and DNA damage-induced apoptosis. esteric-glycoside 35-52 H3 histone pseudogene 16 Homo sapiens 124-127 26113875-6 2015 Moreover, a novel pathway, p21/HIF-1alpha/VEGF, was found to be involved in the inhibitory effect of myricetin on angiogenesis in OVCAR-3 cells. myricetin 101-110 H3 histone pseudogene 16 Homo sapiens 27-30 26131123-9 2015 P53 and p21 were significantly upregulated by honokiol treatment. honokiol 46-54 H3 histone pseudogene 16 Homo sapiens 8-11 25720435-3 2015 In the present study, our results showed that shikonin significantly inhibited the growth of A431 cells in a concentration- and time-dependent manner, and caused cell cycle arrest by upregulation of p21 and p27, and downregulation of cyclins and cyclin-dependent kinases. shikonin 46-54 H3 histone pseudogene 16 Homo sapiens 199-202 25940539-8 2015 The anticancer effect of CUDC-101 was associated with increased expression of p21 and E-cadherin, and reduced expression of survivin, XIAP, beta-catenin, N-cadherin, and Vimentin. 7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide 25-33 H3 histone pseudogene 16 Homo sapiens 78-81 26015807-11 2015 It also revealed overexpression of the ATM/p53/p21 pathway, which is activated in response to DNA damage and induces cell cycle arrest in thiopurine resistant LCLs. 2-mercaptopyrazine 138-148 H3 histone pseudogene 16 Homo sapiens 47-50 25879533-6 2015 Interestingly, in intermittent high glucose, this effect was more pronounced as well as increase of p21 and p16INK4a , senescence related proteins with DNA damage. Glucose 36-43 H3 histone pseudogene 16 Homo sapiens 100-103 25925725-8 2015 p21 overexpression significantly downregulated glutathione peroxidase and superoxide dismutase antioxidant activity (p<0.05) while significantly upregulating hydrogen peroxide and malondialdehyde content (p<0.05), suggesting a role in decreasing antioxidant defense capabilities in UVB-irradiated HaCaT keratinocytes. Hydrogen Peroxide 161-178 H3 histone pseudogene 16 Homo sapiens 0-3 25925725-8 2015 p21 overexpression significantly downregulated glutathione peroxidase and superoxide dismutase antioxidant activity (p<0.05) while significantly upregulating hydrogen peroxide and malondialdehyde content (p<0.05), suggesting a role in decreasing antioxidant defense capabilities in UVB-irradiated HaCaT keratinocytes. Malondialdehyde 183-198 H3 histone pseudogene 16 Homo sapiens 0-3 25914461-8 2015 Alternol activated caspase 3, upregulated p53 and p21 expression, and downregulated Bcl-2 expression in a dose-dependent manner. Alternol 0-8 H3 histone pseudogene 16 Homo sapiens 50-53 25960215-5 2015 Furthermore, we demonstrated that miR-194 could reduce the phosphoinositide 3-kinase (PI3K)/AKT/FoxO3a signaling pathway by suppressing acylglycerol kinase (AGK) directly, resulting in decreasing cyclin D1 expression and increasing expression of p21 in OSCC. mir-194 34-41 H3 histone pseudogene 16 Homo sapiens 246-249 25995861-1 2015 The title compound, C11H13NO6, shows two polymorphs, orange and yellow forms, both of which crystallize in the space group P21/c. c11h13no6 20-29 H3 histone pseudogene 16 Homo sapiens 123-128 25897210-12 2015 Treatment of CQ and NQ repressed expression of cyclin D1 but enhanced expression of p21. Clioquinol 13-15 H3 histone pseudogene 16 Homo sapiens 84-87 25897210-12 2015 Treatment of CQ and NQ repressed expression of cyclin D1 but enhanced expression of p21. nq 20-22 H3 histone pseudogene 16 Homo sapiens 84-87 25751281-5 2015 In temozolomide-resistant GBM cells, decitabine can potentiate the cytotoxic DNA alkylation by counteracting cytosine methylation and reactivating tumor suppressor genes, such as p53 and p21. Decitabine 37-47 H3 histone pseudogene 16 Homo sapiens 187-190 25597952-5 2015 Statistically significant proportional tissue increases in the vitamin D group relative to the placebo group were found in bax (51%), p21 (141%), APC (48%), E-cadherin (78%), MSH2 (179%), the CaSR (39%), and CYP27B1 (159%). Vitamin D 63-72 H3 histone pseudogene 16 Homo sapiens 134-137 25501628-5 2015 SBHA-treated MCF-7 cells showed G0/G1 cell-cycle arrest, coupled with elevated expression levels of p21 and p27 proteins. suberoyl bis-hydroxamic acid 0-4 H3 histone pseudogene 16 Homo sapiens 100-103 25501628-9 2015 In conclusion, these results indicate that SBHA exerts cytotoxic effects against human breast cancer cells, which involves the modulation of p21, p27 and Bcl-2 family proteins, consequently leading to cell-cycle arrest and apoptosis. suberoyl bis-hydroxamic acid 43-47 H3 histone pseudogene 16 Homo sapiens 141-144 25776512-9 2015 Moreover, Western blotting analysis showed that apoptosis induced by RSV-GNPs is associated with the increased Bax, p53, p21, caspase-3 protein levels, and decreased Bcl-2 and NF-kappaB proteins expression, which indicates the involvement of mitochondria-dependent apoptosis in the anticancer efficacy of RSV-GNPs in NCI-H460 cells. Resveratrol 69-72 H3 histone pseudogene 16 Homo sapiens 121-124 25786122-7 2015 Expression of downstream effectors of TGF-beta signaling pathway, cyclinD1, p21 and Pin1, was inhibited along with the down regulation of key mesenchymal markers (Snail and Slug) upon curcumin and emodin treatment. Curcumin 184-192 H3 histone pseudogene 16 Homo sapiens 76-79 25886177-11 2015 The cyproheptadine-induced G1 arrest in HepG2 cells was associated with an increased expression of HBP1 and p16, whereas the G1/S arrest in Huh-7 cells was associated with an increase in p21 and p27 expression and a dramatic decrease in the phosphorylation of the retinoblastoma protein. Cyproheptadine 4-18 H3 histone pseudogene 16 Homo sapiens 187-190 26101699-9 2015 Furthermore, mogrol enhanced p21 expression, resulting in G0/G1 cell cycle arrest. MOGROL 13-19 H3 histone pseudogene 16 Homo sapiens 29-32 26101701-6 2015 SAHA and GDC-0449 cooperatively enhanced G0/G1 cell cycle arrest which was associated with up-regulation of p21(waf). Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 108-111 26101701-6 2015 SAHA and GDC-0449 cooperatively enhanced G0/G1 cell cycle arrest which was associated with up-regulation of p21(waf). HhAntag691 9-17 H3 histone pseudogene 16 Homo sapiens 108-111 25776512-11 2015 CONCLUSIONS: Taken together, the results of our study clearly suggested that the cell death induced by the combination of RSV-GNPs would involve alteration in expression of p53, p21, caspase-3, Bax, Bcl-2 and NF-kappaB, indicating oxidative mechanism in NCI-H460 cells. Resveratrol 122-125 H3 histone pseudogene 16 Homo sapiens 178-181 25948203-4 2015 Chidamide induced cell cycle arrest of RPMI 8226 cells in G0/G1 phase by upregulating the expression of P21. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 0-9 H3 histone pseudogene 16 Homo sapiens 104-107 25948203-4 2015 Chidamide induced cell cycle arrest of RPMI 8226 cells in G0/G1 phase by upregulating the expression of P21. rpmi 39-43 H3 histone pseudogene 16 Homo sapiens 104-107 25785443-9 2015 Sucrose gradient fractionation revealed that co-expression of p21.5 resulted in a spread distribution pattern of core proteins ranging from low to high sucrose densities. Sucrose 0-7 H3 histone pseudogene 16 Homo sapiens 62-65 25785443-9 2015 Sucrose gradient fractionation revealed that co-expression of p21.5 resulted in a spread distribution pattern of core proteins ranging from low to high sucrose densities. Sucrose 152-159 H3 histone pseudogene 16 Homo sapiens 62-65 25747583-7 2015 Mechanistically, SD-208-induced G2/M arrest was accompanied by an increase in levels of p21 in DU145 and PC3 cells as well as elevated phosphorylation of Cdc2 and Cdc25C in DU145 cells. SD-208 17-23 H3 histone pseudogene 16 Homo sapiens 88-91 25595558-7 2015 Consistent with this observation in SK-MEL28 cells, Sp1 was necessary for the tamoxifen-regulated Raf-1:ER to induce p21(CIP1) transcription in U251 cells, in which TP53 is mutated. Tamoxifen 78-87 H3 histone pseudogene 16 Homo sapiens 118-121 25573651-5 2015 Western blot analysis indicated that GA mediated G1-phase cell cycle arrest by upregulation of cyclin-dependent kinase inhibitors (CKIs) (p18, p16, p27 and p21) and inhibition of cyclins (cyclin-D1, -D3 and -E) and cyclin-dependent kinases (CDKs) (CDK4, 6 and 2). Glycyrrhetinic Acid 37-39 H3 histone pseudogene 16 Homo sapiens 156-159 25682003-9 2015 The expressions of genes related with G1/S transition of cell cycle and metastasis were increased by DHT, TCS, and BP-1, while the expression of p21 protein responsible for cell cycle arrest was reduced by DHT, TCS, and BP-1. Dihydrotestosterone 206-209 H3 histone pseudogene 16 Homo sapiens 145-148 25682003-9 2015 The expressions of genes related with G1/S transition of cell cycle and metastasis were increased by DHT, TCS, and BP-1, while the expression of p21 protein responsible for cell cycle arrest was reduced by DHT, TCS, and BP-1. Triclosan 211-214 H3 histone pseudogene 16 Homo sapiens 145-148 26045752-9 2015 Our results also showed that miR-196a mimic accelerated cell cycle progression of MG63 and U2OS cells by down regulation of p21 and p27, and upregulation of cyclin D1. mir-196a 29-37 H3 histone pseudogene 16 Homo sapiens 124-127 25345581-0 2015 Hesperetin inhibit adipocyte differentiation and enhance Bax- and p21-mediated adipolysis in human mesenchymal stem cell adipogenesis. hesperetin 0-10 H3 histone pseudogene 16 Homo sapiens 66-69 25345581-4 2015 The treatment with hesperetin decreased the expression of resistin, adiponectin, aP2, LPL, PPAR-gamma, and TNF-alpha in Groups 1 and 2, whereas a significant increase was observed in Bcl, Bax, and p21 expression in Group 2 compared to untreated preadipocytes. hesperetin 19-29 H3 histone pseudogene 16 Homo sapiens 197-200 25639717-3 2015 In addition, activation of p53 via phosphorylation at Ser15 and subsequent up-regulation of p21(CIP1) showed that CR389 also induces p53-dependent-p21(CIP1)-mediated cell cycle arrest. cr389 114-119 H3 histone pseudogene 16 Homo sapiens 92-95 25639717-3 2015 In addition, activation of p53 via phosphorylation at Ser15 and subsequent up-regulation of p21(CIP1) showed that CR389 also induces p53-dependent-p21(CIP1)-mediated cell cycle arrest. cr389 114-119 H3 histone pseudogene 16 Homo sapiens 147-150 25381309-0 2015 Zinc oxide nanoparticles affect the expression of p53, Ras p21 and JNKs: an ex vivo/in vitro exposure study in respiratory disease patients. Zinc Oxide 0-10 H3 histone pseudogene 16 Homo sapiens 59-62 25738367-7 2015 Subsequently, miR-15/16 activities are reduced and many of their direct targets are de-repressed, including ubiquitin ligase FBXW7 that destabilizes Cyclin E. Conversely, GBM cells expressing low p21 level, or after p21 knock-down, exhibit weaker or no E2F1 response to miR-10b inhibition. mir-15 14-20 H3 histone pseudogene 16 Homo sapiens 196-199 25530218-0 2015 Nitidine chloride induces apoptosis in human hepatocellular carcinoma cells through a pathway involving p53, p21, Bax and Bcl-2. nitidine 0-17 H3 histone pseudogene 16 Homo sapiens 109-112 25407160-10 2015 In addition, TUDCA decreased cellular senescence by reducing levels of p53, p21, and reactive oxygen species and increased nitric oxide. ursodoxicoltaurine 13-18 H3 histone pseudogene 16 Homo sapiens 76-79 25490952-10 2015 Furthermore, Cd-induced superoxide and lipid peroxidation mediated activation of proapoptotic markers p21 and p53 in the developing embryo. Cadmium 13-15 H3 histone pseudogene 16 Homo sapiens 102-105 25490952-10 2015 Furthermore, Cd-induced superoxide and lipid peroxidation mediated activation of proapoptotic markers p21 and p53 in the developing embryo. Superoxides 24-34 H3 histone pseudogene 16 Homo sapiens 102-105 25371069-6 2015 Simultaneously, p21 and ATF3 expression levels were upregulated and downregulated upon TSA stimulation, respectively. trichostatin A 87-90 H3 histone pseudogene 16 Homo sapiens 16-19 25371069-10 2015 Collectively, these data demonstrate that ATF3 acts as an essential negative regulator of TSA-induced cell growth inhibition through interfering with TSA-induced p21 activation. trichostatin A 90-93 H3 histone pseudogene 16 Homo sapiens 162-165 25371069-10 2015 Collectively, these data demonstrate that ATF3 acts as an essential negative regulator of TSA-induced cell growth inhibition through interfering with TSA-induced p21 activation. trichostatin A 150-153 H3 histone pseudogene 16 Homo sapiens 162-165 25544776-0 2015 The anti-leukemic activity of sodium dichloroacetate in p53mutated/null cells is mediated by a p53-independent ILF3/p21 pathway. Dichloroacetic Acid 30-52 H3 histone pseudogene 16 Homo sapiens 116-119 25723170-7 2015 Rather, TGF-beta transcriptionally activates p21, which stabilizes NRF2, thereby markedly enhancing glutathione metabolism and diminishing effectiveness of anti-cancer therapeutics. Glutathione 100-111 H3 histone pseudogene 16 Homo sapiens 45-48 25567764-1 2015 We report in this work that the Abeta peptide directly interacts with tubulin close to the vinblastine and GTP/GDP binding site, inhibits the tubulin polymerization rate, induces tubulin aggregation, causes cell shrinking, enhances Mad2, BubR1, p53, and p21 activation in MCF7 cells and induces the apoptotic death of A549, HeLa and MCF7 cells. Vinblastine 91-102 H3 histone pseudogene 16 Homo sapiens 254-257 25567764-1 2015 We report in this work that the Abeta peptide directly interacts with tubulin close to the vinblastine and GTP/GDP binding site, inhibits the tubulin polymerization rate, induces tubulin aggregation, causes cell shrinking, enhances Mad2, BubR1, p53, and p21 activation in MCF7 cells and induces the apoptotic death of A549, HeLa and MCF7 cells. Guanosine Triphosphate 107-110 H3 histone pseudogene 16 Homo sapiens 254-257 25567764-1 2015 We report in this work that the Abeta peptide directly interacts with tubulin close to the vinblastine and GTP/GDP binding site, inhibits the tubulin polymerization rate, induces tubulin aggregation, causes cell shrinking, enhances Mad2, BubR1, p53, and p21 activation in MCF7 cells and induces the apoptotic death of A549, HeLa and MCF7 cells. Guanosine Diphosphate 111-114 H3 histone pseudogene 16 Homo sapiens 254-257 25719742-9 2015 Moreover, boldine induced apoptosis concomitantly with increasing the expression of bax/bcl2 (p < 0.02) and p21 (p < 0.01) genes. boldine 10-17 H3 histone pseudogene 16 Homo sapiens 111-114 25544776-5 2015 By using a proteomic approach, we demonstrated that DCA up-regulated the ILF3 transcription factor, which is a known regulator of p21 expression. Dichloroacetic Acid 52-55 H3 histone pseudogene 16 Homo sapiens 130-133 25544776-6 2015 The role of the ILF3/p21 axis in mediating the DCA anti-leukemic activity was underscored by knocking-down experiments. Dichloroacetic Acid 47-50 H3 histone pseudogene 16 Homo sapiens 21-24 25544776-7 2015 Indeed, transfection with ILF3 and p21 siRNAs significantly decreased both the DCA-induced p21 expression and the DCA-mediated cytotoxicity. Dichloroacetic Acid 79-82 H3 histone pseudogene 16 Homo sapiens 35-38 25544776-7 2015 Indeed, transfection with ILF3 and p21 siRNAs significantly decreased both the DCA-induced p21 expression and the DCA-mediated cytotoxicity. Dichloroacetic Acid 79-82 H3 histone pseudogene 16 Homo sapiens 91-94 25544776-7 2015 Indeed, transfection with ILF3 and p21 siRNAs significantly decreased both the DCA-induced p21 expression and the DCA-mediated cytotoxicity. Dichloroacetic Acid 114-117 H3 histone pseudogene 16 Homo sapiens 35-38 25445786-6 2015 SIRT7 overexpressing cells when treated with low dose of doxorubicin (0.25 microM) showed delayed onset of senescence, lesser accumulation of DNA damage marker gammaH2AX and lowered levels of growth arrest markers viz., p53 and p21 when compared to doxorubicin treated control GFP expressing cells. Doxorubicin 57-68 H3 histone pseudogene 16 Homo sapiens 228-231 25242579-8 2015 Deguelin induced differentiation of OCI-AML3 cells at a nontoxic concentration which was associated with a decrease in expression of activated caspase-8, p53, p21, and the 30-kD form of CCAAT/enhancer binding protein alpha (C/EBPalpha), whereas no effects were found in OCIM2 cells expressing NPM-wt. deguelin 0-8 H3 histone pseudogene 16 Homo sapiens 159-162 25523931-4 2015 Ba6Ga2SnSe11 crystallizes in a new structure type in the monoclinic centrosymmetric space group P21/c. ba6ga2snse11 0-12 H3 histone pseudogene 16 Homo sapiens 96-101 25434486-8 2015 Diosgenin inhibited Akt phosphorylation and upregulated p21 and p27 expression, but did not alter the expression of p53, suggesting diosgenin-induced upregulation of p21 and p57 is p53-independent in HCC cells. Diosgenin 0-9 H3 histone pseudogene 16 Homo sapiens 56-59 25434486-8 2015 Diosgenin inhibited Akt phosphorylation and upregulated p21 and p27 expression, but did not alter the expression of p53, suggesting diosgenin-induced upregulation of p21 and p57 is p53-independent in HCC cells. Diosgenin 0-9 H3 histone pseudogene 16 Homo sapiens 166-169 25434486-8 2015 Diosgenin inhibited Akt phosphorylation and upregulated p21 and p27 expression, but did not alter the expression of p53, suggesting diosgenin-induced upregulation of p21 and p57 is p53-independent in HCC cells. Diosgenin 132-141 H3 histone pseudogene 16 Homo sapiens 56-59 25434486-8 2015 Diosgenin inhibited Akt phosphorylation and upregulated p21 and p27 expression, but did not alter the expression of p53, suggesting diosgenin-induced upregulation of p21 and p57 is p53-independent in HCC cells. Diosgenin 132-141 H3 histone pseudogene 16 Homo sapiens 166-169 25615717-7 2015 Moreover, low oxygen tension significantly up-regulated VEGF and bFGF mRNA expression and protein secretion while reducing the expression level of tumour suppressor genes p16, p21, p53, and pRb. Oxygen 14-20 H3 histone pseudogene 16 Homo sapiens 176-179 25305450-6 2015 Western blot showed that metformin activated caspase 3, caspase 9, PARP-1, Bak, and p21 and inactivated Mcl-1, HIAP-1, cyclin D1, CDK4, and CDK6. Metformin 25-34 H3 histone pseudogene 16 Homo sapiens 84-87 25092068-8 2015 Delivered cisplatin cooperated with piroxicam in modulating cell cycle regulators as caspase-3, p53 and p21. Cisplatin 10-19 H3 histone pseudogene 16 Homo sapiens 104-107 25092068-8 2015 Delivered cisplatin cooperated with piroxicam in modulating cell cycle regulators as caspase-3, p53 and p21. Piroxicam 36-45 H3 histone pseudogene 16 Homo sapiens 104-107 25625511-9 2015 Treatment with EGCG was found to elevate the expression of p53 and p21, and eventually led to apoptosis of NPC cells via caspase 3 activation. epigallocatechin gallate 15-19 H3 histone pseudogene 16 Homo sapiens 67-70 26477797-0 2015 Chloroform Extract of Solanum lyratum Induced G0/G1 Arrest via p21/p16 and Induced Apoptosis via Reactive Oxygen Species, Caspases and Mitochondrial Pathways in Human Oral Cancer Cell Lines. Chloroform 0-10 H3 histone pseudogene 16 Homo sapiens 63-66 25431333-1 2015 The oxidation of elemental palladium at 100 C in a mixture of fuming nitric acid and a pyridine-SO3 complex leads to the anhydrous nitrate Pd(NO3)2 (monoclinic, P2(1)/n, Z=2, a=469.12(3) pm, b=593.89(3) pm, c=805.72(4) pm, beta=105.989(3) , V=215.79(2) A(3)). Palladium 27-36 H3 histone pseudogene 16 Homo sapiens 162-167 25431333-1 2015 The oxidation of elemental palladium at 100 C in a mixture of fuming nitric acid and a pyridine-SO3 complex leads to the anhydrous nitrate Pd(NO3)2 (monoclinic, P2(1)/n, Z=2, a=469.12(3) pm, b=593.89(3) pm, c=805.72(4) pm, beta=105.989(3) , V=215.79(2) A(3)). Nitric Acid 70-81 H3 histone pseudogene 16 Homo sapiens 162-167 25431333-1 2015 The oxidation of elemental palladium at 100 C in a mixture of fuming nitric acid and a pyridine-SO3 complex leads to the anhydrous nitrate Pd(NO3)2 (monoclinic, P2(1)/n, Z=2, a=469.12(3) pm, b=593.89(3) pm, c=805.72(4) pm, beta=105.989(3) , V=215.79(2) A(3)). pyridine-so3 88-100 H3 histone pseudogene 16 Homo sapiens 162-167 25431333-1 2015 The oxidation of elemental palladium at 100 C in a mixture of fuming nitric acid and a pyridine-SO3 complex leads to the anhydrous nitrate Pd(NO3)2 (monoclinic, P2(1)/n, Z=2, a=469.12(3) pm, b=593.89(3) pm, c=805.72(4) pm, beta=105.989(3) , V=215.79(2) A(3)). Nitrates 132-139 H3 histone pseudogene 16 Homo sapiens 162-167 25431333-1 2015 The oxidation of elemental palladium at 100 C in a mixture of fuming nitric acid and a pyridine-SO3 complex leads to the anhydrous nitrate Pd(NO3)2 (monoclinic, P2(1)/n, Z=2, a=469.12(3) pm, b=593.89(3) pm, c=805.72(4) pm, beta=105.989(3) , V=215.79(2) A(3)). pd(no3)2 140-148 H3 histone pseudogene 16 Homo sapiens 162-167 25431333-3 2015 The reaction of elemental palladium with a mixture of fuming nitric acid and methanesulfonic acid at 120 C leads to single crystals of Pd(CH3SO3)2 (monoclinic, P2(1)/n, Z=2, a=480.44(1) pm, b=1085.53(3) pm, c=739.78(2) pm, beta=102.785(1) , V=376.254(17) A(3)). Palladium 26-35 H3 histone pseudogene 16 Homo sapiens 161-166 25431333-3 2015 The reaction of elemental palladium with a mixture of fuming nitric acid and methanesulfonic acid at 120 C leads to single crystals of Pd(CH3SO3)2 (monoclinic, P2(1)/n, Z=2, a=480.44(1) pm, b=1085.53(3) pm, c=739.78(2) pm, beta=102.785(1) , V=376.254(17) A(3)). Nitric Acid 61-72 H3 histone pseudogene 16 Homo sapiens 161-166 25431333-3 2015 The reaction of elemental palladium with a mixture of fuming nitric acid and methanesulfonic acid at 120 C leads to single crystals of Pd(CH3SO3)2 (monoclinic, P2(1)/n, Z=2, a=480.44(1) pm, b=1085.53(3) pm, c=739.78(2) pm, beta=102.785(1) , V=376.254(17) A(3)). methanesulfonic acid 77-97 H3 histone pseudogene 16 Homo sapiens 161-166 25431333-3 2015 The reaction of elemental palladium with a mixture of fuming nitric acid and methanesulfonic acid at 120 C leads to single crystals of Pd(CH3SO3)2 (monoclinic, P2(1)/n, Z=2, a=480.44(1) pm, b=1085.53(3) pm, c=739.78(2) pm, beta=102.785(1) , V=376.254(17) A(3)). pd(ch3so3)2 136-147 H3 histone pseudogene 16 Homo sapiens 161-166 25625122-10 2015 The drop in PR expression together with altered distribution of p21 and p27 can explain different effects of cyclin E isoforms expression on progesterone responsivity. Progesterone 141-153 H3 histone pseudogene 16 Homo sapiens 64-67 26085404-1 2015 Three new crystal forms of a mononuclear cobalt(II) chloride with 3-pyridinemethanol (3PM), CoCl2(3PM)4, have been prepared: triclinic (P1) and monoclinic (P21/c) polymorphs and its dihydrate which crystallises in the triclinic P1 space group. cobaltous chloride 41-60 H3 histone pseudogene 16 Homo sapiens 156-161 24993871-4 2015 (-)-Loliolide diminished senescence-associated beta-galactosidase activity (SA-beta-gal), the level of p21 protein, and the level of reactive oxygen species in senescent cells induced by adriamycin treatment. loliolide 0-13 H3 histone pseudogene 16 Homo sapiens 103-106 24993871-4 2015 (-)-Loliolide diminished senescence-associated beta-galactosidase activity (SA-beta-gal), the level of p21 protein, and the level of reactive oxygen species in senescent cells induced by adriamycin treatment. Doxorubicin 187-197 H3 histone pseudogene 16 Homo sapiens 103-106 26379747-10 2015 In conclusion, we for the first time demonstrated that hinokitiol upregulates p21 expression and attenuates IFN-gamma secretion in ConA-stimulated T lymphocytes, thereby arresting cell cycle at the G0/G1 phase. beta-thujaplicin 55-65 H3 histone pseudogene 16 Homo sapiens 78-81 25359865-4 2015 APPROACH AND RESULTS: When compared with primary human umbilical vein endothelial cells grown under standard conditions, ECs with chronic homocysteine treatment showed accelerated upregulation of p16, p21, and p53, markers of cellular senescence, during 6 to 10 passages. Homocysteine 138-150 H3 histone pseudogene 16 Homo sapiens 201-204 25701261-6 2015 Interestingly, molecular analysis revealed that estradiol treatment markedly increases expression of cyclin A and B, and decreases p21 and p27 in the insulin-primed cells. Estradiol 48-57 H3 histone pseudogene 16 Homo sapiens 131-134 25411358-6 2015 Early DNA damage checkpoint response, mediated through p53/p21, led to G1 arrest in TPA-exposed cells. terephthalic acid 84-87 H3 histone pseudogene 16 Homo sapiens 59-62 25659606-6 2015 RESULTS: Clozapine inhibited A549 and H1299 proliferation and increased p21 and p27 expression levels, leading to cell cycle arrest. Clozapine 9-18 H3 histone pseudogene 16 Homo sapiens 72-75 25142552-3 2015 The single-modification peptides (P-1-1, P-2-1 and P-3-1) and double-modification peptides (P-1-2, P-2-2 and P-3-2) showed significantly lower immunoglobulin (Ig)E binding with patients" sera compared to osmotin (P < 0 01). osmotin 204-211 H3 histone pseudogene 16 Homo sapiens 41-57 26050346-13 2015 CONCLUSION: SAHA promotes SiHa apoptosis in chemotherapy through up-regulation of mRNA and protein of p21 and Bax which leads to cell cycle arrest in G0/G1 phase. Vorinostat 12-16 H3 histone pseudogene 16 Homo sapiens 102-105 25773855-0 2015 Silibilin-induces apoptosis in breast cancer cells by modulating p53, p21, Bak and Bcl-XL pathways. silibilin 0-9 H3 histone pseudogene 16 Homo sapiens 70-73 25773855-7 2015 Taken together, the results suggest that silibinin inhibits the proliferation and induces apoptosis of MCF-7 cells by down-regulating Bak, P53, P21, BRCA1, BCL-Xl and thus may be considered as an effective adjuvant drug to produce a better chemopreventive response for the cancer therapy. Silybin 41-50 H3 histone pseudogene 16 Homo sapiens 144-147 26235577-6 2015 Results showed that pretreatment with curcumin significantly attenuated the H2O2-induced HUVECs" premature senescence, which was evidenced by a decreased percentage of senescence-associated beta-galactosidase positive cells, improved cell division and decreased expression of senescence-associated protein p21 (all p<0.05). Curcumin 38-46 H3 histone pseudogene 16 Homo sapiens 306-309 26235577-6 2015 Results showed that pretreatment with curcumin significantly attenuated the H2O2-induced HUVECs" premature senescence, which was evidenced by a decreased percentage of senescence-associated beta-galactosidase positive cells, improved cell division and decreased expression of senescence-associated protein p21 (all p<0.05). Hydrogen Peroxide 76-80 H3 histone pseudogene 16 Homo sapiens 306-309 25590413-9 2015 Western blot analysis demonstrated that Wnt-targeting genes, including c-Myc and cyclin D1, were upregulated and were relevant in inhibiting the expression of p21 in MES-SA/Dx5 cells. 2-(N-morpholino)ethanesulfonic acid 166-169 H3 histone pseudogene 16 Homo sapiens 159-162 25590413-10 2015 On the other hand, MES-SA cells expressed high levels of p21 and downregulated cyclin D1 and caused cell cycle arrest. mes-sa 19-25 H3 histone pseudogene 16 Homo sapiens 57-60 26333122-6 2015 The p53 protein was activated and phosphorylated at serines 15 and 392 and accumulated in the nucleus after 24 and 48 h. The Mdm2 protein was present in the cytoplasm with its maximal level after 8 and 16 h. The p21 protein was detected in the nucleus after 24 and 48 h. Increased levels of phosphorylated Chk2 at threonine 68 were observed in the cytoplasmic fraction after 24 and 48 h of mitoxantrone treatment. Threonine 314-323 H3 histone pseudogene 16 Homo sapiens 212-215 26333122-6 2015 The p53 protein was activated and phosphorylated at serines 15 and 392 and accumulated in the nucleus after 24 and 48 h. The Mdm2 protein was present in the cytoplasm with its maximal level after 8 and 16 h. The p21 protein was detected in the nucleus after 24 and 48 h. Increased levels of phosphorylated Chk2 at threonine 68 were observed in the cytoplasmic fraction after 24 and 48 h of mitoxantrone treatment. Mitoxantrone 390-402 H3 histone pseudogene 16 Homo sapiens 212-215 25355277-2 2015 MSCs were treated with high glucose (HG) in order to induce senescence, which was markedly attenuated by pre-treatment with isosorbide dinitrate (ISDN), a commonly used nitrate, as indicated by senescence-associated galactosidase (SA-beta-gal) activity, p21 expression, as well as by the mRNA levels of DNA methyltransferase 1 (DNMT1) and differentiated embryo chondrocyte expressed gene 1 (DEC1), which are senescence-related biomarkers. Isosorbide Dinitrate 124-144 H3 histone pseudogene 16 Homo sapiens 254-257 25092802-5 2015 Inhibition of astrocyte proliferation by ammonia was mediated by a l-methionine sulfoximine-, oxidative stress-, and p38(MAPK) -dependent activation of p53 associated with enhanced transcription of cell cycle inhibitory genes GADD45alpha and p21. Ammonia 41-48 H3 histone pseudogene 16 Homo sapiens 242-245 25355277-2 2015 MSCs were treated with high glucose (HG) in order to induce senescence, which was markedly attenuated by pre-treatment with isosorbide dinitrate (ISDN), a commonly used nitrate, as indicated by senescence-associated galactosidase (SA-beta-gal) activity, p21 expression, as well as by the mRNA levels of DNA methyltransferase 1 (DNMT1) and differentiated embryo chondrocyte expressed gene 1 (DEC1), which are senescence-related biomarkers. Isosorbide Dinitrate 146-150 H3 histone pseudogene 16 Homo sapiens 254-257 25751508-7 2015 In this article, we have shown for the first time that 2DG induced a transient expression of p21 and a continuous expression of p53 in colorectal cancer cells (SW620). Deoxyglucose 55-58 H3 histone pseudogene 16 Homo sapiens 93-96 24578216-6 2015 Compared with the control group, manganese deficiency significantly decreased the proliferative zone width and Bcl-2 mRNA expression level, while significantly increased the apoptotic rates and the expression level of p21 gene in chondrocytes. Manganese 33-42 H3 histone pseudogene 16 Homo sapiens 218-221 26372775-2 2015 In the present study, we investigated the effects of sulforaphane (SFN), a phytochemical from cruciferous vegetables, on the methylation and expression of PTEN and RARbeta2 tumour suppressor genes as well as on the expression of regulators of DNA methylation reaction, DNMT1 , p53 , and p21 , in MCF-7 and MDA-MB-231 human breast cancer cells with different invasive potential. sulforaphane 53-65 H3 histone pseudogene 16 Homo sapiens 287-290 26372775-2 2015 In the present study, we investigated the effects of sulforaphane (SFN), a phytochemical from cruciferous vegetables, on the methylation and expression of PTEN and RARbeta2 tumour suppressor genes as well as on the expression of regulators of DNA methylation reaction, DNMT1 , p53 , and p21 , in MCF-7 and MDA-MB-231 human breast cancer cells with different invasive potential. sulforaphane 67-70 H3 histone pseudogene 16 Homo sapiens 287-290 26016511-6 2015 PA augmented the expression of long-chain acyl-CoA synthetase (ACSL) and the cyclin-dependent kinase inhibitor p21, and enhanced the phosphorylation of p65, a component of NF-kappaB. Palmitic Acid 0-2 H3 histone pseudogene 16 Homo sapiens 111-114 26016511-8 2015 In addition, p21 knockdown suppressed the PA-induced increase in the expression of MCP-1 and ICAM-1. Palmitic Acid 42-44 H3 histone pseudogene 16 Homo sapiens 13-16 26016511-9 2015 EPA suppressed the PA-induced increase in the expression of ACSL and p21, the enhancement of p65 phosphorylation, as well as the associated increase in the expression of ICAM-1, MCP-1, interleukin-6, and PTX3. Palmitic Acid 1-3 H3 histone pseudogene 16 Homo sapiens 69-72 26016511-10 2015 CONCLUSIONS: These results suggest that the ACSL, p21, and NF-kappaB-dependent pathway may possibly be involved in PA-induced vascular endothelial dysfunction, and that EPA ameliorates this at least in part through the regulation of ACSL3 expression. Palmitic Acid 115-117 H3 histone pseudogene 16 Homo sapiens 50-53 25304329-10 2015 The time-course of decreasing ROS coincides with an increase in cell number and decreasing p21 protein levels, indicating a release from radiation-induced growth arrest. Reactive Oxygen Species 30-33 H3 histone pseudogene 16 Homo sapiens 91-94 25705818-3 2015 We proved that the colon cancer cell line HCT116 responded to Liofenol treatment by reducing their proliferation, in association with an increase of p53 and p21 cell cycle gate keepers. liofenol 62-70 H3 histone pseudogene 16 Homo sapiens 158-161 25868784-5 2015 Silibinin with 0.5 or 5 microM arsenic induced G1 or G2/M phase arrest, respectively, and decreased the protein levels of CDK2, -4, and -6 and cyclin D1, D3, and E and increased CDK inhibitors p21 and p27. Silybin 0-9 H3 histone pseudogene 16 Homo sapiens 193-196 25751508-9 2015 The effects of 2DG on p21 and p53 protein levels were totally independent of its inhibitory effect on either hexokinase or ATP levels. Deoxyglucose 15-18 H3 histone pseudogene 16 Homo sapiens 22-25 25922640-10 2015 Our study first shows that LMB produces ROS and is possibly metabolized by CYP3A4, GPX1, and SOD in A549 cells, and combination treatment of LMB and EGCG augments LMB-induced cytotoxicity through enhanced ROS production and the modulation of drug metabolism and p21/survivin pathways. leptomycin B 141-144 H3 histone pseudogene 16 Homo sapiens 262-265 25922640-8 2015 Additionally, these increases of CYP3A4, SOD, and GPX1 were significantly reduced, while p21 was significantly increased in LMB+EGCG-treated cells compared to LMB-treated cells. leptomycin B 124-127 H3 histone pseudogene 16 Homo sapiens 89-92 25922640-10 2015 Our study first shows that LMB produces ROS and is possibly metabolized by CYP3A4, GPX1, and SOD in A549 cells, and combination treatment of LMB and EGCG augments LMB-induced cytotoxicity through enhanced ROS production and the modulation of drug metabolism and p21/survivin pathways. epigallocatechin gallate 149-153 H3 histone pseudogene 16 Homo sapiens 262-265 25922640-8 2015 Additionally, these increases of CYP3A4, SOD, and GPX1 were significantly reduced, while p21 was significantly increased in LMB+EGCG-treated cells compared to LMB-treated cells. epigallocatechin gallate 128-132 H3 histone pseudogene 16 Homo sapiens 89-92 25922640-10 2015 Our study first shows that LMB produces ROS and is possibly metabolized by CYP3A4, GPX1, and SOD in A549 cells, and combination treatment of LMB and EGCG augments LMB-induced cytotoxicity through enhanced ROS production and the modulation of drug metabolism and p21/survivin pathways. leptomycin B 27-30 H3 histone pseudogene 16 Homo sapiens 262-265 25922640-10 2015 Our study first shows that LMB produces ROS and is possibly metabolized by CYP3A4, GPX1, and SOD in A549 cells, and combination treatment of LMB and EGCG augments LMB-induced cytotoxicity through enhanced ROS production and the modulation of drug metabolism and p21/survivin pathways. leptomycin B 141-144 H3 histone pseudogene 16 Homo sapiens 262-265 25118313-7 2015 Inhibitors of BH4 activity or synthesis also inhibited NF-kappaB activation and, similar to MTX, increased JNK, p53, p21 and JUN activity. sapropterin 14-17 H3 histone pseudogene 16 Homo sapiens 117-120 25527123-11 2014 The activation of p53-p21 pathway by SC-III3 was also reversed by Ku55933 treatment. 2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one 66-73 H3 histone pseudogene 16 Homo sapiens 22-25 27012093-1 2015 Human endometrium-derived mesenchymal stem cells (hMESC) under the sublethal oxidative stress induced by H2O2 activate both p53/p21/Rb and p38MAPK/MAPKAPK-2 pathways that are responsible for the induction of hMESC premature senescence (Borodkina et al., 2014). Hydrogen Peroxide 105-109 H3 histone pseudogene 16 Homo sapiens 128-131 25587030-11 2014 In HT-p21 cells, cell cycle arrest was caused by IPTG-inducible p21 and was spontaneously followed by mTOR-dependent geroconversion. Isopropyl Thiogalactoside 49-53 H3 histone pseudogene 16 Homo sapiens 6-9 25587030-11 2014 In HT-p21 cells, cell cycle arrest was caused by IPTG-inducible p21 and was spontaneously followed by mTOR-dependent geroconversion. Isopropyl Thiogalactoside 49-53 H3 histone pseudogene 16 Homo sapiens 64-67 25446094-3 2014 Moreover, HMA upregulated p21 and p27, while it downregulated p53 and Akt. herbimycin 10-13 H3 histone pseudogene 16 Homo sapiens 26-29 25318830-2 2014 of Li[N(SiHMe2)2] in n-hexane) which crystallizes isotypically to its analogues of the rare-earth metal series (space group P21/c). li[n(sihme2)2] 3-17 H3 histone pseudogene 16 Homo sapiens 124-129 25318830-2 2014 of Li[N(SiHMe2)2] in n-hexane) which crystallizes isotypically to its analogues of the rare-earth metal series (space group P21/c). Metals 98-103 H3 histone pseudogene 16 Homo sapiens 124-129 25446094-7 2014 Therefore, we propose that HMA suppresses cell growth, and reverses EMT in conjunction with the activation of E-cadherin, p21 and p27 and the inactivation of p53 and PI3K/Akt signaling in ATC cells. herbimycin 27-30 H3 histone pseudogene 16 Homo sapiens 122-125 25293876-6 2014 Quercetin treatment resulted in an increased cell arrest in G1 phase of the cell cycle, with pronounced decrease in CDK2, CDK6, cyclin D, cyclin E, and cyclin A proteins, decreased Rb phosphorylation and increased p21 and p27 expression. Quercetin 0-9 H3 histone pseudogene 16 Homo sapiens 214-217 25482151-1 2014 BACKGROUND: PA28gamma (also known as Ki, REG gamma, PMSE3), a member of the ubiquitin-and ATP-independent proteasome activator family 11S, has been proved to show proteasome-dependent and -independent effects on several proteins including tumor suppressor p53, cyclin-dependent kinase inhibitor p21 and steroid receptor co-activator 3 (SCR-3). Adenosine Triphosphate 90-93 H3 histone pseudogene 16 Homo sapiens 295-298 25315710-10 2014 CONCLUSIONS: These results suggest that spermidine and DHPS are key contributing factors in NB tumor proliferation through regulation of the p21/Rb signaling axis. Spermidine 40-50 H3 histone pseudogene 16 Homo sapiens 141-144 25445757-5 2014 Mechanistic studies showed that glycyrol induced G0/G1 phase cell cycle arrest as indicated by increase in p21. glycyrol 32-40 H3 histone pseudogene 16 Homo sapiens 107-110 25260383-6 2014 Our results demonstrated that deoxyelephantopin-induced G2/M phase arrest was associated with a marked increase in the levels of p53 and p21 and a decrease in phospho-signal transducer and activator of transcription 3 (pSTAT3-Tyr705), cyclin-dependent kinase 1 (cdc2), and cyclin B1. deoxyelephantopin 30-47 H3 histone pseudogene 16 Homo sapiens 137-140 25260383-9 2014 Our findings provided the first evidence that STAT3/p53/p21 signaling, MAPK pathway, PI3k/Akt/mTOR pathway, caspase cascades, and ROS play critical roles in deoxyelephantopin-induced G2/M phase arrest and apoptosis of SiHa cells. deoxyelephantopin 157-174 H3 histone pseudogene 16 Homo sapiens 56-59 25236744-0 2014 Human OXR1 maintains mitochondrial DNA integrity and counteracts hydrogen peroxide-induced oxidative stress by regulating antioxidant pathways involving p21. Hydrogen Peroxide 65-82 H3 histone pseudogene 16 Homo sapiens 153-156 25236744-5 2014 In sum, these data reveal that human OXR1 upregulates the expression of antioxidant genes via the p21 signaling pathway to suppress hydrogen peroxide-induced oxidative stress and maintain mtDNA integrity. Hydrogen Peroxide 132-149 H3 histone pseudogene 16 Homo sapiens 98-101 25674209-5 2014 On the molecular level, we observed that exposure to formononetin altered the expression levels of cell cycle arrest-associated proteins p21, cyclin A and cyclin D1. formononetin 53-65 H3 histone pseudogene 16 Homo sapiens 137-140 25195135-2 2014 Here we found a significantly higher ratio of phosphorylated beta-catenin (phos-beta-cat) to beta-catenin (beta-cat) as an indicator of an activated Wnt signaling, with significantly higher levels of c-myc and transcription factor activating protein-4 (AP-4) and a significantly lower level of p21 in the resected HCC, compared to the paired adjacent healthy hepatic tissue from the patients. phosphorylethanolamine 46-50 H3 histone pseudogene 16 Homo sapiens 294-297 25469035-10 2014 Our results showed that treatment with 17beta-estradiol and/or ER agonists in human LoVo colorectal cancer cells activated p53 and then up-regulated p21 and p27 protein levels, subsequently inhibiting the downstream target gene, cyclin D1, which regulates cell proliferation. Estradiol 39-55 H3 histone pseudogene 16 Homo sapiens 149-152 25530715-8 2014 RESULTS: We demonstrated MCF-7 and MDA-MB-231 cells exhibited differential responses to curcumin by WST-1 and clonogenic assay (MDA-MB-231 cells was sensitive, and MCF-7 cells was resistant), which were found to be related to the differential curcumin-mediated regulation of SKP2-Cip/Kips (p21 and p27 but not p57) signaling. Curcumin 88-96 H3 histone pseudogene 16 Homo sapiens 290-293 25409512-5 2014 DM-MCM treatment induced HASMC proliferation, decreased p21(Cip1) and p27(Kip1) expressions, and increased microRNA (miR)-17-5p and miR-221 expressions. dm-mcm 0-6 H3 histone pseudogene 16 Homo sapiens 56-59 25622680-12 2014 Cisplatin up-regulated p53, Mdm2 and p21 in both cell lines. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 37-40 23554011-7 2014 Western blotting assay showed that ellagic acid promoted p21, p53 and decreased CDC2 and WEE1 for leading to G0/G1 phase arrest and promoting BAD expression, AIF and Endo G, cytochrome c, caspase-9 and -3 for leading to apoptosis in TSGH8301 cells. Ellagic Acid 35-47 H3 histone pseudogene 16 Homo sapiens 57-60 25409512-7 2014 Inhibition of miR-17-5p abolished DM-MCM-induced p21(Cip1) down-regulation; and inhibition of miR-221 attenuated the DM-MCM-induced p27(Kip1) down-regulation. dm-mcm 34-40 H3 histone pseudogene 16 Homo sapiens 49-52 25242120-6 2014 The results indicated that silymarin effectively suppressed cell growth in a dose- and time-dependent manner, and arrested cell cycle progression at G1/S phase in A2780s and PA-1 cells via up-regulation of p53, p21, and p27 protein expression, and down-regulation of CDK2 protein expression. Silymarin 27-36 H3 histone pseudogene 16 Homo sapiens 211-214 25281925-3 2014 In addition, histone deacetylase inhibitor trichostatin A (TSA)-mediated upregulation of p21 expression was repressed by knockdown of FOXA1/2 in H1299 cells. trichostatin A 43-57 H3 histone pseudogene 16 Homo sapiens 89-92 25281925-3 2014 In addition, histone deacetylase inhibitor trichostatin A (TSA)-mediated upregulation of p21 expression was repressed by knockdown of FOXA1/2 in H1299 cells. trichostatin A 59-62 H3 histone pseudogene 16 Homo sapiens 89-92 26753100-4 2014 The tetramethylguanidine salt (P21/c) exhibits layers of anions hydrogen-bonded to the cations. tetramethylguanidine salt 4-29 H3 histone pseudogene 16 Homo sapiens 31-36 26753100-4 2014 The tetramethylguanidine salt (P21/c) exhibits layers of anions hydrogen-bonded to the cations. Hydrogen 64-72 H3 histone pseudogene 16 Homo sapiens 31-36 25405759-7 2014 The mitotic index and the expression of p21, BubR1 and Securin were all reduced following Nocodazole treatment. Nocodazole 90-100 H3 histone pseudogene 16 Homo sapiens 40-43 25109285-8 2014 Sirt1-Foxp3 signaling-mediated regulation of Bax and p21 mRNA expression was a signature molecular event in TPC1 cells, which showed remarkable resistance to etoposide-induced genotoxic stress. Etoposide 158-167 H3 histone pseudogene 16 Homo sapiens 53-56 25296971-4 2014 Treatment with ganetespib (50 nM) for 24 hours inhibited cyclin D1 and pRb at the transcriptional and translational levels and induced p21, leading to G0/G1 cell cycle arrest in both CRC cell lines (HCT-116 and HT-29). STA 9090 15-25 H3 histone pseudogene 16 Homo sapiens 135-138 25129649-8 2014 Moreover, OA and ALA up-regulated tumor suppressor genes (p53, p21, and p27) and these effects are abolished by AMPK siRNA administration. alpha-Linolenic Acid 17-20 H3 histone pseudogene 16 Homo sapiens 63-66 26027111-13 2014 The results of Western blot assay showed that this ratio of drugs could significantly increase the protein expression of Bax,P53 and P21 and decreased the expression of BCL-2, Casepase-3, p-Erk, p-Ras and p-c-Raf in SMMC-7721 cells. smmc 216-220 H3 histone pseudogene 16 Homo sapiens 133-136 25285637-4 2014 Although delta-T3 induced G1 arrest by up-regulating p21 in PANC-1 cells, more cells accumulated in G1 phase with the combination of delta-T3 and FA. Triiodothyronine 15-17 H3 histone pseudogene 16 Homo sapiens 53-56 25285637-4 2014 Although delta-T3 induced G1 arrest by up-regulating p21 in PANC-1 cells, more cells accumulated in G1 phase with the combination of delta-T3 and FA. delta-t3 9-17 H3 histone pseudogene 16 Homo sapiens 53-56 23994263-11 2014 Taken together the results demonstrate that BaP sensitizes MCF7 cells to E5M antiproliferative activity via enhanced induction of p21, JNK and p-JNK that in turn results by cytochrome P450 CYP1-mediated conversion to the metabolite E5M1. Benzo(a)pyrene 44-47 H3 histone pseudogene 16 Homo sapiens 130-133 25169428-0 2014 Sulforaphane inhibition of TPA-mediated PDCD4 downregulation contributes to suppression of c-Jun and induction of p21-dependent Nrf2 expression. sulforaphane 0-12 H3 histone pseudogene 16 Homo sapiens 114-117 25358785-0 2014 Activation of p38, p21, and NRF-2 mediates decreased proliferation of human dental pulp stem cells cultured under 21% O2. Oxygen 118-120 H3 histone pseudogene 16 Homo sapiens 19-22 25358785-5 2014 Under 21% O2, increased p38 phosphorylation led to activation of p21. Oxygen 10-12 H3 histone pseudogene 16 Homo sapiens 65-68 25358785-8 2014 Activation of p38/p21/NRF-2 in hDPSCs cultured under ambient oxygen tension inhibits stem cell proliferation and upregulates NRF-2 antioxidant defenses. Oxygen 61-67 H3 histone pseudogene 16 Homo sapiens 18-21 25238284-2 2014 Tetrahydroisoquinoline 12 was identified as a potent HDAC6 and HDAC8 dual inhibitor from a focused library through cellular tubulin acetylation and p21 induction screening assays. 1,2,3,4-tetrahydroisoquinoline 0-22 H3 histone pseudogene 16 Homo sapiens 148-151 24499675-0 2014 Arsenite induces premature senescence via p53/p21 pathway as a result of DNA damage in human malignant glioblastoma cells. arsenite 0-8 H3 histone pseudogene 16 Homo sapiens 46-49 25274525-3 2014 These layers host a well resolved R12 dodecameric discrete ring of water clusters built by six independent molecules located around the 2c centrosymmetric Wyckoff positions of the P21/n space group in which the compound crystallizes. Water 67-72 H3 histone pseudogene 16 Homo sapiens 180-183 25244664-3 2014 A P21/c monoclinic structure describes precisely the [(CH3)4N]2MnCl4 crystal in the 0.1-6 GPa range, prior to crystal decomposition and amorphization, while [(CH3)4N]2MnBr4 can be described by a Pmcn orthorhombic structure in its stability pressure range of 0-3 GPa. [(ch3)4n]2mncl4 53-68 H3 histone pseudogene 16 Homo sapiens 2-5 25244664-3 2014 A P21/c monoclinic structure describes precisely the [(CH3)4N]2MnCl4 crystal in the 0.1-6 GPa range, prior to crystal decomposition and amorphization, while [(CH3)4N]2MnBr4 can be described by a Pmcn orthorhombic structure in its stability pressure range of 0-3 GPa. pmcn 195-199 H3 histone pseudogene 16 Homo sapiens 2-5 24930072-6 2014 Up-regulation of p38 MAPK activity in responding the ROS stabilize p53 and activate p21 transcription, the critical regulatory in G1/S checkpoint. Reactive Oxygen Species 53-56 H3 histone pseudogene 16 Homo sapiens 84-87 24499675-4 2014 Dimethyl- and trimethyl-lysine 9 of histone H3 (H3DMK9 and H3TMK9) foci formation was accompanied by p21 accumulation only in U87MG-neo but not in U87MG-E6 cells. dimethyl- and trimethyl-lysine 0-30 H3 histone pseudogene 16 Homo sapiens 101-104 24499675-5 2014 This suggests that arsenite induces premature senescence as a result of DNA damage with heterochromatin forming through a p53/p21 dependent pathway. arsenite 19-27 H3 histone pseudogene 16 Homo sapiens 126-129 24499675-6 2014 p21 and p53 siRNA consistently decreased H3TMK9 foci formation in U87M G-neo but not in U87MG-E6 cells after arsenite treatment. g-neo 71-76 H3 histone pseudogene 16 Homo sapiens 0-3 24499675-7 2014 Taken together, arsenite reduces cell growth independently of p53 and induces premature senescence via p53/p21-dependent pathway following DNA damage. arsenite 16-24 H3 histone pseudogene 16 Homo sapiens 107-110 24535918-1 2014 We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation. Methylcholanthrene 83-103 H3 histone pseudogene 16 Homo sapiens 240-243 25107568-16 2014 Elevated levels of P21 and GADD45, in concert with cyclin D1, also mediated the antiproliferative response of HL-60 in the presence of 1,25-(OH)2D3 and PS121912. Calcitriol 135-147 H3 histone pseudogene 16 Homo sapiens 19-22 25382556-10 2014 To investigate hMED15 localization, we treated human MCF-7 cells with the MDM2 inhibitor Nutlin-3, thus inducing p21 transcription. nutlin 3 89-97 H3 histone pseudogene 16 Homo sapiens 113-116 24535918-1 2014 We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation. Methylcholanthrene 105-108 H3 histone pseudogene 16 Homo sapiens 240-243 24535918-3 2014 Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback. Methylcholanthrene 27-30 H3 histone pseudogene 16 Homo sapiens 62-65 24535918-3 2014 Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback. Methylcholanthrene 27-30 H3 histone pseudogene 16 Homo sapiens 148-151 24535918-4 2014 Downregulation of p21/p27 by siRNA, and cytosolic p21/p27 by the nuclear export blocker leptomycin B, further reduced cell migration in the 3MC-treated cells. leptomycin B 88-100 H3 histone pseudogene 16 Homo sapiens 50-53 24535918-4 2014 Downregulation of p21/p27 by siRNA, and cytosolic p21/p27 by the nuclear export blocker leptomycin B, further reduced cell migration in the 3MC-treated cells. Methylcholanthrene 140-143 H3 histone pseudogene 16 Homo sapiens 18-21 24535918-4 2014 Downregulation of p21/p27 by siRNA, and cytosolic p21/p27 by the nuclear export blocker leptomycin B, further reduced cell migration in the 3MC-treated cells. Methylcholanthrene 140-143 H3 histone pseudogene 16 Homo sapiens 50-53 24535918-9 2014 Our results provide a molecular basis for the therapeutic application of simvastatin to reduce RhoA/PTEN activation, restore cytosolic levels of phosphorylated p21/p27, and induce angiogenic processes. Simvastatin 73-84 H3 histone pseudogene 16 Homo sapiens 160-163 25232279-8 2014 The regulatory targets of miR-106b~25 cluster namely p21 (cyclin-dependent kinase inhibitor) and BIM (pro-apoptotic gene) were elevated, and apoptotic cell death was observed, in RB tumor cells treated with the specific antagomirs of the miR-106b~25 cluster. mir-106b 26-34 H3 histone pseudogene 16 Homo sapiens 53-56 25175641-0 2014 Diallyl disulfide induces G2/M arrest and promotes apoptosis through the p53/p21 and MEK-ERK pathways in human esophageal squamous cell carcinoma. diallyl disulfide 0-17 H3 histone pseudogene 16 Homo sapiens 77-80 25123426-6 2014 Escin induced G2/M-phase cell cycle arrest and thus led to a significant decrease in the expression of cyclinB1 and its activating partner cyclin-dependent kinase 1, with the concomitant induction of p21. Escin 0-5 H3 histone pseudogene 16 Homo sapiens 200-203 25509266-11 2014 Western blot showed the expression of p53 and p21 protein could be increased by DHA combined irradiation, and the expression of Bcl-2 protein down-regulated (P <0.01, P <0. artenimol 80-83 H3 histone pseudogene 16 Homo sapiens 46-49 25144919-1 2014 The crystal structure of 3-quinolinecarboxaldehyde (3QC) has been solved, and the compound has been shown to crystallize in the space group P21/c (monoclinic) with a = 6.306(4), b = 18.551(11), c = 6.999(4) A, beta = 106.111(13) , and Z = 4. 3-quinolinecarboxaldehyde 25-50 H3 histone pseudogene 16 Homo sapiens 140-145 25170649-2 2014 Single-crystal X-ray diffraction reveals that the six complexes are all isomorphous with the monoclinic P21/c space group and with lattice parameters that decrease with the lanthanide contraction. Lanthanoid Series Elements 173-183 H3 histone pseudogene 16 Homo sapiens 104-109 24726874-10 2014 It indicated that aspirin induced adipocyte differentiation through p53-p21 pathway. Aspirin 18-25 H3 histone pseudogene 16 Homo sapiens 72-75 25232279-8 2014 The regulatory targets of miR-106b~25 cluster namely p21 (cyclin-dependent kinase inhibitor) and BIM (pro-apoptotic gene) were elevated, and apoptotic cell death was observed, in RB tumor cells treated with the specific antagomirs of the miR-106b~25 cluster. mir-106b 238-246 H3 histone pseudogene 16 Homo sapiens 53-56 25047426-9 2014 In addition, hesperidin enhanced p53-p21 axis with concomitant decrease in cell cycle regulator. Hesperidin 13-23 H3 histone pseudogene 16 Homo sapiens 37-40 24747221-6 2014 RESULTS: We found that acrolein induced cellular senescence by increasing both p53 and p21. Acrolein 23-31 H3 histone pseudogene 16 Homo sapiens 87-90 24942805-9 2014 Furthermore, berberine-induced miR-23a expression may mediate the transcription activation of p53-related tumor suppressive genes p21 and GADD45alpha. Berberine 13-22 H3 histone pseudogene 16 Homo sapiens 130-133 24894198-5 2014 We found that dihydromyricetin induced increased p21 expression and G2-M cell-cycle arrest, caused DNA damage, activated ATM-CHK2-H2AX signaling pathways, and induced apoptosis in osteosarcoma cells as well as decreasing the sphere formation capability by downregulating Sox2 expression. dihydromyricetin 14-30 H3 histone pseudogene 16 Homo sapiens 49-52 24894198-7 2014 Moreover, GSK3beta deletion or GSK3beta inhibition by LiCl treatment resulted in increased p21 expression and reduced Sox2 expression in osteosarcoma cells. Lithium Chloride 54-58 H3 histone pseudogene 16 Homo sapiens 91-94 23239598-9 2014 CECF increased protein levels of caspase-3, caspase-9, Bax, cytochrome c, GRP78, AIF, ATF-6alpha, Fas, TRAIL, p21, p27, and p16 which were associated with cell-cycle arrest and apoptosis. cecf 0-4 H3 histone pseudogene 16 Homo sapiens 110-113 24568186-13 2014 In conclusion, upregulation of p53 and p21 via HO-1 induction and subsequent release of iron with accumulation of H-ferritin may confer resistance to oxidative damage in cancer cells frequently challenged by redox-cycling anticancer drugs. Iron 88-92 H3 histone pseudogene 16 Homo sapiens 39-42 25564054-4 2014 RESULTS: Western blot showed that the overexpression of RIG-G protein significantly upregulated p21 protein level in the NB4 cells, and the level of p21 protein largely increased along with the induction of endogenous RIG-G protein during the differentiation of NB4 cells treated by all-trans retinoic acid (ATRA). Tretinoin 293-306 H3 histone pseudogene 16 Homo sapiens 149-152 24597985-4 2014 Compared with the use of DEX or low-dose anisomycin alone, co-treatment with them resulted in a significant increase of growth inhibition, apoptosis and cell cycle arrest in CEM-C1 cells through induction of activated caspase-3 and up-regulation of Bim, p21and p27, and down-regulation of Mcl-1, Bcl-2, c-myc, cyclin A and cyclin D1. Anisomycin 41-51 H3 histone pseudogene 16 Homo sapiens 254-257 24996978-10 2014 Exposure of cultured human proximal tubular cells to 25mmol/L, but not 8mmol/L, glucose medium increased the expression of senescence markers, which was suppressed by knock-down of p21 or sodium glucose cotransporter (SGLT) 2. Glucose 80-87 H3 histone pseudogene 16 Homo sapiens 181-184 24597985-4 2014 Compared with the use of DEX or low-dose anisomycin alone, co-treatment with them resulted in a significant increase of growth inhibition, apoptosis and cell cycle arrest in CEM-C1 cells through induction of activated caspase-3 and up-regulation of Bim, p21and p27, and down-regulation of Mcl-1, Bcl-2, c-myc, cyclin A and cyclin D1. Dexamethasone 25-28 H3 histone pseudogene 16 Homo sapiens 254-257 25564054-4 2014 RESULTS: Western blot showed that the overexpression of RIG-G protein significantly upregulated p21 protein level in the NB4 cells, and the level of p21 protein largely increased along with the induction of endogenous RIG-G protein during the differentiation of NB4 cells treated by all-trans retinoic acid (ATRA). Tretinoin 308-312 H3 histone pseudogene 16 Homo sapiens 149-152 24939757-0 2014 Xylarianaphthol-1, a novel dinaphthofuran derivative, activates p21 promoter in a p53-independent manner. xylarianaphthol-1 0-17 H3 histone pseudogene 16 Homo sapiens 64-67 25100434-5 2014 By RT-PCR and western blot assays, Kuding tea polyphenol significantly induced apoptosis in BcaCD885 cancer cells (p < 0.05) by upregulating caspase-3, caspase-8, caspase-9, Fas/FasL, Bax, p53, p21, E2F1, p73 and downregulating Bcl-2, Bcl-xL, HIAP-1, and HIAP-2 mRNA and protein expressions. Polyphenols 46-56 H3 histone pseudogene 16 Homo sapiens 197-200 24858802-3 2014 In the present study, we found that, in human colorectal cancer cells, low-dose camptothecin (CPT) simultaneously induced autophagy and premature senescence through AMPK-TSC2-mTOR pathway and ATM-Chk2-p53-p21 pathway respectively. Camptothecin 80-92 H3 histone pseudogene 16 Homo sapiens 205-208 24858802-3 2014 In the present study, we found that, in human colorectal cancer cells, low-dose camptothecin (CPT) simultaneously induced autophagy and premature senescence through AMPK-TSC2-mTOR pathway and ATM-Chk2-p53-p21 pathway respectively. Camptothecin 94-97 H3 histone pseudogene 16 Homo sapiens 205-208 24679790-5 2014 Azufrado Higuera modified the expression of cell cycle regulation proteins p21 and cyclin B1. azufrado 0-8 H3 histone pseudogene 16 Homo sapiens 75-78 24797896-11 2014 Interestingly, hydralazine restored androgen receptor expression, with upregulation of its target p21 in DU145 cell line. Hydralazine 15-26 H3 histone pseudogene 16 Homo sapiens 98-101 24997578-4 2014 The bicyclic tetrapeptides disulfide showed potent HDAC1 and HDAC4 inhibition and p21 promoting activity. Disulfides 27-36 H3 histone pseudogene 16 Homo sapiens 82-85 24939757-0 2014 Xylarianaphthol-1, a novel dinaphthofuran derivative, activates p21 promoter in a p53-independent manner. dinaphthofuran 27-41 H3 histone pseudogene 16 Homo sapiens 64-67 24939757-4 2014 Expression of p21 protein in the wild-type MG63 cells was also increased by xylarianaphthol-1 treatment. xylarianaphthol-1 76-93 H3 histone pseudogene 16 Homo sapiens 14-17 25003799-0 2014 Vitamin C protects against UV irradiation-induced apoptosis through reactivating silenced tumor suppressor genes p21 and p16 in a Tet-dependent DNA demethylation manner in human skin cancer cells. Ascorbic Acid 0-9 H3 histone pseudogene 16 Homo sapiens 113-116 24632182-12 2014 Inhibition of "over-active" Cathepsin D by the specific, cell-permeable inhibitor pepstatin A abolishes the increase in nuclear p21 protein, ROS formation and degradation of Trx-1 protein, thus leading to blockade of stress-induced premature senescence by stabilizing the cellular redox homeostasis. pepstatin 82-93 H3 histone pseudogene 16 Homo sapiens 128-131 25003799-0 2014 Vitamin C protects against UV irradiation-induced apoptosis through reactivating silenced tumor suppressor genes p21 and p16 in a Tet-dependent DNA demethylation manner in human skin cancer cells. tetramethylenedisulfotetramine 130-133 H3 histone pseudogene 16 Homo sapiens 113-116 25003799-7 2014 To examine the DNA demethylation activity of vitamin C, DNA immunoprecipitation (DIP)-qPCR was performed to determine the relative levels of 5-methylcytosine (5mC) or 5-hydroxymethylcytosine (5hmC) in p16 and p21 promoter regions containing cytosine-phosphorothiolated guanine (CpG) islands. Ascorbic Acid 45-54 H3 histone pseudogene 16 Homo sapiens 209-212 25003799-10 2014 Vitamin C also reactivated the expression of p16 and p21 at mRNA and protein levels. Ascorbic Acid 0-9 H3 histone pseudogene 16 Homo sapiens 53-56 25003799-11 2014 Mechanistically, about 27% 5hmC-positive cells were observed in vitamin C-treated A431 cells, and the 5hmC enrichment at p16 and p21 promoter regions was also largely increased by vitamin C. 5-hydroxymethylcytosine 102-106 H3 histone pseudogene 16 Homo sapiens 129-132 24799378-0 2014 Oligosaccharide G19 inhibits U-87 MG human glioma cells growth in vitro and in vivo by targeting epidermal growth factor (EGF) and activating p53/p21 signaling. oligosaccharide g19 0-19 H3 histone pseudogene 16 Homo sapiens 146-149 25003799-11 2014 Mechanistically, about 27% 5hmC-positive cells were observed in vitamin C-treated A431 cells, and the 5hmC enrichment at p16 and p21 promoter regions was also largely increased by vitamin C. Ascorbic Acid 180-189 H3 histone pseudogene 16 Homo sapiens 129-132 25003799-12 2014 Moreover, the expression of p16 and p21 was decreased in Tet1/2 double-knockdown cells, in which the inhibitory effect of vitamin C on UV-induced apoptosis was dismissed. Ascorbic Acid 122-131 H3 histone pseudogene 16 Homo sapiens 36-39 25003799-13 2014 Furthermore, the inhibition of UV-induced apoptosis on vitamin C treatment nearly disappeared in p16- or p21-knockout primary cultured fibroblasts. Ascorbic Acid 55-64 H3 histone pseudogene 16 Homo sapiens 105-108 25135721-6 2014 Both PDOX and DOX caused an up-regulation of the P53/P21-related signal pathway, and PDOX significantly increased expression of P53 and caspase 3, and arrested the cell cycle at the G1/G2 phase. acetyl-phenylalanyl-lysyl-para-aminobenzyloxycarbonyl-adriamycin 5-9 H3 histone pseudogene 16 Homo sapiens 53-56 24858230-7 2014 DBP, a type of phthalate, was shown to promote LNCaP cell proliferation by upregulating the gene expression of c-myc and cyclin D1 and by downregulating the expression of p21. phthalic acid 15-24 H3 histone pseudogene 16 Homo sapiens 171-174 25135721-6 2014 Both PDOX and DOX caused an up-regulation of the P53/P21-related signal pathway, and PDOX significantly increased expression of P53 and caspase 3, and arrested the cell cycle at the G1/G2 phase. Doxorubicin 6-9 H3 histone pseudogene 16 Homo sapiens 53-56 24526307-6 2014 In vitro temozolomide at the EC50 (10 microM) induced accumulation of cells in the G2/M phase that was unexpectedly accompanied by downregulation of p27 and p21 without modulation of full-length p53 (FLp53). Temozolomide 9-21 H3 histone pseudogene 16 Homo sapiens 157-160 24920214-13 2014 Thus, a 15-fold increase in p21 levels was observed in melatonin-treated cancer cells. Melatonin 55-64 H3 histone pseudogene 16 Homo sapiens 28-31 23727633-7 2014 Increased levels of acetylated p53 as well as increased RNA levels of its pro-senescence effector p21 were evident in dexamethasone-treated tenocytes. Dexamethasone 118-131 H3 histone pseudogene 16 Homo sapiens 98-101 24867323-5 2014 Cell response to homocysteine-induced DNA damage involved the up-regulation of Bax and, at a greater extent, Bcl-2, but not caspase-3, in association with a p53-independent increase of p21 levels; concomitantly, also p16 levels were increased. Homocysteine 17-29 H3 histone pseudogene 16 Homo sapiens 185-188 24867323-7 2014 However, in line with the observed increase of p21 and p16 levels, a five days incubation with homocysteine induced cyclin down-regulation accompanied by a strong reduction of phosphorylated pRB amounts. Homocysteine 95-107 H3 histone pseudogene 16 Homo sapiens 47-50 25254004-10 2014 We found that DAPT treatment results in downregulation of Hes1 and p21 and upregulation of Wnt10b. 24-diamino-5-phenylthiazole 14-18 H3 histone pseudogene 16 Homo sapiens 67-70 25254004-12 2014 The DAPT may modulate human hair follicle stem cell proliferation and differentiation through regulation of p21 and Wnt-10b. 24-diamino-5-phenylthiazole 4-8 H3 histone pseudogene 16 Homo sapiens 108-111 24845028-8 2014 Collectively, our results show that SM inhibits proliferation and induces apoptosis in lung cancer cells through p38 MAPK-mediated suppression of phosphorylation and protein expression of Stat3, followed by inducing Stat3 downstream effector p21. beta-solamarine 36-38 H3 histone pseudogene 16 Homo sapiens 242-245 24919507-9 2014 In in vitro studies, we observed increased expression of p21 and p-ERK1/2 diminution via use of both analogs as compared to use of 5-FU alone. Fluorouracil 131-135 H3 histone pseudogene 16 Homo sapiens 57-60 24919507-12 2014 Our results suggest that the mechanism of potentiation of 5-FU antitumor action by both analogs is realized via increased p21 expression and decreased p-ERK1/2 level which may lead to diminution of thymidylate synthase expression. Fluorouracil 58-62 H3 histone pseudogene 16 Homo sapiens 122-125 24913829-7 2014 RESULTS: In the presence of continuous PGF signaling, PrEC hyperplasia is prevented by androgen binding to AR suppressing c-MYC transcription, resulting in G0 arrest/terminal differentiation independent of Rb, p21, p27, FoxP3, or down regulation of growth factors receptors and instead involves androgen-induced formation of AR/beta-catenin/TCF-4 complexes, which suppress c-MYC transcription. Prostaglandins F 39-42 H3 histone pseudogene 16 Homo sapiens 210-213 25036040-10 2014 Trichostatin A and MS-275 (both HDAC inhibitors) inhibited the downstream pathway of HDAC1 and caused cell growth arrest via activation of p53 and p21; the effects of digoxigenin were totally opposite. trichostatin A 0-14 H3 histone pseudogene 16 Homo sapiens 147-150 25036040-10 2014 Trichostatin A and MS-275 (both HDAC inhibitors) inhibited the downstream pathway of HDAC1 and caused cell growth arrest via activation of p53 and p21; the effects of digoxigenin were totally opposite. entinostat 19-25 H3 histone pseudogene 16 Homo sapiens 147-150 25036040-11 2014 Staurosporine blocked the cell cycle via p53 and p21, but also promoted cell growth via activated HDAC1 and its downstream pathway. Staurosporine 0-13 H3 histone pseudogene 16 Homo sapiens 49-52 24989033-5 2014 Here, we show that the treatment of the novel small molecule, CG500354, into CD133-expressing human primary GBM cells induces growth arrest by cell cycle regulators, p53, p21, p27 and phase-specific cyclins, and neural differentiation, as confirmed by neural progenitor/precursor markers, nestin, GFAP and Tuj1. CG500354 62-70 H3 histone pseudogene 16 Homo sapiens 171-174 24840054-8 2014 In addition, it hindered doxorubicin-induced apoptosis by regulating the expression of c-Myc and p21. Doxorubicin 25-36 H3 histone pseudogene 16 Homo sapiens 97-100 24888707-9 2014 Nimbolide also increased the protein expression of p21 and decreased the cyclins in both the cell lines. nimbolide 0-9 H3 histone pseudogene 16 Homo sapiens 51-54 24962518-5 2014 Indeed, transfection of leukemic cells with p21 siRNAs significantly decreased the DCA+Nutlin-3-induced cytotoxicity. Dichloroacetic Acid 83-86 H3 histone pseudogene 16 Homo sapiens 44-47 24962518-5 2014 Indeed, transfection of leukemic cells with p21 siRNAs significantly decreased the DCA+Nutlin-3-induced cytotoxicity. nutlin 3 87-95 H3 histone pseudogene 16 Homo sapiens 44-47 24892596-8 2014 The third isomer, 1,4-dibromobenzene, is a solid at room temperature and crystallizes as monoclinic, space group P21/a. 1,4-dibromobenzene 18-36 H3 histone pseudogene 16 Homo sapiens 113-116 25009787-4 2014 Initially, DMF increased p21 protein stability through an enhancement in Nrf2 activity without an increase in p21 mRNA. Dimethyl Fumarate 11-14 H3 histone pseudogene 16 Homo sapiens 25-28 25009787-5 2014 Later on, DMF stimulated p21 mRNA expression through a process dependent on p53 activity. Dimethyl Fumarate 10-13 H3 histone pseudogene 16 Homo sapiens 25-28 25009787-10 2014 In conclusion, DMF prevented abnormal proliferation in VSMCs by G1 cell cycle arrest via p21 upregulation driven by Nrf2 and p53 activity, and had a beneficial effect on TNF-alpha-induced apoptosis and dysfunction in endothelial cells through Nrf2-NQO1 activity suggesting that DMF might be a therapeutic drug for patients with vascular disease. Dimethyl Fumarate 15-18 H3 histone pseudogene 16 Homo sapiens 89-92 24794748-0 2014 The pterocarpanquinone LQB-118 inhibits tumor cell proliferation by downregulation of c-Myc and cyclins D1 and B1 mRNA and upregulation of p21 cell cycle inhibitor expression. Pterocarpanquinone 4-22 H3 histone pseudogene 16 Homo sapiens 139-142 24794748-0 2014 The pterocarpanquinone LQB-118 inhibits tumor cell proliferation by downregulation of c-Myc and cyclins D1 and B1 mRNA and upregulation of p21 cell cycle inhibitor expression. LQB 118 23-30 H3 histone pseudogene 16 Homo sapiens 139-142 24789439-6 2014 DHM increased the production of p53 and p21 proteins and downregulated the production of Cdc25A, Cdc2 and P-Cdc2 proteins, which induced cell cycle arrest. dihydromyricetin 0-3 H3 histone pseudogene 16 Homo sapiens 40-43 24646031-3 2014 In many cases, downregulation of CDK activity by ATRA and vitamin D3 is a result of elevated p21- and p27-bound CDKs. Tretinoin 49-53 H3 histone pseudogene 16 Homo sapiens 93-96 24646031-3 2014 In many cases, downregulation of CDK activity by ATRA and vitamin D3 is a result of elevated p21- and p27-bound CDKs. Cholecalciferol 58-68 H3 histone pseudogene 16 Homo sapiens 93-96 24728469-6 2014 This may indicate that the alteration of p21 and CHK1 following zebularine administration was not due to inhibition of methylation of their promoter. pyrimidin-2-one beta-ribofuranoside 64-74 H3 histone pseudogene 16 Homo sapiens 41-44 24710632-8 2014 DNA damage induced p53 stabilization and p21 induction by cisplatin treatment confirmed that wt-AGR2 expression suppressed the p53 pathway. Cisplatin 58-67 H3 histone pseudogene 16 Homo sapiens 41-44 24932256-11 2014 Fractionated IR resulted in a significant increase in p21 expression, which was further enhanced when combined with cisplatin. Cisplatin 116-125 H3 histone pseudogene 16 Homo sapiens 54-57 24682388-5 2014 In addition, ALO induced cell cycle arrest at the G2/M phase with a concomitant increase in p21 and p53 and a decrease in cyclin D1 and B1. aloperine 13-16 H3 histone pseudogene 16 Homo sapiens 92-95 24756776-6 2014 Knockdown of GRP78 rescued the senescence sensitivity of cisplatin-resistant C13K cells to cisplatin through P21 and CDC2. Cisplatin 57-66 H3 histone pseudogene 16 Homo sapiens 109-112 24756776-6 2014 Knockdown of GRP78 rescued the senescence sensitivity of cisplatin-resistant C13K cells to cisplatin through P21 and CDC2. Cisplatin 91-100 H3 histone pseudogene 16 Homo sapiens 109-112 24878898-6 2014 At the early stage of KIOM-C treatment (12 h), cells were arrested in G1 phase, which was accompanied by up-regulation of p21 and p27, down-regulation of cyclin D1, and subsequent increases in apoptotic and autophagic cells. kiom-c 22-28 H3 histone pseudogene 16 Homo sapiens 122-125 24932256-14 2014 As for the apoptosis signaling genes, the combination of cisplatin and fractionated IR therapy resulted in a significant decrease in Bcl-2 expression and a marked upregulation of p21 expression. Cisplatin 57-66 H3 histone pseudogene 16 Homo sapiens 179-182 24684733-3 2014 Altered expressions of cyclin D1 and p21 were observed in MCF-7 human breast cancer cells treated with TCS and OP, which is linked to the G1/S transition of cell cycle, leading to cell proliferation. Triclosan 103-106 H3 histone pseudogene 16 Homo sapiens 37-40 24704462-5 2014 High glucose condition led to significant increase in the expression of PCNA, cyclin D1 and decrease in the expression of PTPN 12, p21 and PTEN. Glucose 5-12 H3 histone pseudogene 16 Homo sapiens 131-134 24847310-1 2014 Physiological concentrations of the green tea extract epigallocatechin-3-gallate (EGCG) caused growth inhibition in estrogen receptor alpha (ERalpha)-positive MCF7 cells that was associated with down-regulation of the ERalpha and reduced insulin-like growth factor binding protein-2 abundance and increased protein abundance of the tumor suppressor genes p53/p21. epigallocatechin gallate 54-80 H3 histone pseudogene 16 Homo sapiens 359-362 24798549-11 2014 Reovirus and irinotecan combination therapy is synergistic, p21 mediated, and represents a novel potential treatment for patients with CRC. Irinotecan 13-23 H3 histone pseudogene 16 Homo sapiens 60-63 24847310-1 2014 Physiological concentrations of the green tea extract epigallocatechin-3-gallate (EGCG) caused growth inhibition in estrogen receptor alpha (ERalpha)-positive MCF7 cells that was associated with down-regulation of the ERalpha and reduced insulin-like growth factor binding protein-2 abundance and increased protein abundance of the tumor suppressor genes p53/p21. epigallocatechin gallate 82-86 H3 histone pseudogene 16 Homo sapiens 359-362 24835555-5 2014 As results, MXC and TCS induced BG-1 cell growth via regulating cyclin D1, p21 and Bax genes related with cell cycle and apoptosis. Triclosan 20-23 H3 histone pseudogene 16 Homo sapiens 75-78 24804719-4 2014 The G1 arrest by piperine correlated with the down-regulation of cyclin D1 and induction of p21. piperine 17-25 H3 histone pseudogene 16 Homo sapiens 92-95 24604009-6 2014 It was demonstrated that isolinderalactone may induce p21 expression and then cause the cell cycle arrest of A549 cells. linderalactone 25-42 H3 histone pseudogene 16 Homo sapiens 54-57 24642253-8 2014 In addition, over-expression of ChDFFA inhibited the transcriptional activities of p53/p21-Luc reporter genes in HEK293T cells. chdffa 32-38 H3 histone pseudogene 16 Homo sapiens 87-90 24593988-8 2014 Moreover, co-treatment of MCF-7 cells with THC and p38 MAPK inhibitor, SB203580, effectively reversed the dissipation in mitochondrial membrane potential (Deltapsim), and blocked THC-mediated Bax up-regulation, Bcl-2 down-regulation, caspase-3 activation as well as p21 up-regulation, suggesting p38 MAPK might mediate THC-induced apoptosis and G2/M arrest. tetrahydrocurcumin 43-46 H3 histone pseudogene 16 Homo sapiens 266-269 24593988-8 2014 Moreover, co-treatment of MCF-7 cells with THC and p38 MAPK inhibitor, SB203580, effectively reversed the dissipation in mitochondrial membrane potential (Deltapsim), and blocked THC-mediated Bax up-regulation, Bcl-2 down-regulation, caspase-3 activation as well as p21 up-regulation, suggesting p38 MAPK might mediate THC-induced apoptosis and G2/M arrest. SB 203580 71-79 H3 histone pseudogene 16 Homo sapiens 266-269 24593988-8 2014 Moreover, co-treatment of MCF-7 cells with THC and p38 MAPK inhibitor, SB203580, effectively reversed the dissipation in mitochondrial membrane potential (Deltapsim), and blocked THC-mediated Bax up-regulation, Bcl-2 down-regulation, caspase-3 activation as well as p21 up-regulation, suggesting p38 MAPK might mediate THC-induced apoptosis and G2/M arrest. tetrahydrocurcumin 179-182 H3 histone pseudogene 16 Homo sapiens 266-269 24593988-8 2014 Moreover, co-treatment of MCF-7 cells with THC and p38 MAPK inhibitor, SB203580, effectively reversed the dissipation in mitochondrial membrane potential (Deltapsim), and blocked THC-mediated Bax up-regulation, Bcl-2 down-regulation, caspase-3 activation as well as p21 up-regulation, suggesting p38 MAPK might mediate THC-induced apoptosis and G2/M arrest. tetrahydrocurcumin 179-182 H3 histone pseudogene 16 Homo sapiens 266-269 24325805-4 2014 Our results demonstrate that polyphyllin D exerts a growth inhibitory effect by arresting cells at G2/M phase and by the induction of apoptosis in K562/A02 human leukaemia drug-resistant cells, G2/M phase arrest was found to be associated with up-regulation of p21 and down-regulation of cyclin B1 and cyclin-dependent protein kinase 1. polyphyllin D 29-42 H3 histone pseudogene 16 Homo sapiens 261-264 24573222-14 2014 The results of this study suggest that 1,25(OH)2D3 potentiates cisplatin-mediated cell growth inhibition and cell apoptosis, which involves the upregulation of Bax, a decrease in ERK and AKT phosphorylation levels, and increased p21 and p27 levels. Calcitriol 39-50 H3 histone pseudogene 16 Homo sapiens 229-232 24573222-14 2014 The results of this study suggest that 1,25(OH)2D3 potentiates cisplatin-mediated cell growth inhibition and cell apoptosis, which involves the upregulation of Bax, a decrease in ERK and AKT phosphorylation levels, and increased p21 and p27 levels. Cisplatin 63-72 H3 histone pseudogene 16 Homo sapiens 229-232 24615755-6 2014 In addition, DHR upregulated the cell cycle repressors p21 and p53. 1',2'-dihydrorotenone 13-16 H3 histone pseudogene 16 Homo sapiens 55-58 24615755-7 2014 DHR also increased the phosphorylation level of p53, suggesting the upregulated transactivation function of p53, which was confirmed by the induction of p21, a substrate of activated p53. 1',2'-dihydrorotenone 0-3 H3 histone pseudogene 16 Homo sapiens 153-156 24604009-8 2014 These novel findings demonstrated that isolinderalactone may cause the cell cycle arrest of A549 cells by induction of p21, and induce apoptosis of A549 human non-small-cell lung carcinoma cells through the Fas/sFasL apoptotic system. linderalactone 39-56 H3 histone pseudogene 16 Homo sapiens 119-122 24676336-12 2014 For the TSA+DAC group, higher levels of p53, p21, cyclin B1 and Chk1 were detected, concomitant with lower levels of CDK1, when compared to the control group. trichostatin A 8-11 H3 histone pseudogene 16 Homo sapiens 45-48 24626782-3 2014 The present preliminary study using DNA microarray and real-time PCR indicates p21 mRNA is upregulated in human colon carcinoma (HT29) cells exposed to pyridoxal (PL, 500 microM). Pyridoxal 152-161 H3 histone pseudogene 16 Homo sapiens 79-82 24626782-3 2014 The present preliminary study using DNA microarray and real-time PCR indicates p21 mRNA is upregulated in human colon carcinoma (HT29) cells exposed to pyridoxal (PL, 500 microM). Pyridoxal 163-165 H3 histone pseudogene 16 Homo sapiens 79-82 24676336-12 2014 For the TSA+DAC group, higher levels of p53, p21, cyclin B1 and Chk1 were detected, concomitant with lower levels of CDK1, when compared to the control group. Decitabine 12-15 H3 histone pseudogene 16 Homo sapiens 45-48 24788149-0 2014 Lipotoxic effect of p21 on free fatty acid-induced steatosis in L02 cells. Fatty Acids, Nonesterified 27-42 H3 histone pseudogene 16 Homo sapiens 20-23 24765160-7 2014 Furthermore, damnacanthal-mediated apoptosis involves the sustained activation of p21, leading to the transcription of p53 and the Bax gene. damnacanthal 13-25 H3 histone pseudogene 16 Homo sapiens 82-85 24765160-8 2014 Overall, the present study provided significant evidence demonstrating that p53-mediated damnacanthal induced apoptosis through the activation of p21 and caspase-7. damnacanthal 89-101 H3 histone pseudogene 16 Homo sapiens 146-149 24788149-4 2014 We therefore analyzed the L02 cells with MG132 and siRNA treatment for different expression of p21 related to lipid accumulation and lipotoxicity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 41-46 H3 histone pseudogene 16 Homo sapiens 95-98 24788149-6 2014 Treatment with 1 mM FFA for 48 hr induced magnificent intracellular lipid accumulation and increased oxidative stress in p21 overload L02 cells compared to that in p21 knockdown L02 cells. Fatty Acids, Nonesterified 20-23 H3 histone pseudogene 16 Homo sapiens 121-124 24765160-0 2014 Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cells. damnacanthal 0-12 H3 histone pseudogene 16 Homo sapiens 94-97 24788149-3 2014 This study aimed to investigate the effects of p21 on free fatty acid (FFA)-induced steatosis in L02 cells. Fatty Acids, Nonesterified 54-69 H3 histone pseudogene 16 Homo sapiens 47-50 24788149-6 2014 Treatment with 1 mM FFA for 48 hr induced magnificent intracellular lipid accumulation and increased oxidative stress in p21 overload L02 cells compared to that in p21 knockdown L02 cells. Fatty Acids, Nonesterified 20-23 H3 histone pseudogene 16 Homo sapiens 164-167 24788149-3 2014 This study aimed to investigate the effects of p21 on free fatty acid (FFA)-induced steatosis in L02 cells. Fatty Acids, Nonesterified 71-74 H3 histone pseudogene 16 Homo sapiens 47-50 24834497-1 2014 : p21 is a master regulator of HIV replication in macrophages through dNTP synthesis block. Parathion 70-74 H3 histone pseudogene 16 Homo sapiens 2-5 24762088-9 2014 A stable overexpression of miR-125b in human melanoma cell line Mel-Juso resulted in a G0/G1 cell cycle block and emergence of large cells expressing senescence markers: senescence-associated beta-galactosidase, p21, p27 and p53. mir-125b 27-35 H3 histone pseudogene 16 Homo sapiens 212-215 24692690-6 2014 At higher concentrations, AsA induced apoptosis of osteosarcoma cells, possibly with the involvement of p21. Ascorbic Acid 26-29 H3 histone pseudogene 16 Homo sapiens 104-107 24398465-2 2014 L-Lys HF (C6H15FN2O2), crystallizes in a monoclinic system with space group P21, a=5.464(1)A, b=7.4717(15)A, c=10.252(2)A, alpha=gamma=90 , beta=99.17(3) , Z=2, rhoc=1.336Mg/m(3), rhom=1.335(2)Mg/m(3). c6h15fn2o2 10-20 H3 histone pseudogene 16 Homo sapiens 76-79 24708484-0 2014 P21 and CD166 as predictive markers of poor response and outcome after fluorouracil-based chemoradiotherapy for the patients with rectal cancer. Fluorouracil 71-83 H3 histone pseudogene 16 Homo sapiens 0-3 24708484-9 2014 CONCLUSION: These show high p21 and CD166 expression at the pretreatment biopsy were associated with tumor regression and poor prognosis in patients treated with 5-FU based CRT. Fluorouracil 162-166 H3 histone pseudogene 16 Homo sapiens 28-31 24485799-4 2014 In this study, we investigate whether combined treatment with romidepsin and bortezomib would induce apoptosis in A549 NSCLC cells by activating cell cycle arrest, enhanced generation of p21 and p53, down-regulation of matrix metalloproteinases (MMPs) 2,9 also altering the acetylation status of histone proteins. Bortezomib 77-87 H3 histone pseudogene 16 Homo sapiens 187-190 24380881-4 2014 BTZ-treated HTLA-230 cells down-regulated p53 and up-regulated p21, favoring cell survival. Bortezomib 0-3 H3 histone pseudogene 16 Homo sapiens 63-66 24380881-5 2014 The inhibition of HO-1 activity obtained by Zinc (II) protoprophyrin IX (ZnPPIX) was able to significantly increase the pro-apoptotic effect of BTZ in a p53- and p21-independent way. zinc (ii) protoprophyrin ix 44-71 H3 histone pseudogene 16 Homo sapiens 162-165 24380881-5 2014 The inhibition of HO-1 activity obtained by Zinc (II) protoprophyrin IX (ZnPPIX) was able to significantly increase the pro-apoptotic effect of BTZ in a p53- and p21-independent way. zinc protoporphyrin 73-79 H3 histone pseudogene 16 Homo sapiens 162-165 24380881-5 2014 The inhibition of HO-1 activity obtained by Zinc (II) protoprophyrin IX (ZnPPIX) was able to significantly increase the pro-apoptotic effect of BTZ in a p53- and p21-independent way. Bortezomib 144-147 H3 histone pseudogene 16 Homo sapiens 162-165 24384472-8 2014 Through this study, we have provided the first evidence on the pivotal role of arginine 213 that determines the p53 mediated functions of p21 in human cancer cells. Arginine 79-87 H3 histone pseudogene 16 Homo sapiens 138-141 24692711-4 2014 Nobiletin induced cell-cycle arrest at the G0/G1 phase by suppressing ERK1/2 activity, with concomitant cyclin-D1 suppression and p21 up-regulation. nobiletin 0-9 H3 histone pseudogene 16 Homo sapiens 130-133 24485799-5 2014 Our data show that combination of romidepsin and bortezomib caused cell cycle arrest at Sub G0-G1 transition, up-regulation of cell cycle protein p21 and tumour suppressor protein p53. Bortezomib 49-59 H3 histone pseudogene 16 Homo sapiens 146-149 24635079-8 2014 ATRA also induced G1 cell-cycle arrest, inhibited the expression of cyclin D1/cyclin-dependent kinase (CDK)4 and cyclinE/CDK2, and increased the expression of the cyclin-dependent kinase inhibitors p21 and p27. Tretinoin 0-4 H3 histone pseudogene 16 Homo sapiens 198-201 24535104-5 2014 Therefore, our studies showed that RC-6 can increase p16 and p21 protein levels and induce cellular senescence in NT2 cells. rc-6 35-39 H3 histone pseudogene 16 Homo sapiens 61-64 24476133-7 2014 We observed that administration of MK-2206, an allosteric AKT inhibitor, increased levels of reactive oxygen species, up-regulated the microRNA miR-182 and several senescence-associated genes (including p16, p53, p21, and beta-galactosidase), and drove leiomyoma cells into stress-induced premature senescence (SIPS). MK 2206 35-42 H3 histone pseudogene 16 Homo sapiens 213-216 24573532-8 2014 In addition, PFT-alpha (a p53 inhibitor) reduced the apoptotic rates and the expression of p53, p21, caspase-3 and caspase-9 induced by tangeretin, indicating that tangeretin-induced apoptosis was p53-dependent. tangeretin 136-146 H3 histone pseudogene 16 Homo sapiens 96-99 24931021-9 2014 CONCLUSIONS: Metformin may inhibit the proliferation of Fadu cells by inducing the cell cycle arrest in G1 phase mediated in part by AMPK and P21. Metformin 13-22 H3 histone pseudogene 16 Homo sapiens 142-145 24931021-6 2014 RESULTS: Metformin inhibited the proliferation of Fadu cells in a dose-and time-dependent manner.Flow cytometry showed that cell cycle arrest in G1 phase was induced by metformin in Fadu cells.Immunocytochemistry showed the expressions of both AMPK and P21 in cells treated with metformin were higher than those in cells untreated with metformin. Metformin 9-18 H3 histone pseudogene 16 Homo sapiens 253-256 24931021-6 2014 RESULTS: Metformin inhibited the proliferation of Fadu cells in a dose-and time-dependent manner.Flow cytometry showed that cell cycle arrest in G1 phase was induced by metformin in Fadu cells.Immunocytochemistry showed the expressions of both AMPK and P21 in cells treated with metformin were higher than those in cells untreated with metformin. Metformin 169-178 H3 histone pseudogene 16 Homo sapiens 253-256 24323562-0 2014 p21 overexpression sensitizes osteosarcoma U2OS cells to cisplatin via evoking caspase-3 and Bax/Bcl-2 cascade. Cisplatin 57-66 H3 histone pseudogene 16 Homo sapiens 0-3 24323562-7 2014 However, U2O3-p21 cells underwent more obvious apoptotic morphological changes than U2OS and U2OS-vec cells after being treated with cisplatin (5 mug) for 72 h. Besides, increased expression of cleaved caspase-3 and Bax/Bcl-2 ratio was observed in cisplatin-treated U2O3-p21 cells. Cisplatin 133-142 H3 histone pseudogene 16 Homo sapiens 14-17 24323562-7 2014 However, U2O3-p21 cells underwent more obvious apoptotic morphological changes than U2OS and U2OS-vec cells after being treated with cisplatin (5 mug) for 72 h. Besides, increased expression of cleaved caspase-3 and Bax/Bcl-2 ratio was observed in cisplatin-treated U2O3-p21 cells. Cisplatin 133-142 H3 histone pseudogene 16 Homo sapiens 271-274 24323562-7 2014 However, U2O3-p21 cells underwent more obvious apoptotic morphological changes than U2OS and U2OS-vec cells after being treated with cisplatin (5 mug) for 72 h. Besides, increased expression of cleaved caspase-3 and Bax/Bcl-2 ratio was observed in cisplatin-treated U2O3-p21 cells. Cisplatin 248-257 H3 histone pseudogene 16 Homo sapiens 14-17 24323562-8 2014 These data clearly indicated that exogenous p21 gene transfection could enhance the cisplatin-induced cytotoxicity against human osteosarcoma U2OS cells, at least in part, by activating caspase-3 cascade and increasing Bax/Bcl-2 ratio. Cisplatin 84-93 H3 histone pseudogene 16 Homo sapiens 44-47 24607898-0 2014 DNA binding of the p21 repressor ZBTB2 is inhibited by cytosine hydroxymethylation. Cytosine 55-63 H3 histone pseudogene 16 Homo sapiens 19-22 24556504-6 2014 Lovastatin supplementation arrested cells in the G0/G1 phase and enhanced expression levels of p21, whereas the conjugate did not demonstrate cell cycle arrest nor increased p21 expression. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 95-98 24559053-4 2014 X-ray crystallography of [Re(CO)3(dppzBr2)Cl] and [Re(CO)3(dppzBr)(py)]PF6 showed these crystallize in space groups triclinic P1 and monoclinic P2(1/n), respectively. [re(co)3(dppzbr2)cl 25-44 H3 histone pseudogene 16 Homo sapiens 144-150 24658119-1 2014 We previously showed that treating vascular endothelial cells with 3-methylcholanthrene (3MC) caused cell-cycle arrest in the Go/G1 phase; this resulted from the induction of p21 and p27 and a decreased level and activity of the cyclin-dependent kinase, Cdk2. Methylcholanthrene 67-87 H3 histone pseudogene 16 Homo sapiens 175-178 24658119-1 2014 We previously showed that treating vascular endothelial cells with 3-methylcholanthrene (3MC) caused cell-cycle arrest in the Go/G1 phase; this resulted from the induction of p21 and p27 and a decreased level and activity of the cyclin-dependent kinase, Cdk2. Methylcholanthrene 89-92 H3 histone pseudogene 16 Homo sapiens 175-178 24451377-0 2014 The Chinese herb isolate yuanhuacine (YHL-14) induces G2/M arrest in human cancer cells by up-regulating p21 protein expression through an p53 protein-independent cascade. Yuanhuacin 25-36 H3 histone pseudogene 16 Homo sapiens 105-108 24467951-2 2014 Resveratrol (Res) is a promising natural chemotherapeutic agent that regulates many cellular targets including p21, a cip/kip family of cyclin kinase inhibitors involved in DNA damage-induced cell cycle arrest and blocking of DNA replication and repair. Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 111-114 24467951-2 2014 Resveratrol (Res) is a promising natural chemotherapeutic agent that regulates many cellular targets including p21, a cip/kip family of cyclin kinase inhibitors involved in DNA damage-induced cell cycle arrest and blocking of DNA replication and repair. Resveratrol 0-3 H3 histone pseudogene 16 Homo sapiens 111-114 24618722-6 2014 Thiacremonone (0-50 mug/ml) inhibited lung cancer cell growth in a concentration dependent manner through induction of apoptotic cell death accompanied by induction of cleaved caspase-3, -8, -9, Bax, p21 and p53, but decrease of xIAP, cIAP and Bcl2 expression. thiacremonone 0-13 H3 histone pseudogene 16 Homo sapiens 200-203 24618722-9 2014 In an allograft in vivo model, thiacremonone (30 mg/kg) also inhibited tumor growth accompanied with the reduction of PRDX6 expression and glutathione peroxidase activity, but increased expression of cleaved caspase-3, -8, -9, Bax, p21 and p53. thiacremonone 31-44 H3 histone pseudogene 16 Homo sapiens 232-235 24451377-0 2014 The Chinese herb isolate yuanhuacine (YHL-14) induces G2/M arrest in human cancer cells by up-regulating p21 protein expression through an p53 protein-independent cascade. Yuanhuacin 38-44 H3 histone pseudogene 16 Homo sapiens 105-108 24598942-5 2014 Further studies demonstrated that zardaverine induced G0/G1 phase cell cycle arrest of sensitive HCC cells through dysregulating cell cycle-associated proteins, including Cdk4, Cdk6, Cdk2, Cyclin A, Cyclin E, p21 and Rb. zardaverine 34-45 H3 histone pseudogene 16 Homo sapiens 209-212 24552166-1 2014 5d and 3d hybrid solid-state oxide Ca2FeOsO6 crystallizes into an ordered double-perovskite structure with a space group of P21/n with high-pressures and temperatures. Oxides 29-34 H3 histone pseudogene 16 Homo sapiens 124-127 24492005-3 2014 We demonstrate that G9a upregulates p21 via interaction with PCAF, and provide evidence that the activating complex is recruited to the p21 promoter upon DNA damage-inducing agent etoposide treatment. Etoposide 180-189 H3 histone pseudogene 16 Homo sapiens 136-139 24552166-1 2014 5d and 3d hybrid solid-state oxide Ca2FeOsO6 crystallizes into an ordered double-perovskite structure with a space group of P21/n with high-pressures and temperatures. ca2feoso6 35-44 H3 histone pseudogene 16 Homo sapiens 124-127 24596384-6 2014 Additionally, quinuclidinone 2 induced G1 phase arrest presumably sensitizing breast cancer cells to apoptosis by increasing expression of p21. 1-azabicyclo[2.2.2]octan-2-one 14-28 H3 histone pseudogene 16 Homo sapiens 139-142 24595168-4 2014 METHODOLOGY/PRINCIPAL FINDINGS: We have shown here that caffeine up-regulates the tumor suppressor proteins p16, p21, p53 and Cav-1, and reduces the expression/secretion of various cytokines (IL-6, TGF-beta, SDF-1 and MMP-2), and down-regulates alpha-SMA. Caffeine 56-64 H3 histone pseudogene 16 Homo sapiens 113-116 24286391-9 2014 OFLX significantly upregulated the expression of p21 and bax genes. Ofloxacin 0-4 H3 histone pseudogene 16 Homo sapiens 49-52 23934182-1 2014 Our recent study showing association of hyperhomocysteinemia and hypomethioninemia in breast cancer and other studies indicating association of hyperhomocysteinemia with metastasis and development of drug resistance in breast cancer cells treated with homocysteine lead us to hypothesize that homocysteine might modulate the expression of certain tumor suppressors, i.e., RASSF1, RARbeta1, CNND1, BRCA1, and p21, and might influence prognostic markers such as BNIP3 by inducing epigenetic alteration. Homocysteine 149-161 H3 histone pseudogene 16 Homo sapiens 408-411 23884787-4 2014 We found that EGCG treatment results in increased expression of KLF4 and alters expression of the KLF4 target genes p21, CDK4, and cyclin D1. epigallocatechin gallate 14-18 H3 histone pseudogene 16 Homo sapiens 116-119 24637250-8 2014 The results indicated that CIT inhibited HUVECs proliferation and the cells were arrested at G0/G1 phase, which is associated with decreased levels of cyclinD1 and increased expression of p53 and p21. citreoviridin 27-30 H3 histone pseudogene 16 Homo sapiens 196-199 24397737-6 2014 Lycopene induced strong and sustained activation of the ERK1/2, with concomitant cyclin D1 suppression and p21 upregulation in these three cell lines. Lycopene 0-8 H3 histone pseudogene 16 Homo sapiens 107-110 24286391-10 2014 In conclusion, the study revealed that photosensitized OFLX induced apoptosis via ROS-mediated DNA damage, destabilization of lysosomal and mitochondrial membrane, and upregulation of p21, bax, and caspase-3 genes. Ofloxacin 55-59 H3 histone pseudogene 16 Homo sapiens 184-187 23934681-7 2014 We also found that GW9662 attenuated OA-induced upregulation of C/EBPbeta, an important regulator of leukemic differentiation, and p21, which is a potent inhibitor of CDKs that can inhibit phosphorylation of Rb by cyclin D1-CDK4 complexes. 2-chloro-5-nitrobenzanilide 19-25 H3 histone pseudogene 16 Homo sapiens 131-134 24218335-12 2014 The influence on the level of cylinB1, CDK1, and p21 was also observed after bufalin treatment, and the relationship between Hsp27 and the cell cycle-related proteins mentioned above deserves much more research. bufalin 77-84 H3 histone pseudogene 16 Homo sapiens 49-52 24365999-5 2014 However, p53-null and p21-null cells were more resistant to the antiproliferative and apoptotic effects of MHY336 than p53-wt cells. MHY336 107-113 H3 histone pseudogene 16 Homo sapiens 22-25 24365999-6 2014 The same result was achieved by knocking down p53 and p21 with siRNA in p53-wt cells, indicating that p53 and p21 play a crucial role in MHY336-induced cell cycle arrest and apoptosis. MHY336 137-143 H3 histone pseudogene 16 Homo sapiens 54-57 24365999-6 2014 The same result was achieved by knocking down p53 and p21 with siRNA in p53-wt cells, indicating that p53 and p21 play a crucial role in MHY336-induced cell cycle arrest and apoptosis. MHY336 137-143 H3 histone pseudogene 16 Homo sapiens 110-113 24399193-5 2014 Moreover, the results clearly showed that kaempferol causes a strong inhibition of the activation of the EGFR/p38 signaling pathways, upregulation of p21 expression and downregulation of cyclin B1 expression in human RCC cells, together with activation of PARP cleavages, induction of apoptotic death and inhibition of cell growth. kaempferol 42-52 H3 histone pseudogene 16 Homo sapiens 150-153 24365999-0 2014 A novel oxiranylchromenone derivative, MHY336, induces apoptosis and cell cycle arrest via a p53- and p21-dependent pathway in HCT116 human colon cancer cells. oxiranylchromenone 8-26 H3 histone pseudogene 16 Homo sapiens 102-105 24365999-0 2014 A novel oxiranylchromenone derivative, MHY336, induces apoptosis and cell cycle arrest via a p53- and p21-dependent pathway in HCT116 human colon cancer cells. MHY336 39-45 H3 histone pseudogene 16 Homo sapiens 102-105 24365999-1 2014 In this study, we compared cytotoxicity, cell cycle distribution, and apoptosis on MHY336 treatment in three human colorectal carcinoma HCT116 cells: p53+/+ (p53-wt), p53-/- (p53-null), and p21-/- (p21-null), as well as investigated the roles of p53 and p21 in cell death. MHY336 83-89 H3 histone pseudogene 16 Homo sapiens 190-193 24365999-1 2014 In this study, we compared cytotoxicity, cell cycle distribution, and apoptosis on MHY336 treatment in three human colorectal carcinoma HCT116 cells: p53+/+ (p53-wt), p53-/- (p53-null), and p21-/- (p21-null), as well as investigated the roles of p53 and p21 in cell death. MHY336 83-89 H3 histone pseudogene 16 Homo sapiens 198-201 24365999-1 2014 In this study, we compared cytotoxicity, cell cycle distribution, and apoptosis on MHY336 treatment in three human colorectal carcinoma HCT116 cells: p53+/+ (p53-wt), p53-/- (p53-null), and p21-/- (p21-null), as well as investigated the roles of p53 and p21 in cell death. MHY336 83-89 H3 histone pseudogene 16 Homo sapiens 198-201 25337571-9 2014 Ethanol also increased the phosphorylation of p53 and p53 activation was followed by an increase in the p21 tumor suppressor protein accompanied by a gradual decrease in phospho-Rb protein. Ethanol 0-7 H3 histone pseudogene 16 Homo sapiens 104-107 24343584-3 2014 Both oxyhydroxides crystallize in a P2(1)/c monoclinic unit cell and have a structure resembling that of the related salts. oxyhydroxides 5-18 H3 histone pseudogene 16 Homo sapiens 36-41 24211300-5 2014 BIM-23244 (SS2R/SS5R) led to p21 increment only in PC-3 cells, and to pERK1/2 reduction in both cell lines. bim 0-3 H3 histone pseudogene 16 Homo sapiens 29-32 24643130-3 2014 Here, we reported that capsaicin had a profound anti-proliferative effect on human colon cancer cells via inducing cell cycle G0/G1 phase arrest and apoptosis, which was associated with an increase of p21, Bax and cleaved PARP. Capsaicin 23-32 H3 histone pseudogene 16 Homo sapiens 201-204 24587053-6 2014 In addition, TCDD exposure altered the expression of senescence marker proteins, such as p16, p21 and p-Rb, in both dose- and time-dependent manners. Polychlorinated Dibenzodioxins 13-17 H3 histone pseudogene 16 Homo sapiens 94-97 24327721-11 2014 Naproxen caused an accumulation of cells at the G1 phase mediated through cyclin-dependent kinase 4, cyclin D1, and p21. Naproxen 0-8 H3 histone pseudogene 16 Homo sapiens 116-119 24516636-9 2014 (-)-Epicatechin enhanced Chk2 phosphorylation and p21 induction when combined with radiation in cancer, but not normal, cells. Catechin 0-15 H3 histone pseudogene 16 Homo sapiens 50-53 24437929-2 2014 (NH4)2PaF7, K2PaF7, Rb2PaF7, and Cs2PaF7 were found to crystallize in the monoclinic space group P21/c for the ammonium compound and C2/c for the K(+)-, Rb(+)-, and Cs(+)-containing compounds, with nine-coordinate Pa forming infinite chains through fluorine bridges. nh4) 1-5 H3 histone pseudogene 16 Homo sapiens 97-102 24437929-2 2014 (NH4)2PaF7, K2PaF7, Rb2PaF7, and Cs2PaF7 were found to crystallize in the monoclinic space group P21/c for the ammonium compound and C2/c for the K(+)-, Rb(+)-, and Cs(+)-containing compounds, with nine-coordinate Pa forming infinite chains through fluorine bridges. Protactinium 6-8 H3 histone pseudogene 16 Homo sapiens 97-102 24384380-0 2014 Shikonin induces cell cycle arrest in human gastric cancer (AGS) by early growth response 1 (Egr1)-mediated p21 gene expression. shikonin 0-8 H3 histone pseudogene 16 Homo sapiens 108-111 24241211-6 2014 In addition, BI-D1870 also induced G2/M arrest by modulating the expression of p21 and other cell cycle regulators. BI D1870 13-21 H3 histone pseudogene 16 Homo sapiens 79-82 24189165-4 2014 It was also identified that the transcriptional activation of p53 and the activation of p21 promoter by spermine are related to the induction of autophagy in reporter gene assay. Spermine 104-112 H3 histone pseudogene 16 Homo sapiens 88-91 24342076-9 2014 These findings identify p21 as a key determinant of DOX resistance downstream of FAK in cardiomyocytes and indicate that cardiac-restricted enhancement of the FAK/p21 signaling axis might be an effective strategy to preserve myocardial function in patients receiving anthracycline chemotherapy. Doxorubicin 52-55 H3 histone pseudogene 16 Homo sapiens 24-27 24430184-5 2014 Using cultured lung cancer cells, we showed that SAG knockdown suppressed growth and survival, inactivated both NF-kappaB and mTOR pathways, and resulted in accumulation of tumor suppressor substrates, including p21, p27, NOXA, and BIM. sagopilone 49-52 H3 histone pseudogene 16 Homo sapiens 212-215 24342076-9 2014 These findings identify p21 as a key determinant of DOX resistance downstream of FAK in cardiomyocytes and indicate that cardiac-restricted enhancement of the FAK/p21 signaling axis might be an effective strategy to preserve myocardial function in patients receiving anthracycline chemotherapy. Anthracyclines 267-280 H3 histone pseudogene 16 Homo sapiens 24-27 24297112-8 2014 Furthermore, the activation of the p38 kinase promoted the activation of p53 and its downstream target p21, and further caused caspase-9 and -3 activation, as demonstrated by evidence showing that the p38 inhibitor SB203580 not only blocked the phosphorylation of p38 but also reduced the activation of p53, p21 and caspase-9 and -3. SB 203580 215-223 H3 histone pseudogene 16 Homo sapiens 103-106 24293651-5 2014 Multiple nanometer distances in the p21-RE and BAX-RE, measured using a nucleotide-independent nitroxide probe and double-electron-electron-resonance spectroscopy, were used to derive molecular models of unbound REs from pools of all-atom structures generated by Monte-Carlo simulations, thus enabling analyses to reveal sequence-dependent DNA shape features of unbound REs in solution. Hydroxylamine 95-104 H3 histone pseudogene 16 Homo sapiens 36-39 24297112-5 2014 Moreover, oridonin increased the expression of p-p53 with a concomitant increase in p21 in the SW1990 cells. oridonin 10-18 H3 histone pseudogene 16 Homo sapiens 84-87 24297112-8 2014 Furthermore, the activation of the p38 kinase promoted the activation of p53 and its downstream target p21, and further caused caspase-9 and -3 activation, as demonstrated by evidence showing that the p38 inhibitor SB203580 not only blocked the phosphorylation of p38 but also reduced the activation of p53, p21 and caspase-9 and -3. SB 203580 215-223 H3 histone pseudogene 16 Homo sapiens 308-311 25551711-3 2014 The product 3,3"-[(4-Hydroxyphenyl)methyl]bis-(4-hydroxy-2H-chromen-2-one) ethanol crystallizes in the monoclinic system, space group P2(1)/n. 3,3"-[(4-hydroxyphenyl)methyl]bis-(4-hydroxy-2h-chromen-2-one) ethanol 12-84 H3 histone pseudogene 16 Homo sapiens 136-141 24640606-5 2014 Further studies indicated that kirenol treatment triggered the arrest of cell cycle S period which might resulted from the up-regulation of phosphorylation of p53 (Ser 6 and Ser 37) and expression of p21 protein. kirenol 31-38 H3 histone pseudogene 16 Homo sapiens 200-203 24339045-1 2014 The reaction of (NO2 )(CF3 SO3 ) and elemental palladium in oleum (65 % SO3 ) leads to violet single crystals of Pd(HS2 O7 )2 (monoclinic, P21 /c, Z=2, a=927.80(9), b=682.58(7), c=920.84(9) pm, beta=117.756(2) , wR2 =0.0439). Nitrogen Dioxide 17-20 H3 histone pseudogene 16 Homo sapiens 139-142 24339045-1 2014 The reaction of (NO2 )(CF3 SO3 ) and elemental palladium in oleum (65 % SO3 ) leads to violet single crystals of Pd(HS2 O7 )2 (monoclinic, P21 /c, Z=2, a=927.80(9), b=682.58(7), c=920.84(9) pm, beta=117.756(2) , wR2 =0.0439). Palladium 47-56 H3 histone pseudogene 16 Homo sapiens 139-142 24339045-1 2014 The reaction of (NO2 )(CF3 SO3 ) and elemental palladium in oleum (65 % SO3 ) leads to violet single crystals of Pd(HS2 O7 )2 (monoclinic, P21 /c, Z=2, a=927.80(9), b=682.58(7), c=920.84(9) pm, beta=117.756(2) , wR2 =0.0439). Palladium 113-115 H3 histone pseudogene 16 Homo sapiens 139-142 24289924-3 2014 We further show that cellular ATP level might act as a molecular switch for Thr55 phosphorylation on the p21 promoter, indicating that TAF1 is a cellular ATP sensor. Adenosine Triphosphate 30-33 H3 histone pseudogene 16 Homo sapiens 105-108 24289924-3 2014 We further show that cellular ATP level might act as a molecular switch for Thr55 phosphorylation on the p21 promoter, indicating that TAF1 is a cellular ATP sensor. Adenosine Triphosphate 154-157 H3 histone pseudogene 16 Homo sapiens 105-108 24289924-4 2014 Upon DNA damage, cells undergo PARP-1-dependent ATP depletion, which is correlated with reduced TAF1 kinase activity and Thr55 phosphorylation, resulting in p21 activation. Adenosine Triphosphate 48-51 H3 histone pseudogene 16 Homo sapiens 157-160 24415827-1 2014 The crystal structure of the anticancer drug oxaliplatin, [Pt(R,R-DACH)(oxalate)] (DACH = diaminocyclohexane), was first reported in the non-centrosymmetric space group P21, confirming the sole presence of the R,R enantiomer of the DACH ligand [M. A. Bruck et al., Inorg. Oxaliplatin 45-56 H3 histone pseudogene 16 Homo sapiens 169-172 24415827-1 2014 The crystal structure of the anticancer drug oxaliplatin, [Pt(R,R-DACH)(oxalate)] (DACH = diaminocyclohexane), was first reported in the non-centrosymmetric space group P21, confirming the sole presence of the R,R enantiomer of the DACH ligand [M. A. Bruck et al., Inorg. pt(r,r-dach)(oxalate) 59-80 H3 histone pseudogene 16 Homo sapiens 169-172 24415827-1 2014 The crystal structure of the anticancer drug oxaliplatin, [Pt(R,R-DACH)(oxalate)] (DACH = diaminocyclohexane), was first reported in the non-centrosymmetric space group P21, confirming the sole presence of the R,R enantiomer of the DACH ligand [M. A. Bruck et al., Inorg. 1,2-cyclohexanediamine 83-87 H3 histone pseudogene 16 Homo sapiens 169-172 24337632-7 2014 LY294002 induced cell cycle arrest at G0/G1 in SNU-449 and Mahlavu cells by decreasing expression of CDK2, CDK4, CycD1, CycD3, CycE, CycA and increasing expression of p21 and p27 as well; it also caused a decrease in the E2F1 transcriptional activity through declining phosphorylated Rb. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 0-8 H3 histone pseudogene 16 Homo sapiens 167-170 24401087-12 2014 Moreover, Stat6 overexpression and knockdown, respectively, increased or prevented the induction of p21 and p27 gene expression by progesterone. Progesterone 131-143 H3 histone pseudogene 16 Homo sapiens 100-103 24467547-3 2014 FUR concentration-dependently inhibited cell proliferation and blocked the cell cycle progressions in G1 phase by down-regulating the protein levels of cyclin D1 and CDK6, and up-regulating those of p21 and p27 in 95-D cells. furanodiene 0-3 H3 histone pseudogene 16 Homo sapiens 199-202 24036327-9 2014 CONCLUSIONS: PPARgamma signaling pathway, via stimulating p21 and inhibiting cyclin D1, may play an important role in the anti-proliferative effects of carotenoid and rosiglitazone combination on K562 cells. Carotenoids 152-162 H3 histone pseudogene 16 Homo sapiens 58-61 23983146-8 2014 In addition, neferine could induce p53 and its effector protein p21 and downregulation of cell cycle regulatory protein cyclin D1 thereby inducing G1 cell cycle arrest. neferine 13-21 H3 histone pseudogene 16 Homo sapiens 64-67 24036327-9 2014 CONCLUSIONS: PPARgamma signaling pathway, via stimulating p21 and inhibiting cyclin D1, may play an important role in the anti-proliferative effects of carotenoid and rosiglitazone combination on K562 cells. Rosiglitazone 167-180 H3 histone pseudogene 16 Homo sapiens 58-61 24036327-8 2014 Moreover, GW9662 and PPARgamma siRNA also significantly attenuated the up-regulation of p21 and down-regulation of cyclin D1 caused by carotenoids and rosiglitazone. Carotenoids 135-146 H3 histone pseudogene 16 Homo sapiens 88-91 24877132-5 2014 3beta-Adiol (10 nM) is the sole ligand decreasing cell proliferation and increasing p21 levels. 3beta-adiol 0-11 H3 histone pseudogene 16 Homo sapiens 84-87 24036327-8 2014 Moreover, GW9662 and PPARgamma siRNA also significantly attenuated the up-regulation of p21 and down-regulation of cyclin D1 caused by carotenoids and rosiglitazone. Rosiglitazone 151-164 H3 histone pseudogene 16 Homo sapiens 88-91 25162034-7 2014 Additionally, H2O2 treatment reduced eNOS expression, enhanced p21 expression, and dephosphorylated (activated) retinoblastoma (Rb) protein. Hydrogen Peroxide 14-18 H3 histone pseudogene 16 Homo sapiens 63-66 24345738-6 2014 Conversely, nutlin-3 induced a p21-dependent growth arrest, rather than apoptosis, and was slightly toxic on HMC-hTERT. nutlin 3 12-20 H3 histone pseudogene 16 Homo sapiens 31-34 25482947-7 2014 Synthetic inhibitors of mTOR (temsirolimus, LY294.002 and PP242) also impaired actinomycin D triggered p53 stabilization and induction of p21. ly294 44-49 H3 histone pseudogene 16 Homo sapiens 138-141 25482947-7 2014 Synthetic inhibitors of mTOR (temsirolimus, LY294.002 and PP242) also impaired actinomycin D triggered p53 stabilization and induction of p21. PP242 58-63 H3 histone pseudogene 16 Homo sapiens 138-141 25482947-7 2014 Synthetic inhibitors of mTOR (temsirolimus, LY294.002 and PP242) also impaired actinomycin D triggered p53 stabilization and induction of p21. Dactinomycin 79-92 H3 histone pseudogene 16 Homo sapiens 138-141 25486476-4 2014 We have previously shown that PD0332991 inhibits not only CDK4/6 activity but also the activation by phosphorylation of the bulk of cyclin D-CDK4 complexes stabilized by p21 binding. palbociclib 30-39 H3 histone pseudogene 16 Homo sapiens 170-173 25486476-6 2014 Indeed, whereas PD0332991 inhibits the phosphorylation and activity of p21-bound CDK4/6, it specifically stabilized activated cyclin D3-CDK4/6 complexes devoid of p21 and p27. palbociclib 16-25 H3 histone pseudogene 16 Homo sapiens 71-74 25700359-5 2014 TEA treatment also caused significant increases in mRNA and protein levels of tumor-suppressor proteins p53 and p21, and the upregulation was attenuated by pretreatment of NAC. Tetraethylammonium 0-3 H3 histone pseudogene 16 Homo sapiens 112-115 26166893-2 2014 Orange-yellow tetrakis(4-methylpyridinium) bis(4-methylpyridine)-gamma-octamolybdate 1 crystallizes in space group P21/c with a = 11.586(2) A, b = 15.526(2) A, c = 16.247(2) A, beta = 118.753(1)o, Z = 2. orange-yellow tetrakis(4-methylpyridinium) bis(4-methylpyridine)-gamma-octamolybdate 0-84 H3 histone pseudogene 16 Homo sapiens 115-118 26629942-11 2014 In addition, calcitriol increased p21 expression and promoter activity. Calcitriol 13-23 H3 histone pseudogene 16 Homo sapiens 34-37 26629942-13 2014 Thus, our results suggested that calcitriol inhibited HeLa S3 cell proliferation by decreasing HCCR-1 expression and increasing p21 expression. Calcitriol 33-43 H3 histone pseudogene 16 Homo sapiens 128-131 25116350-0 2014 Up-regulation of P21 inhibits TRAIL-mediated extrinsic apoptosis, contributing resistance to SAHA in acute myeloid leukemia cells. Vorinostat 93-97 H3 histone pseudogene 16 Homo sapiens 17-20 25116350-2 2014 In this study we examined the effect of altered p21 expression on the sensitivity of acute myeloid leukemia cells in response to HDAC inhibitor SAHA treatment and investigated the underlying mechanism. Vorinostat 144-148 H3 histone pseudogene 16 Homo sapiens 48-51 25116350-8 2014 Enforced expression of p21 in HL60 cells reduced sensitivity to SAHA and blocked TRAIL-mediated apoptosis. Vorinostat 64-68 H3 histone pseudogene 16 Homo sapiens 23-26 25116350-9 2014 Conversely, p21 silencing in NB4 cells enhanced SAHA-mediated apoptosis and lethality. Vorinostat 48-52 H3 histone pseudogene 16 Homo sapiens 12-15 25116350-10 2014 Finally, we found that combined treatment with SAHA and rapamycin down-regulated p21 and enhanced apoptosis in AML cells. Vorinostat 47-51 H3 histone pseudogene 16 Homo sapiens 81-84 25116350-10 2014 Finally, we found that combined treatment with SAHA and rapamycin down-regulated p21 and enhanced apoptosis in AML cells. Sirolimus 56-65 H3 histone pseudogene 16 Homo sapiens 81-84 25116350-11 2014 CONCLUSION: We conclude that up-regulated p21 expression mediates resistance to SAHA via inhibition of TRAIL apoptotic pathway. Vorinostat 80-84 H3 histone pseudogene 16 Homo sapiens 42-45 25116350-12 2014 P21 may serve as a candidate biomarker to predict responsiveness or resistance to SAHA-based therapy in AML patients. Vorinostat 82-86 H3 histone pseudogene 16 Homo sapiens 0-3 25116350-13 2014 In addition, rapamycin may be an effective agent to override p21-mediated resistance to SAHA in AML patients. Sirolimus 13-22 H3 histone pseudogene 16 Homo sapiens 61-64 25116350-13 2014 In addition, rapamycin may be an effective agent to override p21-mediated resistance to SAHA in AML patients. Vorinostat 88-92 H3 histone pseudogene 16 Homo sapiens 61-64 24169561-9 2014 Furthermore, CRT knock-down suppressed the ovarian steroid-stimulated PRL and IGFBP1 expression and morphological differentiation, and silencing of EPAC2 or CRT significantly increased senescence-associated beta-galactosidase activity with enhanced p21 expression and decreased p53 expression. Steroids 51-58 H3 histone pseudogene 16 Homo sapiens 249-252 26168133-7 2014 Berberine induced cell cycle arrest at the G2/M phase by upregulation of p53 and p21 expression and suppressed cyclin B1, cyclin-dependent kinase 1 (cdc2), cdc25c, and phosphorylated retinoblastoma tumor-suppressor protein (pRb) expression. Berberine 0-9 H3 histone pseudogene 16 Homo sapiens 81-84 26168133-9 2014 Inhibition of phosphatidylinositol 3-kinase (PI3K)/Akt with LY294002 (LY) and p38 kinase with SB203580 (SB), respectively, decreased berberine-induced p53 and p21 expression and restored cell proliferation and expression of cyclin B1, cdc2, cdc25c, and pRb cell cycle progression proteins. Berberine 133-142 H3 histone pseudogene 16 Homo sapiens 159-162 24177866-2 2014 The Cl1 Single crystals were successfully grown by the slow evaporation method at a constant temperature 35 C. Single crystal XRD confirms the Cl1 molecule belongs to monoclinic crystal system and space group P21/C with a=10.114, b=11.127, c=14.929 and V=1668.9 and Z=4. cl1 4-7 H3 histone pseudogene 16 Homo sapiens 209-212 24177866-2 2014 The Cl1 Single crystals were successfully grown by the slow evaporation method at a constant temperature 35 C. Single crystal XRD confirms the Cl1 molecule belongs to monoclinic crystal system and space group P21/C with a=10.114, b=11.127, c=14.929 and V=1668.9 and Z=4. cl1 143-146 H3 histone pseudogene 16 Homo sapiens 209-212 24262031-3 2013 [Mn2LAc](ClO4) (DMF)0.5, [Mn2LAc](ClO4) (ACN)0.5, and [Zn2LAc](PF6) crystallized in the space group P2(1)/c, with nearly identical unit-cell dimensions and geometric structures. [Mn2LAc](ClO4) 0-14 H3 histone pseudogene 16 Homo sapiens 100-107 24311505-1 2013 4-Oxo-N-phenyl-4H-chromene-2-carboxamide, C16H11NO3, crystallizes in the space group P2(1)/n and its derivative 7-methoxy-4-oxo-N-p-tolyl-4H-chromene-2-carboxamide, C18H15NO4, forms two polymorphs which crystallize in the space groups P2(1)/c and P1. 4-Oxo-N-phenyl-4H-chromene-2-carboxamide 0-40 H3 histone pseudogene 16 Homo sapiens 85-90 24311505-1 2013 4-Oxo-N-phenyl-4H-chromene-2-carboxamide, C16H11NO3, crystallizes in the space group P2(1)/n and its derivative 7-methoxy-4-oxo-N-p-tolyl-4H-chromene-2-carboxamide, C18H15NO4, forms two polymorphs which crystallize in the space groups P2(1)/c and P1. 4-Oxo-N-phenyl-4H-chromene-2-carboxamide 0-40 H3 histone pseudogene 16 Homo sapiens 235-240 24311505-1 2013 4-Oxo-N-phenyl-4H-chromene-2-carboxamide, C16H11NO3, crystallizes in the space group P2(1)/n and its derivative 7-methoxy-4-oxo-N-p-tolyl-4H-chromene-2-carboxamide, C18H15NO4, forms two polymorphs which crystallize in the space groups P2(1)/c and P1. Anhydrolycorinone 42-51 H3 histone pseudogene 16 Homo sapiens 85-90 24311505-1 2013 4-Oxo-N-phenyl-4H-chromene-2-carboxamide, C16H11NO3, crystallizes in the space group P2(1)/n and its derivative 7-methoxy-4-oxo-N-p-tolyl-4H-chromene-2-carboxamide, C18H15NO4, forms two polymorphs which crystallize in the space groups P2(1)/c and P1. Anhydrolycorinone 42-51 H3 histone pseudogene 16 Homo sapiens 235-240 25552063-3 2014 In experimental studies it was showed that synthetic antineoplastons (A10-3-phenyl-acetyl-amino-2,6-piperidinedione and AS2-1--a mixture of phenylacetic acid and phenylacetylglutamine) were able to prevent the introduction of glutamine into the cell, to block the action of Bcl-2, to activate p53 and p21, to inhibit histone deacetylase, to induce apoptosis. a10-3-phenyl-acetyl-amino-2,6-piperidinedione 70-115 H3 histone pseudogene 16 Homo sapiens 301-304 25552063-3 2014 In experimental studies it was showed that synthetic antineoplastons (A10-3-phenyl-acetyl-amino-2,6-piperidinedione and AS2-1--a mixture of phenylacetic acid and phenylacetylglutamine) were able to prevent the introduction of glutamine into the cell, to block the action of Bcl-2, to activate p53 and p21, to inhibit histone deacetylase, to induce apoptosis. as2-1--a 120-128 H3 histone pseudogene 16 Homo sapiens 301-304 24161784-6 2013 Cell viability assays and cytometric analysis of p53 and p21 null cells indicated that BBR3610-DACH-induced cell cycle arrest was p21-dependent and partially p53-dependent. BBR3610 87-94 H3 histone pseudogene 16 Homo sapiens 57-60 24161784-6 2013 Cell viability assays and cytometric analysis of p53 and p21 null cells indicated that BBR3610-DACH-induced cell cycle arrest was p21-dependent and partially p53-dependent. BBR3610 87-94 H3 histone pseudogene 16 Homo sapiens 130-133 24161784-6 2013 Cell viability assays and cytometric analysis of p53 and p21 null cells indicated that BBR3610-DACH-induced cell cycle arrest was p21-dependent and partially p53-dependent. 1,2-cyclohexanediamine 95-99 H3 histone pseudogene 16 Homo sapiens 57-60 24161784-6 2013 Cell viability assays and cytometric analysis of p53 and p21 null cells indicated that BBR3610-DACH-induced cell cycle arrest was p21-dependent and partially p53-dependent. 1,2-cyclohexanediamine 95-99 H3 histone pseudogene 16 Homo sapiens 130-133 23948751-8 2013 Further studies revealed that LY and PD significantly reversed the inhibitory effect of BA145 on cell cycle regulatory proteins by upregulating hyperphosphorylated retinoblastoma, pRB (S795) and downregulating p21 and cyclin E. More importantly, all these events were reversed by caspase inhibition by Z-VAD-fmk, suggesting that both LY and PD act at the level of caspases to diminish the apoptosis induced by BA145. ba145 88-93 H3 histone pseudogene 16 Homo sapiens 210-213 24203813-4 2013 The structure of Cs[B(S2O7)(SO4)] (P2(1)/c; a=10.4525(6), b=11.3191(14), c=8.2760(8) A; beta=103.206(1); Z=4) combines, for the first time, sulfate and disulfate units into a chain structure. Cesium 17-19 H3 histone pseudogene 16 Homo sapiens 35-42 24203813-4 2013 The structure of Cs[B(S2O7)(SO4)] (P2(1)/c; a=10.4525(6), b=11.3191(14), c=8.2760(8) A; beta=103.206(1); Z=4) combines, for the first time, sulfate and disulfate units into a chain structure. b(s2o7)(so4) 20-32 H3 histone pseudogene 16 Homo sapiens 35-42 24309939-0 2013 Wentilactone A as a novel potential antitumor agent induces apoptosis and G2/M arrest of human lung carcinoma cells, and is mediated by HRas-GTP accumulation to excessively activate the Ras/Raf/ERK/p53-p21 pathway. wentilactone 0-12 H3 histone pseudogene 16 Homo sapiens 202-205 24309939-10 2013 Molecular docking analysis suggested that WA could bind to HRas-GTP, causing accumulation of Ras-GTP and excessive activation of Raf/ERK/p53-p21. Guanosine Triphosphate 64-67 H3 histone pseudogene 16 Homo sapiens 141-144 24309939-10 2013 Molecular docking analysis suggested that WA could bind to HRas-GTP, causing accumulation of Ras-GTP and excessive activation of Raf/ERK/p53-p21. ras-gtp 60-67 H3 histone pseudogene 16 Homo sapiens 141-144 24161692-5 2013 Simultaneously, quinocetone induced HepG2 cell cycle arrest, which was supported by overexpression of p21. quinocetone 16-27 H3 histone pseudogene 16 Homo sapiens 102-105 24304587-6 2013 Low dose SVP treatment also increased acetylation of histone H3 and H4 on p21 promoter, accompanied by up-regulation of p21 and down-regulation of RB phosphorylation. Valproic Acid 9-12 H3 histone pseudogene 16 Homo sapiens 74-77 24304587-6 2013 Low dose SVP treatment also increased acetylation of histone H3 and H4 on p21 promoter, accompanied by up-regulation of p21 and down-regulation of RB phosphorylation. Valproic Acid 9-12 H3 histone pseudogene 16 Homo sapiens 120-123 24304587-7 2013 These observations suggested that a low dose of SVP could induce cell senescence in hepatocarcinoma cells, which might correlate with hyperacetylation of histone H3 and H4, up-regulation of p21, and inhibition of RB phosphorylation. Valproic Acid 48-51 H3 histone pseudogene 16 Homo sapiens 190-193 23787902-8 2013 Ectopic expression of DACH1 enhanced chemosensitivity to 5-fluorouracil (5-FU) by inducing p21 expression in HCC cells. Fluorouracil 57-71 H3 histone pseudogene 16 Homo sapiens 91-94 23787902-8 2013 Ectopic expression of DACH1 enhanced chemosensitivity to 5-fluorouracil (5-FU) by inducing p21 expression in HCC cells. Fluorouracil 73-77 H3 histone pseudogene 16 Homo sapiens 91-94 23625774-9 2013 Furthermore, miR-302a-enhanced cisplatin sensitivity was partially mediated through the down-regulation of p21 in NT2 cells. Cisplatin 31-40 H3 histone pseudogene 16 Homo sapiens 107-110 24085108-7 2013 EA treatment resulted in the increased expression of the tumor suppressor protein p21 and increased the percentage of apoptotic cells. Ellagic Acid 0-2 H3 histone pseudogene 16 Homo sapiens 82-85 25337562-8 2013 The expression of p21 was increased but the phosphorylation of Akt was inhibited in BS-IV-treated YD-10B cells. yd-10b 98-104 H3 histone pseudogene 16 Homo sapiens 18-21 23418094-4 2013 H2 O2 induced apoptosis in the cells through activation of pro-apoptotic p21, Bax, and caspase-3. Hydrogen Peroxide 0-5 H3 histone pseudogene 16 Homo sapiens 73-76 24263099-6 2013 Importantly, Bortezomib inhibits G2/M transition by inhibiting proteasomal degradation of cell cycle regulatory proteins such as p21, thereby preventing cells to enter mitosis, the cell cycle phase in which they are most vulnerable to antitubulin chemotherapeutics. Bortezomib 13-23 H3 histone pseudogene 16 Homo sapiens 129-132 24114842-8 2013 By inhibiting HDAC activity, CQ induced expression of p21, p27, and p53, cell cycle arrest at G1 phase, and cell apoptosis. Clioquinol 29-31 H3 histone pseudogene 16 Homo sapiens 54-57 23907579-4 2013 The result showed that the proliferation rate and colony-forming abilities of gastric cancer cells were significantly suppressed by DHA together with significant suppression of the expressions of proliferation markers (PCNA, cyclin E, and cyclin D1), and upregulation of p21 and p27. artenimol 132-135 H3 histone pseudogene 16 Homo sapiens 271-274 24076166-10 2013 Carbocysteine in CSE stimulated bronchial epithelial cells, reduced: (1) TLR4, LPS binding and p21; (2) IL-8 mRNA and IL-8 release due to IL-1 stimulation; (3) neutrophil chemotactic migration. Carbocysteine 0-13 H3 histone pseudogene 16 Homo sapiens 95-98 23999988-3 2013 Single crystals of LiCN3H4 were obtained using a solvothermal route in liquid ammonia, and the crystal structure was determined at 100 K using single-crystal X-ray diffraction (monoclinic, P2(1)/c, Z = 4, a = 7.251(2) A, b = 4.532(2) A, c = 9.051(2) A, beta = 103.315(3) ). licn3h4 19-26 H3 histone pseudogene 16 Homo sapiens 189-196 23995341-2 2013 The symmetry ambiguity between P2(1) and P2(1)/m of the high temperature polymorph of BiPO4 has been resolved by a neutron diffraction study. bipo4 86-91 H3 histone pseudogene 16 Homo sapiens 31-36 23995341-2 2013 The symmetry ambiguity between P2(1) and P2(1)/m of the high temperature polymorph of BiPO4 has been resolved by a neutron diffraction study. bipo4 86-91 H3 histone pseudogene 16 Homo sapiens 41-46 23933099-0 2013 Simvastatin rises reactive oxygen species levels and induces senescence in human melanoma cells by activation of p53/p21 pathway. Simvastatin 0-11 H3 histone pseudogene 16 Homo sapiens 117-120 23933099-4 2013 Also, the main pathways leading to cell senescence were examined in simvastatin-treated human melanoma cells, and the expression levels of phospho-p53 and p21 were upregulated by simvastatin, suggesting that cell cycle regulators and DNA damage pathways are involved in the onset of senescence. Simvastatin 68-79 H3 histone pseudogene 16 Homo sapiens 155-158 23933099-4 2013 Also, the main pathways leading to cell senescence were examined in simvastatin-treated human melanoma cells, and the expression levels of phospho-p53 and p21 were upregulated by simvastatin, suggesting that cell cycle regulators and DNA damage pathways are involved in the onset of senescence. Simvastatin 179-190 H3 histone pseudogene 16 Homo sapiens 155-158 23933099-7 2013 Collectively, our results demonstrated that simvastatin can induce senescence in human melanoma cells by activation of p53/p21 pathway, and that oxidative stress may be related to this process. Simvastatin 44-55 H3 histone pseudogene 16 Homo sapiens 123-126 23954467-4 2013 Teroxirone caused transient elevation of p53 that activates downstream p21 and procaspase-3 cleavage. teroxirone 0-10 H3 histone pseudogene 16 Homo sapiens 71-74 23831333-3 2013 MDA-MB-231 cells cultured in the presence of DIOA exhibited an increase in cell volume, a decrease in intracellular Cl(-) concentration, and reduction in cell proliferation with the G0/G1 phase arrest, which was accompanied with down-regulation of cyclin D1 and cyclin E2, and up-regulation of p21. ((dihydroindenyl)oxy)alkanoic acid 45-49 H3 histone pseudogene 16 Homo sapiens 294-297 24236158-6 2013 In contrast, SAHA increased expression of Caspase-3, p21 and p53 mRNA, and upregulated acetyl-Histones H3 and H4, Caspase-8, and p53 proteins. Vorinostat 13-17 H3 histone pseudogene 16 Homo sapiens 53-56 24223226-0 2013 Branched-chain amino acids enhance premature senescence through mammalian target of rapamycin complex I-mediated upregulation of p21 protein. Amino Acids, Branched-Chain 0-26 H3 histone pseudogene 16 Homo sapiens 129-132 24223226-10 2013 Interestingly, the protein levels of p21, a p53 target and well-known gene essential for the execution of cellular senescence, were upregulated in the presence of BCAAs. Amino Acids, Branched-Chain 163-168 H3 histone pseudogene 16 Homo sapiens 37-40 24192163-4 2013 Crystals of (+-)-threo-ritalinic acid belong to the P21/n space group and form intermolecular hydrogen bonds. (+-)-threo-ritalinic acid 12-37 H3 histone pseudogene 16 Homo sapiens 52-55 24269881-6 2013 Ceramide treatment also upregulated (p<0.05) p53 and p21 protein expression, that was reversed by either pifithrin-alpha or shRNA for p53. Ceramides 0-8 H3 histone pseudogene 16 Homo sapiens 56-59 23911866-5 2013 The resulting accumulation of p53 proteins from phosphorylation at Ser-15 and Ser-392 correlated with an increase in p21 and caspase activation. Serine 67-70 H3 histone pseudogene 16 Homo sapiens 117-120 23911866-5 2013 The resulting accumulation of p53 proteins from phosphorylation at Ser-15 and Ser-392 correlated with an increase in p21 and caspase activation. Serine 78-81 H3 histone pseudogene 16 Homo sapiens 117-120 24082141-0 2013 p21-mediated RNR2 repression restricts HIV-1 replication in macrophages by inhibiting dNTP biosynthesis pathway. Parathion 86-90 H3 histone pseudogene 16 Homo sapiens 0-3 24042364-3 2013 Two stable crystalline structures of tris(tertrazolyl)amine were located belonging to P1 and P21 space groups. tris(tertrazolyl)amine 37-59 H3 histone pseudogene 16 Homo sapiens 93-96 24144209-12 2013 Furthermore, phosphorylation of p21-activated kinase PAK downstream of Rac-1 was reduced by DMOG in a HIF-1alpha-dependent manner. oxalylglycine 92-96 H3 histone pseudogene 16 Homo sapiens 32-35 24204428-2 2013 6,7,8,9-Tetrafluoro-4-methyl-1,3-dihydro-2H-1,5-benzodiazepin-2-one crystallizes in the monoclinic P21/c space group and 6,7,8,9-tetrafluoro-1,4-dimethyl-1,3-dihydro-2H-1,5-benzodiazepin-2-one in the triclinic P-1 space group. 6,7,8,9-tetrafluoro-4-methyl-1,3-dihydro-2h-1,5-benzodiazepin-2-one 0-67 H3 histone pseudogene 16 Homo sapiens 99-104 24082141-3 2013 In the attempt to understand the p21-mediated restriction mechanisms, we found that p21 impairs HIV-1 and simian immunodeficiency virus (SIV)mac reverse transcription in macrophages by reducing the intracellular deoxyribonucleotide (dNTP) pool to levels below those required for viral cDNA synthesis by a SAM domain and HD domain-containing protein 1 (SAMHD1)-independent pathway. Deoxyribonucleotides 212-231 H3 histone pseudogene 16 Homo sapiens 33-36 24082141-3 2013 In the attempt to understand the p21-mediated restriction mechanisms, we found that p21 impairs HIV-1 and simian immunodeficiency virus (SIV)mac reverse transcription in macrophages by reducing the intracellular deoxyribonucleotide (dNTP) pool to levels below those required for viral cDNA synthesis by a SAM domain and HD domain-containing protein 1 (SAMHD1)-independent pathway. Deoxyribonucleotides 212-231 H3 histone pseudogene 16 Homo sapiens 84-87 24082141-3 2013 In the attempt to understand the p21-mediated restriction mechanisms, we found that p21 impairs HIV-1 and simian immunodeficiency virus (SIV)mac reverse transcription in macrophages by reducing the intracellular deoxyribonucleotide (dNTP) pool to levels below those required for viral cDNA synthesis by a SAM domain and HD domain-containing protein 1 (SAMHD1)-independent pathway. Parathion 233-237 H3 histone pseudogene 16 Homo sapiens 33-36 24082141-3 2013 In the attempt to understand the p21-mediated restriction mechanisms, we found that p21 impairs HIV-1 and simian immunodeficiency virus (SIV)mac reverse transcription in macrophages by reducing the intracellular deoxyribonucleotide (dNTP) pool to levels below those required for viral cDNA synthesis by a SAM domain and HD domain-containing protein 1 (SAMHD1)-independent pathway. Parathion 233-237 H3 histone pseudogene 16 Homo sapiens 84-87 24082141-4 2013 We found that p21 blocks dNTP biosynthesis by down-regulating the expression of the RNR2 subunit of ribonucleotide reductase, an enzyme essential for the reduction of ribonucleotides to dNTP. Parathion 25-29 H3 histone pseudogene 16 Homo sapiens 14-17 24082141-4 2013 We found that p21 blocks dNTP biosynthesis by down-regulating the expression of the RNR2 subunit of ribonucleotide reductase, an enzyme essential for the reduction of ribonucleotides to dNTP. Parathion 186-190 H3 histone pseudogene 16 Homo sapiens 14-17 23904037-2 2013 [Th(H2O)4(edta)] (Th1) crystallized in monoclinic space group P2(1)/c with unit cell parameters of a = 8.5275(5) A, b = 12.0635(7) A, c = 15.8825(9) A, and beta = 105.340(2) . [th(h2o)4 0-9 H3 histone pseudogene 16 Homo sapiens 62-67 24051088-2 2013 However, in this study we found that adenosine treatment results in cellular senescence in A549 lung cancer cells both in vitro and in vivo; adenosine induces cell cycle arrest and senescence in a p53/p21 dependent manner; adenosine elevates the level of phosphor-gammaH2AX, pCHK2 and pBRCA1, the markers for prolonged DNA damage response which are likely responsible for initiating the cellular senescence. Adenosine 37-46 H3 histone pseudogene 16 Homo sapiens 201-204 24051088-2 2013 However, in this study we found that adenosine treatment results in cellular senescence in A549 lung cancer cells both in vitro and in vivo; adenosine induces cell cycle arrest and senescence in a p53/p21 dependent manner; adenosine elevates the level of phosphor-gammaH2AX, pCHK2 and pBRCA1, the markers for prolonged DNA damage response which are likely responsible for initiating the cellular senescence. Adenosine 141-150 H3 histone pseudogene 16 Homo sapiens 201-204 24051088-2 2013 However, in this study we found that adenosine treatment results in cellular senescence in A549 lung cancer cells both in vitro and in vivo; adenosine induces cell cycle arrest and senescence in a p53/p21 dependent manner; adenosine elevates the level of phosphor-gammaH2AX, pCHK2 and pBRCA1, the markers for prolonged DNA damage response which are likely responsible for initiating the cellular senescence. Adenosine 141-150 H3 histone pseudogene 16 Homo sapiens 201-204 24113589-5 2013 Pretreatment with nitric oxide (NO) scavengers suppressed the apoptotic biochemical changes induced by 20 muM emodin, and attenuated emodin-induced p53 and p21 expression involved in apoptotic signaling. Nitric Oxide 18-30 H3 histone pseudogene 16 Homo sapiens 156-159 24028450-2 2013 Their crystal structures have been studied by X-ray and neutron powder diffraction at room temperature (RT) and 2 K. At RT, these oxides crystallize in the monoclinic space group P2(1)/n with unit-cell parameters a 2a0, b 2a0, and c 2a0, and beta 90 . Oxides 130-136 H3 histone pseudogene 16 Homo sapiens 179-184 23904037-2 2013 [Th(H2O)4(edta)] (Th1) crystallized in monoclinic space group P2(1)/c with unit cell parameters of a = 8.5275(5) A, b = 12.0635(7) A, c = 15.8825(9) A, and beta = 105.340(2) . Edetic Acid 10-14 H3 histone pseudogene 16 Homo sapiens 62-67 23729655-4 2013 In vitro, DAPM suppressed cell proliferation and induced the expression of Kruppel-like factor 4 (KLF4) and p21 in human colon cancer cells. dapm 10-14 H3 histone pseudogene 16 Homo sapiens 108-111 23729655-5 2013 Interestingly, p21-null HCT 116 cells were largely resistant to the suppressive effects of DAPM on cell proliferation compared with the parental cells. dapm 91-95 H3 histone pseudogene 16 Homo sapiens 15-18 23729655-11 2013 Our results suggest that inhibition of Notch signaling by DAPM provides a potential chemopreventive strategy for patients with tubular adenomas, in part via activation of the KLF4-p21 axis. dapm 58-62 H3 histone pseudogene 16 Homo sapiens 180-183 23716467-0 2013 Bortezomib induces apoptosis of endometrial cancer cells through microRNA-17-5p by targeting p21. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 93-96 23716467-7 2013 The transfection of miR-17-5p mimics or siRNA-p21 reversed the effect of bortezomib on HTB-111 and Ishikawa cells, indicating that miR-17-5p may mediate the function of bortezomib by targeting p21 in endometrial cancer cells. Bortezomib 73-83 H3 histone pseudogene 16 Homo sapiens 46-49 23939040-5 2013 Notably, the level of p21(Cip1) and p27(Kip1) was increased dose-dependently by piperine treatment in both LNCaP and DU145 but not in PC-3 cells, in line with more robust cell cycle arrest in the former two cell lines than the latter one. piperine 80-88 H3 histone pseudogene 16 Homo sapiens 22-25 23716467-7 2013 The transfection of miR-17-5p mimics or siRNA-p21 reversed the effect of bortezomib on HTB-111 and Ishikawa cells, indicating that miR-17-5p may mediate the function of bortezomib by targeting p21 in endometrial cancer cells. Bortezomib 73-83 H3 histone pseudogene 16 Homo sapiens 193-196 23716467-7 2013 The transfection of miR-17-5p mimics or siRNA-p21 reversed the effect of bortezomib on HTB-111 and Ishikawa cells, indicating that miR-17-5p may mediate the function of bortezomib by targeting p21 in endometrial cancer cells. Bortezomib 169-179 H3 histone pseudogene 16 Homo sapiens 46-49 23716467-7 2013 The transfection of miR-17-5p mimics or siRNA-p21 reversed the effect of bortezomib on HTB-111 and Ishikawa cells, indicating that miR-17-5p may mediate the function of bortezomib by targeting p21 in endometrial cancer cells. Bortezomib 169-179 H3 histone pseudogene 16 Homo sapiens 193-196 24270384-3 2013 Further examination showed that Celergen enhanced expression of the p21(CIPl1WAF1), GADD153 genes and downregulated the c-myc gene. celergen 32-40 H3 histone pseudogene 16 Homo sapiens 68-71 24026251-12 2013 The present study also showed that treatment with ethanol resulted in significant increases in the expression of p21, but not the levels of p53 and p53 target genes such as Bax, Puma, and Bcl-2. Ethanol 50-57 H3 histone pseudogene 16 Homo sapiens 113-116 24026251-13 2013 Furthermore, the inhibition of p75NTR expression or Sp1 activity suppressed ethanol-induced p21 expression, cell cycle arrest, and apoptosis. Ethanol 76-83 H3 histone pseudogene 16 Homo sapiens 92-95 23873413-4 2013 In the course of this study, the single-crystal X-ray structure of lisinopril dihydrate, [a = 14.550(2), b = 5.8917(8), c = 14.238(2) A, beta = 112.832(3) at T = 173(2) K, space group P21 , Z = 2], was determined for the first time, revealing its double zwitterionic character in the solid state. Lisinopril 67-87 H3 histone pseudogene 16 Homo sapiens 185-188 23900299-6 2013 Triptolide treatment resulted in a significant decrease in mRNA expression levels in genes encoding Bcl-2, cyclin D1, p27 and survivin and an increase in those encoding Bax and p21 in THP-1 cells. triptolide 0-10 H3 histone pseudogene 16 Homo sapiens 177-180 23797319-6 2013 The results of present study showed that MK-2206-induced G1-phase arrest was associated with a marked decrease in the protein expression of cyclin D1 with concomitant induction of p21 and p27. MK 2206 41-48 H3 histone pseudogene 16 Homo sapiens 180-183 24109558-6 2013 Our data indicate that harmine exhibits a pronounced cytotoxicity and induces an anti-proliferation state in MCF-7 cells which is accompanied by a significant inhibition of telomerase activity and an induction of an accelerated senescence phenotype by over-expressing elements of the p53/p21 pathway. Harmine 23-30 H3 histone pseudogene 16 Homo sapiens 288-291 24137434-7 2013 However, pre-treatment of the cells with tanshinone IIA inhibited p65/NF-kappaB nuclear translocation and p53/p21 pathway activation. tanshinone 41-55 H3 histone pseudogene 16 Homo sapiens 110-113 24113128-0 2013 Notch3 inhibition enhances sorafenib cytotoxic efficacy by promoting GSK3b phosphorylation and p21 down-regulation in hepatocellular carcinoma. Sorafenib 27-36 H3 histone pseudogene 16 Homo sapiens 95-98 24113128-3 2013 Here we found that p21 and pGSK3betaSer9 are major players in the resistance to sorafenib. Sorafenib 80-89 H3 histone pseudogene 16 Homo sapiens 19-22 24113128-5 2013 In this study we first found that Notch3 inhibition significantly increased the apoptosis inducing effect of sorafenib in HCC cells via specific down-regulation of p21 and up-regulation of pGSK3betaSer9. Sorafenib 109-118 H3 histone pseudogene 16 Homo sapiens 164-167 24113128-7 2013 Interestingly, we showed that, upon exposure to sorafenib treatment, Notch3 depleted xenografts maintain lower levels of p21 and higher levels of pGSK3betaSer9 than control xenografts. Sorafenib 48-57 H3 histone pseudogene 16 Homo sapiens 121-124 23994334-7 2013 Our results showed that GCCs can induce HPMC apoptosis by unregulated apoptosis associated with cleaved caspase3, cleaved caspase9, and p21 proteins. gccs 24-28 H3 histone pseudogene 16 Homo sapiens 136-139 23953587-6 2013 The results demonstrate that choline substitution leads to: (i) an improved preservation of oocytes and follicular cells; (ii) the recovery of a higher percentage of grade-1 follicles negative for p53, p21 and Apaf-1 apoptotic markers; (iii) a reduced mitochondrial damage as observed at an ultrastructural level; and (iv) a better preservation of ovarian tissue stroma. Choline 29-36 H3 histone pseudogene 16 Homo sapiens 202-205 24086266-0 2013 Hepatocyte expression of the senescence marker p21 is linked to fibrosis and an adverse liver-related outcome in alcohol-related liver disease. Alcohols 113-120 H3 histone pseudogene 16 Homo sapiens 47-50 24198727-4 2013 Both H2O2 treatment and AdRas12V infection induced senescence in VECs, as assessed by senescence-associated beta-Gal activity and the expression of proteins such as p53 and p21(CIP1). Hydrogen Peroxide 5-9 H3 histone pseudogene 16 Homo sapiens 173-176 24086266-3 2013 In previous studies increased hepatocyte nuclear area and hepatocyte expression of p21, both markers of senescence, were associated with increased fibrosis stage and a poor outcome in non-alcohol-related fatty liver disease, while increased hepatocyte nuclear area was related to liver dysfunction in ALD cirrhosis. Alcohols 188-195 H3 histone pseudogene 16 Homo sapiens 83-86 23828041-1 2013 Phosphorylation of histone H4 serine 47 (H4S47ph) is catalyzed by Pak2, a member of the p21-activated serine/threonine protein kinase (Pak) family and regulates the deposition of histone variant H3.3. Serine 30-36 H3 histone pseudogene 16 Homo sapiens 88-91 23645216-0 2013 Azidothymidine hinders arsenic trioxide-induced apoptosis in acute promyelocytic leukemia cells by induction of p21 and attenuation of G2/M arrest. Zidovudine 0-14 H3 histone pseudogene 16 Homo sapiens 112-115 23645216-0 2013 Azidothymidine hinders arsenic trioxide-induced apoptosis in acute promyelocytic leukemia cells by induction of p21 and attenuation of G2/M arrest. Arsenic Trioxide 23-39 H3 histone pseudogene 16 Homo sapiens 112-115 23645216-6 2013 QRT-PCR assay revealed that induction of p21expression by the combined AZT/ATO compared to ATO alone could be a reason for the relative decline of cells accumulation in G2/M and the increase of cells in G1 and S phases. Zidovudine 71-74 H3 histone pseudogene 16 Homo sapiens 41-44 23645216-6 2013 QRT-PCR assay revealed that induction of p21expression by the combined AZT/ATO compared to ATO alone could be a reason for the relative decline of cells accumulation in G2/M and the increase of cells in G1 and S phases. Arsenic Trioxide 75-78 H3 histone pseudogene 16 Homo sapiens 41-44 23645216-6 2013 QRT-PCR assay revealed that induction of p21expression by the combined AZT/ATO compared to ATO alone could be a reason for the relative decline of cells accumulation in G2/M and the increase of cells in G1 and S phases. Arsenic Trioxide 91-94 H3 histone pseudogene 16 Homo sapiens 41-44 23903894-1 2013 INTRODUCTION: Vorinostat is a small molecule inhibitor of class I and II histone deacetylase enzymes which alters the expression of target genes including the cell cycle gene p21, leading to cell cycle arrest and apoptosis. Vorinostat 14-24 H3 histone pseudogene 16 Homo sapiens 175-178 23903894-8 2013 p21, a downstream target of Nur77, was significantly decreased on day 9, 2 and 6 h after administration of vorinostat and bortezomib, 0.67 (0.41-1.03) (p < 0.01); 0.44 (0.25-1.3) (p < 0.01), respectively. Vorinostat 107-117 H3 histone pseudogene 16 Homo sapiens 0-3 23903894-8 2013 p21, a downstream target of Nur77, was significantly decreased on day 9, 2 and 6 h after administration of vorinostat and bortezomib, 0.67 (0.41-1.03) (p < 0.01); 0.44 (0.25-1.3) (p < 0.01), respectively. Bortezomib 122-132 H3 histone pseudogene 16 Homo sapiens 0-3 23903894-9 2013 The ChIP assay demonstrated a protein-DNA interaction, in this case interaction of Nur77, HSP70 and p21 with acetylated histone H3, at baseline and at day 9 after treatment with vorinostat in tissue biopsies in most patients. Vorinostat 178-188 H3 histone pseudogene 16 Homo sapiens 100-103 23903894-10 2013 CONCLUSION: Vorinostat inhibits Nur77 expression, which in turn may decrease p21 and AKT expression in PBMCs. Vorinostat 12-22 H3 histone pseudogene 16 Homo sapiens 77-80 23723074-4 2013 Cell-cycle analysis revealed that miR-133a induced a G0/G1-phase arrest, concomitant with the upregulation of the key G1-phase regulator p21(Cip1). mir-133a 34-42 H3 histone pseudogene 16 Homo sapiens 137-140 23723074-5 2013 We further revealed that miR-133a markedly increased p53 protein and induced p21(Cip1) transcription. mir-133a 25-33 H3 histone pseudogene 16 Homo sapiens 77-80 24005866-4 2013 Accumulation of reactive oxygen species (ROS) was observed in the progression of cell cycle arrest, which was associated with the increased expression of cell cycle regulating factors, p53 and p21. Reactive Oxygen Species 16-39 H3 histone pseudogene 16 Homo sapiens 193-196 24005866-4 2013 Accumulation of reactive oxygen species (ROS) was observed in the progression of cell cycle arrest, which was associated with the increased expression of cell cycle regulating factors, p53 and p21. Reactive Oxygen Species 41-44 H3 histone pseudogene 16 Homo sapiens 193-196 23752064-3 2013 Subsequent treatment with 4-hydroxy-tamoxifen (4-OHT) induced ER-beta nuclear translocation, upregulated pS2 and p21 levels and reduced cell viability. 4'-hydroxytamoxifen 26-45 H3 histone pseudogene 16 Homo sapiens 113-116 23752064-3 2013 Subsequent treatment with 4-hydroxy-tamoxifen (4-OHT) induced ER-beta nuclear translocation, upregulated pS2 and p21 levels and reduced cell viability. 4,17 beta-dihydroxy-4-androstene-3-one 47-52 H3 histone pseudogene 16 Homo sapiens 113-116 23810214-6 2013 By contrast, 5-fluorouracil induced G2 cell-cycle arrest and apoptosis that may be associated with p53 activation and p21 up-regulation. Fluorouracil 13-27 H3 histone pseudogene 16 Homo sapiens 118-121 24067199-0 2013 Cisplatin induces cell cycle arrest and senescence via upregulating P53 and P21 expression in HepG2 cells. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 76-79 24067199-9 2013 Western blotting confirmed P53 and P21 expression changes similar to their mRNA expressions during cisplatin-induced cellular senescence in HepG2 cells. Cisplatin 99-108 H3 histone pseudogene 16 Homo sapiens 35-38 23828041-1 2013 Phosphorylation of histone H4 serine 47 (H4S47ph) is catalyzed by Pak2, a member of the p21-activated serine/threonine protein kinase (Pak) family and regulates the deposition of histone variant H3.3. h4s47ph 41-48 H3 histone pseudogene 16 Homo sapiens 88-91 24618550-9 2013 It was found that let-7d could inhibit the proliferation of PASMCs through upregulation of p21. pasmcs 60-66 H3 histone pseudogene 16 Homo sapiens 91-94 23881456-4 2013 Treatment with cudraflavone B triggered the mitochondrial apoptotic pathway (indicated by induction of the proapoptotic protein p53 and the p21 and p27 effector proteins), downregulation of cell cycle regulatory proteins (e.g., p-Rb, changing Bax/Bcl-2 ratios, cytochrome-c release), and caspase-3 activation. cudraflavone B 15-29 H3 histone pseudogene 16 Homo sapiens 140-143 23881456-6 2013 SIRT1 activator, resveratrol, dose-dependently attenuated the growth-inhibitory and apoptosis-inducing effect of cudraflavone B and blocked cudraflavone B-induced regulatory protein expressions in the mitochondrial pathway such as p53, p21, p27, Bax, caspase-3, and cytochrome-c. Conversely, treatment with SIRT1 inhibitor sirtinol caused opposite effects. Resveratrol 17-28 H3 histone pseudogene 16 Homo sapiens 236-239 23881456-6 2013 SIRT1 activator, resveratrol, dose-dependently attenuated the growth-inhibitory and apoptosis-inducing effect of cudraflavone B and blocked cudraflavone B-induced regulatory protein expressions in the mitochondrial pathway such as p53, p21, p27, Bax, caspase-3, and cytochrome-c. Conversely, treatment with SIRT1 inhibitor sirtinol caused opposite effects. cudraflavone B 113-127 H3 histone pseudogene 16 Homo sapiens 236-239 23907891-1 2013 The title compound, C17H13NO4, crystallizes in two polymorphic forms, each with two molecules in the asymmetric unit and in the monoclinic space group P21/c. c17h13no4 20-29 H3 histone pseudogene 16 Homo sapiens 151-156 23901880-6 2013 At low temperature, RbMnPO4 exhibits a canted antiferromagnetic structure characterized by the propagation vector k1 = 0, resulting in the magnetic symmetry P2(1)". rbmnpo4 20-27 H3 histone pseudogene 16 Homo sapiens 157-162 23906417-3 2013 We report the structure of a new monoclinic P2(1)/n perovskite phase of ScMnO3 synthesized from the hexagonal phase under high-pressure and high-temperature conditions. perovskite 52-62 H3 histone pseudogene 16 Homo sapiens 44-49 23906417-3 2013 We report the structure of a new monoclinic P2(1)/n perovskite phase of ScMnO3 synthesized from the hexagonal phase under high-pressure and high-temperature conditions. scmno3 72-78 H3 histone pseudogene 16 Homo sapiens 44-49 23899521-5 2013 SL-01 modulated the expressions of p-ATM, p53 and p21 and decrease of cyclin D1 in MCF-7 cells. dodecyl-3-((1-(3,3-difluoro-4-hydroxy-5-(hydroxymethyl)-tetrahydrofuran-2-yl)-2-oxo-1,2-dihydropyrimidin-4-yl)carbamoyl)pyrazine-2-carboxylate 0-5 H3 histone pseudogene 16 Homo sapiens 50-53 23977108-7 2013 Treatment of SK-N-DZ with PCI-24781 also induced cell cycle arrest in G2/M phase and activated apoptosis signaling pathways via the up-regulation of DR4, p21, p53 and caspase 3. sk-n-dz 13-20 H3 histone pseudogene 16 Homo sapiens 154-157 23977108-7 2013 Treatment of SK-N-DZ with PCI-24781 also induced cell cycle arrest in G2/M phase and activated apoptosis signaling pathways via the up-regulation of DR4, p21, p53 and caspase 3. abexinostat 26-35 H3 histone pseudogene 16 Homo sapiens 154-157 23754252-6 2013 In combination with cerulenin and oxaliplatin, activation of the p53-p21 pathway and p38 occurred in a smaller concentration and finally induced caspase-3 cleavage in a smaller concentration of cerulenin and oxaliplatin. Oxaliplatin 208-219 H3 histone pseudogene 16 Homo sapiens 69-72 23695011-5 2013 Mechanistic studies showed that JH-induced C8161 cell cycle arrest at the G0/G1 transition, which was accompanied by overexpression of the cell cycle-suppressive genes p21 and p27 at higher doses. jh 32-34 H3 histone pseudogene 16 Homo sapiens 168-171 23607751-10 2013 On the contrary, doxorubicin abolished p21 activation and elicited p53 induction both in SSc- and HC-MSCs. Doxorubicin 17-28 H3 histone pseudogene 16 Homo sapiens 39-42 23936432-0 2013 Inhibition of proliferation and induction of autophagy by atorvastatin in PC3 prostate cancer cells correlate with downregulation of Bcl2 and upregulation of miR-182 and p21. Atorvastatin 58-70 H3 histone pseudogene 16 Homo sapiens 170-173 23754252-5 2013 Oxaliplatin induced activation of the p53-p21 pathway and p38. Oxaliplatin 0-11 H3 histone pseudogene 16 Homo sapiens 42-45 23754252-6 2013 In combination with cerulenin and oxaliplatin, activation of the p53-p21 pathway and p38 occurred in a smaller concentration and finally induced caspase-3 cleavage in a smaller concentration of cerulenin and oxaliplatin. Cerulenin 20-29 H3 histone pseudogene 16 Homo sapiens 69-72 23754252-6 2013 In combination with cerulenin and oxaliplatin, activation of the p53-p21 pathway and p38 occurred in a smaller concentration and finally induced caspase-3 cleavage in a smaller concentration of cerulenin and oxaliplatin. Oxaliplatin 34-45 H3 histone pseudogene 16 Homo sapiens 69-72 23754252-6 2013 In combination with cerulenin and oxaliplatin, activation of the p53-p21 pathway and p38 occurred in a smaller concentration and finally induced caspase-3 cleavage in a smaller concentration of cerulenin and oxaliplatin. Cerulenin 194-203 H3 histone pseudogene 16 Homo sapiens 69-72 23299388-6 2013 Induction of acetyl-H3, acetyl-H4 and p21 by vorinostat were transient and rapidly reversed within 12 h of drug removal. Vorinostat 45-55 H3 histone pseudogene 16 Homo sapiens 38-41 23299388-7 2013 In contrast, panobinostat-induced acetyl-H3, acetyl-H4, and p21 persisted for 48 h after an initial 3 h exposure. Panobinostat 13-25 H3 histone pseudogene 16 Homo sapiens 60-63 23514434-4 2013 AgNP exposure increased apoptosis, as demonstrated by an increase in 4 ,6-diamidino-2-phenylindole-stained apoptotic nuclei, BAX/BCL-XL ratio, cleaved poly(ADP-ribose) polymerase, p53, p21 and caspases 3, 8 and 9, and by a decrease in the levels of AKT and NF-kappaB. agnp 0-4 H3 histone pseudogene 16 Homo sapiens 185-212 23936432-10 2013 Bcl2 was downregulated and p21 was upregulated in PC3 cells exposed to ATO. Atorvastatin 71-74 H3 histone pseudogene 16 Homo sapiens 27-30 23998584-2 2013 Apoptosis of HL-60 cells was detected by flow cytometry, the expression of P21, P27 and P53 proteins in HL-60 cells treated with MG132 was assayed by Western blot. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 129-134 H3 histone pseudogene 16 Homo sapiens 75-78 23998584-7 2013 The expression of P21 and P27 protein increased after treatment of HL-60 cells with MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 84-89 H3 histone pseudogene 16 Homo sapiens 18-21 23998584-10 2013 The P21 and P27 protein may be involved in MG132 induced HL-60 cell apoptosis. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 43-48 H3 histone pseudogene 16 Homo sapiens 4-7 23692869-7 2013 BPDE-induced cdc2 down-regulation corresponded with accumulation of the cell cycle inhibitor protein p21 (transactivation product of p53). 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 0-4 H3 histone pseudogene 16 Homo sapiens 101-104 25206494-7 2013 Ethanol also increased p53 phosphorylation, followed by an increase in p21 tumor suppressor protein and a decrease in phospho-Rb (retinoblastoma) protein, leading to alterations in the expressions and activity of cyclin dependent protein kinases. Ethanol 0-7 H3 histone pseudogene 16 Homo sapiens 71-74 23869224-9 2013 The anti-fibrotic action of rupatadine might relate to its attenuation of BLM- or PAF-induced premature senescence because rupatadine treatment protected against the in vivo and in vitro activation of the p53/p21-dependent senescence pathway. rupatadine 28-38 H3 histone pseudogene 16 Homo sapiens 209-212 23869224-9 2013 The anti-fibrotic action of rupatadine might relate to its attenuation of BLM- or PAF-induced premature senescence because rupatadine treatment protected against the in vivo and in vitro activation of the p53/p21-dependent senescence pathway. rupatadine 123-133 H3 histone pseudogene 16 Homo sapiens 209-212 23887718-8 2013 Treatment of A549 cells with PA resulted in a strong inhibition of NF-kappaB activation, which was consistent with a decrease in nuclear levels of NF-kappaB/p65 and NF-kappaB/p50 and the elevation of p53 and p21. panduratin A 29-31 H3 histone pseudogene 16 Homo sapiens 208-211 23475945-8 2013 Additionally, BMJ decreased survivin and X-linked inhibitor of apoptosis protein but increased p21, CHOP and phosphorylated mitogen-activated protein kinases (extracellular signal-regulated kinase 1/2 and p38) levels. (12R)-12-methyltetradecanoic acid 14-17 H3 histone pseudogene 16 Homo sapiens 95-98 23832026-1 2013 Bis(4-picoline-kappaN)gold(I) dibromidoaurate(I), [Au(C6H7N)2][AuBr2], (I), crystallizes in the monoclinic space group P21/n, with two half cations and one general anion in the asymmetric unit. bis(4-picoline-kappan)gold 0-26 H3 histone pseudogene 16 Homo sapiens 119-122 23832026-1 2013 Bis(4-picoline-kappaN)gold(I) dibromidoaurate(I), [Au(C6H7N)2][AuBr2], (I), crystallizes in the monoclinic space group P21/n, with two half cations and one general anion in the asymmetric unit. dibromidoaurate 30-45 H3 histone pseudogene 16 Homo sapiens 119-122 23546866-0 2013 Reactive oxygen species-mediated activation of the Akt/ASK1/p38 signaling cascade and p21(Cip1) downregulation are required for shikonin-induced apoptosis. Reactive Oxygen Species 0-23 H3 histone pseudogene 16 Homo sapiens 86-89 23546866-3 2013 Here, we demonstrated that shikonin-induced apoptosis is caused by reactive oxygen species (ROS)-mediated activation of Akt/ASK1/p38 mitogen-activated protein kinase (MAPK) and downregulation of p21(Cip1). shikonin 27-35 H3 histone pseudogene 16 Homo sapiens 195-198 23546866-3 2013 Here, we demonstrated that shikonin-induced apoptosis is caused by reactive oxygen species (ROS)-mediated activation of Akt/ASK1/p38 mitogen-activated protein kinase (MAPK) and downregulation of p21(Cip1). Reactive Oxygen Species 92-95 H3 histone pseudogene 16 Homo sapiens 195-198 23546866-10 2013 Depletion of p21(Cip1) facilitated shikonin-induced apoptosis, implying that p21(Cip1) delayed shikonin-induced apoptosis via G1 arrest. shikonin 35-43 H3 histone pseudogene 16 Homo sapiens 13-16 23546866-13 2013 These findings suggest that shikonin-induced ROS activated ASK1 by decreasing Ser83 phosphorylation and by dissociation of the negative regulator p21(Cip1), leading to p38 MAPK activation, and finally, promoting apoptosis. shikonin 28-36 H3 histone pseudogene 16 Homo sapiens 146-149 23546866-13 2013 These findings suggest that shikonin-induced ROS activated ASK1 by decreasing Ser83 phosphorylation and by dissociation of the negative regulator p21(Cip1), leading to p38 MAPK activation, and finally, promoting apoptosis. Reactive Oxygen Species 45-48 H3 histone pseudogene 16 Homo sapiens 146-149 23692084-7 2013 In addition, p21 and p27 protein levels were higher when Notch signalling was activated by EDTA treatment. Edetic Acid 91-95 H3 histone pseudogene 16 Homo sapiens 13-16 23585524-5 2013 ATM dysfunction leads to impaired p21 induction after doxorubicin exposure. Doxorubicin 54-65 H3 histone pseudogene 16 Homo sapiens 34-37 23579097-6 2013 The combined treatment with BLU and gemcitabine further activated p53 and p21 expression, whereas the productions of Bcl-2, Bcl-xL, and nuclear factor-kappa B proteins were decreased, with BLU possibly being more effective in the treatment of ovarian cancer when given in combination with gemcitabine, rather than as a single agent. gemcitabine 36-47 H3 histone pseudogene 16 Homo sapiens 74-77 24022933-6 2013 L-OHP induced S cell cycle arrest in HepG2 cell; down-regulated the levels of CDK4, cyclinD1 and up-regulated the levels of p21, p53. Oxaliplatin 0-5 H3 histone pseudogene 16 Homo sapiens 124-127 23744352-8 2013 Consequently, cells responded to NS1643 by developing a senescence-like phenotype associated with increased protein levels of the tumor suppressors p21 and p16(INK4a) and by a positive beta-galactosidase assay. 1,3-bis(2-hydroxy-5-trifluoromethylphenyl)urea 33-39 H3 histone pseudogene 16 Homo sapiens 148-151 23874066-5 2013 Notably, tolfenamic acid increased apoptosis-related proteins, such as p53 and p21, within 48 h. Furthermore, in vivo experiments showed that tolfenamic acid treatment resulted in a significant reduction in tumor volume over 5 weeks. tolfenamic acid 9-24 H3 histone pseudogene 16 Homo sapiens 79-82 23874066-5 2013 Notably, tolfenamic acid increased apoptosis-related proteins, such as p53 and p21, within 48 h. Furthermore, in vivo experiments showed that tolfenamic acid treatment resulted in a significant reduction in tumor volume over 5 weeks. tolfenamic acid 142-157 H3 histone pseudogene 16 Homo sapiens 79-82 23098692-5 2013 1,25(OH)2D3 augmented the effect of cisplatin in an embryonal carcinoma-derived cell line (NTera2), possibly through downregulation of pluripotency genes and simultaneous upregulation of the cell cycle regulators p21, p27, p53, p73 and FOXO1, while no significant effects were found in TCam-2 and 2102Ep cell lines (derived from seminoma and embryonal carcinoma, respectively). Cisplatin 36-45 H3 histone pseudogene 16 Homo sapiens 213-216 23098692-7 2013 In xenograft tumors, co-treatment with 1,25(OH)2D3 and cisplatin resulted in downregulation of OCT4 and simultaneous upregulation of p21 and p73, but did not reduce tumor growth significantly more than cisplatin alone. Calcitriol 39-50 H3 histone pseudogene 16 Homo sapiens 133-136 23098692-7 2013 In xenograft tumors, co-treatment with 1,25(OH)2D3 and cisplatin resulted in downregulation of OCT4 and simultaneous upregulation of p21 and p73, but did not reduce tumor growth significantly more than cisplatin alone. Cisplatin 55-64 H3 histone pseudogene 16 Homo sapiens 133-136 23559092-6 2013 The mechanism is due partially to DHA, and Rac1 siRNA deactivates NFkappaB activity, so as to decrease tremendously the expression of its target gene products, such as PCNA, cyclin D1, and CDK4; and increase the expression of p21, cleaved-caspase-3, and cleaved-PARP. artenimol 34-37 H3 histone pseudogene 16 Homo sapiens 226-229 23651583-6 2013 p53 activation is an important factor in Nanog suppression and treatment with resveratrol was also found to activate the p53/p21 pathway. Resveratrol 78-89 H3 histone pseudogene 16 Homo sapiens 125-128 23676219-7 2013 By phosphorylating p53 on its serine-15, HIPK1 favored its transactivation potential, which led to a rise in p21 protein level and a decline in cell proliferation. Serine 30-36 H3 histone pseudogene 16 Homo sapiens 109-112 23744385-2 2013 The crystal structure shows a completely planar geometry of the TTN core, crystallizing in the monoclinic space group P2(1)/c. Tartronic acid 64-67 H3 histone pseudogene 16 Homo sapiens 118-125 23602914-7 2013 Exposure of PA to HCT116 and SW480 cells activated p21 expression and suppressed the expressions of cyclin D1 and cyclin-dependent kinase 4 (CDK4) in a dose-dependent manner. patchouli alcohol 12-14 H3 histone pseudogene 16 Homo sapiens 51-54 23386415-0 2013 Inhibition of p21 and Akt potentiates SU6656-induced caspase-independent cell death in FRO anaplastic thyroid carcinoma cells. SU 6656 38-44 H3 histone pseudogene 16 Homo sapiens 14-17 23386415-2 2013 The aim of the present study was to investigate the influence of SU6656 on cell survival and to assess the role of p21 and PI3K/Akt signaling in cell survival resulting from SU6656 treatment in anaplastic thyroid carcinoma (ATC) cells. SU 6656 174-180 H3 histone pseudogene 16 Homo sapiens 115-118 23386415-7 2013 Regarding FRO ATC cells, the decrement of cell viability, the increment of cleaved PARP-1 protein levels, and the decrement of phospho-Src protein levels were shown in p21 siRNA- or LY294002-pretreated cells compared to SU6656-treated control cells. SU 6656 220-226 H3 histone pseudogene 16 Homo sapiens 168-171 23386415-9 2013 In conclusion, these results suggest that SU6656 induces caspase-independent death of FRO ATC cells by overcoming the resistance mechanism involving p21 and Akt. SU 6656 42-48 H3 histone pseudogene 16 Homo sapiens 149-152 23386415-10 2013 Suppression of p21 and Akt enhances the cytotoxic effect of SU6656 in FRO ATC cells. SU 6656 60-66 H3 histone pseudogene 16 Homo sapiens 15-18 23298900-6 2013 The mRNA expression levels of VDR, CYP24A1, and p21 were increased significantly following 1,25-dihydroxyvitamin D3 treatment. Calcitriol 91-115 H3 histone pseudogene 16 Homo sapiens 48-51 23628417-5 2013 As expected, the Bax and p21 activities were enhanced by BLU or paclitaxel, while a combination of BLU and paclitaxel were additively promoted, whereas Bcl-xL and NF-kappaB including Bcl-2 activity were inactivated. Paclitaxel 64-74 H3 histone pseudogene 16 Homo sapiens 25-28 23547259-7 2013 Disrupting formation of SG by inactivation of mTOR with its specific inhibitor pp242 or by depletion of eIF4E or eIF4GI blocks the SG-associated antiapoptotic p21 pathway. PP242 79-84 H3 histone pseudogene 16 Homo sapiens 159-162 23178160-4 2013 We found that the synthetic progestin medroxyprogesterone acetate (MPA) upregulates p21(CIP1) protein expression via c-Src, signal transducer and activator of transcription 3 (Stat3) and ErbB-2 phosphorylation. Medroxyprogesterone Acetate 38-65 H3 histone pseudogene 16 Homo sapiens 84-87 23501710-2 2013 The Centro-symmetric single crystal of S-benzyl isothiouronium nitrate (SBTN), which crystallizes in monoclinic crystal system with space group P21/C, exhibits second order non-linear optical (NLO) susceptibility, due to intermolecular charge transfer. s-benzyl isothiouronium nitrate 39-70 H3 histone pseudogene 16 Homo sapiens 144-149 23646986-4 2013 The Co(II)-Ln(III) and Ni(II)-Ln(III) complexes are crystallized in an isomorphous monoclinic space group P2(1)/c, where the Co(II) or Ni(II) ion at the high-spin state has an octahedral coordination environment with N2O2 donor atoms of 3-MeOsaltn at the equatorial sites, and one oxygen atom of the bridged acetato and a methanol oxygen atom at the two axial sites. Nickel(2+) 23-29 H3 histone pseudogene 16 Homo sapiens 106-113 23615119-1 2013 The perovskite form of the Mn2FeSbO6 oxide has been obtained at 5.5 GPa and 1523 K. X-ray and neutron diffraction data reveal that this compound crystallizes in the monoclinic P21/n space group with a = 0.5234 nm, b = 0.5389 nm, c = 0.7642 nm and beta = 90.372 lattice parameters. perovskite 4-14 H3 histone pseudogene 16 Homo sapiens 176-179 23615119-1 2013 The perovskite form of the Mn2FeSbO6 oxide has been obtained at 5.5 GPa and 1523 K. X-ray and neutron diffraction data reveal that this compound crystallizes in the monoclinic P21/n space group with a = 0.5234 nm, b = 0.5389 nm, c = 0.7642 nm and beta = 90.372 lattice parameters. mn2fesbo6 oxide 27-42 H3 histone pseudogene 16 Homo sapiens 176-179 23501710-2 2013 The Centro-symmetric single crystal of S-benzyl isothiouronium nitrate (SBTN), which crystallizes in monoclinic crystal system with space group P21/C, exhibits second order non-linear optical (NLO) susceptibility, due to intermolecular charge transfer. sbtn 72-76 H3 histone pseudogene 16 Homo sapiens 144-149 23637829-9 2013 Additionally, DMF regulates cell cycle-related proteins, such as p21, pRb, and cyclin D. DMF treatment markedly inhibited differentiation medium-induced STAT3 phosphorylation and inhibited STAT3 transcriptional activation of a reporter construct composed of four synthetic STAT3-response elements. Dimethyl Fumarate 14-17 H3 histone pseudogene 16 Homo sapiens 65-68 23590630-1 2013 Single crystals of Ca4SiN4 were found in the product prepared by heating Ba, Ca, Si, NaN3, and Na at 900 C. Ca4SiN4 [space group P2(1)/c (No. ca4sin4 19-26 H3 histone pseudogene 16 Homo sapiens 130-137 23468063-5 2013 Following pretreatment with subcytotoxic concentrations of copper sulfate, U87-MG tumor cells showed typical aging characteristics, including reduced cell proliferation, cell enlargement, increased level of senescence-associated beta-galactosidase (SA beta-gal) activity, and overexpression of several senescence-associated genes, p16, p21, transforming growth factor beta-1 (TGF-beta1), insulin growth factor binding protein 3 (IGFBP3) and apolipoprotein J (ApoJ). Copper Sulfate 59-73 H3 histone pseudogene 16 Homo sapiens 336-339 23262037-3 2013 Our data indicated that due to the repression by p53, FoxM1 played a critical role in oxaliplatin-induced senescence via regulating cycle-related proteins p21, p27, cyclins B1 and D1. Oxaliplatin 86-97 H3 histone pseudogene 16 Homo sapiens 155-158 23597199-6 2013 The detailed in vitro and in vivo study on the molecular mechanisms of this compound demonstrated that IVHD-valtrate exposure modulated the expression of numerous molecules involved in cell cycle progression and apoptosis regardless of p53 status, leading to increase the level of p53, Rb, p21, p27 and decrease Mdm2, E2F1, Cyclin B1, Cdc25C and Cdc2. valtrate 108-116 H3 histone pseudogene 16 Homo sapiens 290-293 22290509-6 2013 The decreased cell viability observed in SkBr3 cells when curcumin was combined with TSA led to a G0/G1 cell cycle arrest and increased p21 and p27, and decreased Cyclin D1 protein expression. Curcumin 58-66 H3 histone pseudogene 16 Homo sapiens 136-139 22290509-6 2013 The decreased cell viability observed in SkBr3 cells when curcumin was combined with TSA led to a G0/G1 cell cycle arrest and increased p21 and p27, and decreased Cyclin D1 protein expression. trichostatin A 85-88 H3 histone pseudogene 16 Homo sapiens 136-139 23541946-4 2013 Treatments of BxPC-3 or PANC-1 pancreatic cancer cell lines with chidamide resulted in dose- and time-dependent growth arrest, accompanied by induction of p21 expression. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 65-74 H3 histone pseudogene 16 Homo sapiens 155-158 23637829-9 2013 Additionally, DMF regulates cell cycle-related proteins, such as p21, pRb, and cyclin D. DMF treatment markedly inhibited differentiation medium-induced STAT3 phosphorylation and inhibited STAT3 transcriptional activation of a reporter construct composed of four synthetic STAT3-response elements. Dimethyl Fumarate 89-92 H3 histone pseudogene 16 Homo sapiens 65-68 23462712-8 2013 Similarly to cisplatin this compound interacts with nuclear DNA and induces both p53 and p21(waf), and thus it represents an interesting starting point for future optimisation of new Pt(II) complexes forming DNA adducts. Cisplatin 13-22 H3 histone pseudogene 16 Homo sapiens 89-92 23079474-11 2013 Over-expression was associated with cell G1 arrest and p21 induction irrespective of p53 proficiency, while IRF-1 silencing reduced the induction of p21 by CDDP. Cisplatin 156-160 H3 histone pseudogene 16 Homo sapiens 149-152 23521517-5 2013 Structural analysis of 1, i.e., the complex of L(1) 4PF6 containing methyl as a wingtip substituent, and Ag2O shows the formation of a bimetallic silver NHC (NHC-Ag) complex, [(L(1)-4H) 2Ag] 2PF6, which is rotationally disordered over an inversion of symmetry of the space group P2(1)/c. silver nhc 146-156 H3 histone pseudogene 16 Homo sapiens 279-286 23459358-1 2013 Both 10-(2-hydroxyethyl)acridin-9(10H)-one, C15H13NO2, and 10-(2-chloroethyl)acridin-9(10H)-one, C15H12ClNO, have monoclinic (P21/c) symmetry and supramolecular three-dimensional networks. 10-(2-hydroxyethyl)acridin-9(10H)-one 5-42 H3 histone pseudogene 16 Homo sapiens 126-131 23459358-1 2013 Both 10-(2-hydroxyethyl)acridin-9(10H)-one, C15H13NO2, and 10-(2-chloroethyl)acridin-9(10H)-one, C15H12ClNO, have monoclinic (P21/c) symmetry and supramolecular three-dimensional networks. 10-(2-chloroethyl)acridin-9(10H)-one 59-95 H3 histone pseudogene 16 Homo sapiens 126-131 23459358-1 2013 Both 10-(2-hydroxyethyl)acridin-9(10H)-one, C15H13NO2, and 10-(2-chloroethyl)acridin-9(10H)-one, C15H12ClNO, have monoclinic (P21/c) symmetry and supramolecular three-dimensional networks. c15h12clno 97-107 H3 histone pseudogene 16 Homo sapiens 126-131 23476627-1 2013 A new polymorph of the title compound, C8H8BrNO, has been determined at 173 K in the space group P21/c. c8h8brno 39-47 H3 histone pseudogene 16 Homo sapiens 97-102 23376478-4 2013 Our data showed that LH effectively inhibited mitotic proliferation of Hey1B cells (half maximal inhibitory concentration=1.2muM) with very low toxicity, resulting in cell cycle arrest at the G2/M transition through enhanced expression of the cell cycle inhibitor p21 and marked down-regulation of cyclin D3 expression. lycorine 21-23 H3 histone pseudogene 16 Homo sapiens 264-267 23352703-0 2013 Salinomycin induces apoptosis and senescence in breast cancer: upregulation of p21, downregulation of survivin and histone H3 and H4 hyperacetylation. salinomycin 0-11 H3 histone pseudogene 16 Homo sapiens 79-82 23352703-10 2013 Interestingly, treatment with low concentrations of Salinomycin induced a transient G1 arrest at earlier time point and G2 arrest at later point and senescence associated with enlarged cellmorphology, upregulation of p21 protein, increase in histone H3 and H4 hyperacetylation and expression of SA-beta-Gal activity. salinomycin 52-63 H3 histone pseudogene 16 Homo sapiens 217-220 23430755-6 2013 By double labeling of senescent cells, first by SA-beta-Gal and then by antibodies against genes related to cellular senescence, we found that p21, p16, and RARbeta, but not p53, were upregulated by bexarotene in mammary tumors and in breast cancer cell lines, suggesting involvement of multiple signaling pathways in mediating the senescence program of rexinoids. 2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid 48-59 H3 histone pseudogene 16 Homo sapiens 143-146 23430755-6 2013 By double labeling of senescent cells, first by SA-beta-Gal and then by antibodies against genes related to cellular senescence, we found that p21, p16, and RARbeta, but not p53, were upregulated by bexarotene in mammary tumors and in breast cancer cell lines, suggesting involvement of multiple signaling pathways in mediating the senescence program of rexinoids. Bexarotene 199-209 H3 histone pseudogene 16 Homo sapiens 143-146 23430755-6 2013 By double labeling of senescent cells, first by SA-beta-Gal and then by antibodies against genes related to cellular senescence, we found that p21, p16, and RARbeta, but not p53, were upregulated by bexarotene in mammary tumors and in breast cancer cell lines, suggesting involvement of multiple signaling pathways in mediating the senescence program of rexinoids. rexinoids 354-363 H3 histone pseudogene 16 Homo sapiens 143-146 23515411-11 2013 Ex vivo exposure of leukemia cells to plasma obtained from patients after alvocidib treatment blocked vorinostat-mediated p21(CIP1) induction and downregulated Mcl-1 and p-RNA Pol II for some specimens, although parallel in vivo bone marrow responses were infrequent. alvocidib 74-83 H3 histone pseudogene 16 Homo sapiens 122-125 23515411-11 2013 Ex vivo exposure of leukemia cells to plasma obtained from patients after alvocidib treatment blocked vorinostat-mediated p21(CIP1) induction and downregulated Mcl-1 and p-RNA Pol II for some specimens, although parallel in vivo bone marrow responses were infrequent. Vorinostat 102-112 H3 histone pseudogene 16 Homo sapiens 122-125 22773548-9 2013 Cell line studies showed that metformin inhibits hepatocyte proliferation and induces cell cycle arrest at G0/G1 phase via AMP-activated protein kinase and its upstream kinase LKB1 to upregulate p21/Cip1 and p27/Kip1 and downregulate cyclin D1 in a dose-dependent manner, but independent of p53. Metformin 30-39 H3 histone pseudogene 16 Homo sapiens 195-198 23128353-6 2013 Glucosamine at 50 mM was demonstrated to elevate both the mRNA and protein expression of p53 and heme oxygenase-1 (HO-1), but also caused a reduction in p21 protein expression. Glucosamine 0-11 H3 histone pseudogene 16 Homo sapiens 153-156 23128353-7 2013 In addition, glucosamine attenuated p21 protein stability via the proteasomal proteolytic pathway, as well as inducing p21 nuclear accumulation. Glucosamine 13-24 H3 histone pseudogene 16 Homo sapiens 36-39 23128353-7 2013 In addition, glucosamine attenuated p21 protein stability via the proteasomal proteolytic pathway, as well as inducing p21 nuclear accumulation. Glucosamine 13-24 H3 histone pseudogene 16 Homo sapiens 119-122 23128353-8 2013 Altogether, our results suggest that a high dose of glucosamine may inhibit cell proliferation through apoptosis and disturb cell cycle progression with a halt at G(0)/G(1) phase, and that this occurs, at least in part, by a reduction in Rb phosphorylation together with modulation of p21, p53 and HO-1 expression, and nuclear p21 accumulation. Glucosamine 52-63 H3 histone pseudogene 16 Homo sapiens 285-288 23128353-8 2013 Altogether, our results suggest that a high dose of glucosamine may inhibit cell proliferation through apoptosis and disturb cell cycle progression with a halt at G(0)/G(1) phase, and that this occurs, at least in part, by a reduction in Rb phosphorylation together with modulation of p21, p53 and HO-1 expression, and nuclear p21 accumulation. Glucosamine 52-63 H3 histone pseudogene 16 Homo sapiens 327-330 23448150-1 2013 Previously, we demonstrated that magnolol, a hydroxylated biphenyl compound isolated from the bark of Magnolia officinalis, at low concentrations (3-10 muM) exerted an antiproliferation effect in colon cancer, hepatoma, and glioblastoma (U373) cell lines through upregulation of the p21/Cip1 protein. magnolol 33-41 H3 histone pseudogene 16 Homo sapiens 283-286 23268707-9 2013 Celecoxib treatment activated Cdc25C and inhibited p21 expression in both unirradiated and irradiated cells, regardless of COX-2 expression. Celecoxib 0-9 H3 histone pseudogene 16 Homo sapiens 51-54 23268707-11 2013 These results imply that celecoxib deactivates the G2 checkpoint via both Cdc25C- and p21-dependent pathways in irradiated cells, which subsequently die by secondary apoptosis. Celecoxib 25-34 H3 histone pseudogene 16 Homo sapiens 86-89 23184057-4 2013 Furthermore, hSSB1 also associates with the acetyltransferase p300 and is required for efficient transcriptional activation of the p53 target gene p21 by affecting the acetylation of p53 at lysine382. lysine382 190-199 H3 histone pseudogene 16 Homo sapiens 147-150 23434523-7 2013 DNA damage induced by AAI led to an arrest of cells in the S-phase which was associated with the increased expression of p53 and p21 proteins. aristolochic acid I 22-25 H3 histone pseudogene 16 Homo sapiens 129-132 23219618-7 2013 Therefore, these data suggest that CD34(+) cells from patients with lower-risk MDS present p21 dependent premature senescence, increased accumulation of ROS and DNA damage in CD34(+)CD38(-) cells could contribute to this process; however, CD34(+) cells from patients with higher-risk MDS could develop some mechanisms to uncouple ROS and DNA damage induced senescence. Reactive Oxygen Species 330-333 H3 histone pseudogene 16 Homo sapiens 91-94 23275086-11 2013 Moreover, overexpression of PTEN could induce ASMCs arrested in the G0/G1 phase through the downregulation of Cyclin D1 and upregulation of p21 expressions. asmcs 46-51 H3 histone pseudogene 16 Homo sapiens 140-143 22619007-6 2013 In addition, Silibinin caused an increase in p53 and p21 protein level as well as mRNA levels. Silybin 13-22 H3 histone pseudogene 16 Homo sapiens 53-56 22986577-10 2013 Furthermore, ethanol in combination with TRAIL increased the expression of cyclin-dependent kinase inhibitor p21 and decreased the levels of Bcl-2 and phosphorylated-AKT. Ethanol 13-20 H3 histone pseudogene 16 Homo sapiens 109-112 23146690-6 2013 The inhibition of phosphoinositide 3-kinase using Ly294002 augmented a decrease in the p21 level induced by their combination, but it showed no significant effects on expression of Sp1 and cyclin D1. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 50-58 H3 histone pseudogene 16 Homo sapiens 87-90 23449448-3 2013 In this study, we show that bortezomib induced apoptosis, which was demonstrated by the downregulation of antiapoptotic molecules (Bcl-2, Bcl-XL, p-Bad, and p-AKT) and the upregulation of proapoptotic proteins (p21, p27, and cleaved-Bid) in ovarian cancer cell lines. Bortezomib 28-38 H3 histone pseudogene 16 Homo sapiens 211-214 23361053-2 2013 The p21-regulated serine/threonine kinase PAK1, implicated in tamoxifen resistance, phosphorylates EBP1 in vitro and in vivo at T261. Tamoxifen 62-71 H3 histone pseudogene 16 Homo sapiens 4-7 22815158-6 2013 Activation of p53 by FK866 involved increased acetylation of p53 at lysine 382 with subsequent increase in the expression of p21 and BAX. N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide 21-26 H3 histone pseudogene 16 Homo sapiens 125-128 22815158-6 2013 Activation of p53 by FK866 involved increased acetylation of p53 at lysine 382 with subsequent increase in the expression of p21 and BAX. Lysine 68-74 H3 histone pseudogene 16 Homo sapiens 125-128 22815158-7 2013 Further, knockdown of p53 attenuated the effects of FK866 on apoptosis and cell cycle arrest, which was partly associated with decreased expression of p21 and BAX. N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide 52-57 H3 histone pseudogene 16 Homo sapiens 151-154 23395165-2 2013 A new study shows that, upon serine starvation, the tumor suppressor p53 activates p21 to shift metabolic flux from purine biosynthesis to glutathione production, which enhances cellular proliferation and viability by combating ROS (Maddocks et al., 2013). Serine 29-35 H3 histone pseudogene 16 Homo sapiens 83-86 23395165-2 2013 A new study shows that, upon serine starvation, the tumor suppressor p53 activates p21 to shift metabolic flux from purine biosynthesis to glutathione production, which enhances cellular proliferation and viability by combating ROS (Maddocks et al., 2013). purine 116-122 H3 histone pseudogene 16 Homo sapiens 83-86 23395165-2 2013 A new study shows that, upon serine starvation, the tumor suppressor p53 activates p21 to shift metabolic flux from purine biosynthesis to glutathione production, which enhances cellular proliferation and viability by combating ROS (Maddocks et al., 2013). Glutathione 139-150 H3 histone pseudogene 16 Homo sapiens 83-86 23395165-2 2013 A new study shows that, upon serine starvation, the tumor suppressor p53 activates p21 to shift metabolic flux from purine biosynthesis to glutathione production, which enhances cellular proliferation and viability by combating ROS (Maddocks et al., 2013). ros 228-231 H3 histone pseudogene 16 Homo sapiens 83-86 23065571-4 2013 Combination of 2DG and FA also increased the levels of p21 and GADD45A in NCI-H460 cells. Deoxyglucose 15-18 H3 histone pseudogene 16 Homo sapiens 55-58 23124852-5 2013 After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs. Reactive Oxygen Species 17-20 H3 histone pseudogene 16 Homo sapiens 180-183 23124852-5 2013 After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs. Acetylcysteine 26-42 H3 histone pseudogene 16 Homo sapiens 180-183 23065571-8 2013 Taken together, the results of our study clearly suggested that the cell death induced by the combination of 2DG and FA along with irradiation would involve alteration in expression of p53, p21, NF-kappaB, Bax, and caspase-3, indicating oxidative mechanism in NCI-H460 cells. Deoxyglucose 109-112 H3 histone pseudogene 16 Homo sapiens 190-193 23878945-5 2013 One of the adduct bis(O-butyldithiocarbonato)bis(3,5-dimethylpyridine)nickel(II) crystallizes in the monoclinic space group P21/c with unit cell parameters. bis(o-butyldithiocarbonato)bis(3,5-dimethylpyridine)nickel 18-76 H3 histone pseudogene 16 Homo sapiens 124-127 24088253-4 2013 Furthermore, sesamin suppressed the constitutive and interleukin (IL)-6-induced signal transducer and activator of transcription 3 (STAT3) signalling pathway in HepG2 cells, leading to regulate the downstream genes, including p53, p21, cyclin proteins and the Bcl-2 protein family. sesamin 13-20 H3 histone pseudogene 16 Homo sapiens 231-234 23278893-8 2013 Further evidences of AzA anti-senescence effect were repression of p53 and p21, increase in type I pro-collagen and abrogation of the enhanced expression of growth factors, such as HGF and SCF. azelaic acid 21-24 H3 histone pseudogene 16 Homo sapiens 75-78 24141202-4 2013 The resulting accumulation of p53 proteins from phosphorylation at serine-15 and serine-392 was correlated with an increase in p21 and caspase activation. Serine 67-73 H3 histone pseudogene 16 Homo sapiens 127-130 24141202-4 2013 The resulting accumulation of p53 proteins from phosphorylation at serine-15 and serine-392 was correlated with an increase in p21 and caspase activation. Serine 81-87 H3 histone pseudogene 16 Homo sapiens 127-130 22918703-0 2013 CCAAT/Enhancer-binding protein-homologous protein sensitizes to SU5416 by modulating p21 and PI3K/Akt signal pathway in FRO anaplastic thyroid carcinoma cells. Semaxinib 64-70 H3 histone pseudogene 16 Homo sapiens 85-88 22918703-12 2013 In conclusion, these results suggest that CHOP may sensitize FRO ATC cells to SU5416 thereby inhibiting cell survival by modulating p21 and PI3K/Akt signal pathway. Semaxinib 78-84 H3 histone pseudogene 16 Homo sapiens 132-135 22918703-8 2013 In SU5416-treated situation, cell viability was not different before and after administration of either p21 siRNA or LY294002 whereas it was lessened after co-administration of p21 siRNA and LY294002. Semaxinib 3-9 H3 histone pseudogene 16 Homo sapiens 177-180 23154268-5 2013 Most of the PCV patients showed no overexpression of p53 and high expression of p21, cyclin A, and Ki67. penciclovir 12-15 H3 histone pseudogene 16 Homo sapiens 80-83 22674530-8 2013 Remarkably, Pi/doxorubicin combination-induced cytotoxicity was accompanied by an increase of p53 protein levels and of p53 target genes mdm2, p21 and Bax, and was significantly reduced by the p53 inhibitor pifithrine-alpha. Doxorubicin 15-26 H3 histone pseudogene 16 Homo sapiens 143-146 22674530-8 2013 Remarkably, Pi/doxorubicin combination-induced cytotoxicity was accompanied by an increase of p53 protein levels and of p53 target genes mdm2, p21 and Bax, and was significantly reduced by the p53 inhibitor pifithrine-alpha. pifithrine 207-217 H3 histone pseudogene 16 Homo sapiens 143-146 23067223-6 2013 Anisomycin also induced cell cycle arrest at G0/G1 phase in CEM-C1 cells through increasing expressions of p21 and p27, and attenuating the expression of cyclinA. Anisomycin 0-10 H3 histone pseudogene 16 Homo sapiens 107-110 23476648-0 2013 Enhancement of Cisplatin-Mediated Apoptosis in Ovarian Cancer Cells through Potentiating G2/M Arrest and p21 Upregulation by Combinatorial Epigallocatechin Gallate and Sulforaphane. Cisplatin 15-24 H3 histone pseudogene 16 Homo sapiens 105-108 23476648-0 2013 Enhancement of Cisplatin-Mediated Apoptosis in Ovarian Cancer Cells through Potentiating G2/M Arrest and p21 Upregulation by Combinatorial Epigallocatechin Gallate and Sulforaphane. combinatorial 125-138 H3 histone pseudogene 16 Homo sapiens 105-108 23476648-0 2013 Enhancement of Cisplatin-Mediated Apoptosis in Ovarian Cancer Cells through Potentiating G2/M Arrest and p21 Upregulation by Combinatorial Epigallocatechin Gallate and Sulforaphane. epigallocatechin gallate 139-163 H3 histone pseudogene 16 Homo sapiens 105-108 23476648-0 2013 Enhancement of Cisplatin-Mediated Apoptosis in Ovarian Cancer Cells through Potentiating G2/M Arrest and p21 Upregulation by Combinatorial Epigallocatechin Gallate and Sulforaphane. sulforaphane 168-180 H3 histone pseudogene 16 Homo sapiens 105-108 23476648-8 2013 EGCG and SFN combinational treatment upregulated p21 expression induced by cisplatin in cisplatin-sensitive ovarian cancer cells, while p27 expression was not regulated by these treatments. epigallocatechin gallate 0-4 H3 histone pseudogene 16 Homo sapiens 49-52 23476648-8 2013 EGCG and SFN combinational treatment upregulated p21 expression induced by cisplatin in cisplatin-sensitive ovarian cancer cells, while p27 expression was not regulated by these treatments. sulforaphane 9-12 H3 histone pseudogene 16 Homo sapiens 49-52 23476648-8 2013 EGCG and SFN combinational treatment upregulated p21 expression induced by cisplatin in cisplatin-sensitive ovarian cancer cells, while p27 expression was not regulated by these treatments. Cisplatin 75-84 H3 histone pseudogene 16 Homo sapiens 49-52 23476648-8 2013 EGCG and SFN combinational treatment upregulated p21 expression induced by cisplatin in cisplatin-sensitive ovarian cancer cells, while p27 expression was not regulated by these treatments. Cisplatin 88-97 H3 histone pseudogene 16 Homo sapiens 49-52 23360998-7 2013 In human osteosarcoma cells, stictic acid exhibits dose-dependent reactivation of p21 expression for mutant R175H more strongly than does PRIMA-1. stictic acid 29-41 H3 histone pseudogene 16 Homo sapiens 82-85 23530650-6 2013 Western blotting showed that 75 muM of DAS-induced G0/G1 phase arrest was mediated through the increased expression of p21, p27, and p53 with a simultaneous decrease in CDK2, CDK6, and CHK2 expression. allyl sulfide 39-42 H3 histone pseudogene 16 Homo sapiens 119-122 23950593-8 2013 In addition, BDMC activated the pro-apoptotic protein p53 and its downstream effector p21 as well as the cell cycle regulatory proteins p16 and its downstream effector retinoblastoma protein (Rb). bisdemethoxycurcumin 13-17 H3 histone pseudogene 16 Homo sapiens 86-89 23064281-7 2013 In addition, sequential or concomitant treatment of bortezomib and cisplatin stimulated the expression of p53, hScrib and p21 and the stimulation was markedly influenced by the order of drugs in HeLa cells. Bortezomib 52-62 H3 histone pseudogene 16 Homo sapiens 134-137 23064281-7 2013 In addition, sequential or concomitant treatment of bortezomib and cisplatin stimulated the expression of p53, hScrib and p21 and the stimulation was markedly influenced by the order of drugs in HeLa cells. Cisplatin 67-76 H3 histone pseudogene 16 Homo sapiens 134-137 23950593-10 2013 CONCLUSIONS: These results suggested that BDMC-induced ROS accumulation may contribute to its inhibitory effect on MCF-7 cell viability through regulation of p53/p21 and p16/Rb pathways. bisdemethoxycurcumin 42-46 H3 histone pseudogene 16 Homo sapiens 162-165 23950593-10 2013 CONCLUSIONS: These results suggested that BDMC-induced ROS accumulation may contribute to its inhibitory effect on MCF-7 cell viability through regulation of p53/p21 and p16/Rb pathways. ros 55-58 H3 histone pseudogene 16 Homo sapiens 162-165 23085518-6 2012 Mechanistically, enhancement of ROS production by T63 induced FOXO3a expression and nuclear translocation through activation of p38MAPK and inhibition of AKT, subsequently elevating the expression of FOXO3a target genes, including p21, p27, and Bim, and then increased the levels of activated caspase-3 and decreased the levels of cyclin D1. Reactive Oxygen Species 32-35 H3 histone pseudogene 16 Homo sapiens 231-234 23349840-13 2013 Along with an additive stimulatory effect of cAMP and TGFbeta on p21 expression an additive inhibitory effect of these agents on proliferation was observed. Cyclic AMP 45-49 H3 histone pseudogene 16 Homo sapiens 65-68 23349842-4 2013 Our results demonstrated that homocysteine inhibited hepatocyte proliferation by up-regulating protein levels of p53 as well as mRNA and protein levels of p21(Cip1) in primary cultured hepatocytes. Homocysteine 30-42 H3 histone pseudogene 16 Homo sapiens 155-158 23349842-6 2013 A p53 inhibitor pifithrin-alpha inhibited the expression of p21(Cip1) and attenuated homocysteine-induced cell growth arrest. pifithrin 16-31 H3 histone pseudogene 16 Homo sapiens 60-63 23349842-10 2013 These results demonstrate that both TRB3 and p21(Cip1) are critical molecules in the homocysteine signaling cascade and provide a mechanistic explanation for impairment of liver regeneration in hyperhomocysteinemia. Homocysteine 85-97 H3 histone pseudogene 16 Homo sapiens 45-48 23859040-3 2013 ECG induced cell cycle arrest at the G0/G1-S phase border associated with the stimulation of p21, p-p53, and p53 and the suppression of cyclins D1 and B1. epicatechin gallate 0-3 H3 histone pseudogene 16 Homo sapiens 93-96 23451128-6 2013 An up-regulated expression of CDK inhibitor p21 along with suppressed expression of mutated p53 was observed in MDA-MB-231 cells treated with alpha-santalol. a-santalol 142-156 H3 histone pseudogene 16 Homo sapiens 44-47 23256041-3 2012 Doxorubicin stimulates proteolytic cleavage of CREB3L1 by Site-1 Protease and Site-2 Protease, allowing the NH(2)-terminal domain of CREB3L1 to enter the nucleus where it activates transcription of genes encoding inhibitors of the cell cycle, including p21. Doxorubicin 0-11 H3 histone pseudogene 16 Homo sapiens 253-256 23160189-1 2012 A La(2)NiMnO(6) polycrystalline sample prepared by the sol-gel method showed monoclinic crystal structure with the P2(1)/n space group and a saturation magnetization of 4.63 mu(B)/f.u. la(2)nimno 2-12 H3 histone pseudogene 16 Homo sapiens 115-120 23160189-1 2012 A La(2)NiMnO(6) polycrystalline sample prepared by the sol-gel method showed monoclinic crystal structure with the P2(1)/n space group and a saturation magnetization of 4.63 mu(B)/f.u. polycrystalline 16-31 H3 histone pseudogene 16 Homo sapiens 115-120 22843228-7 2012 The FA-inhibited [3H]thymidine incorporation was completely blocked when the expressions of p21 and p27 were knocked-down together. Tritium 18-20 H3 histone pseudogene 16 Homo sapiens 92-95 23192018-2 2012 The availability of Mn2+ during the crystallization process appears to play an important role in inducing different crystal packings that lead to crystals belonging to the two space groups P2(1) and P6(5). Manganese(2+) 20-24 H3 histone pseudogene 16 Homo sapiens 189-194 22843228-7 2012 The FA-inhibited [3H]thymidine incorporation was completely blocked when the expressions of p21 and p27 were knocked-down together. Thymidine 21-30 H3 histone pseudogene 16 Homo sapiens 92-95 22634494-4 2012 RITA promoted apoptosis in association with upregulation of p21, BAX, and cleaved caspase-3; notably, the apoptotic response was blocked by pifithrin-alpha, demonstrating its p53 dependence. RITA 0-4 H3 histone pseudogene 16 Homo sapiens 60-63 22644070-7 2012 p21 was associated with a lower response to sunitinib (35.9 vs. 65.4; p = 0.025). Sunitinib 44-53 H3 histone pseudogene 16 Homo sapiens 0-3 22957647-5 2012 In human prostate cancer DU145 cells with mutated RB, flavone increased cyclin-dependent kinase (CDK) inhibitors p21 and p27, and reduced cdk4 and cdk6, resulting in decrement of phosphorylated RB family proteins p130 and p107. flavone 54-61 H3 histone pseudogene 16 Homo sapiens 113-116 22644070-12 2012 PTEN and p21 may be important in predicting response to sunitinib. Sunitinib 56-65 H3 histone pseudogene 16 Homo sapiens 9-12 22814742-0 2012 Cyclin D1 degradation and p21 induction contribute to growth inhibition of colorectal cancer cells induced by epigallocatechin-3-gallate. epigallocatechin gallate 110-136 H3 histone pseudogene 16 Homo sapiens 26-29 22814742-8 2012 RESULTS: We identified cyclin D1 and p21 as molecular targets of EGCG in human colorectal cancer cells. epigallocatechin gallate 65-69 H3 histone pseudogene 16 Homo sapiens 37-40 22814742-9 2012 We observed that cyclin D1 was down-regulated, while p21 expression was up-regulated by EGCG in dose- and time-dependent manners. epigallocatechin gallate 88-92 H3 histone pseudogene 16 Homo sapiens 53-56 22814742-11 2012 Meanwhile, EGCG increased p21 promoter activity, resulting in up-regulation of p21 mRNA and protein, which was likely dependent on extracellular-signal-regulated kinase (ERK), inhibitor of nuclear factor kappa-B kinase (IKK) and phosphoinositide 3-kinase (PI3 K). epigallocatechin gallate 11-15 H3 histone pseudogene 16 Homo sapiens 26-29 22814742-11 2012 Meanwhile, EGCG increased p21 promoter activity, resulting in up-regulation of p21 mRNA and protein, which was likely dependent on extracellular-signal-regulated kinase (ERK), inhibitor of nuclear factor kappa-B kinase (IKK) and phosphoinositide 3-kinase (PI3 K). epigallocatechin gallate 11-15 H3 histone pseudogene 16 Homo sapiens 79-82 22814742-13 2012 Namely, EGCG-induced cyclin D1 degradation and p21 transcriptional activation partially contribute to growth suppression in these cells. epigallocatechin gallate 8-12 H3 histone pseudogene 16 Homo sapiens 47-50 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. 3-deazaneplanocin 80-85 H3 histone pseudogene 16 Homo sapiens 220-223 23257465-5 2012 The roles of p53-p21 and p16-Rb pathways can induce hematopoietic dysfunction and lead to ROS-induced HSC senescence. Reactive Oxygen Species 90-93 H3 histone pseudogene 16 Homo sapiens 17-20 22956150-3 2012 Aim of investigation was to study the effects of cholinergic precursors (choline, CDP-choline, Acetylcholine and alpha-Glyceril-Phosphorylcholine) on HO-1 and p21 expression during astroglial cell proliferation and differentiation in primary cultures at 14 and 35 days in vitro (DIV) treated for 24 h with choline metabolites. Choline 49-56 H3 histone pseudogene 16 Homo sapiens 159-162 22956150-3 2012 Aim of investigation was to study the effects of cholinergic precursors (choline, CDP-choline, Acetylcholine and alpha-Glyceril-Phosphorylcholine) on HO-1 and p21 expression during astroglial cell proliferation and differentiation in primary cultures at 14 and 35 days in vitro (DIV) treated for 24 h with choline metabolites. Acetylcholine 95-108 H3 histone pseudogene 16 Homo sapiens 159-162 22956150-3 2012 Aim of investigation was to study the effects of cholinergic precursors (choline, CDP-choline, Acetylcholine and alpha-Glyceril-Phosphorylcholine) on HO-1 and p21 expression during astroglial cell proliferation and differentiation in primary cultures at 14 and 35 days in vitro (DIV) treated for 24 h with choline metabolites. alpha-glyceril-phosphorylcholine 113-145 H3 histone pseudogene 16 Homo sapiens 159-162 22956150-3 2012 Aim of investigation was to study the effects of cholinergic precursors (choline, CDP-choline, Acetylcholine and alpha-Glyceril-Phosphorylcholine) on HO-1 and p21 expression during astroglial cell proliferation and differentiation in primary cultures at 14 and 35 days in vitro (DIV) treated for 24 h with choline metabolites. Choline 73-80 H3 histone pseudogene 16 Homo sapiens 159-162 22956150-10 2012 Instead, ACh treatment induced a marked increment of p21 expression at 35 DIV. Acetylcholine 9-12 H3 histone pseudogene 16 Homo sapiens 53-56 22962266-5 2012 Unexpectedly, when CAFs were analyzed, p53 accumulation and induction of p21 was observed only in tumors with constitutively low p53 protein and accumulation upon cisplatin treatment. Cisplatin 163-172 H3 histone pseudogene 16 Homo sapiens 73-76 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Panobinostat 90-92 H3 histone pseudogene 16 Homo sapiens 220-223 23037503-0 2012 Inhibition of tumor promotion by parthenolide: epigenetic modulation of p21. parthenolide 33-45 H3 histone pseudogene 16 Homo sapiens 72-75 22828135-7 2012 In addition, a reduction in the number of cells in S-phase, characterized by a concomitant increase in the levels of p21 and p53 proteins, together with a strong inhibition of pRb protein phosphorylation, was observed in DHS-treated cells. 4,4'-dihydroxystilbene 221-224 H3 histone pseudogene 16 Homo sapiens 117-120 23037503-2 2012 We investigated whether the NF-kB inhibitor, parthenolide, currently in cancer clinical trials, attenuates tumor promotion by modulating the epigenetically regulated NF-kB target genes, p21 and cyclin D1. parthenolide 45-57 H3 histone pseudogene 16 Homo sapiens 186-189 23038051-2 2012 The results showed that this semiconducting polymer crystallizes in the monoclinic space group P2(1)/c with nontilted pi-stacks at a distance of 3.9 A (see picture). Polymers 44-51 H3 histone pseudogene 16 Homo sapiens 95-100 23037503-5 2012 Furthermore, parthenolide decreased tumor promoter-induced NF-kB activity, increased p21, and decreased cyclin D1 expression. parthenolide 13-25 H3 histone pseudogene 16 Homo sapiens 85-88 23037503-6 2012 In parthenolide-treated cells, p21 transcription correlated with relaxed chromatin and p65/NF-kB binding at the p21 promoter. parthenolide 3-15 H3 histone pseudogene 16 Homo sapiens 31-34 23037503-6 2012 In parthenolide-treated cells, p21 transcription correlated with relaxed chromatin and p65/NF-kB binding at the p21 promoter. parthenolide 3-15 H3 histone pseudogene 16 Homo sapiens 112-115 23037503-9 2012 Because p21 expression by parthenolide was sustained, we used p21-siRNA and p21 -/- cancer cells and showed that the loss of p21 is cytoprotective against parthenolide. parthenolide 26-38 H3 histone pseudogene 16 Homo sapiens 8-11 23037503-12 2012 These results show that low doses of parthenolide inhibit tumor promotion and epigenetically modulate p21 expression, highlighting the potential role of this drug as a chemopreventive agent and in epigenetic cancer therapy. parthenolide 37-49 H3 histone pseudogene 16 Homo sapiens 102-105 23146670-5 2012 Whereas doxorubicin treatment in early-passaged cells results in nucleosome density changes near the p53 binding sites of the p21 promoter, our studies show that senescent cells with a high p21 transcription activity had a comparable nucleosome distribution as unstressed young cells. Doxorubicin 8-19 H3 histone pseudogene 16 Homo sapiens 126-129 23110523-11 2012 Lastly, we performed cell cycle array analysis of Cl-amidine treated and control MCF10DCIS cells, and found that the PADI inhibitor strongly affects the expression of several cell cycle genes implicated in tumor progression, including p21, GADD45alpha, and Ki67. N-alpha-benzoyl-N5-(2-chloro-1-iminoethyl)-L-ornithine amide 50-60 H3 histone pseudogene 16 Homo sapiens 235-238 22841670-5 2012 Further mechanistic studies revealed that bufotalin treatment induced cell cycle arrest at G(2)/M phase through down-regulation of Aurora A, CDC25, CDK1, cyclin A and cyclin B1, as well as up-regulation of p53 and p21. bufotalin 42-51 H3 histone pseudogene 16 Homo sapiens 214-217 22872685-6 2012 Treatment with low doses of Peg IFN-alpha 2a combined with Nutlin-3 increased phospho-p53 and p21 protein levels in PV CD34(+) cells and increased the degree of apoptosis. Polyethylene Glycols 28-31 H3 histone pseudogene 16 Homo sapiens 94-97 22707243-8 2012 Furthermore, Rosiglitazone affects the expression of Smad3/Smad4 associated regulators of gene expression, including p21 and c-Myc. Rosiglitazone 13-26 H3 histone pseudogene 16 Homo sapiens 117-120 22903553-10 2012 The p53 and p21 promoter luciferase activities were promoted by either sMEK1 or gemcitabine, and sMEK1 and gemcitabine combined additively activated the promoter further. gemcitabine 80-91 H3 histone pseudogene 16 Homo sapiens 12-15 22903553-10 2012 The p53 and p21 promoter luciferase activities were promoted by either sMEK1 or gemcitabine, and sMEK1 and gemcitabine combined additively activated the promoter further. gemcitabine 107-118 H3 histone pseudogene 16 Homo sapiens 12-15 23013131-0 2012 Aldosterone induces p21-regulated apoptosis via increased synthesis and secretion of tumour necrosis factor-alpha in human proximal tubular cells. Aldosterone 0-11 H3 histone pseudogene 16 Homo sapiens 20-23 23013131-4 2012 The aim of the present study was to investigate the hypothesis that aldosterone increases proximal tubular apoptosis by increasing the secretion of apoptosis-inducing factors through a p21-dependent mechanism. Aldosterone 68-79 H3 histone pseudogene 16 Homo sapiens 185-188 23182046-5 2012 Flow cytometric analysis showed that quinuclidinone derivative 6 reduced the percentage of MCF-7 cells in G(2)/M which is confirmed by increased expression levels of cyclin B, while it arrests MCF12a in G1 phase judging from increased p21. 1-azabicyclo[2.2.2]octan-2-one 38-52 H3 histone pseudogene 16 Homo sapiens 236-239 22711363-8 2012 Dracorhodin perchlorate induced up-regulation of p53, thereby resulting in the activation of its downstream targets p21 and Bax following the dissipation of mitochondrial membrane potential and activation of caspase-3 and its substrate, PARP. dracorhodin 0-23 H3 histone pseudogene 16 Homo sapiens 116-119 23013131-9 2012 Exposure of cells to aldosterone for 3 or 5 days increased senescence-associated beta-galactosidase staining, p21 and TNF-alpha mRNA expression and secretion of TNF-alpha into the culture medium. Aldosterone 21-32 H3 histone pseudogene 16 Homo sapiens 110-113 23013131-15 2012 These findings indicate that aldosterone increases TNF-alpha synthesis and secretion in proximal tubular cells via p21/senescence-dependent cell phenotypic changes and that the TNF-alpha secreted plays an important role as a paracrine factor in mediating cell apoptosis, indicating a possible involvement in aldosterone-induced renal damage. Aldosterone 29-40 H3 histone pseudogene 16 Homo sapiens 115-118 22859066-5 2012 Furthermore, the low concentration of DHT induced lower mRNA levels in the p53 and p21 genes in HNTEP cells. Dihydrotestosterone 38-41 H3 histone pseudogene 16 Homo sapiens 83-86 22859066-6 2012 In turn, high DHT concentrations induced a significant increase in the expression of the p53 and p21 genes. Dihydrotestosterone 14-17 H3 histone pseudogene 16 Homo sapiens 97-100 22787116-9 2012 Low concentrations of MG262 provoked growth arrest, inhibited DNA replication and retinoblastoma phosphorylation, and increased expression of the cell cycle inhibitors p21 and p27. MG 262 22-27 H3 histone pseudogene 16 Homo sapiens 168-171 22799769-2 2012 We proposed PTHLH-activated network that upstream included the regulation of apoptosis, signal transduction resulting in induction of apoptosis, signal transduction by p53 class mediator resulting in transcription of p21 class mediator, negative regulation of centriole replication, negative regulation of fatty acid biosynthesis, negative regulation of Wnt receptor signaling pathway, anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolism, apoptosis, induction of apoptosis, and negative regulation of phosphorylation. Fatty Acids 306-316 H3 histone pseudogene 16 Homo sapiens 217-220 22627294-5 2012 The global analysis and quantitative PCR demonstrated that mRNA levels of p21(Cip1), an inhibitor of cyclins D and E, and of GADD45alpha, a growth arrest and DNA damage-inducible protein, were significantly increased by clioquinol treatment in SH-SY5Y and IMR-32 neuroblastoma cells. Clioquinol 220-230 H3 histone pseudogene 16 Homo sapiens 74-77 22723548-4 2012 Furthermore, Treg-mediated molecular control of senescence in responder T cells was associated with selective modulation of p38 and ERK1/2 signaling and cell-cycle-regulatory molecules p16, p21, and p53. treg 13-17 H3 histone pseudogene 16 Homo sapiens 190-193 23017148-5 2012 Moreover, AQP3 siRNA significantly blocked other effects of nucleoside analogs, including G1/S cell cycle arrest, p21 and FAS up-regulation, and cell growth inhibition. Nucleosides 60-70 H3 histone pseudogene 16 Homo sapiens 114-117 25585933-5 2012 A limitation for this biosensor system was that it might give false positive results in response to sodium butyrate and any other agents, which can trans-activate the p21 gene in a p53-independent manner. Butyric Acid 100-115 H3 histone pseudogene 16 Homo sapiens 167-170 22993307-6 2012 administration of CHO27 suppressed the growth of established PCa 22Rv1 xenograft tumors accompanied with p53 and p21(Cip1) induction. cho27 18-23 H3 histone pseudogene 16 Homo sapiens 113-116 22460505-4 2012 Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1, cyclin A and CDK4, and the induction of p21 and p27, a cyclin-dependent kinase inhibitor. Thioridazine 30-42 H3 histone pseudogene 16 Homo sapiens 125-128 22705644-11 2012 CIL-102-treatment induced apoptosis in MCF-7 cells in association with increased nuclear accumulation of p53 and p21 suggesting that apoptosis is triggered through a p53-p21 dependent pathway. 1-(4-(furo(2,3-b)quinolin-4-ylamino)phenyl)ethanone 0-7 H3 histone pseudogene 16 Homo sapiens 113-116 22705644-11 2012 CIL-102-treatment induced apoptosis in MCF-7 cells in association with increased nuclear accumulation of p53 and p21 suggesting that apoptosis is triggered through a p53-p21 dependent pathway. 1-(4-(furo(2,3-b)quinolin-4-ylamino)phenyl)ethanone 0-7 H3 histone pseudogene 16 Homo sapiens 170-173 22591064-2 2012 We previously reported that Asp-hemolysin-related synthetic peptide (P21) composed of 21 amino acid residues markedly inhibits the bioactivities of oxidized low-density lipoprotein and lysophosphatidylcholine, by directly binding to oxidized low-density lipoprotein and lysophosphatidylcholine. Lysophosphatidylcholines 185-208 H3 histone pseudogene 16 Homo sapiens 69-72 22814677-9 2012 DHCF treatment resulted in upregulation of p21(Cip1) and downregulation of cyclin A in all three PCa cell lines. 23,24-dihydrocucurbitacin F 0-4 H3 histone pseudogene 16 Homo sapiens 43-46 22591064-2 2012 We previously reported that Asp-hemolysin-related synthetic peptide (P21) composed of 21 amino acid residues markedly inhibits the bioactivities of oxidized low-density lipoprotein and lysophosphatidylcholine, by directly binding to oxidized low-density lipoprotein and lysophosphatidylcholine. Lysophosphatidylcholines 270-293 H3 histone pseudogene 16 Homo sapiens 69-72 22591064-3 2012 Here, to clarify whether P21 specifically binds to lysophosphatidylcholine and what forms of lysophosphatidylcholine with which P21 interact, we investigated the interaction between P21 containing two tryptophan residues and lysophosphatidylcholine by using fluorescence spectroscopy, polyacrylamide gel electrophoresis, and surface plasmon resonance. Lysophosphatidylcholines 51-74 H3 histone pseudogene 16 Homo sapiens 25-28 22591064-4 2012 From tryptophan fluorescence measurements, N-terminally biotinylated P21 specifically interacted with lysophosphatidylcholine, at concentrations exceeding the critical micelle concentration. Tryptophan 5-15 H3 histone pseudogene 16 Homo sapiens 69-72 22591064-4 2012 From tryptophan fluorescence measurements, N-terminally biotinylated P21 specifically interacted with lysophosphatidylcholine, at concentrations exceeding the critical micelle concentration. Lysophosphatidylcholines 102-125 H3 histone pseudogene 16 Homo sapiens 69-72 22591064-5 2012 From tryptophan fluorescence quenching, the tryptophan residues in biotinylated P21 in the presence of lysophosphatidylcholine were mostly exposed on the outer side of the peptide. Tryptophan 5-15 H3 histone pseudogene 16 Homo sapiens 80-83 22591064-5 2012 From tryptophan fluorescence quenching, the tryptophan residues in biotinylated P21 in the presence of lysophosphatidylcholine were mostly exposed on the outer side of the peptide. Tryptophan 44-54 H3 histone pseudogene 16 Homo sapiens 80-83 22591064-5 2012 From tryptophan fluorescence quenching, the tryptophan residues in biotinylated P21 in the presence of lysophosphatidylcholine were mostly exposed on the outer side of the peptide. Lysophosphatidylcholines 103-126 H3 histone pseudogene 16 Homo sapiens 80-83 22591064-7 2012 These results indicate that biotinylated P21 specifically recognizes lysophosphatidylcholine micelles. Lysophosphatidylcholines 69-92 H3 histone pseudogene 16 Homo sapiens 41-44 22591064-8 2012 Further study of the interaction between biotinylated P21 and lysophosphatidylcholine micelles may provide important information for the prevention and treatment for many inflammatory diseases caused by lysophosphatidylcholine micelles. Lysophosphatidylcholines 62-85 H3 histone pseudogene 16 Homo sapiens 54-57 22591064-8 2012 Further study of the interaction between biotinylated P21 and lysophosphatidylcholine micelles may provide important information for the prevention and treatment for many inflammatory diseases caused by lysophosphatidylcholine micelles. Lysophosphatidylcholines 203-226 H3 histone pseudogene 16 Homo sapiens 54-57 23018309-9 2012 Vitamin K2 also attenuated the downregulation of p21 expression induced by sorafenib, which may represent the mechanism by which vitamin K2 promotes the inhibitory effects of sorafenib on cell proliferation. Vitamin K 2 0-10 H3 histone pseudogene 16 Homo sapiens 49-52 23018309-9 2012 Vitamin K2 also attenuated the downregulation of p21 expression induced by sorafenib, which may represent the mechanism by which vitamin K2 promotes the inhibitory effects of sorafenib on cell proliferation. Sorafenib 75-84 H3 histone pseudogene 16 Homo sapiens 49-52 23018309-9 2012 Vitamin K2 also attenuated the downregulation of p21 expression induced by sorafenib, which may represent the mechanism by which vitamin K2 promotes the inhibitory effects of sorafenib on cell proliferation. Vitamin K 2 129-139 H3 histone pseudogene 16 Homo sapiens 49-52 23018309-9 2012 Vitamin K2 also attenuated the downregulation of p21 expression induced by sorafenib, which may represent the mechanism by which vitamin K2 promotes the inhibitory effects of sorafenib on cell proliferation. Sorafenib 175-184 H3 histone pseudogene 16 Homo sapiens 49-52 22018604-7 2012 In addition, GCTI increased the expression of cell cycle inhibitory proteins (p21, p27 and p53) and the Bax-to-Bcl-2 ratio to induce apoptosis. gcti 13-17 H3 histone pseudogene 16 Homo sapiens 78-81 22752086-6 2012 This revealed that the methanol extract increased the levels of p21 and this may have caused cell cycle attenuation. Methanol 23-31 H3 histone pseudogene 16 Homo sapiens 64-67 22770909-4 2012 The enzyme 15-lipoxygenase type 1 (15-LOX-1), which is involved in arachidonic and linoleic acid metabolism, has the potential to down-regulate the expression of p21. arachidonic 67-78 H3 histone pseudogene 16 Homo sapiens 162-165 22770909-4 2012 The enzyme 15-lipoxygenase type 1 (15-LOX-1), which is involved in arachidonic and linoleic acid metabolism, has the potential to down-regulate the expression of p21. Linoleic Acid 83-96 H3 histone pseudogene 16 Homo sapiens 162-165 22970038-9 2012 Furthermore, downregulation of CDK4 and upregulation of p21 and Bak by AEA were observed. anandamide 71-74 H3 histone pseudogene 16 Homo sapiens 56-59 21769450-3 2012 MTT and cell cycle analysis results indicated that perifosine inhibited the growth of HUVECs in a dose-dependent manner, arrested cell cycle progression at the G(2) phase with regulation the expression of p21 and cyclinB1. perifosine 51-61 H3 histone pseudogene 16 Homo sapiens 205-208 22766505-6 2012 The protein levels of cyclin-dependent kinase inhibitors, p21 and p27(Kip), which inhibit cell proliferation by blocking cell cycle progression at G1/S phase, increased after RA treatment. Tretinoin 175-177 H3 histone pseudogene 16 Homo sapiens 58-61 22750490-6 2012 NAG-1 and p21 expression was not blocked by PPARgamma-specific antagonist GW9662, suggesting that MCC-555-induced NAG-1 and p21 expression is independent of PPARgamma activation. netoglitazone 98-105 H3 histone pseudogene 16 Homo sapiens 10-13 22750490-6 2012 NAG-1 and p21 expression was not blocked by PPARgamma-specific antagonist GW9662, suggesting that MCC-555-induced NAG-1 and p21 expression is independent of PPARgamma activation. netoglitazone 98-105 H3 histone pseudogene 16 Homo sapiens 124-127 22617025-4 2012 Berberine arrested SW480 cell cycle at G2/M phase, which was supported by induction of p21 expression. Berberine 0-9 H3 histone pseudogene 16 Homo sapiens 87-90 22862878-8 2012 Antp-p21 killed cancer cells selectively that were malignant as a result of mutations or nuclear exclusion of the p53 and p21 genes and over-expression of MDM2. antp 0-4 H3 histone pseudogene 16 Homo sapiens 5-8 22561451-7 2012 In addition, resveratrol suppressed Ang II-induced induction of p53 and its downstream target gene p21, both of which play an important role in the induction of senescence. Resveratrol 13-24 H3 histone pseudogene 16 Homo sapiens 99-102 22561451-8 2012 Resveratrol suppressed senescence of VSMC possibly through inhibition of AT1R-dependent induction of p53/p21. Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 105-108 22561451-8 2012 Resveratrol suppressed senescence of VSMC possibly through inhibition of AT1R-dependent induction of p53/p21. vsmc 37-41 H3 histone pseudogene 16 Homo sapiens 105-108 22789129-2 2012 The crystal structure of Cl(3)SiSiCl(3) TMEDA displays one tetrahedrally and one octahedrally bonded Si atom (monoclinic, P2(1)/n). Silicon 30-32 H3 histone pseudogene 16 Homo sapiens 122-127 22862878-8 2012 Antp-p21 killed cancer cells selectively that were malignant as a result of mutations or nuclear exclusion of the p53 and p21 genes and over-expression of MDM2. antp 0-4 H3 histone pseudogene 16 Homo sapiens 122-125 22904824-0 2012 Diosgenone: a second P2(1) polymorph. diosgenone 0-10 H3 histone pseudogene 16 Homo sapiens 21-26 22862878-9 2012 Non-specific toxicity was excluded by showing that Antp-p21 penetrated but did not kill p53- or p21- wild-type cells. antp 51-55 H3 histone pseudogene 16 Homo sapiens 56-59 22862878-10 2012 Antp-p21 was not immunogenic in normal New Zealand White rabbits. antp 0-4 H3 histone pseudogene 16 Homo sapiens 5-8 22711276-7 2012 Exposure to valproic acid and suberoylanilide hydroxamic acid was associated with increased levels of p21 and FOXO3 and reduced expression of survivin. Valproic Acid 12-25 H3 histone pseudogene 16 Homo sapiens 102-105 21695420-6 2012 WI-38 fibroblasts exposed to a subcytotoxic concentration of copper sulfate presented inhibition of cell proliferation, cell enlargement, increased SA beta-gal activity, and mRNA overexpression of several senescence-associated genes such as p21, apolipoprotein J (ApoJ), fibronectin, transforming growth factor beta-1 (TGF beta1), insulin growth factor binding protein 3, and heme oxygenase 1. Copper Sulfate 61-75 H3 histone pseudogene 16 Homo sapiens 241-244 21695420-7 2012 Western blotting results confirmed enhanced intracellular p21, ApoJ, and TGF beta1 in copper-treated cells. Copper 86-92 H3 histone pseudogene 16 Homo sapiens 58-61 21573958-4 2012 Sal treatment also reduced p21 levels in radiation-treated cells. salinomycin 0-3 H3 histone pseudogene 16 Homo sapiens 27-30 21573958-5 2012 Considering that Sal sensitizes doxorubicin (DOX)- or etoposide (ETO)-treated cancer cells by causing DNA damage and reducing p21 expression, the results from our study suggest that the mechanism underlying Sal sensitization is conserved in both chemo- and radiation-treated cells. salinomycin 17-20 H3 histone pseudogene 16 Homo sapiens 126-129 21573958-5 2012 Considering that Sal sensitizes doxorubicin (DOX)- or etoposide (ETO)-treated cancer cells by causing DNA damage and reducing p21 expression, the results from our study suggest that the mechanism underlying Sal sensitization is conserved in both chemo- and radiation-treated cells. Doxorubicin 32-43 H3 histone pseudogene 16 Homo sapiens 126-129 21573958-5 2012 Considering that Sal sensitizes doxorubicin (DOX)- or etoposide (ETO)-treated cancer cells by causing DNA damage and reducing p21 expression, the results from our study suggest that the mechanism underlying Sal sensitization is conserved in both chemo- and radiation-treated cells. Doxorubicin 45-48 H3 histone pseudogene 16 Homo sapiens 126-129 21573958-5 2012 Considering that Sal sensitizes doxorubicin (DOX)- or etoposide (ETO)-treated cancer cells by causing DNA damage and reducing p21 expression, the results from our study suggest that the mechanism underlying Sal sensitization is conserved in both chemo- and radiation-treated cells. Etoposide 54-63 H3 histone pseudogene 16 Homo sapiens 126-129 21573958-5 2012 Considering that Sal sensitizes doxorubicin (DOX)- or etoposide (ETO)-treated cancer cells by causing DNA damage and reducing p21 expression, the results from our study suggest that the mechanism underlying Sal sensitization is conserved in both chemo- and radiation-treated cells. Etoposide 65-68 H3 histone pseudogene 16 Homo sapiens 126-129 21573958-5 2012 Considering that Sal sensitizes doxorubicin (DOX)- or etoposide (ETO)-treated cancer cells by causing DNA damage and reducing p21 expression, the results from our study suggest that the mechanism underlying Sal sensitization is conserved in both chemo- and radiation-treated cells. salinomycin 207-210 H3 histone pseudogene 16 Homo sapiens 126-129 22349439-8 2012 The acetylation levels of histone H3 at lysine 9 and p21 mRNA expression were decreased in human GCs treated with dihydrotestosterone in vitro (P < 0.05). Dihydrotestosterone 114-133 H3 histone pseudogene 16 Homo sapiens 53-56 22711276-7 2012 Exposure to valproic acid and suberoylanilide hydroxamic acid was associated with increased levels of p21 and FOXO3 and reduced expression of survivin. Vorinostat 30-61 H3 histone pseudogene 16 Homo sapiens 102-105 22348919-7 2012 Notably, 5-epi-sinuleptolide up-regulated p53 and p21 expression and inhibited G2/M phase regulators of cyclin B1 and cyclin-dependent kinease 1 (CDK1) in SCC25 cells. 5-episinuleptolide 9-28 H3 histone pseudogene 16 Homo sapiens 50-53 22534328-9 2012 The protein levels of p21(Cip1)and 14-3-3sigma were increased with both AZA and MPA mix treatments without any change in the DNA methylation profiles of the genes. Decitabine 72-75 H3 histone pseudogene 16 Homo sapiens 22-25 22932460-7 2012 On the protein level, LiCl downregulates expression of cdc 6, cyclins A and cyclins E, and cdc 25C, and upregulates expression of the CDK inhibitor p21(CIP1). Lithium Chloride 22-26 H3 histone pseudogene 16 Homo sapiens 148-151 22484732-0 2012 Vorinostat enhances protein stability of p27 and p21 through negative regulation of Skp2 and Cks1 in human breast cancer cells. Vorinostat 0-10 H3 histone pseudogene 16 Homo sapiens 49-52 22702647-3 2012 Several in vitro assays were used to characterize the prototype aminothiol, PrC-210, for efficacy: protection against reactive oxygen species-induced plasmid DNA nicking, mass spectrometry to detect aminothiol-reactive oxygen species by-products, S. typhimurium mutagenesis, human cell growth inhibition, Western blot for p21 expression, and FACS analysis. Aminothiol 64-74 H3 histone pseudogene 16 Homo sapiens 324-327 22547681-6 2012 The other subset of miR-519 target mRNAs encoded proteins that control intracellular calcium levels (notably, ATP2C1 and ORAI1); their downregulation by miR-519 aberrantly elevated levels of cytosolic [Ca(2+)] storage in HeLa cells, similarly increasing p21 levels in a manner dependent on the Ca(2+)-activated kinases CaMKII and GSK3beta. Calcium 85-92 H3 histone pseudogene 16 Homo sapiens 254-257 22547681-8 2012 As a consequence, ATP levels increased, and the level of activity of the AMP-activated protein kinase (AMPK) declined, further contributing to the elevation in the abundance of p21. Adenosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 177-180 22484732-3 2012 Vorinostat significantly reduced BrdU incorporation in MDA-MB-231 and MCF-7 cells, which was associated with increased p27 and p21 protein levels without concomitant induction of p27 mRNA. Vorinostat 0-10 H3 histone pseudogene 16 Homo sapiens 151-154 22484732-3 2012 Vorinostat significantly reduced BrdU incorporation in MDA-MB-231 and MCF-7 cells, which was associated with increased p27 and p21 protein levels without concomitant induction of p27 mRNA. Bromodeoxyuridine 45-49 H3 histone pseudogene 16 Homo sapiens 151-154 22484732-4 2012 Vorinostat-induced accumulation of p27 and p21 proteins was inversely correlated with the mRNA and protein levels of Skp2 and Cks1. Vorinostat 0-10 H3 histone pseudogene 16 Homo sapiens 43-46 22484732-5 2012 Cycloheximide chase analysis revealed that vorinostat increased the half-life of p27 and p21 proteins. Vorinostat 55-65 H3 histone pseudogene 16 Homo sapiens 101-104 22484732-6 2012 The accumulation of p27 and p21 proteins was attenuated by forced expression of Skp2 and Cks1, which conferred resistance to the vorinostat-induced S-phase reduction. Vorinostat 153-163 H3 histone pseudogene 16 Homo sapiens 40-43 22484732-7 2012 These results suggest that vorinostat-induced growth arrest may be in part due to the enhanced protein stability of p27 and p21 through the downregulation of Skp2 and Cks1. Vorinostat 27-37 H3 histone pseudogene 16 Homo sapiens 136-139 22670709-8 2012 In p53 positive LNCaP cells, pterostilbene blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression. pterostilbene 29-42 H3 histone pseudogene 16 Homo sapiens 146-149 22446789-2 2012 The structure of the title compound which crystallizes in the non-centrosymmetric monoclinic space group P2(1) consists of a molecule of L-asparagine and a molecule of free l-tartaric acid both of which are interlinked by three varieties of H-bonding interactions namely O-H O, N-H O and C-H O. Asparagine 137-149 H3 histone pseudogene 16 Homo sapiens 105-110 22428663-0 2012 Cell cycle regulation by carboxylated multiwalled carbon nanotubes through p53-independent induction of p21 under the control of the BMP signaling pathway. Carbon 50-56 H3 histone pseudogene 16 Homo sapiens 104-107 22428663-1 2012 This report describes how carboxylated multiwalled carbon nanotubes (MWCNTs) induce p53-independent p21 expression and cell cycle arrest. Carbon 51-57 H3 histone pseudogene 16 Homo sapiens 100-103 22542654-4 2012 In in vitro experiments, P21, one of the peptides, bound to both PAF and lyso-PAF in a dose-dependent manner and markedly inhibited PAF-induced apoptosis in human umbilical vein endothelial cells. Platelet Activating Factor 65-68 H3 histone pseudogene 16 Homo sapiens 25-28 22542654-4 2012 In in vitro experiments, P21, one of the peptides, bound to both PAF and lyso-PAF in a dose-dependent manner and markedly inhibited PAF-induced apoptosis in human umbilical vein endothelial cells. O-deacetyl platelet activating factor 73-81 H3 histone pseudogene 16 Homo sapiens 25-28 22542654-4 2012 In in vitro experiments, P21, one of the peptides, bound to both PAF and lyso-PAF in a dose-dependent manner and markedly inhibited PAF-induced apoptosis in human umbilical vein endothelial cells. Platelet Activating Factor 78-81 H3 histone pseudogene 16 Homo sapiens 25-28 22547059-0 2012 RNA processing and modification protein, carbon catabolite repression 4 (Ccr4), arrests the cell cycle through p21-dependent and p53-independent pathway. carbon catabolite 41-58 H3 histone pseudogene 16 Homo sapiens 111-114 22464014-0 2012 Triptolide inhibits colon-rectal cancer cells proliferation by induction of G1 phase arrest through upregulation of p21. triptolide 0-10 H3 histone pseudogene 16 Homo sapiens 116-119 22464014-8 2012 Further detection for the expression of cell cycle-related proteins suggesting that triptolide stimulate expression of p21 and repress cyclin A1. triptolide 84-94 H3 histone pseudogene 16 Homo sapiens 119-122 22231280-5 2012 Here we show that single-agent bortezomib treatment of MCL cell lines leads to G2/M arrest and induction of apoptosis accompanied by downregulation of EIF4E and CCND1 mRNA but upregulation of p15(INK4B) and p21 mRNA. Bortezomib 31-41 H3 histone pseudogene 16 Homo sapiens 207-210 22417066-6 2012 The antiproliferative effect of XRT/RSV treatment correlated with increased expression of p15, p21, and mutant p53 and decreased expression of cyclin B, cyclin D, and cdk2. Resveratrol 36-39 H3 histone pseudogene 16 Homo sapiens 95-98 22324515-7 2012 Bad, p53, p21 and p27 were downregulated by neuropeptides in PC-3, and these effects were reversed with the addition of bortezomib. Bortezomib 120-130 H3 histone pseudogene 16 Homo sapiens 10-13 22041988-7 2012 When bladder cancer cell lines were treated with SB plus CDDP, Western blotting showed increased expression of p21 but not p27 in T24 cells, whereas both p21 and p27 increased in 253J and UMUC3 cells. Butyric Acid 49-51 H3 histone pseudogene 16 Homo sapiens 154-157 22041988-7 2012 When bladder cancer cell lines were treated with SB plus CDDP, Western blotting showed increased expression of p21 but not p27 in T24 cells, whereas both p21 and p27 increased in 253J and UMUC3 cells. Cisplatin 57-61 H3 histone pseudogene 16 Homo sapiens 111-114 22041988-7 2012 When bladder cancer cell lines were treated with SB plus CDDP, Western blotting showed increased expression of p21 but not p27 in T24 cells, whereas both p21 and p27 increased in 253J and UMUC3 cells. Butyric Acid 49-51 H3 histone pseudogene 16 Homo sapiens 111-114 22041988-7 2012 When bladder cancer cell lines were treated with SB plus CDDP, Western blotting showed increased expression of p21 but not p27 in T24 cells, whereas both p21 and p27 increased in 253J and UMUC3 cells. Cisplatin 57-61 H3 histone pseudogene 16 Homo sapiens 154-157 22654424-5 2012 We also observed the effect of DAC on the methylation status of hTERT promoter and the expression of regulatory genes, such as c-myc, p15, p16, p21, E2F1, and WT1. Decitabine 31-34 H3 histone pseudogene 16 Homo sapiens 144-147 22484326-7 2012 In addition, Chidamide induced apoptosis and up-regulated p21 mRNA expression. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 13-22 H3 histone pseudogene 16 Homo sapiens 58-61 22484326-8 2012 These results suggest that Chidamide may arrest the cell cycle and inhibit the growth of hepatocellular carcinoma cells through up-regulation of p21. N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide 27-36 H3 histone pseudogene 16 Homo sapiens 145-148 22802695-4 2012 Western blotting on the expression of cell cycle inhibitors showed that p21 and p27 was up-regulated as ethanol concentration increases from 0 to 1.5% whilst the cell cycle regulators, cdk1, cdk2, and cdk4 as well as Cyclin A, Cyclin B1 and Cyclin E1, were gradually down-regulated. Ethanol 104-111 H3 histone pseudogene 16 Homo sapiens 72-75 22559167-7 2012 The effects of rapamycin and/or bortezomib on the mRNA expression levels of p53, p27, p21 and Bcl-2 family in HCCLM3 cells were evaluated by RT-PCR. Sirolimus 15-24 H3 histone pseudogene 16 Homo sapiens 86-89 22427654-0 2012 Sulforaphane induction of p21(Cip1) cyclin-dependent kinase inhibitor expression requires p53 and Sp1 transcription factors and is p53-dependent. sulforaphane 0-12 H3 histone pseudogene 16 Homo sapiens 26-29 22542944-7 2012 The expression levels of p53 and p21 were also induced by SKLB70326 treatment. 3-amino-6-(3-methoxyphenyl)thieno(2.3-b)pyridine-2-carboxamide 58-67 H3 histone pseudogene 16 Homo sapiens 33-36 22559167-7 2012 The effects of rapamycin and/or bortezomib on the mRNA expression levels of p53, p27, p21 and Bcl-2 family in HCCLM3 cells were evaluated by RT-PCR. Bortezomib 32-42 H3 histone pseudogene 16 Homo sapiens 86-89 22648623-0 2012 2"-Hydroxyflavanone induces apoptosis through Egr-1 involving expression of Bax, p21, and NAG-1 in colon cancer cells. 2'-hydroxyflavanone 0-19 H3 histone pseudogene 16 Homo sapiens 81-84 22342732-4 2012 The induction of p21 and the inhibition of cyclin B and CDC25C contributed to DHA-induced G2/M arrest. artenimol 78-81 H3 histone pseudogene 16 Homo sapiens 17-20 22241506-1 2012 OBJECTIVE: To investigate the effect of total flavonoids of Hedysarum polybotry on the proliferation, cell cycle, and expressions of p21(Ras) and proliferating cell nuclear antigen (PCNA) gene in erythroleukemia cell line K562. Flavonoids 46-56 H3 histone pseudogene 16 Homo sapiens 133-136 22241506-5 2012 The immunocytochemistry method was applied to quantitatively analyze the effects of flavonoids of Hedysarum polybotry on changes p21(Ras) and PCNA gene expressions. Flavonoids 84-94 H3 histone pseudogene 16 Homo sapiens 129-132 22241506-8 2012 Compared with the control group, p21(Ras) and PCNA gene expressions were decreased significantly in K562 cells treated with total flavonoids of Hedysarum polybotry (40 and 80 mug/mL, respectively) for 48 h. CONCLUSION: The inhibitory effect on proliferation of K562 cells was observed in the groups treated with flavonoids of Hedysarum polybotry, which might be related to cells arresting. Flavonoids 130-140 H3 histone pseudogene 16 Homo sapiens 33-36 22241506-8 2012 Compared with the control group, p21(Ras) and PCNA gene expressions were decreased significantly in K562 cells treated with total flavonoids of Hedysarum polybotry (40 and 80 mug/mL, respectively) for 48 h. CONCLUSION: The inhibitory effect on proliferation of K562 cells was observed in the groups treated with flavonoids of Hedysarum polybotry, which might be related to cells arresting. Flavonoids 312-322 H3 histone pseudogene 16 Homo sapiens 33-36 22142405-11 2012 The exposure of DPSCs and HDFs to cisplatin provoked an increase in p53 and p21 expression and p53 phosphorylation of serine 15. Cisplatin 34-43 H3 histone pseudogene 16 Homo sapiens 76-79 22307313-0 2012 Treatment with bisphenol A and methoxychlor results in the growth of human breast cancer cells and alteration of the expression of cell cycle-related genes, cyclin D1 and p21, via an estrogen receptor-dependent signaling pathway. bisphenol A 15-26 H3 histone pseudogene 16 Homo sapiens 195-198 22307313-0 2012 Treatment with bisphenol A and methoxychlor results in the growth of human breast cancer cells and alteration of the expression of cell cycle-related genes, cyclin D1 and p21, via an estrogen receptor-dependent signaling pathway. Methoxychlor 31-43 H3 histone pseudogene 16 Homo sapiens 195-198 22328720-7 2012 At the molecular level, cisplatin treatment resulted in elevated p53 levels, enhanced caspase-3 activation, and reduced p21 levels in E6-suppressed cells. Cisplatin 24-33 H3 histone pseudogene 16 Homo sapiens 120-123 22589186-6 2012 Furthermore, we show that Tam- and siE6AP-mediated inhibition of E6AP leads to enhanced G0-G1 growth arrest and apoptosis, which is also evident from significant upregulation of cytochrome-c, Bax, p21, and PARP cleavage. Tamoxifen 26-29 H3 histone pseudogene 16 Homo sapiens 197-200 22369716-3 2012 Melatonin"s SERM actions include modulation of estrogen-regulated cell proliferation, invasiveness and expression of proteins, growth factors and proto-oncogenes (hTERT, p53, p21, TGFbeta, E-cadherin, etc.). Melatonin 0-9 H3 histone pseudogene 16 Homo sapiens 175-178 22294050-9 2012 Everolimus +- 5 Gy suppressed endothelin 1 and lactate dehydrogenase expression and increased VEGFA, p21, hypoxia-inducible factor-1alpha and SLC2A1 (facilitated glucose transporter 1). Everolimus 0-10 H3 histone pseudogene 16 Homo sapiens 113-116 22589186-6 2012 Furthermore, we show that Tam- and siE6AP-mediated inhibition of E6AP leads to enhanced G0-G1 growth arrest and apoptosis, which is also evident from significant upregulation of cytochrome-c, Bax, p21, and PARP cleavage. sie6ap 35-41 H3 histone pseudogene 16 Homo sapiens 197-200 22421144-8 2012 Mechanistically, metformin caused G 1 arrest, which coincided with a decrease in the protein levels of CDKs (2, 4 and 6), cyclins (D1 and E) and CDK inhibitors (p15, p16, p18 and p27), but no change in p19 and p21. Metformin 17-26 H3 histone pseudogene 16 Homo sapiens 210-213 22385209-1 2012 Mutations of human oncoprotein p21(Ras) (hereafter Ras) at glutamine 61 are known to slow the rate of guanosine triphosphate (GTP) hydrolysis and transform healthy cells into malignant cells. Glutamine 59-68 H3 histone pseudogene 16 Homo sapiens 31-34 22385209-1 2012 Mutations of human oncoprotein p21(Ras) (hereafter Ras) at glutamine 61 are known to slow the rate of guanosine triphosphate (GTP) hydrolysis and transform healthy cells into malignant cells. Guanosine Triphosphate 102-124 H3 histone pseudogene 16 Homo sapiens 31-34 22385209-1 2012 Mutations of human oncoprotein p21(Ras) (hereafter Ras) at glutamine 61 are known to slow the rate of guanosine triphosphate (GTP) hydrolysis and transform healthy cells into malignant cells. Guanosine Triphosphate 126-129 H3 histone pseudogene 16 Homo sapiens 31-34 20946258-4 2012 Our previous study has demonstrated that simvastatin inhibits VSMC proliferation in high glucose status without dyslipidemia, inducing a G0/G1 phase cell cycle growth arrest by acting on multiple steps upstream of pRb, including inhibition of CDK2/4 expression and upregulation of p53, p21, p16, and p27. Simvastatin 41-52 H3 histone pseudogene 16 Homo sapiens 286-289 22147199-6 2012 Effect of DI on up-regulation of p21 expression and down-regulation of cyclin B1, p34(cdc2) expression in irradiated HeLa cell was concomitant with cell cycle arrest in G(2) phase. di 10-12 H3 histone pseudogene 16 Homo sapiens 33-36 22134899-3 2012 Chromatin immunoprecipitation assays demonstrated that JMJD2A was recruited together with p53 to the promoter of the p21 cell cycle inhibitor upon stimulation with the DNA damaging agent, adriamycin. Doxorubicin 188-198 H3 histone pseudogene 16 Homo sapiens 117-120 22307336-5 2012 Knockdown of p21 or p27 by each siRNA significantly repressed G1 phase arrest induced by brassinin. brassinin 101-110 H3 histone pseudogene 16 Homo sapiens 13-16 22315229-2 2012 Earlier studies suggest that upon DNA damage, a specific B subunit, B56gamma, bridges the PP2A AC core to p53, leading to dephosphorylation of p53 at Thr-55, induction of the p53 transcriptional target p21, and the inhibition of cell proliferation and transformation. Threonine 150-153 H3 histone pseudogene 16 Homo sapiens 202-205 22470341-6 2012 Bilirubin-mediated inhibition of neointimal thickening was associated with a significant decrease in ERK activity and cyclin D1 and A protein expression, and an increase in p21 and p53 protein expression in injured blood vessels. Bilirubin 0-9 H3 histone pseudogene 16 Homo sapiens 173-176 21801466-4 2012 It was associated with PTEN induction as well as DNA methyltransferase down-regulation and p21 up-regulation after treatments with vitamin D3 and resveratrol, suggesting a complex regulation of the DNA methylation machinery. Cholecalciferol 131-141 H3 histone pseudogene 16 Homo sapiens 91-94 21801466-4 2012 It was associated with PTEN induction as well as DNA methyltransferase down-regulation and p21 up-regulation after treatments with vitamin D3 and resveratrol, suggesting a complex regulation of the DNA methylation machinery. Resveratrol 146-157 H3 histone pseudogene 16 Homo sapiens 91-94 22307336-0 2012 Brassinin induces G1 phase arrest through increase of p21 and p27 by inhibition of the phosphatidylinositol 3-kinase signaling pathway in human colon cancer cells. brassinin 0-9 H3 histone pseudogene 16 Homo sapiens 54-57 22307336-4 2012 Brassinin increased the expression of p21 and p27, resulting in hypophosphorylation of the retinoblastoma gene (RB). brassinin 0-9 H3 histone pseudogene 16 Homo sapiens 50-53 22160773-8 2012 Downregulation of p21 expression and increased expression of Akt, the mammalian target of rapamycin (mTOR), and some of its downstream effectors were significantly reversed by 2-OHE. 2-ohe 176-181 H3 histone pseudogene 16 Homo sapiens 18-21 22404134-1 2012 INTRODUCTION: The p21-activated kinase (PAK) family of serine/threonine protein kinases is activated by binding to the small (p21) GTP-binding proteins Cdc42 and Rac. Guanosine Triphosphate 131-134 H3 histone pseudogene 16 Homo sapiens 18-21 22404134-1 2012 INTRODUCTION: The p21-activated kinase (PAK) family of serine/threonine protein kinases is activated by binding to the small (p21) GTP-binding proteins Cdc42 and Rac. Guanosine Triphosphate 131-134 H3 histone pseudogene 16 Homo sapiens 126-129 22134754-7 2012 Belinostat induced the expression of p21 and p27, acetylation of p53 and G2/M arrest associated with Bcl2 and Bcl-Xl downmodulation and significant reduction of survivin, IAPs and Akt/pAkt and increased caspase-8 and -9 expression/activity. belinostat 0-10 H3 histone pseudogene 16 Homo sapiens 37-40 22135025-13 2012 However, incorporating p21 into a multivariable Cox model did contribute to improved model quality for predicting CSS. thiocysteine 114-117 H3 histone pseudogene 16 Homo sapiens 23-26 22307336-8 2012 These results suggest the possibility that brassinin inhibits the PI3K signaling pathway and upregulates the expression of p21 and p27, thereby inducing G1 phase arrest. brassinin 55-64 H3 histone pseudogene 16 Homo sapiens 147-150 22545405-5 2012 The structure of dimerized griseofulvin, C34H32C12O12 x C2H6O x H2O, at 100 K has monoclinic (P2(1)) symmetry. Griseofulvin 27-39 H3 histone pseudogene 16 Homo sapiens 94-99 22238365-7 2012 In addition, (212)Pb-TCMC-trastuzumab treatment delayed open chromatin structure and expression of p21 until 72 hours, suggesting a correlation between induction of p21 protein and modification in chromatin structure of p21 in response to (212)Pb-TCMC-trastuzumab treatment. Lead-212 13-20 H3 histone pseudogene 16 Homo sapiens 99-102 22238365-7 2012 In addition, (212)Pb-TCMC-trastuzumab treatment delayed open chromatin structure and expression of p21 until 72 hours, suggesting a correlation between induction of p21 protein and modification in chromatin structure of p21 in response to (212)Pb-TCMC-trastuzumab treatment. Lead-212 13-20 H3 histone pseudogene 16 Homo sapiens 165-168 22238365-7 2012 In addition, (212)Pb-TCMC-trastuzumab treatment delayed open chromatin structure and expression of p21 until 72 hours, suggesting a correlation between induction of p21 protein and modification in chromatin structure of p21 in response to (212)Pb-TCMC-trastuzumab treatment. Lead-212 13-20 H3 histone pseudogene 16 Homo sapiens 165-168 22238365-7 2012 In addition, (212)Pb-TCMC-trastuzumab treatment delayed open chromatin structure and expression of p21 until 72 hours, suggesting a correlation between induction of p21 protein and modification in chromatin structure of p21 in response to (212)Pb-TCMC-trastuzumab treatment. tcmc 21-25 H3 histone pseudogene 16 Homo sapiens 99-102 22238365-7 2012 In addition, (212)Pb-TCMC-trastuzumab treatment delayed open chromatin structure and expression of p21 until 72 hours, suggesting a correlation between induction of p21 protein and modification in chromatin structure of p21 in response to (212)Pb-TCMC-trastuzumab treatment. tcmc 21-25 H3 histone pseudogene 16 Homo sapiens 165-168 22545405-5 2012 The structure of dimerized griseofulvin, C34H32C12O12 x C2H6O x H2O, at 100 K has monoclinic (P2(1)) symmetry. c34h32c12o12 41-53 H3 histone pseudogene 16 Homo sapiens 94-99 22238365-7 2012 In addition, (212)Pb-TCMC-trastuzumab treatment delayed open chromatin structure and expression of p21 until 72 hours, suggesting a correlation between induction of p21 protein and modification in chromatin structure of p21 in response to (212)Pb-TCMC-trastuzumab treatment. tcmc 21-25 H3 histone pseudogene 16 Homo sapiens 165-168 22238365-7 2012 In addition, (212)Pb-TCMC-trastuzumab treatment delayed open chromatin structure and expression of p21 until 72 hours, suggesting a correlation between induction of p21 protein and modification in chromatin structure of p21 in response to (212)Pb-TCMC-trastuzumab treatment. tcmc 247-251 H3 histone pseudogene 16 Homo sapiens 165-168 22238365-7 2012 In addition, (212)Pb-TCMC-trastuzumab treatment delayed open chromatin structure and expression of p21 until 72 hours, suggesting a correlation between induction of p21 protein and modification in chromatin structure of p21 in response to (212)Pb-TCMC-trastuzumab treatment. tcmc 247-251 H3 histone pseudogene 16 Homo sapiens 165-168 22545405-5 2012 The structure of dimerized griseofulvin, C34H32C12O12 x C2H6O x H2O, at 100 K has monoclinic (P2(1)) symmetry. Ethanol 56-61 H3 histone pseudogene 16 Homo sapiens 94-99 22545405-5 2012 The structure of dimerized griseofulvin, C34H32C12O12 x C2H6O x H2O, at 100 K has monoclinic (P2(1)) symmetry. Water 64-67 H3 histone pseudogene 16 Homo sapiens 94-99 22244892-7 2012 In addition, Sal treatment increased pH2AX levels and reduced p21 levels in antimitotic drugs-treated cells. sal 13-16 H3 histone pseudogene 16 Homo sapiens 62-65 22159450-6 2012 In contrast, CG-1521 significantly induces the expression of several p53 target genes associated with apoptosis including Bnip3/Bnip3L, p21/p21B and Gdf15. cysteinylglycine 13-15 H3 histone pseudogene 16 Homo sapiens 160-163 22294184-6 2012 A marked rise in the cell-cycle inhibitor p21, together with reduction of aurora kinases A and B, cyclins B1 and D1 proteins was induced by lovastatin alone or in combination with docetaxel. Lovastatin 140-150 H3 histone pseudogene 16 Homo sapiens 42-45 22294184-6 2012 A marked rise in the cell-cycle inhibitor p21, together with reduction of aurora kinases A and B, cyclins B1 and D1 proteins was induced by lovastatin alone or in combination with docetaxel. Docetaxel 180-189 H3 histone pseudogene 16 Homo sapiens 42-45 22002102-6 2012 Wild type p53 function inhibits the efficacy of a combined IR and ABT-737 treatment via a p21-dependent G1 cell cycle arrest. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 66-69 H3 histone pseudogene 16 Homo sapiens 90-93 22305266-0 2012 Cytoplasmic p21 induced by p65 prevents doxorubicin-induced cell death in pancreatic carcinoma cell line. Doxorubicin 40-51 H3 histone pseudogene 16 Homo sapiens 12-15 22305266-2 2012 Our previous study indicates that DOX-induced p65 is able to bind the p21 promoter to activate its transactivation in the cells. Doxorubicin 34-37 H3 histone pseudogene 16 Homo sapiens 70-73 22305266-7 2012 RESULTS: Here we showed that over-expression of p65 decreased the cytotoxic effect of DOX on PANC1 cells, correlating with increased induction of cytoplasmic p21. Doxorubicin 86-89 H3 histone pseudogene 16 Homo sapiens 158-161 22305266-11 2012 More, we present evidence that over-expression of p53 or p53/p65 in the PANC1 cells were more sensitive to DOX treatment, correlated with activation of caspase-3 and clear elevation of nuclear p21 level. Doxorubicin 107-110 H3 histone pseudogene 16 Homo sapiens 193-196 22305266-12 2012 Our previous data suggested that expression of p21 increases Gefitinib-induced cell death by blocking the cell cycle at the G1 and G2 phases. Gefitinib 61-70 H3 histone pseudogene 16 Homo sapiens 47-50 22305266-13 2012 The present findings here reinforced this idea by showing p21"s ability of potentiality of DOX-induced cell death correlated with its inhibition of cell cycle progression after over-expression of p53 or p53/p65. Doxorubicin 91-94 H3 histone pseudogene 16 Homo sapiens 58-61 22020984-9 2012 Moreover, 4-PB led to a dose-dependent overexpression of the cell cycle regulator p21 in tumour cells. 4-phenylbutyric acid 10-14 H3 histone pseudogene 16 Homo sapiens 94-97 21983885-12 2012 Furthermore, induced levels of total p53 and its transcriptional target p21 declined at higher BPDE concentrations correlating with reduced rates of apoptosis. 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 95-99 H3 histone pseudogene 16 Homo sapiens 72-75 22112863-7 2012 Furthermore, we also demonstrated that phosphorylation of p53 at Thr18 is required for p53 acetylation at lysine 373/382 and for p21 expression in response to depsipeptide treatment. UNII-PYZ33YLR8A 65-70 H3 histone pseudogene 16 Homo sapiens 129-132 22112863-8 2012 Our results demonstrate that depsipeptide plays an anti-neoplastic role by generating ROS to elicit p53/p21 pathway activation. Depsipeptides 29-41 H3 histone pseudogene 16 Homo sapiens 104-107 22112863-8 2012 Our results demonstrate that depsipeptide plays an anti-neoplastic role by generating ROS to elicit p53/p21 pathway activation. Reactive Oxygen Species 86-89 H3 histone pseudogene 16 Homo sapiens 104-107 22012578-6 2012 Immunoblotting analysis of key cell cycle regulators demonstrated that andrographolide treatment caused a dose-dependent increase in the expression of cell-cycle inhibitors p21 and p27 and a concomitant reduction of cyclin-dependent kinase 4. andrographolide 71-86 H3 histone pseudogene 16 Homo sapiens 173-176 22020547-7 2012 Our results showed that the TPA-induced up-regulation of p21 and down-regulation of p53 was reversed by UO126 (a MEK1/2 inhibitor), but not by SP600125 (a JNK inhibitor) or SB203580 (a p38 inhibitor), although TPA increased the phosphorylation of ERK and JNK in MCF-7 cells. Tetradecanoylphorbol Acetate 246-249 H3 histone pseudogene 16 Homo sapiens 69-72 22075951-6 2012 Suppression of p21 induction by p21 siRNA reversed the suppressive effect of vorinostat on the replication of CRAd, but still failed to reverse the antagonistic interaction. Vorinostat 77-87 H3 histone pseudogene 16 Homo sapiens 32-35 22075951-6 2012 Suppression of p21 induction by p21 siRNA reversed the suppressive effect of vorinostat on the replication of CRAd, but still failed to reverse the antagonistic interaction. Vorinostat 77-87 H3 histone pseudogene 16 Homo sapiens 15-18 21993902-9 2012 The data presented an increase of G0/G1 phase cells and decrease of S phase cells after rapamycin treatment, and the decreased expression of cyclinD1, higher expression of p21 at mRNA level was also detected in K562 with rapamycin. Sirolimus 245-254 H3 histone pseudogene 16 Homo sapiens 196-199 22020547-0 2012 TPA-induced p21 expression augments G2/M arrest through a p53-independent mechanism in human breast cancer cells. Tetradecanoylphorbol Acetate 0-3 H3 histone pseudogene 16 Homo sapiens 12-15 22020547-4 2012 Our results showed that TPA increased the level of p21 expression in MCF-7 cells with wild-type p53 and MDA-MB-231 cells with mutant p53 in a dose-dependent manner. Tetradecanoylphorbol Acetate 24-27 H3 histone pseudogene 16 Homo sapiens 51-54 22020547-6 2012 We next examined the regulatory mechanism of TPA on p21 and p53 expression. Tetradecanoylphorbol Acetate 45-48 H3 histone pseudogene 16 Homo sapiens 64-67 22020547-7 2012 Our results showed that the TPA-induced up-regulation of p21 and down-regulation of p53 was reversed by UO126 (a MEK1/2 inhibitor), but not by SP600125 (a JNK inhibitor) or SB203580 (a p38 inhibitor), although TPA increased the phosphorylation of ERK and JNK in MCF-7 cells. Tetradecanoylphorbol Acetate 28-31 H3 histone pseudogene 16 Homo sapiens 69-72 22020547-11 2012 Taken together, we suggest that TPA reciprocally regulates the level of p21 and p53 expression via a MEK/ERK-dependent pathway. Tetradecanoylphorbol Acetate 44-47 H3 histone pseudogene 16 Homo sapiens 84-87 22020547-7 2012 Our results showed that the TPA-induced up-regulation of p21 and down-regulation of p53 was reversed by UO126 (a MEK1/2 inhibitor), but not by SP600125 (a JNK inhibitor) or SB203580 (a p38 inhibitor), although TPA increased the phosphorylation of ERK and JNK in MCF-7 cells. U 0126 116-121 H3 histone pseudogene 16 Homo sapiens 69-72 22020547-12 2012 The up-regulation of p21 in response to TPA is mediated through a p53-independent mechanism in breast cancer cells. Tetradecanoylphorbol Acetate 40-43 H3 histone pseudogene 16 Homo sapiens 21-24 22273506-6 2012 The histone acetyltransferase (HAT) inhibitor curcumin was able to abrogate microgravity-induced p21 mRNA expression, whereas expression was enhanced by a histone deacetylase (HDAC) inhibitor. Curcumin 46-54 H3 histone pseudogene 16 Homo sapiens 97-100 22679561-9 2012 The comparison to HeLa and SiHa cells revealed a higher sensitivity of the novel cell lines to cisplatin treatment, which caused p53 accumulation and transcriptional induction of p21. Cisplatin 95-104 H3 histone pseudogene 16 Homo sapiens 179-182 21351099-8 2012 In vitro, low-dose DOC, which did not induce G2/M arrest, increased p53 and p21 and resulted in down-regulation of TS in C4-2 cells, and down-regulation of TS is considered to be responsible for the synergistic effect of S-1 in vivo. Docetaxel 19-22 H3 histone pseudogene 16 Homo sapiens 76-79 22076474-0 2012 Role of p21 as a determinant of 1,6-Bis[4-(4-amino-3-hydroxyphenoxy)phenyl] diamantane response in human HCT-116 colon carcinoma cells. 1,6-Bis(4-(4-amino-3-hydroxyphenoxy)phenyl)diamantane 32-98 H3 histone pseudogene 16 Homo sapiens 8-11 21927533-0 2012 Kaempferol inhibits VEGF expression and in vitro angiogenesis through a novel ERK-NFkappaB-cMyc-p21 pathway. kaempferol 0-10 H3 histone pseudogene 16 Homo sapiens 96-99 21927533-6 2012 Kaempferol down-regulated ERK phosphorelation as well as NFkappaB and cMyc expression, but promoted p21 expression. kaempferol 0-10 H3 histone pseudogene 16 Homo sapiens 100-103 21927533-7 2012 Examination of relationship between these genes suggested a novel ERK-NFkappaB-cMyc-p21-VEGF pathway, which accounts for kaempferol"s angioprevention effects in ovarian cancer cells. kaempferol 121-131 H3 histone pseudogene 16 Homo sapiens 84-87 22213289-7 2012 Treatment of p53-wild-type cells with 50 muM quercetin reduced drug-induced up-regulation of p53, p21 and BAX. Quercetin 45-54 H3 histone pseudogene 16 Homo sapiens 98-101 23167335-0 2012 MDM2 T309G has a synergistic effect with P21 ser31arg single nucleotide polymorphisms on the risk of acute myeloid leukemia. ser31arg 45-53 H3 histone pseudogene 16 Homo sapiens 41-44 23464429-16 2012 CONCLUSION: Ginsenoside Rg1 can induce a state of senescence in human leukemia K562 cells, which is associated with p21-Rb and p16-Rb pathways. Ginsenosides 12-23 H3 histone pseudogene 16 Homo sapiens 116-119 23167335-9 2012 RESULTS: We found that the P21 ser31arg heterozygous polymorphism increases the risk of AML (P value=0.017, OR=2.946, 95% CI=1.216-7.134). ser31arg 31-39 H3 histone pseudogene 16 Homo sapiens 27-30 23167335-10 2012 Although the MDM2 309G allele was itself without affect, it showed a synergistic effect with P21 ser/arg polymorphism (P value=0.003, OR= 6.807, 95% CI= 1.909-24.629). Serine 97-100 H3 histone pseudogene 16 Homo sapiens 93-96 23167335-10 2012 Although the MDM2 309G allele was itself without affect, it showed a synergistic effect with P21 ser/arg polymorphism (P value=0.003, OR= 6.807, 95% CI= 1.909-24.629). Arginine 101-104 H3 histone pseudogene 16 Homo sapiens 93-96 23167335-13 2012 CONCLUSION: We suggest that SNPs in the P53 pathway, especially the P21 ser31arg polymorphism and combined polymorphisms especially the P21/ MDM2 might be genetic susceptibility factors in the pathogenesis of AML. ser31arg 72-80 H3 histone pseudogene 16 Homo sapiens 68-71 23075671-7 2012 EIPA-induced lowered [Cl(-)](c) up-regulated expression of p21associated with phosphorylation of MAPKs, suppressing proliferation associated with G(0)/G(1) arrest. ethylisopropylamiloride 0-4 H3 histone pseudogene 16 Homo sapiens 59-62 22223345-5 2012 PA inhibited cell proliferation and induced sub-G(1) arrest, elevating the mRNA levels of the apoptotic genes p53 and p21. pomolic acid 0-2 H3 histone pseudogene 16 Homo sapiens 118-121 22236190-0 2012 Direct short-term cytotoxic effects of BIBR 1532 on acute promyelocytic leukemia cells through induction of p21 coupled with downregulation of c-Myc and hTERT transcription. bibr 39-43 H3 histone pseudogene 16 Homo sapiens 108-111 22236190-4 2012 Our results also suggest that induction of p21 and subsequent disturbance of Bax/Bcl-2 balanced ratio as well as decreased telomerase activity may be rational mechanisms for the potent/direct short-term cytotoxicity of high doses of BIBR1532 against NB4 cells. BIBR 1532 233-241 H3 histone pseudogene 16 Homo sapiens 43-46 22272214-0 2012 Cucurbitacin E Induces G(2)/M Phase Arrest through STAT3/p53/p21 Signaling and Provokes Apoptosis via Fas/CD95 and Mitochondria-Dependent Pathways in Human Bladder Cancer T24 Cells. cucurbitacin E 0-14 H3 histone pseudogene 16 Homo sapiens 61-64 22119126-2 2012 The benzimidazole (L) crystallizes in the space group P2(1)/c with a = 8.6660(3) A, b = 16.6739(7) A, c = 9.8611(4) A and beta = 113.505(3) and forms an infinite chain structure with a trans-zigzag type along the crystallographic axis "a", through the intermolecular H-bond. benzimidazole 4-17 H3 histone pseudogene 16 Homo sapiens 54-59 22745580-0 2012 Oridonin up-regulates expression of P21 and induces autophagy and apoptosis in human prostate cancer cells. oridonin 0-8 H3 histone pseudogene 16 Homo sapiens 36-39 22272214-7 2012 Our findings provided the first evidence that STAT3/p53/p21 signaling, Fas/CD95 and mitochondria-dependent pathways play critical roles in cucurbitacin E-induced G(2)/M phase arrest and apoptosis of T24 cells. cucurbitacin E 139-153 H3 histone pseudogene 16 Homo sapiens 56-59 22454691-6 2012 The expression of p53 protein was markedly upregulated, and the p21 level was also obviously elevated in zerumbone-treated PANC-1 cells. zerumbone 105-114 H3 histone pseudogene 16 Homo sapiens 64-67 22919418-7 2012 PEITC induced G(0)/G(1) phase arrest through the effects of associated protein such as p53, p21, p17, CDK2 and cyclin E, and it triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (DeltaPsi(m)), and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in HSC-3 cells. phenethyl isothiocyanate 0-5 H3 histone pseudogene 16 Homo sapiens 92-95 22583615-5 2012 Ataxia telangiectasia mutated protein kinase (ATM) was activated by GL331 through its autophosphorylation at Ser1981, which led to the activation of DNA damage signaling pathways including p53/p21 and Chk2/Cdc25A cascades. GL 331 68-73 H3 histone pseudogene 16 Homo sapiens 193-196 23049256-6 2012 Under the same conditions, LMWP-SOD1 abolished activation of the cell cycle regulator proteins, p53 and p21(Cip1), induced by hydrogen peroxide. Hydrogen Peroxide 126-143 H3 histone pseudogene 16 Homo sapiens 104-107 22642109-8 2012 Likewise, p21 protein reached its maximal expression in 4 h after the irradiation of VA-treated cells. Valproic Acid 85-87 H3 histone pseudogene 16 Homo sapiens 10-13 21993662-6 2012 PL up-regulated the expression of p53 in U2OS cells and p21 in the two osteosarcoma cell lines causing cell cycle arrest by decreasing the expression of murine double minute 2 (MDM2)/cyclin B1 and cyclin D1. plumbagin 0-2 H3 histone pseudogene 16 Homo sapiens 56-59 21842375-9 2012 Zebularine induced regional chromatin remodeling by local histone H4 acetylation and histone H3-K4 methylation in promoter sites of methylated E-cadherin and also in the promoter of unmethylated p21 as evidenced by chromatin immunoprecipitation assay. pyrimidin-2-one beta-ribofuranoside 0-10 H3 histone pseudogene 16 Homo sapiens 195-198 22642109-11 2012 The 24-hour treatment of MOLT-4 leukemia cells with 2 mM VA results in radiosensitizing, increases apoptosis induction, H2AX phosphorylation, and also p53 and p21 activation. Valproic Acid 57-59 H3 histone pseudogene 16 Homo sapiens 159-162 21922150-9 2012 Treatment of PA-1 cells with 10 microM tamoxifen resulted in an increase in the levels of p21, p27, p16 and phospho-pRb, indicating typical G1 arrest. Tamoxifen 39-48 H3 histone pseudogene 16 Homo sapiens 102-105 22862161-5 2012 Roscovitine decreased production of the cell cycle inhibitor p21 and induced apoptosis. Roscovitine 0-11 H3 histone pseudogene 16 Homo sapiens 61-64 21947091-12 2012 In conclusion, SB induces G1 and G2 arrest by increasing p21 expression resulting in CDK2, CDK4 and CDK6 down-regulation. Butyric Acid 27-29 H3 histone pseudogene 16 Homo sapiens 69-72 23251689-8 2012 Treatments with MGCD0103 (a class I-selective HDACI) resulted in dose-dependent growth arrest, cell death/apoptosis, and cell cycle arrest in G2/M phase, accompanied by induction of p21 and DNA double-strand breaks (DSBs). mocetinostat 16-24 H3 histone pseudogene 16 Homo sapiens 182-185 23193914-0 2012 Quinacrine-mediated autophagy and apoptosis in colon cancer cells is through a p53- and p21-dependent mechanism. Quinacrine 0-10 H3 histone pseudogene 16 Homo sapiens 88-91 23193914-1 2012 We previously showed that quinacrine (QC), a small molecule antimalarial agent, also presented anticancer activity in breast cancer cells through activation of p53, p21, and inhibition of topoisomerase activity. Quinacrine 26-36 H3 histone pseudogene 16 Homo sapiens 165-168 23251689-11 2012 Although MC1568 or Tubastatin A alone had no obvious effects on DNA DSBs and p21 expression, their combination with MGCD0103 resulted in cooperative induction of p21 in the cells. MC1568 9-15 H3 histone pseudogene 16 Homo sapiens 162-165 23251689-11 2012 Although MC1568 or Tubastatin A alone had no obvious effects on DNA DSBs and p21 expression, their combination with MGCD0103 resulted in cooperative induction of p21 in the cells. tubastatin A 19-31 H3 histone pseudogene 16 Homo sapiens 162-165 23251689-11 2012 Although MC1568 or Tubastatin A alone had no obvious effects on DNA DSBs and p21 expression, their combination with MGCD0103 resulted in cooperative induction of p21 in the cells. mocetinostat 116-124 H3 histone pseudogene 16 Homo sapiens 162-165 23272171-6 2012 DEX co-treatment cells exhibited the decrease of DNA damage signaling pathway proteins, the lower expression of p53 and p21(CIP1), the lower cellular secretory program and down-regulation of NF-kappaB and its signaling cascade. Dexamethasone 0-3 H3 histone pseudogene 16 Homo sapiens 120-123 23133524-0 2012 Gatifloxacin induces S and G2-phase cell cycle arrest in pancreatic cancer cells via p21/p27/p53. Gatifloxacin 0-12 H3 histone pseudogene 16 Homo sapiens 85-88 23152782-11 2012 Western blot analysis suggested that pretreatment with Ki-67-7 sensitized bladder cancer cells to curcumin-mediated apoptosis and cell cycle arrest by p53- and p21-independent mechanisms. Curcumin 98-106 H3 histone pseudogene 16 Homo sapiens 160-163 23133524-6 2012 Our study is of interest because fluoroquinolones have the ability to penetrate pancreatic tissue which can be very effective in combating pancreatic cancers that are usually associated with loss or downregulation of CDK inhibitors p21/p27 as well as mutational inactivation of p53. Fluoroquinolones 33-49 H3 histone pseudogene 16 Homo sapiens 232-235 23049949-6 2012 15d-PGJ2 induced the tumor suppressor gene p21, a G(2)/M arrest and inhibited tumor cell migration. 15-deoxyprostaglandin J2 0-8 H3 histone pseudogene 16 Homo sapiens 43-46 23071787-7 2012 The median mRNA levels of p21 and BAX in the tumors of Pro-allele carriers were significantly reduced to 55.7% and 76.9% compared to Arg/Arg patients, whereas p53, MDM2 and PERP expression were hardly altered. Arginine 133-136 H3 histone pseudogene 16 Homo sapiens 26-29 23071787-7 2012 The median mRNA levels of p21 and BAX in the tumors of Pro-allele carriers were significantly reduced to 55.7% and 76.9% compared to Arg/Arg patients, whereas p53, MDM2 and PERP expression were hardly altered. Arginine 137-140 H3 histone pseudogene 16 Homo sapiens 26-29 23056370-4 2012 Here, we demonstrate that replicating mutants deleted in small E1A-domains, binding pRb (dl1108), p300/CBP (dl1104) and p400/TRRAP or p21 (dl1102) sensitize human prostate cancer cells (PC-3, DU145, 22Rv1) to mitoxantrone and docetaxel. Mitoxantrone 209-221 H3 histone pseudogene 16 Homo sapiens 134-137 23056207-9 2012 Also, decreased androgen receptor, prostate specific antigen, p53 and p21 protein levels were demonstrated in response to treatment with NU9056. 1,2-bis(isothiazol-5-yl)disulfane 137-143 H3 histone pseudogene 16 Homo sapiens 70-73 23056370-4 2012 Here, we demonstrate that replicating mutants deleted in small E1A-domains, binding pRb (dl1108), p300/CBP (dl1104) and p400/TRRAP or p21 (dl1102) sensitize human prostate cancer cells (PC-3, DU145, 22Rv1) to mitoxantrone and docetaxel. Docetaxel 226-235 H3 histone pseudogene 16 Homo sapiens 134-137 22808086-0 2012 Lin28 mediates paclitaxel resistance by modulating p21, Rb and Let-7a miRNA in breast cancer cells. Paclitaxel 15-25 H3 histone pseudogene 16 Homo sapiens 51-54 23028803-7 2012 p21 and BIM, which were identified as target genes of miR-106b-93-25 cluster, increased in TSA treated tumor cells and were responsible for cell cycle arrest and apoptosis. trichostatin A 91-94 H3 histone pseudogene 16 Homo sapiens 0-3 23028803-8 2012 We further identified MYC as a regulator of miR-106b-93-25 cluster and demonstrated its down-regulation in the presence of TSA resulted in the reduction of miR-106b-93-25 cluster and up-regulation of p21 and BIM. trichostatin A 123-126 H3 histone pseudogene 16 Homo sapiens 200-203 22860097-4 2012 Our results show that activation of the p14ARF-p53-p21-Rb pathway in the estrogen sensitive MCF-7 breast cancer cells induces many hallmarks of senescence including a large flat cell morphology, multinucleation, senescence-associated-beta-gal staining, and rapid G1 and G2/M phase cell cycle arrest. beta-D-galactose 234-242 H3 histone pseudogene 16 Homo sapiens 51-54 22574207-9 2012 It is possible that the elevated cAMP levels inhibit growth and induce apoptosis in Hela cells through induction of p21 and cleaved caspase-3/PARP-1 expression, and causing down-regulation of PCNA and cell cycle arrest with accumulation of cells in the G0/G1 and G2/M fractions. Cyclic AMP 33-37 H3 histone pseudogene 16 Homo sapiens 116-119 22679478-5 2012 The anti-mitogenic effect of H(2)S was accompanied by G(1)-phase cell cycle arrest and the induction of the cyclin-dependent kinase inhibitor p21(Cip). Hydrogen Sulfide 29-34 H3 histone pseudogene 16 Homo sapiens 142-145 22514710-9 2012 In conclusion, the results indicate that H(2)O(2) at low concentrations causes premature senescence in human keratinocytes by activating p53-p21(CIP1) signaling and that these effects can be prevented by acute AMPK activation and enhanced by AMPK downregulation. Hydrogen Peroxide 41-49 H3 histone pseudogene 16 Homo sapiens 141-144 22514698-10 2012 Combination of ZnPP and Gem enhanced the release of cytochrome c and increased p21 levels. zinc protoporphyrin 15-19 H3 histone pseudogene 16 Homo sapiens 79-82 22514698-10 2012 Combination of ZnPP and Gem enhanced the release of cytochrome c and increased p21 levels. gemcitabine 24-27 H3 histone pseudogene 16 Homo sapiens 79-82 22514710-3 2012 The increase in SA-gal staining was preceded by increases in both p53 phosphorylation (S15) (1 h) and transactivation (6 h) and the abundance of the cyclin inhibitor p21(CIP1) (16 h). sa-gal 16-22 H3 histone pseudogene 16 Homo sapiens 166-169 22514710-4 2012 Incubation with AICAR or resveratrol, both of which activated AMPK, prevented the H(2)O(2)-induced increases in both SA-Gal staining and p21 abundance. Resveratrol 25-36 H3 histone pseudogene 16 Homo sapiens 137-140 22558087-0 2012 JKA97, a novel benzylidene analog of harmine, exerts anti-cancer effects by inducing G1 arrest, apoptosis, and p53-independent up-regulation of p21. Harmine 37-44 H3 histone pseudogene 16 Homo sapiens 144-147 22514710-4 2012 Incubation with AICAR or resveratrol, both of which activated AMPK, prevented the H(2)O(2)-induced increases in both SA-Gal staining and p21 abundance. h(2) 82-86 H3 histone pseudogene 16 Homo sapiens 137-140 22448262-7 2012 The cell lines exhibited different sensitivity to cadmium, and 24-hour exposure to different CdCl(2) concentrations induced dose- and cell type-dependent apoptotic response and inhibition of cell proliferation that correlated with accumulation of functional p53 and overexpression of p21 in wild type p53-expressing cell lines. Cadmium Chloride 93-100 H3 histone pseudogene 16 Homo sapiens 284-287 22575193-5 2012 Meanwhile, Rb expression was significantly downregulated, E2F-1 and p21 expression upregulated by Zta. zta 98-101 H3 histone pseudogene 16 Homo sapiens 68-71 22412944-7 2012 In comparison with control groups, the levels of p53, phospho-p53 (ser15), and p21 proteins were significantly increased while phospho-p53 (Thr55) and survivin were significantly decreased after treatments of pre-DOX and LMB (P<0.05). Doxorubicin 213-216 H3 histone pseudogene 16 Homo sapiens 79-82 22032700-10 2012 The positive rate of SA-beta-gal staining was increased; the telomere length was shortened; and the expressions of p16 and p21 were increased. 2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine 21-23 H3 histone pseudogene 16 Homo sapiens 123-126 22032700-12 2012 Tanshinone IIA may delay the process of senescence of HPMC induced by high glucose by increasing cell generations and growth rate, decreasing the rate of G1 phase and the positive rate of SA-beta-gal staining, lengthening the telomere, and decreasing the expression of p16 and p21. hydroxypropylmethylcellulose-lactose matrix 54-58 H3 histone pseudogene 16 Homo sapiens 277-280 22072715-4 2011 A marked increase in the levels of p53 and p21 induced by Ang II was blunted by the treatment with GW501516. GW 501516 99-107 H3 histone pseudogene 16 Homo sapiens 43-46 22347457-0 2012 Caffeic acid phenethyl ester causes p21 induction, Akt signaling reduction, and growth inhibition in PC-3 human prostate cancer cells. caffeic acid phenethyl ester 0-28 H3 histone pseudogene 16 Homo sapiens 36-39 22575193-6 2012 CONCLUSION: Zta could promote G(0)/G(1) phase to S phase transition in Daudi cells, which might be associated with the reduced expression of Rb and increased expression of E2F-1 and p21 protein. zta 12-15 H3 histone pseudogene 16 Homo sapiens 182-185 21952585-9 2011 BCAA also inhibited phosphorylation of GSK-3beta, increased cellular levels of p21(CIP1), caused cell-cycle arrest in G(0)/G(1) phase, and induced apoptosis in HCC cells in the presence of visfatin. Amino Acids, Branched-Chain 0-4 H3 histone pseudogene 16 Homo sapiens 79-82 21903181-7 2011 In addition, the cytoplasm sequestration of Cdc25C, Cip1/p21 induction and tubulin dyspolymerization also contributed to the TBMS1-mediated cell cycle arrest on the G2/M phase. tubeimoside I 125-130 H3 histone pseudogene 16 Homo sapiens 57-60 21969371-0 2011 Inhibition or ablation of p21-activated kinase (PAK1) disrupts glucose homeostatic mechanisms in vivo. Glucose 63-70 H3 histone pseudogene 16 Homo sapiens 26-29 22074820-4 2011 The proteasome inhibitors MG132, lactacystin, and proteasome inhibitor I dramatically inhibited cell proliferation and induced apoptosis of PEL cells through the accumulation of p21 and p27. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 26-31 H3 histone pseudogene 16 Homo sapiens 178-181 22074820-4 2011 The proteasome inhibitors MG132, lactacystin, and proteasome inhibitor I dramatically inhibited cell proliferation and induced apoptosis of PEL cells through the accumulation of p21 and p27. lactacystin 33-44 H3 histone pseudogene 16 Homo sapiens 178-181 21431842-6 2011 RESULTS: Surgical specimens from COX-2 positive endometrial cancer patients treated with etodolac had significantly reduced expression levels of COX-2, Ki-67, p53, p21, p27, and cyclin D1 as determined by immunohistochemistry, while AI was not affected. Etodolac 89-97 H3 histone pseudogene 16 Homo sapiens 164-167 21907187-4 2011 Western blot analysis revealed that lovastatin caused an increase of the protein level of p27 and cyclin-dependent kinase (CDK)4 and a decrease of the protein level of cyclin A2, cyclin D3, and phosphorylated Rb (pRb), but did not significantly change the protein levels of p21, cyclins D1 and E, and CDK2, in ARO cells. Lovastatin 36-46 H3 histone pseudogene 16 Homo sapiens 274-295 21225623-7 2011 Moreover, the different stilbenes also elicited diverse cellular and signaling responses in MCF-7 and MDA-MB-231 cells, as evidenced by analysis of colony formation, cell proliferation, cell cycle phase transition, the extent of phosphorylation of p53 at Ser15 and p53-inducible proteins, p21 and p53R2, respectively. Stilbenes 24-33 H3 histone pseudogene 16 Homo sapiens 289-292 22101335-0 2011 Curcumin induces Apaf-1-dependent, p21-mediated caspase activation and apoptosis. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 35-38 22101335-10 2011 Importantly, p21-deficiency resulted in reduced expression of Apaf-1 during curcumin treatment, indicating a requirement of p21 in Apaf-1 dependent caspase activation and apoptosis. Curcumin 76-84 H3 histone pseudogene 16 Homo sapiens 13-16 22101335-11 2011 Together, our findings demonstrate that Apaf-1, Bax, and p21 as novel potential targets for curcumin or curcumin-based anticancer agents. Curcumin 92-100 H3 histone pseudogene 16 Homo sapiens 57-60 22101335-11 2011 Together, our findings demonstrate that Apaf-1, Bax, and p21 as novel potential targets for curcumin or curcumin-based anticancer agents. Curcumin 104-112 H3 histone pseudogene 16 Homo sapiens 57-60 21914449-4 2011 Here, we found that grifolin induced dephosphorylation of DAPK1 (Ser308) to activate DAPK1 and subsequent phosphorylation of its potential downstream effector p21 (Thr145) in nasopharyngeal carcinoma cell CNE1. grifolin 20-28 H3 histone pseudogene 16 Homo sapiens 159-162 22409043-0 2011 Toxicity of carbon nanotubes to p21 and hus1 gene deficient mammalian cells. Carbon 12-18 H3 histone pseudogene 16 Homo sapiens 32-35 22409043-3 2011 The aim of this study is to investigate the role of the p21 and hus1 genes in the toxicity of carbon nanotubes. Carbon 94-100 H3 histone pseudogene 16 Homo sapiens 56-59 22409043-5 2011 Our results show that the yield of the micronucleus ratio in p21 gene knock-out MEF cells is lower than that in the wild type counterpart, indicating that p21 may play as anti-apoptosis factor during the signal transduction of DNA damage caused by carbon nanotubes in mammalian cells. Carbon 248-254 H3 histone pseudogene 16 Homo sapiens 61-64 22409043-5 2011 Our results show that the yield of the micronucleus ratio in p21 gene knock-out MEF cells is lower than that in the wild type counterpart, indicating that p21 may play as anti-apoptosis factor during the signal transduction of DNA damage caused by carbon nanotubes in mammalian cells. Carbon 248-254 H3 histone pseudogene 16 Homo sapiens 155-158 22009179-4 2011 Importantly, radiation enhancement by BEZ235 coincides with a prominent p53-dependent accelerated senescence phenotype characterized by positive beta-galactosidase staining, G(2)-M cell-cycle arrest, enlarged and flattened cellular morphology, and increased p21 expression and senescence-associated cytokine secretion. dactolisib 38-44 H3 histone pseudogene 16 Homo sapiens 258-261 22169296-4 2011 The results showed that compared with cells treated with 2-ME2 or Bor alone, the proliferative potential of cells in combination group was significantly inhibited (p < 0.05), and apoptosis rate markedly increased (p < 0.05), cell cycle was arrested at G(1)-S phase, the mRNA expressive level of P21 and BAX increased, while the expression of BCL-2 decreased. 2-Methoxyestradiol 57-62 H3 histone pseudogene 16 Homo sapiens 301-304 22169296-4 2011 The results showed that compared with cells treated with 2-ME2 or Bor alone, the proliferative potential of cells in combination group was significantly inhibited (p < 0.05), and apoptosis rate markedly increased (p < 0.05), cell cycle was arrested at G(1)-S phase, the mRNA expressive level of P21 and BAX increased, while the expression of BCL-2 decreased. Bortezomib 66-69 H3 histone pseudogene 16 Homo sapiens 301-304 20458559-0 2011 Essential role of cell cycle regulatory genes p21 and p27 expression in inhibition of breast cancer cells by arsenic trioxide. Arsenic Trioxide 109-125 H3 histone pseudogene 16 Homo sapiens 46-49 20458559-6 2011 Notably, As2O3 treatment increased the mRNA and protein levels of the cell cycle inhibitory proteins, p21 and p27. Arsenic Trioxide 9-14 H3 histone pseudogene 16 Homo sapiens 102-105 20458559-7 2011 Interestingly, knocking down p21 or p27 individually did not alter As2O3-induced apoptosis and cell cycle arrest; however, the simultaneous down-regulation of both p21 and p27 resulted in attenuating of G1, G2/M arrest and reduction in apoptosis, thus indicating that p21 and p27 as the primary molecular targets of As2O3 against breast cancer. Arsenic Trioxide 316-321 H3 histone pseudogene 16 Homo sapiens 164-167 20458559-7 2011 Interestingly, knocking down p21 or p27 individually did not alter As2O3-induced apoptosis and cell cycle arrest; however, the simultaneous down-regulation of both p21 and p27 resulted in attenuating of G1, G2/M arrest and reduction in apoptosis, thus indicating that p21 and p27 as the primary molecular targets of As2O3 against breast cancer. Arsenic Trioxide 316-321 H3 histone pseudogene 16 Homo sapiens 164-167 21775055-6 2011 When KIM-1 cells, which are very low in NDRG1/Cap43 expression, were treated with mimosine, a G0/G1 cell cycle blocker, expression of NDRG1/Cap43 was induced in a dose dependent manner, together with p21 induction and CDK4 reduction. Mimosine 82-90 H3 histone pseudogene 16 Homo sapiens 200-203 22127059-3 2011 Here we show the pressure-induced formation of a partially ionic phase (monoclinic P2(1) structure) consisting of coupled alternate layers of (OH)(delta-) and (H(3)O)(delta+) (delta=0.62) in water ice predicted by particle-swarm optimization structural search at zero temperature and pressures of >14 Mbar. Water 191-196 H3 histone pseudogene 16 Homo sapiens 83-88 21889949-7 2011 At the doses used, ATO did not interfere with cell cycle progression, but SAHA induced p21 expression and led to G1 arrest. Vorinostat 74-78 H3 histone pseudogene 16 Homo sapiens 87-90 21552291-8 2011 Although p53 and its classical targets such as p21 and Mdm2 are activated by both H(2)O(2) and CDDP, we found that the expression of haeme-oxygenase-1 (HO-1)-an antioxidant and antiapoptotic protein-was directly induced only upon H(2)O(2) treatment in a p53-dependent manner. Hydrogen Peroxide 82-90 H3 histone pseudogene 16 Homo sapiens 47-50 21552291-8 2011 Although p53 and its classical targets such as p21 and Mdm2 are activated by both H(2)O(2) and CDDP, we found that the expression of haeme-oxygenase-1 (HO-1)-an antioxidant and antiapoptotic protein-was directly induced only upon H(2)O(2) treatment in a p53-dependent manner. Cisplatin 95-99 H3 histone pseudogene 16 Homo sapiens 47-50 21553143-3 2011 METHODS: We treated human glioblastoma cells with BP and found a dose-dependent decrease in human telomerase reverse transcriptase (hTERT) mRNA expression and a concomitant increase in p16 and p21 expression. butylidenephthalide 50-52 H3 histone pseudogene 16 Homo sapiens 193-196 21878748-0 2011 Sorafenib attenuates p21 in kidney cancer cells and augments cell death in combination with DNA-damaging chemotherapy. Sorafenib 0-9 H3 histone pseudogene 16 Homo sapiens 21-24 21878748-6 2011 We now show that sorafenib markedly decreases p21 levels in several RCC and hepatocellular carcinoma cells. Sorafenib 17-26 H3 histone pseudogene 16 Homo sapiens 46-49 21878748-8 2011 In cells treated with doxorubicin to augment p21, sorafenib markedly decreases this protein, and the combinations of paclitaxel or doxorubicin with sorafenib show additive cytotoxicity as a function of the VHL status of the cells, suggesting that lower doses of each agent could be used in the clinical setting. Doxorubicin 22-33 H3 histone pseudogene 16 Homo sapiens 45-48 21878748-8 2011 In cells treated with doxorubicin to augment p21, sorafenib markedly decreases this protein, and the combinations of paclitaxel or doxorubicin with sorafenib show additive cytotoxicity as a function of the VHL status of the cells, suggesting that lower doses of each agent could be used in the clinical setting. Sorafenib 50-59 H3 histone pseudogene 16 Homo sapiens 45-48 21878748-9 2011 In summary, we show a novel signaling pathway by which sorafenib exerts its salutary effects in RCC; future work will focus on the use of these drug combinations in the context of conventional therapeutics, and novel compounds and protocols targeting p21 in conjunction with sorafenib should be pursued. Sorafenib 55-64 H3 histone pseudogene 16 Homo sapiens 251-254 22037398-8 2011 In hMSCs isolated from a chronic lymphocytic leukemia (CLL) patient, p53 and p21 were induced by cisplatin and gamma-irradiation, while RPA2 was phosphorylated on serine4/8 in particular following cisplatin. Cisplatin 197-206 H3 histone pseudogene 16 Homo sapiens 77-80 21908486-7 2011 Honokiol down-regulated the expression of cyclin D1, cyclin D2, Cdk2, Cdk4 and Cdk6 proteins and up-regulated the expression of Cdk"s inhibitor proteins p21 and p27. honokiol 0-8 H3 histone pseudogene 16 Homo sapiens 153-156 21803488-0 2011 All-trans retinoic acid induces cellular senescence via upregulation of p16, p21, and p27. Tretinoin 10-23 H3 histone pseudogene 16 Homo sapiens 77-80 21803488-3 2011 ATRA also upregulated levels of p16, p21, and p27 which lead to activation of Rb and subsequent inactivation of E2F1. Tretinoin 0-4 H3 histone pseudogene 16 Homo sapiens 37-40 21956589-5 2011 VO(CH(3)SO(3))(2) (P2(1)/c, a=1136.5(1), b=869.87(7), c=915.5(1) pm, beta=113.66(1) , V=0.8290(2) nm(3), Z=4) contains [VO] units connected by methanesulfonate anions to form corrugated layers parallel to (100). Vanadium(II) oxide 0-2 H3 histone pseudogene 16 Homo sapiens 19-26 22037398-4 2011 Cisplatin and gamma-irradiation activated the DNA damage response in hMSCs, including induction of p53 and p21, and activation of PI3 kinase-related protein kinase (PIKK)-dependent phosphorylation of histone H2AX on serine 139, and replication protein A2 on serine4/serine8. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 107-110 22037398-8 2011 In hMSCs isolated from a chronic lymphocytic leukemia (CLL) patient, p53 and p21 were induced by cisplatin and gamma-irradiation, while RPA2 was phosphorylated on serine4/8 in particular following cisplatin. Cisplatin 97-106 H3 histone pseudogene 16 Homo sapiens 77-80 21816217-0 2011 Autophagy regulates ROS-induced cellular senescence via p21 in a p38 MAPKalpha dependent manner. Reactive Oxygen Species 20-23 H3 histone pseudogene 16 Homo sapiens 56-59 21816217-5 2011 Further studies showed that Atg5 regulates H2O2-induced senescence primarily by up-regulating the expression of p21 at the level of post-transcription. Hydrogen Peroxide 43-47 H3 histone pseudogene 16 Homo sapiens 112-115 21878644-11 2011 Further studies provided evidence for the stabilization of Nrf2 due to reduced 26 S proteasome activity and increased p21 association as the driving signaling event that contributes to the transition from a high ROS quiescent state to a low ROS proliferating stage in drug-induced tumor stem cell enrichment. Reactive Oxygen Species 212-215 H3 histone pseudogene 16 Homo sapiens 118-121 22065906-0 2011 Apoptotic effects of genistein, biochanin-A and apigenin on LNCaP and PC-3 cells by p21 through transcriptional inhibition of polo-like kinase-1. Genistein 21-30 H3 histone pseudogene 16 Homo sapiens 84-87 22065906-8 2011 In conclusion, flavonoids treatment induces up-regulation of p21 expression, and p21 inhibits transcription of PLK-1, which promotes apoptosis of cancer cells. Flavonoids 15-25 H3 histone pseudogene 16 Homo sapiens 61-64 21811764-9 2011 These results suggest that KLF4 as an important cellular target of ABL mediates the growth inhibition of HT-29 cells induced by ABL via upregulation of p21 expression. lauric acid 67-70 H3 histone pseudogene 16 Homo sapiens 152-155 21811764-9 2011 These results suggest that KLF4 as an important cellular target of ABL mediates the growth inhibition of HT-29 cells induced by ABL via upregulation of p21 expression. lauric acid 128-131 H3 histone pseudogene 16 Homo sapiens 152-155 21878644-11 2011 Further studies provided evidence for the stabilization of Nrf2 due to reduced 26 S proteasome activity and increased p21 association as the driving signaling event that contributes to the transition from a high ROS quiescent state to a low ROS proliferating stage in drug-induced tumor stem cell enrichment. Reactive Oxygen Species 241-244 H3 histone pseudogene 16 Homo sapiens 118-121 21617849-0 2011 Aspirin reduces the apoptotic effect of etoposide via Akt activation and up-regulation of p21(cip). Aspirin 0-7 H3 histone pseudogene 16 Homo sapiens 90-93 22029423-10 2011 RSV enhanced IR-induced expression of DNA damage (gammaH2Ax) and apoptosis (cleaved-caspase 3) markers as well as of the cell cycle regulators p53, p21(cip1) and p27(kip1). Resveratrol 0-3 H3 histone pseudogene 16 Homo sapiens 148-151 22029423-12 2011 CONCLUSIONS: Our results suggest that RSV arrests cell cycle, promotes apoptosis and sensitizes PrCa cells to IR likely through a desirable dual action to activate the ATM-AMPK-p53-p21(cip1)/p27(kip1) and inhibit the Akt signalling pathways. Resveratrol 38-41 H3 histone pseudogene 16 Homo sapiens 181-184 21840268-6 2011 p53 was activated and phosphorylated at Serine15 followed by p21 gene activation through both p53-dependent and -independent pathways. serine15 40-48 H3 histone pseudogene 16 Homo sapiens 61-64 21786165-5 2011 Growth inhibitory effects of celastrol correlated with a decrease in the levels of cyclin D1 and cyclin E, but concomitant increase in the levels of p21 and p27. celastrol 29-38 H3 histone pseudogene 16 Homo sapiens 149-152 21311948-0 2011 Role of p21 in SP600125-induced cell cycle arrest, endoreduplication, and apoptosis. pyrazolanthrone 15-23 H3 histone pseudogene 16 Homo sapiens 8-11 21311948-2 2011 However the role of p21 in SP600125-mediated G(2)/M distribution is not fully understood. pyrazolanthrone 27-35 H3 histone pseudogene 16 Homo sapiens 20-23 21311948-3 2011 Our results showed that the transcriptional activation of p21 by SP600125 is mediated through the proximal regions of multiple Sp1 sites in the p21 promoter following ERK-dependent phosphorylation of Sp1. pyrazolanthrone 65-73 H3 histone pseudogene 16 Homo sapiens 58-61 21311948-3 2011 Our results showed that the transcriptional activation of p21 by SP600125 is mediated through the proximal regions of multiple Sp1 sites in the p21 promoter following ERK-dependent phosphorylation of Sp1. pyrazolanthrone 65-73 H3 histone pseudogene 16 Homo sapiens 144-147 21311948-5 2011 Furthermore, SP600125 induces the phosphorylation of p21 at Thr 145 through the PI3K/Akt pathway. pyrazolanthrone 13-21 H3 histone pseudogene 16 Homo sapiens 53-56 21311948-5 2011 Furthermore, SP600125 induces the phosphorylation of p21 at Thr 145 through the PI3K/Akt pathway. Threonine 60-63 H3 histone pseudogene 16 Homo sapiens 53-56 21617849-0 2011 Aspirin reduces the apoptotic effect of etoposide via Akt activation and up-regulation of p21(cip). Etoposide 40-49 H3 histone pseudogene 16 Homo sapiens 90-93 21617849-7 2011 Our data showed that the protein expression and ser146 phosphorylation levels of p21(cip) were significantly increased after treatment with aspirin, whereas p53 or p27 showed no change. Aspirin 140-147 H3 histone pseudogene 16 Homo sapiens 81-84 21617849-8 2011 The increase of p21(cip) protein levels was also scavenged by wortmannin but not by U0126. Wortmannin 62-72 H3 histone pseudogene 16 Homo sapiens 16-19 21617849-9 2011 Moreover, reduction of caspase-3 activity induced by aspirin was attenuated by silencing p21(cip) expression. Aspirin 53-60 H3 histone pseudogene 16 Homo sapiens 89-92 21617849-10 2011 These results indicated that the anti-apoptotic effect of aspirin was dependent on activation of Akt which inhibited cell apoptosis by up-regulating p21(cip) and blocking caspase-3 activation. Aspirin 58-65 H3 histone pseudogene 16 Homo sapiens 149-152 21872575-11 2011 Furthermore, p53 siRNA and p21 siRNA transfection attenuated adriamycin-induced SA-beta-gal staining. Doxorubicin 61-71 H3 histone pseudogene 16 Homo sapiens 27-30 21933400-12 2011 However, p21 was significantly increased by SAHA and combination treatment as compared to HIT only in the two sarcoma cell lines--again in contrast to the osteoblast cell line. Vorinostat 44-48 H3 histone pseudogene 16 Homo sapiens 9-12 21933400-13 2011 Changes in the repair kinetics of DSB p53-independent apoptosis with p21 involvement may be part of the underlying mechanisms for radio-sensitization by SAHA. Vorinostat 153-157 H3 histone pseudogene 16 Homo sapiens 69-72 21815631-5 2011 We further characterized the DNA damage, generation of highly reactive oxygen species (hROS), and expression of proteins p21 and p53 in cells after exposure to iAs(III), DMA(III), and DMMTA(V). N-myristoyl-alaninol 170-173 H3 histone pseudogene 16 Homo sapiens 121-124 21815631-5 2011 We further characterized the DNA damage, generation of highly reactive oxygen species (hROS), and expression of proteins p21 and p53 in cells after exposure to iAs(III), DMA(III), and DMMTA(V). dmmta 184-189 H3 histone pseudogene 16 Homo sapiens 121-124 21815631-6 2011 Cellular exposure to DMMTA(V) resulted in reduced protein expression of p53 and p21, increased DNA damage, and increased intracellular hROS (hydroxyl radical). dmmta 21-26 H3 histone pseudogene 16 Homo sapiens 80-83 21872575-11 2011 Furthermore, p53 siRNA and p21 siRNA transfection attenuated adriamycin-induced SA-beta-gal staining. 2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid 80-91 H3 histone pseudogene 16 Homo sapiens 27-30 21843507-0 2011 All-trans retinoic acid induces cellular senescence by up-regulating levels of p16 and p21 via promoter hypomethylation. Tretinoin 10-23 H3 histone pseudogene 16 Homo sapiens 87-90 21742020-5 2011 Upregulation of hHR23 expression by low-dose cisplatin was accompanied by an increase in p53, p21, and XPC protein levels. Cisplatin 45-54 H3 histone pseudogene 16 Homo sapiens 94-97 21843507-1 2011 All-trans retinoic acid (ATRA) induces cellular senescence via up-regulation of p16 and p21; however, the action mechanism of ATRA is unknown. Tretinoin 0-23 H3 histone pseudogene 16 Homo sapiens 88-91 21843507-1 2011 All-trans retinoic acid (ATRA) induces cellular senescence via up-regulation of p16 and p21; however, the action mechanism of ATRA is unknown. Tretinoin 25-29 H3 histone pseudogene 16 Homo sapiens 88-91 21843507-2 2011 Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells. Tretinoin 19-23 H3 histone pseudogene 16 Homo sapiens 68-71 21843507-2 2011 Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells. Tretinoin 19-23 H3 histone pseudogene 16 Homo sapiens 199-202 21719763-7 2011 In cultured SMCs, inorganic phosphate (Pi) stimulation dose-dependently increased SAbeta-gal-positive cells, and Pi-induced senescence was associated with downregulation of SIRT1 expression, leading to p21 activation. Phosphates 18-37 H3 histone pseudogene 16 Homo sapiens 202-205 21868512-10 2011 The p53 pathway was involved in the synergism of RAD001 and carboplatin on breast cancer cell proliferation and apoptosis, since the synergistic effect was demonstrated in all tested breast cancer cell lines with wild-type p53 and the use of p53 inhibitor partially antagonized the effect of RAD001 and carboplatin on p53 and p21 expression, as well as their inhibitory effect on cell proliferation. Carboplatin 60-71 H3 histone pseudogene 16 Homo sapiens 326-329 21709443-10 2011 These data also suggest the novel finding that the enhanced antitumor activity of topotecan following low-dose exposure correlates to alterations in cell cycle and increased p21 expression. Topotecan 82-91 H3 histone pseudogene 16 Homo sapiens 174-177 21570766-4 2011 This synergistic effect was associated with abrogation of CDDP-induced G2/M arrest by down-regulations of phospho-Cdc2 and p21, and inhibitions of phospho-AKT, phospho-ERK and NF-kappaB. Cisplatin 58-62 H3 histone pseudogene 16 Homo sapiens 123-126 21940317-8 2011 When pathological factors were also introduced in the analysis, the positive prognostic role on CSS was obtained for p21 and lymphatic invasion; CFS was positively influenced by the presence of p21 protein and lymphatic invasion. thiocysteine 96-99 H3 histone pseudogene 16 Homo sapiens 117-120 21869603-6 2011 In drug sensitive MCF-7 cells which have wild-type p53; ERK, p53 and downstream p21 (Cip-1 ) were induced upon exposure to doxorubicin. Doxorubicin 123-134 H3 histone pseudogene 16 Homo sapiens 80-83 21869603-7 2011 In contrast, in the drug resistant cells which expressed activated Akt-1, much lower levels of p53 and p21 (Cip1) were induced upon exposure to doxorubicin. Doxorubicin 144-155 H3 histone pseudogene 16 Homo sapiens 103-106 21940317-9 2011 For patients with pN0, p21 protein was an independent predictive marker for CSS and CFS. thiocysteine 76-79 H3 histone pseudogene 16 Homo sapiens 23-26 21067279-5 2011 Both types of TiO2 nanoparticles transiently upregulated mRNA expression of p53 and its downstream regulated DNA damage responsive genes (mdm2, gadd45alpha, p21), providing additional evidence that TiO2 nanoparticles are genotoxic. titanium dioxide 14-18 H3 histone pseudogene 16 Homo sapiens 157-160 21229291-10 2011 Inhibiting DNMTs by 5-azacytidine (DNMT inhibitor) treatment led to significant inhibition of expression of DNMT1 and DNMT3B and enhanced expression of TSGs such as PTEN and p21 analyzed in this study. Azacitidine 20-33 H3 histone pseudogene 16 Homo sapiens 174-177 21737444-5 2011 Induction of the cyclin-dependent kinase inhibitor p21 by MS-275 was attenuated by IGFBP-3 down-regulation, providing an explanation for IGFBP-3-dependent effects of MS-275 on cell cycle activity. entinostat 58-64 H3 histone pseudogene 16 Homo sapiens 51-54 21737444-5 2011 Induction of the cyclin-dependent kinase inhibitor p21 by MS-275 was attenuated by IGFBP-3 down-regulation, providing an explanation for IGFBP-3-dependent effects of MS-275 on cell cycle activity. entinostat 166-172 H3 histone pseudogene 16 Homo sapiens 51-54 21620794-7 2011 These carotenoids up-regulated the expression of PPARgamma and p21 and down-regulated the expression of cyclin D1 in a dose-dependent manner. Carotenoids 6-17 H3 histone pseudogene 16 Homo sapiens 63-66 21864408-8 2011 We used the inhibitors LY294002, Akti-1/2, and rapamycin, to show that p21 induction is dependent upon PI3-kinase and AKT activity, and partially dependent on mTOR. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 23-31 H3 histone pseudogene 16 Homo sapiens 71-74 21864408-9 2011 We treated the cells with proteasome inhibitor MG-132 and found that p21 may be degraded in the proteasome to regulate protein levels. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 47-53 H3 histone pseudogene 16 Homo sapiens 69-72 21864408-11 2011 Treatment of cells with the GSK-3beta inhibitor SB-216763 increased p21 levels, while exogenous expression of GSK-3beta caused a decrease in p21, indicating that GSK-3beta actively reduces p21 levels. SB 216763 48-57 H3 histone pseudogene 16 Homo sapiens 68-71 21669554-6 2011 We demonstrate that oxLDL activates ATM and downstream p21 expression in normal fibroblasts and endothelial cells. oxldl 20-25 H3 histone pseudogene 16 Homo sapiens 55-58 21739974-0 2011 4-acetylantroquinonol B isolated from Antrodia cinnamomea arrests proliferation of human hepatocellular carcinoma HepG2 cell by affecting p53, p21 and p27 levels. 4-acetylantroquinonol B 0-23 H3 histone pseudogene 16 Homo sapiens 143-146 21739974-4 2011 The protein levels of p53 and p21 proteins were also increased when the cells were treated with low dosage (0.1 mug/mL) of 4-acetylantroquinonol B. 4-acetylantroquinonol 123-144 H3 histone pseudogene 16 Homo sapiens 30-33 21739974-10 2011 Our finding suggested that the 4-acetylantroquinonol B inhibits proliferation of HepG2 cells via affecting p53, p21 and p27 proteins, and can be considered as a potential cancer drug. 4-acetylantroquinonol B 31-54 H3 histone pseudogene 16 Homo sapiens 112-115 21656826-0 2011 Resistance to docetaxel-induced apoptosis in prostate cancer cells by p38/p53/p21 signaling. Docetaxel 14-23 H3 histone pseudogene 16 Homo sapiens 78-81 21656826-9 2011 Docetaxel stabilizes p53 protein level and upregulates p21 in a p53-dependent manner in LNCaP cells. Docetaxel 0-9 H3 histone pseudogene 16 Homo sapiens 55-58 21656826-11 2011 Treatment with p38-specific inhibitor SB203580 or knocking down p38 by siRNA significantly impaired the upregulation of p53 and p21 by docetaxel. SB 203580 38-46 H3 histone pseudogene 16 Homo sapiens 128-131 21656826-11 2011 Treatment with p38-specific inhibitor SB203580 or knocking down p38 by siRNA significantly impaired the upregulation of p53 and p21 by docetaxel. Docetaxel 135-144 H3 histone pseudogene 16 Homo sapiens 128-131 21656826-12 2011 Knocking down p38 or p21 sensitizes LNCaP cells to docetaxel treatment and the antiapoptotic effect of p21 can be reversed by p38 siRNA in LNCaP cells. Docetaxel 51-60 H3 histone pseudogene 16 Homo sapiens 21-24 21656826-13 2011 CONCLUSIONS: Stimulation of the p38/p53/p21 signaling axis could be important for regulating the susceptibility towards docetaxel in prostate cancer. Docetaxel 120-129 H3 histone pseudogene 16 Homo sapiens 40-43 21906442-5 2011 The expression levels of caspase-3, -8, -9, c-FLIP, Bcl-2, p53, and p21 in the FLS changed after epirubicin treatment. Epirubicin 97-107 H3 histone pseudogene 16 Homo sapiens 68-71 21628527-6 2011 UBCH8, a member of the UBE2E family of UBCs, ubiquitylates and promotes the degradation of p21, both during the normal cell cycle and in UV-irradiated cells. ubcs 39-43 H3 histone pseudogene 16 Homo sapiens 91-94 21906442-6 2011 CONCLUSION: Epirubicin may coordinate with AD5-10 in inducing FLS apoptosis through affecting the levels of p53, p21, c-FLIP, and Bcl-2. Epirubicin 12-22 H3 histone pseudogene 16 Homo sapiens 113-116 21565979-4 2011 Induction of p21 was inhibited by miR-22 after exposure to the genotoxic agent Adriamycin (doxorubicin; Bedford Laboratories), sensitizing cells to p53-dependent apoptosis. Doxorubicin 79-89 H3 histone pseudogene 16 Homo sapiens 13-16 21634433-6 2011 On the other hand, MAP2c and, to a lesser degree, p21(Cip1), which carry out their functions by partner binding and accompanying partially induced folding, show signs of local structuring and also some global compaction upon crowded conditions, in particular in the presence of TMAO. trimethyloxamine 278-282 H3 histone pseudogene 16 Homo sapiens 50-53 21565979-4 2011 Induction of p21 was inhibited by miR-22 after exposure to the genotoxic agent Adriamycin (doxorubicin; Bedford Laboratories), sensitizing cells to p53-dependent apoptosis. Doxorubicin 91-102 H3 histone pseudogene 16 Homo sapiens 13-16 21565980-6 2011 Nicotinamide modulates the p53-dependent genes p21, NOXA, BAX, and Mcl-1, indicating an activation of the p53 pathway and of caspase-3. Niacinamide 0-12 H3 histone pseudogene 16 Homo sapiens 47-50 21515331-0 2011 Induction of ROS, p53, p21 in DEHP- and MEHP-exposed LNCaP cells-protection by selenium compounds. Selenium 79-87 H3 histone pseudogene 16 Homo sapiens 23-26 21515331-1 2011 This study was designed to investigate the hypothesis that the toxic effects of di(2-ethylhexyl)phthalate (DEHP), the most abundantly used plasticizer and ubiquitous environmental contaminant that cause alterations in endocrine and spermatogenic functions in animals is mediated through the induction of reactive oxygen species (ROS) and activation of nuclear p53 and p21 proteins in LNCaP human prostate adenocarcinoma cell line. Diethylhexyl Phthalate 80-105 H3 histone pseudogene 16 Homo sapiens 368-371 21515332-10 2011 In conclusion, both limonoids induced apoptosis by activation of intrinsic apoptosis pathway and activation of p21 leading to arresting cells at G2/M phase of the cell cycle. Limonins 20-29 H3 histone pseudogene 16 Homo sapiens 111-114 21515331-1 2011 This study was designed to investigate the hypothesis that the toxic effects of di(2-ethylhexyl)phthalate (DEHP), the most abundantly used plasticizer and ubiquitous environmental contaminant that cause alterations in endocrine and spermatogenic functions in animals is mediated through the induction of reactive oxygen species (ROS) and activation of nuclear p53 and p21 proteins in LNCaP human prostate adenocarcinoma cell line. Diethylhexyl Phthalate 107-111 H3 histone pseudogene 16 Homo sapiens 368-371 21726064-9 2011 The protein levels of both total Smad3 and phosphorylated Smad3 were both up-regulated after berbamine treatment, together with decreased c-Myc and cyclin D1 and increased p21. berbamine 93-102 H3 histone pseudogene 16 Homo sapiens 172-175 22207897-5 2011 Knockdown of miR-203 following cisplatin treatment enhances p53, p21, and Bax protein expression. Cisplatin 31-40 H3 histone pseudogene 16 Homo sapiens 65-68 21479363-4 2011 Moreover, resveratrol enhanced apoptosis of MCF-7/ASPP1 cells, accompanied by higher expression of bax and p21. Resveratrol 10-21 H3 histone pseudogene 16 Homo sapiens 107-110 21374800-6 2011 SFN treatment also selectively decreased HDAC activity, and Class I and II HDAC proteins, increased acetylated histone H3 at the promoter for P21, induced p21 expression and increased tubulin acetylation in prostate cancer cells. sulforaphane 0-3 H3 histone pseudogene 16 Homo sapiens 142-145 21374800-6 2011 SFN treatment also selectively decreased HDAC activity, and Class I and II HDAC proteins, increased acetylated histone H3 at the promoter for P21, induced p21 expression and increased tubulin acetylation in prostate cancer cells. sulforaphane 0-3 H3 histone pseudogene 16 Homo sapiens 155-158 21396949-7 2011 Moreover, our results demonstrated that attenuation of GTP by almost 60% augmented the intracellular ROS and nuclear localization of p21 and subsequently led to cell death. Guanosine Triphosphate 55-58 H3 histone pseudogene 16 Homo sapiens 133-136 21396949-7 2011 Moreover, our results demonstrated that attenuation of GTP by almost 60% augmented the intracellular ROS and nuclear localization of p21 and subsequently led to cell death. ros 101-104 H3 histone pseudogene 16 Homo sapiens 133-136 21663649-11 2011 However, after repeated NA exposure, BrdU induced epithelial cell (Clara cell) senescence, as demonstrated by a DNA damage response, p21 overexpression, increased senescence-associated beta-galactosidase activity, and growth arrest, which resulted in impaired epithelial regeneration. Bromodeoxyuridine 37-41 H3 histone pseudogene 16 Homo sapiens 133-136 21325480-0 2011 Hepatitis B virus X protein overcomes all-trans retinoic acid-induced cellular senescence by downregulating levels of p16 and p21 via DNA methylation. 2-octenal 42-47 H3 histone pseudogene 16 Homo sapiens 126-129 21325480-0 2011 Hepatitis B virus X protein overcomes all-trans retinoic acid-induced cellular senescence by downregulating levels of p16 and p21 via DNA methylation. Tretinoin 48-61 H3 histone pseudogene 16 Homo sapiens 126-129 21325480-4 2011 In addition, HBx suppressed ATRA-mediated induction of p16 and p21 in HepG2 cells via promoter hypermethylation, resulting in inactivation of retinoblastoma protein. Tretinoin 28-32 H3 histone pseudogene 16 Homo sapiens 63-66 21325480-5 2011 Furthermore, the ability of HBx to overcome ATRA-induced cellular senescence almost completely disappeared when the levels of p16 and p21 in the HBx-expressing cells became similar to those in the control cells by complementation in the former by exogenous expression, knockdown of their expression in the latter using specific small interfering RNA or treatment with a DNA methylation inhibitor, 5-Aza-2"-deoxycytidine. Tretinoin 44-48 H3 histone pseudogene 16 Homo sapiens 134-137 21677879-0 2011 Induction of p21-dependent senescence by an NAE inhibitor, MLN4924, as a mechanism of growth suppression. N-lauroylethanolamine 44-47 H3 histone pseudogene 16 Homo sapiens 13-16 21677879-0 2011 Induction of p21-dependent senescence by an NAE inhibitor, MLN4924, as a mechanism of growth suppression. pevonedistat 59-66 H3 histone pseudogene 16 Homo sapiens 13-16 21466819-10 2011 Nickel was able to activate p21, and its activation was offset by the over-expression of DeltaNp63. Nickel 0-6 H3 histone pseudogene 16 Homo sapiens 28-31 21466819-12 2011 The present study demonstrated that nickel decreased interferon regulatory proteins IRF3 and IRF7, and activated NF-kappaB, resulting in DeltaNp63 suppression and then p21 up-regulation. Nickel 36-42 H3 histone pseudogene 16 Homo sapiens 168-171 21740780-9 2011 In resveratrol sensitive cells, capan-2 and colo357, the activation of caspase-3 was detected and showed significant caspase-3 activation upon resveratrol treatment; p53 and p21 were also detected up-regulated upon resveratrol treatment. Resveratrol 3-14 H3 histone pseudogene 16 Homo sapiens 174-177 21740780-9 2011 In resveratrol sensitive cells, capan-2 and colo357, the activation of caspase-3 was detected and showed significant caspase-3 activation upon resveratrol treatment; p53 and p21 were also detected up-regulated upon resveratrol treatment. Resveratrol 143-154 H3 histone pseudogene 16 Homo sapiens 174-177 21740780-9 2011 In resveratrol sensitive cells, capan-2 and colo357, the activation of caspase-3 was detected and showed significant caspase-3 activation upon resveratrol treatment; p53 and p21 were also detected up-regulated upon resveratrol treatment. Resveratrol 143-154 H3 histone pseudogene 16 Homo sapiens 174-177 21372224-7 2011 Exposure of cells to the ADC demonstrated signaling pathways leading to PARP cleavage, but differences versus free SN-38 in p53 and p21 upregulation were noted. Irinotecan 115-120 H3 histone pseudogene 16 Homo sapiens 132-135 21454683-5 2011 Furthermore, enhanced p21 expression in p53-72R-expressing cells, which is dependent on phosphorylation at Ser-6, was demonstrated. Serine 107-110 H3 histone pseudogene 16 Homo sapiens 22-25 21417953-7 2011 Importantly, blocking the induction of p21 in CaSki-Tam67-expressing cells accelerated their proliferation rate to that of CaSki, implicating p21 as a key player in the growth arrest induced by Tam67. tam67 52-57 H3 histone pseudogene 16 Homo sapiens 39-42 21454715-7 2011 A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression. Citrulline 2-12 H3 histone pseudogene 16 Homo sapiens 209-212 21454715-7 2011 A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression. Arginine 23-26 H3 histone pseudogene 16 Homo sapiens 209-212 21454715-7 2011 A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression. Glutamine 31-34 H3 histone pseudogene 16 Homo sapiens 209-212 21417953-7 2011 Importantly, blocking the induction of p21 in CaSki-Tam67-expressing cells accelerated their proliferation rate to that of CaSki, implicating p21 as a key player in the growth arrest induced by Tam67. tam67 52-57 H3 histone pseudogene 16 Homo sapiens 142-145 21310484-6 2011 Altogether our results showed that 7-b mediated its growth inhibitory effects on Raji cells via the activation of a ROS-mediated mitochondrial pathway and cell cycle checkpoint signaling pathway which subsequently targeted p21. 7-b 35-38 H3 histone pseudogene 16 Homo sapiens 223-226 21321187-7 2011 MG treatment of VSMCs led to increased DNA synthesis (EC(50)=5.8 muM), cell proliferation, phosphorylation of p21 and glycogen synthase kinase-3alpha/beta (GSK-3alpha/beta), and increased cyclin-dependent kinase 2 (CDK2) activity. vsmcs 16-21 H3 histone pseudogene 16 Homo sapiens 110-113 20614134-6 2011 RESULTS: The treatment with LiCl increased the percent of cells at S phase and G phase and the expression of c-MYC and Skp2 and decreased the expression of p21. Lithium Chloride 28-32 H3 histone pseudogene 16 Homo sapiens 156-159 20614134-8 2011 Notch3-siRNA weakened the effect of LiCl on the cell cycle and resulted in attenuation of the LiCl-induced increment of c-MYC and Skp2 and the LiCl-induced decrement of p21. Lithium Chloride 36-40 H3 histone pseudogene 16 Homo sapiens 169-172 21310484-6 2011 Altogether our results showed that 7-b mediated its growth inhibitory effects on Raji cells via the activation of a ROS-mediated mitochondrial pathway and cell cycle checkpoint signaling pathway which subsequently targeted p21. Reactive Oxygen Species 116-119 H3 histone pseudogene 16 Homo sapiens 223-226 21346197-3 2011 Upon serum addition or activation of Rac1, VIF are rapidly phosphorylated at Ser-38, a p21-activated kinase phosphorylation site. Serine 77-80 H3 histone pseudogene 16 Homo sapiens 87-90 24052824-3 2011 The compound (IIb), C28H25NO, crystallizes in the monoclinic system, space group P21/a, with a = 11.376(5) A, b = 14.139(3) A, c = 13.237(4) A, beta = 97.41(3) ( ) , and Z = 4. c28h25no 20-28 H3 histone pseudogene 16 Homo sapiens 81-84 21504622-9 2011 RESULTS: Isochaihulactone caused cell cycle arrest at G2/M phase in LNCaP cells, which was correlated with an increase of p53 and p21 levels and downregulation of the checkpoint proteins cdc25c, cyclin B1, and cdc2. isochaihulactone 9-25 H3 histone pseudogene 16 Homo sapiens 130-133 20891011-6 2011 The unreported zolpidem tartrate monohydrate instead crystallizes in monoclinic P21 , which, for comparison purposes, we treated in the nonstandard setting P1121 with a = 20.7582(9) A, b = 15.2331(5) A, c = 7.2420(2) A, gamma = 90.826(2) , and V = 2289.73(14) A(3) . zolpidem tartrate monohydrate 15-44 H3 histone pseudogene 16 Homo sapiens 80-83 21308745-1 2011 Using short hairpin RNA against p53, transient ectopic expression of wild-type p53 or mutant p53 (R248W or R175H), and a p53- and p21-dependent luciferase reporter assay, we demonstrated that growth arrest and apoptosis of FaDu (human pharyngeal squamous cell carcinoma), Hep3B (hepatoma), and MG-63 (osteosarcoma) cells induced by aloe-emodin (AE) are p53-independent. fadu 223-227 H3 histone pseudogene 16 Homo sapiens 130-133 21205092-7 2011 Furthermore, vorinostat-induced RUNX3 significantly enhanced p21 expression and growth inhibition of Mz-ChA-2 cells through restoration of TGF-beta signaling. Vorinostat 13-23 H3 histone pseudogene 16 Homo sapiens 61-64 21209038-0 2011 (-)-Epigallocatechin-3-gallate reactivates silenced tumor suppressor genes, Cip1/p21 and p16INK4a, by reducing DNA methylation and increasing histones acetylation in human skin cancer cells. epigallocatechin gallate 0-30 H3 histone pseudogene 16 Homo sapiens 81-84 21209038-8 2011 Additionally, EGCG treatment resulted in re-expression of the mRNA and proteins of silenced tumor suppressor genes, p16INK4a and Cip1/p21. epigallocatechin gallate 14-18 H3 histone pseudogene 16 Homo sapiens 134-137 21462329-0 2011 The p53-, Bax- and p21-dependent inhibition of colon cancer cell growth by 5-hydroxy polymethoxyflavones. 5-hydroxy polymethoxyflavones 75-104 H3 histone pseudogene 16 Homo sapiens 19-22 21220410-6 2011 Thus, we examined the effects of amitriptyline on histone 3 (H3) acetylation and demonstrated that amitriptyline increased acetylation of H3 and expression of p27 and p21. Amitriptyline 99-112 H3 histone pseudogene 16 Homo sapiens 167-170 21462329-5 2011 All three 5OH-PMFs increased G0/G1 cell population of HCT116 (p53(+/+) ) cells, and these effects were abolished in HCT116 (p53(-/-) ) and HCT116 (p21(-/-) ) cells. 5oh 10-13 H3 histone pseudogene 16 Homo sapiens 147-150 21462329-7 2011 CONCLUSION: Our results demonstrated that 5OH-PMFs, especially 5HHMF and 5HTMF, induce apoptosis and cell-cycle arrest by p53-, Bax- and p21-dependent mechanism. 5oh-pmfs 42-50 H3 histone pseudogene 16 Homo sapiens 137-140 21462329-7 2011 CONCLUSION: Our results demonstrated that 5OH-PMFs, especially 5HHMF and 5HTMF, induce apoptosis and cell-cycle arrest by p53-, Bax- and p21-dependent mechanism. 5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone 63-68 H3 histone pseudogene 16 Homo sapiens 137-140 21462329-7 2011 CONCLUSION: Our results demonstrated that 5OH-PMFs, especially 5HHMF and 5HTMF, induce apoptosis and cell-cycle arrest by p53-, Bax- and p21-dependent mechanism. 5-hydroxy-6,7,8,4'-tetramethoxyflavone 73-78 H3 histone pseudogene 16 Homo sapiens 137-140 21426504-6 2011 Indoxyl sulfate effects were associated with a dose-dependent induction of intracellular reactive oxygen species and up-regulation of p21 and p27 protein expression. Indican 0-15 H3 histone pseudogene 16 Homo sapiens 134-137 21490707-0 2011 Genome-wide meta-analysis identifies regions on 7p21 (AHR) and 15q24 (CYP1A2) as determinants of habitual caffeine consumption. Caffeine 106-114 H3 histone pseudogene 16 Homo sapiens 49-52 21360677-6 2011 Ormeloxifen also inhibits proliferation of K562 cells by blocking them in G0-G1 phase by inhibiting c-myc promoter via ormeloxifen-induced MBP-1 (c-myc promoter-binding protein) and upregulation of p21 expression. Centchroman 0-11 H3 histone pseudogene 16 Homo sapiens 198-201 21360677-6 2011 Ormeloxifen also inhibits proliferation of K562 cells by blocking them in G0-G1 phase by inhibiting c-myc promoter via ormeloxifen-induced MBP-1 (c-myc promoter-binding protein) and upregulation of p21 expression. Centchroman 119-130 H3 histone pseudogene 16 Homo sapiens 198-201 21360677-8 2011 Thus, ormeloxifen induces apoptosis in K562 cells via phosphorylation of ERK and arrests them in G0-G1 phase by reciprocal regulation of p21 and c-myc. Centchroman 6-17 H3 histone pseudogene 16 Homo sapiens 137-140 21408143-3 2011 Icaritin-inhibited cell growth was associated with increased levels of p21 and p27 expression and reduced cyclinD1 and cdk 4 expression. icaritin 0-8 H3 histone pseudogene 16 Homo sapiens 71-74 21087144-5 2011 The current study demonstrates that DC cells signal a DNA damage response through p53 and its downstream mediator, p21(WAF/CIP), which is accompanied by an elevation in steady-state levels of superoxide and percent glutathione disulfide, both indicators of oxidative stress. Superoxides 192-202 H3 histone pseudogene 16 Homo sapiens 115-118 21087144-5 2011 The current study demonstrates that DC cells signal a DNA damage response through p53 and its downstream mediator, p21(WAF/CIP), which is accompanied by an elevation in steady-state levels of superoxide and percent glutathione disulfide, both indicators of oxidative stress. Glutathione Disulfide 215-236 H3 histone pseudogene 16 Homo sapiens 115-118 21087144-7 2011 Further, restoring telomerase activity or inhibiting p53 or p21(WAF/CIP) significantly mitigated growth inhibition as well as caused a significant decrease in steady-state levels of superoxide. Superoxides 182-192 H3 histone pseudogene 16 Homo sapiens 60-63 21087144-8 2011 Our results support a model in which telomerase insufficiency in DC leads to p21(WAF/CIP) signaling, via p53, to cause increased steady-state levels of superoxide, metabolic oxidative stress, and senescence. Superoxides 152-162 H3 histone pseudogene 16 Homo sapiens 77-80 21300767-2 2011 Of all the extracts tested, chloroform and ethyl acetate extracts of M piperita showed significant dose- and time-dependent anticarcinogenic activity leading to G1 cell cycle arrest and mitochondrial-mediated apoptosis, perturbation of oxidative balance, upregulation of Bax gene, elevated expression of p53 and p21 in the treated cells, acquisition of senescence phenotype, while inducing pro-inflammatory cytokines response. Chloroform 28-38 H3 histone pseudogene 16 Homo sapiens 312-315 20839231-5 2011 Cd-induced cell-cycle arrest was associated with a decrease in CDK2 protein and with increase in p21 expression and p53 phosphorylation. Cadmium 0-2 H3 histone pseudogene 16 Homo sapiens 97-100 20839231-6 2011 Cd treatment caused a distinct increase in the formation of p21-cyclin E-CDK2 complex, as revealed by immunoprecipitation. Cadmium 0-2 H3 histone pseudogene 16 Homo sapiens 60-63 21257625-5 2011 In this study, we found that 1 muM ATO promoted MSC senescence mainly through p21, although it had no effect on apoptosis at this dose. Arsenic Trioxide 35-38 H3 histone pseudogene 16 Homo sapiens 78-81 21300767-2 2011 Of all the extracts tested, chloroform and ethyl acetate extracts of M piperita showed significant dose- and time-dependent anticarcinogenic activity leading to G1 cell cycle arrest and mitochondrial-mediated apoptosis, perturbation of oxidative balance, upregulation of Bax gene, elevated expression of p53 and p21 in the treated cells, acquisition of senescence phenotype, while inducing pro-inflammatory cytokines response. ethyl acetate 43-56 H3 histone pseudogene 16 Homo sapiens 312-315 21244075-7 2011 Enhanced p21 expression was also induced by largazole and its C2 epimer. largazole 44-53 H3 histone pseudogene 16 Homo sapiens 9-12 21169275-6 2011 The results show that promoter methylation of p14, p15, p16, p21, p27, p57 and p73 was far more common in ESCC samples with CIMP+ than those with CIMP-. cimp+ 124-129 H3 histone pseudogene 16 Homo sapiens 61-64 20940449-8 2011 Treatment of HUVECs with aspirin suppressed TGFbeta1 and enhanced TGFbeta-R1 mRNA expression during HR (both P < .05 vs HR alone) without a change in p53 and p21 (P-NS). Aspirin 25-32 H3 histone pseudogene 16 Homo sapiens 161-164 21468560-10 2011 The AngII + losartan group displayed longer telomere lengths, further reduced beta-galactosidase staining and decreased P53 and P21 expression compared to the AngII group. Losartan 12-20 H3 histone pseudogene 16 Homo sapiens 128-131 20979106-9 2011 Restored GPR43 expression, coupled with propionate treatment, induced an upregulation of p21 and a decrease in the levels of cyclin D3 and cyclin-dependent kinases (CDKs) 1 and 2, while the CDK4 and CDK6 levels remained unchanged. Propionates 40-50 H3 histone pseudogene 16 Homo sapiens 89-92 21541041-3 2011 In the current study, pretreatment with nitric oxide (NO) scavengers inhibited PDT-induced mitochondrial membrane potential (MMP) changes, activation of caspase-9, caspase-3, p21-activated protein kinase 2 (PAK2) and c-Jun N-terminal kinase (JNK), and gene expression of p53 and p21 involved in apoptotic signaling. Nitric Oxide 40-52 H3 histone pseudogene 16 Homo sapiens 175-178 21106726-5 2011 At the molecular level, Dasatinib significantly counteracted the Nutlin-3-mediated induction of the p53 transcriptional targets MDM2 and p21 observed in p53(wild-type) leukemic cells. Dasatinib 24-33 H3 histone pseudogene 16 Homo sapiens 137-140 21114963-0 2011 Methotrexate induces apoptosis through p53/p21-dependent pathway and increases E-cadherin expression through downregulation of HDAC/EZH2. Methotrexate 0-12 H3 histone pseudogene 16 Homo sapiens 43-46 21114963-6 2011 The apoptosis and inhibition of cell viability induced by MTX were dependent on p53 and, partially, on p21. Methotrexate 58-61 H3 histone pseudogene 16 Homo sapiens 103-106 21288367-8 2011 Furthermore, the ECRG4 and ECRG1 co-expression remarkably upregulatd p21 protein level by Western blot (P < 0.001), induced cell cycle G1 phase block by flow cytometric analysis (P < 0.001) and suppressed cell proliferation by MTT and BrdU assay (both P < 0.01) in ESCC cells. monooxyethylene trimethylolpropane tristearate 233-236 H3 histone pseudogene 16 Homo sapiens 69-72 20948431-9 2011 Low concentrations of boningmycin led to a senescent phenotype with an increase in senescence-associated beta-galactosidase activity and the time-dependent increase of p21, p27, and p53 expressions from 48 to120 h. Taken together, the results showed that boningmycin exhibits potent antitumor actions through the induction of apoptosis and cellular senescence. boningmycin 22-33 H3 histone pseudogene 16 Homo sapiens 168-171 21138753-0 2011 The antiprogestin Lonaprisan inhibits breast cancer cell proliferation by inducing p21 expression. lonaprisan 18-28 H3 histone pseudogene 16 Homo sapiens 83-86 21138753-6 2011 Reduction of p21 levels blunted the antiproliferative effects of Lonaprisan. lonaprisan 65-75 H3 histone pseudogene 16 Homo sapiens 13-16 21145737-3 2011 A subset of the designed compounds selectively induced p21 over klf2 relative to the clinical reference compound SNDX-275. entinostat 113-121 H3 histone pseudogene 16 Homo sapiens 55-58 21216934-6 2011 Furthermore, the MAP/ERK kinase inhibitor PD98059 partially abolished modulation of p21 and cyclin D1 expression by p53R2. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 42-49 H3 histone pseudogene 16 Homo sapiens 84-87 20875401-7 2011 Furthermore, TPT-dependent induction of p53, p21 and apoptosis were found 24-72h after treatment and were increased by PJ34 both in PARP-1 proficient and silenced cells. Topotecan 13-16 H3 histone pseudogene 16 Homo sapiens 45-48 21378327-5 2011 The effect of zeranol-serum on mRNA expression of cell cycle regulating gene (cyclin D1) and tumor suppressor genes (p53, and p21) was evaluated using real-time RT-PCR. Zeranol 14-21 H3 histone pseudogene 16 Homo sapiens 126-129 21378327-7 2011 Zeranol-serum up-regulated cyclin D1 and down-regulated p53 and p21 expression in PCHBECs compared with control serum. Zeranol 0-7 H3 histone pseudogene 16 Homo sapiens 64-67 20973777-0 2011 Salinomycin sensitizes cancer cells to the effects of doxorubicin and etoposide treatment by increasing DNA damage and reducing p21 protein. salinomycin 0-11 H3 histone pseudogene 16 Homo sapiens 128-131 20973777-0 2011 Salinomycin sensitizes cancer cells to the effects of doxorubicin and etoposide treatment by increasing DNA damage and reducing p21 protein. Doxorubicin 54-65 H3 histone pseudogene 16 Homo sapiens 128-131 20973777-0 2011 Salinomycin sensitizes cancer cells to the effects of doxorubicin and etoposide treatment by increasing DNA damage and reducing p21 protein. Etoposide 70-79 H3 histone pseudogene 16 Homo sapiens 128-131 20973777-9 2011 The level of anti-apoptotic p21 protein was increased by DOX or ETO but decreased by Sal, which increased proteasome activity. Doxorubicin 57-60 H3 histone pseudogene 16 Homo sapiens 28-31 20973777-9 2011 The level of anti-apoptotic p21 protein was increased by DOX or ETO but decreased by Sal, which increased proteasome activity. Etoposide 64-67 H3 histone pseudogene 16 Homo sapiens 28-31 20973777-9 2011 The level of anti-apoptotic p21 protein was increased by DOX or ETO but decreased by Sal, which increased proteasome activity. salinomycin 85-88 H3 histone pseudogene 16 Homo sapiens 28-31 20973777-11 2011 Overall, we demonstrated that the ability of Sal to sensitize cancer cells to the effects of DOX or ETO is associated with an increase in DNA damage and a decrease in anti-apoptotic protein p21 levels. salinomycin 45-48 H3 histone pseudogene 16 Homo sapiens 190-193 20973777-11 2011 Overall, we demonstrated that the ability of Sal to sensitize cancer cells to the effects of DOX or ETO is associated with an increase in DNA damage and a decrease in anti-apoptotic protein p21 levels. Doxorubicin 93-96 H3 histone pseudogene 16 Homo sapiens 190-193 20973777-11 2011 Overall, we demonstrated that the ability of Sal to sensitize cancer cells to the effects of DOX or ETO is associated with an increase in DNA damage and a decrease in anti-apoptotic protein p21 levels. Etoposide 100-103 H3 histone pseudogene 16 Homo sapiens 190-193 21241187-0 2011 The RNA activator ds-p21 potentiates the cytotoxicity induced by fludarabine in Dohh2 cells. fludarabine 65-76 H3 histone pseudogene 16 Homo sapiens 21-24 21241187-9 2011 In contrast, the exposure of Dohh2 cells transfected with ds-p21 to fludarabine potentiates the cytotoxicity of the drug, suggesting the RNA activator p21 complements the fludarabine-dependent cell death pathways. fludarabine 68-79 H3 histone pseudogene 16 Homo sapiens 61-64 21241187-9 2011 In contrast, the exposure of Dohh2 cells transfected with ds-p21 to fludarabine potentiates the cytotoxicity of the drug, suggesting the RNA activator p21 complements the fludarabine-dependent cell death pathways. fludarabine 68-79 H3 histone pseudogene 16 Homo sapiens 151-154 21241187-9 2011 In contrast, the exposure of Dohh2 cells transfected with ds-p21 to fludarabine potentiates the cytotoxicity of the drug, suggesting the RNA activator p21 complements the fludarabine-dependent cell death pathways. fludarabine 171-182 H3 histone pseudogene 16 Homo sapiens 61-64 21241187-9 2011 In contrast, the exposure of Dohh2 cells transfected with ds-p21 to fludarabine potentiates the cytotoxicity of the drug, suggesting the RNA activator p21 complements the fludarabine-dependent cell death pathways. fludarabine 171-182 H3 histone pseudogene 16 Homo sapiens 151-154 21283757-0 2011 The microbe-derived short chain fatty acid butyrate targets miRNA-dependent p21 gene expression in human colon cancer. short chain fatty acid butyrate 20-51 H3 histone pseudogene 16 Homo sapiens 76-79 21283757-2 2011 The chemopreventative effects of the SCFA butyrate are, in part, mediated through induction of p21 gene expression. scfa butyrate 37-50 H3 histone pseudogene 16 Homo sapiens 95-98 21283757-3 2011 In this study, we assessed the role of microRNA(miRNA) in butyrate"s induction of p21 expression. Butyrates 58-66 H3 histone pseudogene 16 Homo sapiens 82-85 21283757-8 2011 Butyrate-induced p21 protein expression was dampened by treatment with a miR-106b mimic. Butyrates 0-8 H3 histone pseudogene 16 Homo sapiens 17-20 20309941-3 2011 Our results showed that YSV significantly inhibited the proliferation of human lung carcinoma A549, NCIH460, NCIH292 and NCIH1299 cells, induced G(0) /G(1) cell cycle arrest and increased protein and mRNA levels of p21 and p27. CHEMBL1214620 24-27 H3 histone pseudogene 16 Homo sapiens 215-218 20309941-4 2011 Moreover, YSV treatment significantly inhibited histone deacetylase (HDAC) activity and resulted in the accumulation of acetylated histones H3 and H4 in total cellular chromatin and p21 gene-associated chromatin regions. CHEMBL1214620 10-13 H3 histone pseudogene 16 Homo sapiens 182-185 20309941-5 2011 Together these data suggest that the antitumor effects of YSV might be mediated by its inhibition of HDAC activity, selectively upregulating the expression of p21 by increasing the acetylation of histones associated with p21 gene regions, resulting in an induction of G0/G1 cell cycle arrest and inhibition of the proliferation of tumor cells. CHEMBL1214620 58-61 H3 histone pseudogene 16 Homo sapiens 159-162 20309941-5 2011 Together these data suggest that the antitumor effects of YSV might be mediated by its inhibition of HDAC activity, selectively upregulating the expression of p21 by increasing the acetylation of histones associated with p21 gene regions, resulting in an induction of G0/G1 cell cycle arrest and inhibition of the proliferation of tumor cells. CHEMBL1214620 58-61 H3 histone pseudogene 16 Homo sapiens 221-224 21790217-4 2011 p21 expression was significantly higher in HHUA cells transfected with the proline variant gene than in those transfected with the arginine variant gene. Proline 75-82 H3 histone pseudogene 16 Homo sapiens 0-3 21790217-4 2011 p21 expression was significantly higher in HHUA cells transfected with the proline variant gene than in those transfected with the arginine variant gene. Arginine 131-139 H3 histone pseudogene 16 Homo sapiens 0-3 21790217-5 2011 We consider that the presence of an upstream ERE promotes the transcriptional effects of the exogenous p53 gene with the proline variant, which strengthens the expression of p21, and results in lower transfection rates through cell cycle inhibition. Proline 121-128 H3 histone pseudogene 16 Homo sapiens 174-177 21045015-8 2011 Exposure to resveratrol or triacetyl-resveratrol activated p53, increased p21 and p53R2 and decreased PSA expression in LNCaP cells. Resveratrol 12-23 H3 histone pseudogene 16 Homo sapiens 74-77 21045015-8 2011 Exposure to resveratrol or triacetyl-resveratrol activated p53, increased p21 and p53R2 and decreased PSA expression in LNCaP cells. triacetylresveratrol 27-48 H3 histone pseudogene 16 Homo sapiens 74-77 21045015-12 2011 CWR22Rv1 cells exposed to resveratrol and triacetyl-resveratrol showed a G1S block, concomitant with increased p53 and p21 expression; however, identically treated PC-3 cells showed attenuated progression through the SG2M phases. triacetylresveratrol 42-63 H3 histone pseudogene 16 Homo sapiens 119-122 21045015-12 2011 CWR22Rv1 cells exposed to resveratrol and triacetyl-resveratrol showed a G1S block, concomitant with increased p53 and p21 expression; however, identically treated PC-3 cells showed attenuated progression through the SG2M phases. Resveratrol 26-37 H3 histone pseudogene 16 Homo sapiens 119-122 21035837-9 2011 Exposure to thioridazine induced G(0)/G(1) arrest and down-regulated the cell cycle regulator, Cyclin D1 and CDK4, and up-regulated p21, p16, and p-CDC25A. Thioridazine 12-24 H3 histone pseudogene 16 Homo sapiens 132-135 21931487-7 2011 Moreover, the copolymer of 2ME with MNPs- Fe(3)O(4) blocked a nearly two-fold increase in SKM-1 cells located in G(2)/M phase than in 2ME alone, which may be associated with an accompanying increase of p21 as well as a decrease in cyclin B1 and cdc2 expression, but there was no obvious difference between the MNPs-Fe(3)O(4) and control group. copolymer 14-23 H3 histone pseudogene 16 Homo sapiens 202-205 22174603-4 2011 Western blot analysis indicated that aaptamine induced p21 expression in K562 cells. aaptamine 37-46 H3 histone pseudogene 16 Homo sapiens 55-58 22174603-5 2011 Moreover, p21 promoter was activated by aaptamine treatment in p21 transfected K562 cells. aaptamine 40-49 H3 histone pseudogene 16 Homo sapiens 10-13 22174603-5 2011 Moreover, p21 promoter was activated by aaptamine treatment in p21 transfected K562 cells. aaptamine 40-49 H3 histone pseudogene 16 Homo sapiens 63-66 22174603-6 2011 Since K562 is p53 negative, aaptamine was demonstrated to be a p53-independent p21 inducer in CML cells. aaptamine 28-37 H3 histone pseudogene 16 Homo sapiens 79-82 21931487-7 2011 Moreover, the copolymer of 2ME with MNPs- Fe(3)O(4) blocked a nearly two-fold increase in SKM-1 cells located in G(2)/M phase than in 2ME alone, which may be associated with an accompanying increase of p21 as well as a decrease in cyclin B1 and cdc2 expression, but there was no obvious difference between the MNPs-Fe(3)O(4) and control group. fe(3)o 42-48 H3 histone pseudogene 16 Homo sapiens 202-205 22870140-0 2011 Nordihydroguaiaretic acid inhibits growth of cervical cancer SiHa cells by up-regulating p21. Masoprocol 0-25 H3 histone pseudogene 16 Homo sapiens 89-92 21886803-5 2011 By using DNA template depletion steps that include DNA template immobilization, Trizol extraction and DNase I treatment, we have successfully enriched p21 promoter-driven transcripts over DNA templates. trizol 80-86 H3 histone pseudogene 16 Homo sapiens 151-154 21776823-5 2011 Metformin induced apoptosis by arresting cells in G1 phase and reducing cyclin D level and increasing the expression of p21 and cyclin E. Molecular and cellular studies indicated that metformin significantly elevated p53 and Bax levels and reduced STAT3 and Bcl-2. Metformin 0-9 H3 histone pseudogene 16 Homo sapiens 120-123 21776823-5 2011 Metformin induced apoptosis by arresting cells in G1 phase and reducing cyclin D level and increasing the expression of p21 and cyclin E. Molecular and cellular studies indicated that metformin significantly elevated p53 and Bax levels and reduced STAT3 and Bcl-2. Metformin 184-193 H3 histone pseudogene 16 Homo sapiens 120-123 22022534-5 2011 METHODOLOGY: During induction of senescence by low levels of endogenous p53 and ectopic p21, cells were co-treated with nocodazole, which eliminated proliferating cells. Nocodazole 120-130 H3 histone pseudogene 16 Homo sapiens 88-91 21858171-0 2011 Apoptosis induced by piroxicam plus cisplatin combined treatment is triggered by p21 in mesothelioma. Piroxicam 21-30 H3 histone pseudogene 16 Homo sapiens 81-84 21858171-0 2011 Apoptosis induced by piroxicam plus cisplatin combined treatment is triggered by p21 in mesothelioma. Cisplatin 36-45 H3 histone pseudogene 16 Homo sapiens 81-84 21858171-6 2011 Here we show that apoptotic increase following combined treatment is mediated by p21, since apoptotic increase in piroxicam/cisplatin combined treatment is abolished upon p21 silencing. Piroxicam 114-123 H3 histone pseudogene 16 Homo sapiens 81-84 21858171-6 2011 Here we show that apoptotic increase following combined treatment is mediated by p21, since apoptotic increase in piroxicam/cisplatin combined treatment is abolished upon p21 silencing. Piroxicam 114-123 H3 histone pseudogene 16 Homo sapiens 171-174 21858171-6 2011 Here we show that apoptotic increase following combined treatment is mediated by p21, since apoptotic increase in piroxicam/cisplatin combined treatment is abolished upon p21 silencing. Cisplatin 124-133 H3 histone pseudogene 16 Homo sapiens 81-84 22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Bortezomib 19-29 H3 histone pseudogene 16 Homo sapiens 160-163 22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Tretinoin 34-38 H3 histone pseudogene 16 Homo sapiens 160-163 21980390-9 2011 Resveratrol induced cell cycle arrest by up-regulating the expression of p21/CIP1, p27/KIP1 and inhibiting the expression of cyclin D1. Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 73-76 21858218-5 2011 p21, an important regulator of cell senescence, was induced ~3 fold in HCT116 PTTG1(-/-) cells upon doxorubicin or Trichostatin A treatment. Doxorubicin 100-111 H3 histone pseudogene 16 Homo sapiens 0-3 21858218-5 2011 p21, an important regulator of cell senescence, was induced ~3 fold in HCT116 PTTG1(-/-) cells upon doxorubicin or Trichostatin A treatment. trichostatin A 115-129 H3 histone pseudogene 16 Homo sapiens 0-3 21858218-8 2011 PTTG1 also regulated SW620 colon cancer cells response to doxorubicin and TSA mediated by p21. trichostatin A 74-77 H3 histone pseudogene 16 Homo sapiens 90-93 21858171-6 2011 Here we show that apoptotic increase following combined treatment is mediated by p21, since apoptotic increase in piroxicam/cisplatin combined treatment is abolished upon p21 silencing. Cisplatin 124-133 H3 histone pseudogene 16 Homo sapiens 171-174 21858171-7 2011 CONCLUSIONS/SIGNIFICANCE: Piroxicam/cisplatin combined treatment determines an apoptosis increase in MM cells, which is dependent on the p21 expression. Piroxicam 26-35 H3 histone pseudogene 16 Homo sapiens 137-140 21858171-7 2011 CONCLUSIONS/SIGNIFICANCE: Piroxicam/cisplatin combined treatment determines an apoptosis increase in MM cells, which is dependent on the p21 expression. Cisplatin 36-45 H3 histone pseudogene 16 Homo sapiens 137-140 21858171-8 2011 The results provided suggest that piroxicam/cisplatin combination might be tested in clinical settings in tumor specimens that express p21. Piroxicam 34-43 H3 histone pseudogene 16 Homo sapiens 135-138 21858171-8 2011 The results provided suggest that piroxicam/cisplatin combination might be tested in clinical settings in tumor specimens that express p21. Cisplatin 44-53 H3 histone pseudogene 16 Homo sapiens 135-138 20970453-4 2011 More than 10 sphingolipids and glycosphingolipids selectively mediate expressions of approximately 50 genes including c-myc, p21, c-fos, telomerase reverse transcriptase, caspase-9, Bcl-x, cyclooxygenase-2, matrix metalloproteinases, integrins, Oct-4, glucosylceramide synthase and multidrug-resistant gene 1. Sphingolipids 13-26 H3 histone pseudogene 16 Homo sapiens 125-128 20970453-4 2011 More than 10 sphingolipids and glycosphingolipids selectively mediate expressions of approximately 50 genes including c-myc, p21, c-fos, telomerase reverse transcriptase, caspase-9, Bcl-x, cyclooxygenase-2, matrix metalloproteinases, integrins, Oct-4, glucosylceramide synthase and multidrug-resistant gene 1. Glycosphingolipids 31-49 H3 histone pseudogene 16 Homo sapiens 125-128 21628989-12 2011 Panaxydol dose-dependently decreased the expression of regulatory factors Id1 and increased the protein levels of p21 and p-ERK1/2 correspondingly. panaxydol 0-9 H3 histone pseudogene 16 Homo sapiens 114-117 21150324-0 2010 Lessons learned from testicular cancer: identification of cytoplasmic p21 as an Achilles" heel of cisplatin resistance. Cisplatin 98-107 H3 histone pseudogene 16 Homo sapiens 70-73 21429402-9 2011 BTZ alone significantly increased the proportion of cells in G(2)/M phase (P < 0.01) in a dose-dependent manner and up-regulated the expression level of P21. Bortezomib 0-3 H3 histone pseudogene 16 Homo sapiens 156-159 20880848-9 2010 In further studies, we found that activation of AMPK is involved in TMZ-induced p53 activation and subsequent p21, Noxa, and Bax up-regulation. Temozolomide 68-71 H3 histone pseudogene 16 Homo sapiens 110-113 20952396-3 2010 We show here that induction of p21 by trichostatin A involves MAP kinase signaling. trichostatin A 38-52 H3 histone pseudogene 16 Homo sapiens 31-34 20952396-4 2010 Activation of the MAP kinase signaling pathway by growth factors or stress signals results in histone H3 serine 10 phosphorylation at the p21 promoter and is crucial for acetylation of the neighboring lysine 14 and recruitment of activated RNA polymerase II in response to trichostatin A treatment. Serine 105-111 H3 histone pseudogene 16 Homo sapiens 138-141 20952396-7 2010 The dual modification mark H3S10phK14ac at the activated p21 promoter is recognized by the phospho-binding protein 14-3-3zeta, which protects the phosphoacetylation mark from being processed by PP2A. h3s10phk14ac 27-39 H3 histone pseudogene 16 Homo sapiens 57-60 21311676-8 2010 With the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 25-32 H3 histone pseudogene 16 Homo sapiens 73-76 20633010-6 2010 5-FU induced p53 and p21 accumulation together with a decrease in cyclin B1 and Bcl-2 levels in treated keloid fibroblasts. Fluorouracil 0-4 H3 histone pseudogene 16 Homo sapiens 21-24 19777160-0 2010 Synergistic efficacy of sorafenib and genistein in growth inhibition by down regulating angiogenic and survival factors and increasing apoptosis through upregulation of p53 and p21 in malignant neuroblastoma cells having N-Myc amplification or non-amplification. Sorafenib 24-33 H3 histone pseudogene 16 Homo sapiens 177-180 19777160-0 2010 Synergistic efficacy of sorafenib and genistein in growth inhibition by down regulating angiogenic and survival factors and increasing apoptosis through upregulation of p53 and p21 in malignant neuroblastoma cells having N-Myc amplification or non-amplification. Genistein 38-47 H3 histone pseudogene 16 Homo sapiens 177-180 21181363-8 2010 Chrysoeriol could significantly reduce the expression of p-AKT (s473) and p-4eBP1 (t37/46) protein, meanwhile enhanced Cyclin B1 and p21 protein expression. chrysoeriol 0-11 H3 histone pseudogene 16 Homo sapiens 133-136 21311676-6 2010 Melatonin increased the expressions of p53, p21, and p27. Melatonin 0-9 H3 histone pseudogene 16 Homo sapiens 44-47 21311676-7 2010 Treatment with mitogen-activated protein kinase (MAPK) inhibitors, PD98059 (ERK inhibitor), SP600125 (JNK inhibitor) and SB202190 (p38 inhibitor), confirmed that the melatonin-induced apoptosis was p21-dependent, but ERK-independent. Melatonin 166-175 H3 histone pseudogene 16 Homo sapiens 198-201 21204767-3 2010 This study reports on the characterization in vitro of a fully phosphorothioated 20-mer oligonucleotide, complementary to p21 mRNA, radiolabeled with fluorine-18 using a thiol reactive prosthetic group. mer oligonucleotide 84-103 H3 histone pseudogene 16 Homo sapiens 122-125 21204767-3 2010 This study reports on the characterization in vitro of a fully phosphorothioated 20-mer oligonucleotide, complementary to p21 mRNA, radiolabeled with fluorine-18 using a thiol reactive prosthetic group. Fluorine-18 150-161 H3 histone pseudogene 16 Homo sapiens 122-125 21204767-3 2010 This study reports on the characterization in vitro of a fully phosphorothioated 20-mer oligonucleotide, complementary to p21 mRNA, radiolabeled with fluorine-18 using a thiol reactive prosthetic group. Sulfhydryl Compounds 170-175 H3 histone pseudogene 16 Homo sapiens 122-125 20924037-5 2010 RESULTS: Significantly higher LI was seen in IF compared with TC for p21, p53 and COX2. Technetium 62-64 H3 histone pseudogene 16 Homo sapiens 69-72 21221951-6 2010 An exopolysaccharide purified from the acidophilic strain was added to cultured U937 cells, resulting in significantly increased transcription levels of p53 and p21 genes. exopolysaccharide 3-20 H3 histone pseudogene 16 Homo sapiens 161-164 21311680-7 2010 Moreover, decreased (cyclin A) and increased (p21 and p27) expression of these E2F4 downstream genes by curcumin was restored by pretreatment of cells with NAC and E2F4 overexpression which is induced by doxycycline. nac 156-159 H3 histone pseudogene 16 Homo sapiens 46-49 21311676-8 2010 With the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease. Melatonin 37-46 H3 histone pseudogene 16 Homo sapiens 73-76 21311680-7 2010 Moreover, decreased (cyclin A) and increased (p21 and p27) expression of these E2F4 downstream genes by curcumin was restored by pretreatment of cells with NAC and E2F4 overexpression which is induced by doxycycline. Doxycycline 204-215 H3 histone pseudogene 16 Homo sapiens 46-49 21311676-9 2010 These effects were opposite to the expression of p-p53, p21, and MDM2 observed with SP600125 and SB202190 treatments. pyrazolanthrone 84-92 H3 histone pseudogene 16 Homo sapiens 56-59 20013077-4 2010 These effects were blocked by the MAP kinase blocker PD98059 (25 muM), indicating that MAPK plays a role in VDR and p21 upregulation. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 53-60 H3 histone pseudogene 16 Homo sapiens 116-119 21311680-6 2010 Expression of several genes, cyclin A, p21, and p27, which has been shown to be regulated in E2F4-dependent manner and involved in the cell cycle progression was also affected by curcumin. Curcumin 179-187 H3 histone pseudogene 16 Homo sapiens 39-42 20013077-6 2010 One (p21 VDRE Luc) has the vitamin D response element (VDRE) in the p21 promoter region; the other (p21 NO-VDRE Luc) does not. Vitamin D 27-36 H3 histone pseudogene 16 Homo sapiens 5-8 20013077-6 2010 One (p21 VDRE Luc) has the vitamin D response element (VDRE) in the p21 promoter region; the other (p21 NO-VDRE Luc) does not. Vitamin D 27-36 H3 histone pseudogene 16 Homo sapiens 68-71 20013077-6 2010 One (p21 VDRE Luc) has the vitamin D response element (VDRE) in the p21 promoter region; the other (p21 NO-VDRE Luc) does not. Vitamin D 27-36 H3 histone pseudogene 16 Homo sapiens 68-71 21311680-7 2010 Moreover, decreased (cyclin A) and increased (p21 and p27) expression of these E2F4 downstream genes by curcumin was restored by pretreatment of cells with NAC and E2F4 overexpression which is induced by doxycycline. Curcumin 104-112 H3 histone pseudogene 16 Homo sapiens 46-49 20665144-8 2010 SAHA treatment added to ad-p63/p73 gene delivery caused an increase in p21 expression and cleaved poly-ADP ribose polymerase. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 71-74 20554189-0 2010 12-O-Tetradecanoyl phorbol-13-acetate (TPA)-induced growth arrest is increased by silibinin by the down-regulation of cyclin B1 and cdc2 and the up-regulation of p21 expression in MDA-MB231 human breast cancer cells. Tetradecanoylphorbol Acetate 0-37 H3 histone pseudogene 16 Homo sapiens 162-165 20554189-0 2010 12-O-Tetradecanoyl phorbol-13-acetate (TPA)-induced growth arrest is increased by silibinin by the down-regulation of cyclin B1 and cdc2 and the up-regulation of p21 expression in MDA-MB231 human breast cancer cells. Tetradecanoylphorbol Acetate 39-42 H3 histone pseudogene 16 Homo sapiens 162-165 20554189-0 2010 12-O-Tetradecanoyl phorbol-13-acetate (TPA)-induced growth arrest is increased by silibinin by the down-regulation of cyclin B1 and cdc2 and the up-regulation of p21 expression in MDA-MB231 human breast cancer cells. Silybin 82-91 H3 histone pseudogene 16 Homo sapiens 162-165 20554189-7 2010 In contrast, TPA-induced p21 expression was further increased by silibinin. Tetradecanoylphorbol Acetate 13-16 H3 histone pseudogene 16 Homo sapiens 25-28 20554189-7 2010 In contrast, TPA-induced p21 expression was further increased by silibinin. Silybin 65-74 H3 histone pseudogene 16 Homo sapiens 25-28 20554189-10 2010 In addition, TPA-induced down-regulation of cyclin B1 was inhibited by LY294002; however, the basal level of p21 was increased by TPA and TPA-induced p21 expression was further increased by LY294002. Tetradecanoylphorbol Acetate 13-16 H3 histone pseudogene 16 Homo sapiens 109-112 20554189-10 2010 In addition, TPA-induced down-regulation of cyclin B1 was inhibited by LY294002; however, the basal level of p21 was increased by TPA and TPA-induced p21 expression was further increased by LY294002. Tetradecanoylphorbol Acetate 13-16 H3 histone pseudogene 16 Homo sapiens 150-153 20554189-10 2010 In addition, TPA-induced down-regulation of cyclin B1 was inhibited by LY294002; however, the basal level of p21 was increased by TPA and TPA-induced p21 expression was further increased by LY294002. Tetradecanoylphorbol Acetate 130-133 H3 histone pseudogene 16 Homo sapiens 109-112 20554189-10 2010 In addition, TPA-induced down-regulation of cyclin B1 was inhibited by LY294002; however, the basal level of p21 was increased by TPA and TPA-induced p21 expression was further increased by LY294002. Tetradecanoylphorbol Acetate 130-133 H3 histone pseudogene 16 Homo sapiens 109-112 20554189-10 2010 In addition, TPA-induced down-regulation of cyclin B1 was inhibited by LY294002; however, the basal level of p21 was increased by TPA and TPA-induced p21 expression was further increased by LY294002. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 190-198 H3 histone pseudogene 16 Homo sapiens 109-112 20554189-10 2010 In addition, TPA-induced down-regulation of cyclin B1 was inhibited by LY294002; however, the basal level of p21 was increased by TPA and TPA-induced p21 expression was further increased by LY294002. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 190-198 H3 histone pseudogene 16 Homo sapiens 150-153 20564478-5 2010 GA-treated cells resulted in significant growth inhibition in a dose-dependent manner accompanied by a decrease in cyclin-dependent kinases (Cdk1), Cyclin B1, and Cdc25C, but significant increases in p-cdc2 (Tyr-15) and Cip1/p21 by western blotting. Gallic Acid 0-2 H3 histone pseudogene 16 Homo sapiens 225-228 21139994-5 2010 RESULTS: To reveal primary effects, we examined digitoxin"s effect 6 h post-treatment with the highest dose, 1mug/ml, and found upregulation of the stress response genes EGR-1 and NAB2, lipid biosynthetic genes and the tumor suppressor gene p21, and downregulation of the mitotic cell cycle gene CDC16 and the replication gene PolR3B. Digitoxin 48-57 H3 histone pseudogene 16 Homo sapiens 241-244 21083937-8 2010 Both rapamycin and Dex can induce up-regulation of cyclin-dependent kinase (CDK) inhibitors of p21 and p27 and co-treatment of rapamycin with Dex resulted in a synergistic induction of their expressions. Sirolimus 5-14 H3 histone pseudogene 16 Homo sapiens 95-98 21083937-8 2010 Both rapamycin and Dex can induce up-regulation of cyclin-dependent kinase (CDK) inhibitors of p21 and p27 and co-treatment of rapamycin with Dex resulted in a synergistic induction of their expressions. Dexamethasone 19-22 H3 histone pseudogene 16 Homo sapiens 95-98 20878062-9 2010 P53 staining was decreased, while PCNA and TGFbeta3 staining were increased by indomethacin in tumor areas with high presence of COX-2, which correlated to staining of BAX, TUNEL, Bcl-2, c-jun, p21, p27, p53 and NM23. Indomethacin 79-91 H3 histone pseudogene 16 Homo sapiens 194-197 21083937-8 2010 Both rapamycin and Dex can induce up-regulation of cyclin-dependent kinase (CDK) inhibitors of p21 and p27 and co-treatment of rapamycin with Dex resulted in a synergistic induction of their expressions. Dexamethasone 142-145 H3 histone pseudogene 16 Homo sapiens 95-98 20964307-8 2010 The magnetic ordering temperature decreases monotonously with increasing oxygen deficiency, while pronounced extrema are observed for the paramagnetic moment and the Curie-Weiss temperature at an oxygen deficiency delta 0.10, which corresponds to the P2(1)/n I2/m phase transformation. Oxygen 196-202 H3 histone pseudogene 16 Homo sapiens 253-258 21078189-0 2010 Cell death by the quinoxaline dioxide DCQ in human colon cancer cells is enhanced under hypoxia and is independent of p53 and p21. Quinoxalines 18-29 H3 histone pseudogene 16 Homo sapiens 126-129 21078189-0 2010 Cell death by the quinoxaline dioxide DCQ in human colon cancer cells is enhanced under hypoxia and is independent of p53 and p21. Decylubiquinol 38-41 H3 histone pseudogene 16 Homo sapiens 126-129 22993626-7 2010 The mechanisms involved in the MCF-7 cell proliferation stimulated by zeranol-containing sera may include up-regulation of cyclin D1 and down-regulation of p53 and p21 expression at the mRNA and protein levels in the cells. Zeranol 70-77 H3 histone pseudogene 16 Homo sapiens 164-167 20878071-7 2010 Cantharidin-induced G0/G1 arrest was associated with a marked decrease in the protein expressions of cyclin E and Cdc25c but promoted the levels of p21 and p-p53. Cantharidin 0-11 H3 histone pseudogene 16 Homo sapiens 148-151 20943401-7 2010 Mechanistic studies have shown that this quinoxalinyl-piperazine compound is a G2/M-specific cell cycle inhibitor and inhibits anti-apoptotic Bcl-2 protein with p21 induction. quinoxalinyl-piperazine 41-64 H3 histone pseudogene 16 Homo sapiens 161-164 21078189-13 2010 CONCLUSIONS: Collectively, our findings indicate that DCQ reduces the colony survival of HCT116 and induces apoptosis even in cells that are null for p53 or p21, which makes it a molecule of clinical significance, since many resistant colon tumors harbor mutations in p53. Decylubiquinol 54-57 H3 histone pseudogene 16 Homo sapiens 157-160 20878062-10 2010 Net tumor growth was predicted by EGF-R, p21 and p27 proteins in tumor tissue during indomethacin treatment (multivariate analysis). Indomethacin 85-97 H3 histone pseudogene 16 Homo sapiens 41-44 20583132-1 2010 BACKGROUND: 1-Alpha, 25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) inhibits proliferation of multiple cancer cell types including prostate cells and upregulates p21 and/or p27, while loss of Pten and PI3K/AKT activation stimulates survival and downregulates p21 and p27. Calcitriol 12-45 H3 histone pseudogene 16 Homo sapiens 158-161 21035481-3 2010 We found that salidroside considerably reversed senescence-like phenotypes in the oxidant challenged model, including alterations of morphology, cell cycle, SA-beta-gal staining, DNA damage, as well as related molecules expression such as p53, p21 and p16. rhodioloside 14-25 H3 histone pseudogene 16 Homo sapiens 244-247 20583132-1 2010 BACKGROUND: 1-Alpha, 25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) inhibits proliferation of multiple cancer cell types including prostate cells and upregulates p21 and/or p27, while loss of Pten and PI3K/AKT activation stimulates survival and downregulates p21 and p27. Calcitriol 12-45 H3 histone pseudogene 16 Homo sapiens 255-258 20659543-10 2010 Caspase-8, caspase-3, Bax, P53 and P21 mRNAs as well as proteins were increased while Bcl-2 mRNA and protein were decreased significantly by 24 h of PE treatment. pe 149-151 H3 histone pseudogene 16 Homo sapiens 35-38 20444544-0 2010 p53-Dependent p21-mediated growth arrest pre-empts and protects HCT116 cells from PUMA-mediated apoptosis induced by EGCG. epigallocatechin gallate 117-121 H3 histone pseudogene 16 Homo sapiens 14-17 20444544-3 2010 Cells expressing p53 and p21 accumulate in G1 upon treatment with EGCG. epigallocatechin gallate 66-70 H3 histone pseudogene 16 Homo sapiens 25-28 20444544-5 2010 Treatment with EGCG leads to induction of p53, p21 and PUMA in p21 wild-type, and p53 and PUMA in p21(-/-) cells. epigallocatechin gallate 15-19 H3 histone pseudogene 16 Homo sapiens 47-50 20444544-5 2010 Treatment with EGCG leads to induction of p53, p21 and PUMA in p21 wild-type, and p53 and PUMA in p21(-/-) cells. epigallocatechin gallate 15-19 H3 histone pseudogene 16 Homo sapiens 63-66 20444544-5 2010 Treatment with EGCG leads to induction of p53, p21 and PUMA in p21 wild-type, and p53 and PUMA in p21(-/-) cells. epigallocatechin gallate 15-19 H3 histone pseudogene 16 Homo sapiens 63-66 20444544-6 2010 Ablation of p53 by RNAi protects p21(-/-) cells, thus indicating a p53-dependent apoptosis by EGCG. epigallocatechin gallate 94-98 H3 histone pseudogene 16 Homo sapiens 33-36 20444544-7 2010 Furthermore, analysis of cells lacking PUMA or Bax with or without p21 but with p53 reveals that all the cells expressing p53 and p21 survived after EGCG treatment. epigallocatechin gallate 149-153 H3 histone pseudogene 16 Homo sapiens 67-70 20444544-7 2010 Furthermore, analysis of cells lacking PUMA or Bax with or without p21 but with p53 reveals that all the cells expressing p53 and p21 survived after EGCG treatment. epigallocatechin gallate 149-153 H3 histone pseudogene 16 Homo sapiens 130-133 21184665-7 2010 Our results demonstrate that glycerol guaiacolate inhibits MUC1 protein and mRNA expression levels and significantly increased p21 expression in human breast cancer cells as well as induced PARP cleavage. Guaifenesin 29-49 H3 histone pseudogene 16 Homo sapiens 127-130 20807809-3 2010 The aim of this study was to examine the expression of NER gene transcripts, p53, and p21 in melanoma cell lines treated with cisplatin compared with melanocytes. Cisplatin 126-135 H3 histone pseudogene 16 Homo sapiens 86-89 21184665-8 2010 Similarly, glycerol guaiacolate inhibited breast tumor growth in vivo as well as enhanced p21 expression and decreased breast tumor cell proliferation (ki-67 expression). Guaifenesin 11-31 H3 histone pseudogene 16 Homo sapiens 90-93 21036715-4 2010 RESULTS: Curcumin significantly caused radiation induced expression of p21 and Bax, and reduced BclXl, Mcl1 with only marginal Bcl2 modulation. Curcumin 9-17 H3 histone pseudogene 16 Homo sapiens 71-74 21184665-9 2010 Collectively, our results demonstrate that glycerol guaiacolate decreased MUC1 expression and enhanced cell growth inhibition by inducing p21 expression in breast cancer cells. Guaifenesin 43-63 H3 histone pseudogene 16 Homo sapiens 138-141 21059291-1 2010 OBJECTIVE: To investigate the effects of simvastatin on the proliferation, cell cycle and expression of cyclin-dependent kinase inhibitor p21 protein in human hepatocellular carcinoma (HepG2) cells in vitro. Simvastatin 41-52 H3 histone pseudogene 16 Homo sapiens 138-141 20876807-7 2010 Atorvastatin-induced AMPK activation could induce p21 expression, which was also positively correlated with beclin-1 expression in CRC patients. Atorvastatin 0-12 H3 histone pseudogene 16 Homo sapiens 50-53 20876807-10 2010 In summary, activation of AMPK by atorvastatin enhances p21 expression and ER stress response, leading to autophagy, which promotes survival of cancer cells. Atorvastatin 34-46 H3 histone pseudogene 16 Homo sapiens 56-59 20503249-3 2010 A short-term treatment of cells with 10 mM SAA for 2 h revealed a destabilization of the lysosomes and subsequent induction of cell death, whereas 10 mM SBA triggered a remarkable production of reactive oxidative species, phosphorylation of survival kinase AKT, expression of cyclin kinase-dependent inhibitor p21, and induction of transient growth arrest. Ascorbic Acid 43-46 H3 histone pseudogene 16 Homo sapiens 310-313 20503249-3 2010 A short-term treatment of cells with 10 mM SAA for 2 h revealed a destabilization of the lysosomes and subsequent induction of cell death, whereas 10 mM SBA triggered a remarkable production of reactive oxidative species, phosphorylation of survival kinase AKT, expression of cyclin kinase-dependent inhibitor p21, and induction of transient growth arrest. sba 153-156 H3 histone pseudogene 16 Homo sapiens 310-313 21059291-7 2010 Simvastatin could also increase cyclin-dependent kinase inhibitor p21 protein expression (F = 512.133, P value less than 0.001). Simvastatin 0-11 H3 histone pseudogene 16 Homo sapiens 66-69 21059291-8 2010 CONCLUSION: Simvastatin can inhibit the growth of HepG2 cells in vitro, which may be explained by its effects of enhancing cyclin-dependent kinase inhibitor p21 protein expression and arresting HepG2 cells at G0/G1 phase of cell cycle. Simvastatin 12-23 H3 histone pseudogene 16 Homo sapiens 157-160 20732856-4 2010 We observed an increased risk of cervical cancer associated with the p53 Arg/Arg (OR, 2.25; 95% CI, 1.11-4.54) or p21 Ser/Ser (OR, 2.09; 95% CI, 1.04-4.19) genotype, compared with the p53 Pro/Pro or p21 Arg/Arg genotype, respectively. Serine 118-121 H3 histone pseudogene 16 Homo sapiens 114-117 20799737-2 2010 The [Pt{(+/-)-Me(2)dab}(9-EtG)(2)](NO(3))(2) (Me(2)dab = N,N"-dimethyl-2,3-diaminobutane, 9-EtG = 9-ethyl-guanine) complex crystallizes in the P2(1)/n space group, and the crystal contains a racemic mixture of complex molecules. Platinum 5-7 H3 histone pseudogene 16 Homo sapiens 143-148 20562916-5 2010 Inhibiting DUSP26 expression in the IMR-32 neuroblastoma cell line enhanced doxorubicin-induced p53 phosphorylation at Ser20 and Ser37, p21, Puma, Bax expression as well as apoptosis. Doxorubicin 76-87 H3 histone pseudogene 16 Homo sapiens 136-139 20562916-6 2010 In contrast, DUSP26 overexpression in the SK-N-SH cell line inhibited doxorubicin-induced p53 phosphorylation at Ser20 and Ser37, p21, Puma, Bax expression and apoptosis. Doxorubicin 70-81 H3 histone pseudogene 16 Homo sapiens 130-133 20732856-5 2010 In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes. Arginine 208-211 H3 histone pseudogene 16 Homo sapiens 49-52 20732856-5 2010 In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes. Arginine 208-211 H3 histone pseudogene 16 Homo sapiens 220-223 20732856-5 2010 In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes. Arginine 212-215 H3 histone pseudogene 16 Homo sapiens 49-52 20732856-5 2010 In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes. Arginine 212-215 H3 histone pseudogene 16 Homo sapiens 220-223 20732856-5 2010 In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes. Serine 224-227 H3 histone pseudogene 16 Homo sapiens 49-52 20732856-5 2010 In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes. Serine 224-227 H3 histone pseudogene 16 Homo sapiens 220-223 20732856-5 2010 In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes. Serine 228-231 H3 histone pseudogene 16 Homo sapiens 49-52 20732856-5 2010 In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes. Serine 228-231 H3 histone pseudogene 16 Homo sapiens 220-223 20682400-0 2010 Chronic myeloid leukemia with a novel four-way t(6;13;9;22)(p21;q32;q34;q11.2) successfully treated with imatinib mesylate. Imatinib Mesylate 105-122 H3 histone pseudogene 16 Homo sapiens 60-63 20206442-3 2010 Lunasin caused cytotoxicity to HT-29 cells and induced G2/M cell cycle arrest with simultaneous increased in p21 expression. LUNASINE 0-7 H3 histone pseudogene 16 Homo sapiens 109-112 20558185-7 2010 While the benzofurylquinazolines increased the expression level of the pro-inflammatory gene IL1-alpha as well as p21 and p53 in the PC3 cell line, a phenylpyrrolocarbazole had the converse effect on p53 expression. benzofurylquinazolines 10-32 H3 histone pseudogene 16 Homo sapiens 114-117 20681654-4 2010 Notably, quercetin increased cell cycle arrest in the G1 phase and up-regulated apoptosis-related proteins, such as AMPK, p53, and p21, within 48 h. Furthermore, in vivo experiments showed that quercetin treatment resulted in a significant reduction in tumor volume over 6 weeks, and apoptosis-related protein induction by quercetin was significantly higher in the 100 mg/kg treated group compared to the control group. Quercetin 9-18 H3 histone pseudogene 16 Homo sapiens 131-134 20681654-4 2010 Notably, quercetin increased cell cycle arrest in the G1 phase and up-regulated apoptosis-related proteins, such as AMPK, p53, and p21, within 48 h. Furthermore, in vivo experiments showed that quercetin treatment resulted in a significant reduction in tumor volume over 6 weeks, and apoptosis-related protein induction by quercetin was significantly higher in the 100 mg/kg treated group compared to the control group. Quercetin 194-203 H3 histone pseudogene 16 Homo sapiens 131-134 20681654-4 2010 Notably, quercetin increased cell cycle arrest in the G1 phase and up-regulated apoptosis-related proteins, such as AMPK, p53, and p21, within 48 h. Furthermore, in vivo experiments showed that quercetin treatment resulted in a significant reduction in tumor volume over 6 weeks, and apoptosis-related protein induction by quercetin was significantly higher in the 100 mg/kg treated group compared to the control group. Quercetin 194-203 H3 histone pseudogene 16 Homo sapiens 131-134 20534756-5 2010 Resveratrol also abrogated the inhibitory effects of estradiol on positive growth regulators (cyclin A, cyclin D, MAPK phosphorylation) and the stimulatory effects of estradiol on negative growth regulators (p21, p27). Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 208-211 20664969-7 2010 Immunoblot analysis demonstrated that oridonin treatment increased expression levels of p-JNK, p-p38, p-p53 and p21, elevated the level of cyclin B1/p-Cdc2 (Tyr15) complex, and inhibited the expression of p-ERK. oridonin 38-46 H3 histone pseudogene 16 Homo sapiens 112-115 19450997-7 2010 p21 Expression decreased basal caspase-3 expression compared with the untreated group, and reversed camptothecin-induced caspase-3 activity compared with camptothecin alone group. Camptothecin 100-112 H3 histone pseudogene 16 Homo sapiens 0-3 19450997-7 2010 p21 Expression decreased basal caspase-3 expression compared with the untreated group, and reversed camptothecin-induced caspase-3 activity compared with camptothecin alone group. Camptothecin 154-166 H3 histone pseudogene 16 Homo sapiens 0-3 20682800-7 2010 CP-31398 inhibited proliferation in a manner associated with co-induction of SOX9 and p21. CP 31398 0-8 H3 histone pseudogene 16 Homo sapiens 86-89 20596601-10 2010 In the core signaling pathways of glioblastoma, curcumin either significantly influences the p53 pathway by enhancing p53 and p21 and suppressing cdc2 or significantly inhibits the RB pathway by enhancing CDKN2A/p16 and suppressing phosphorylated RB. Curcumin 48-56 H3 histone pseudogene 16 Homo sapiens 126-129 20682078-0 2010 Up-regulation of p21 and TNF-alpha is mediated in lycorine-induced death of HL-60 cells. lycorine 50-58 H3 histone pseudogene 16 Homo sapiens 17-20 20682078-8 2010 RESULTS: When HL-60 cells were treated with different concentration of lycorine, the expression of p21 and TNF-alpha was up-regulated in a concentration-dependent manner as shown by real-time quantitative reverse transcriptase-polymerase chain reaction and Western blotting. lycorine 71-79 H3 histone pseudogene 16 Homo sapiens 99-102 20682078-9 2010 Lycorine also down-regulated p21-related gene expression, including Cdc2, Cyclin B, Cdk2 and Cyclin E, promoted Bid truncation, decreased IkappaB phosphorylation and blocked NF-kappaB nuclear import. lycorine 0-8 H3 histone pseudogene 16 Homo sapiens 29-32 20682078-11 2010 CONCLUSIONS: The TNF-alpha signal transduction pathway and p21-mediated cell-cycle inhibition were involved in the apoptosis of HL-60 cells induced by lycorine. lycorine 151-159 H3 histone pseudogene 16 Homo sapiens 59-62 20493187-8 2010 Treatment with GA and 17-AAG led to growth arrests in G1 and S phases, increased sub-G1 hypodipoid cell population, induced apoptotic cell death, and upregulated P53 and P21 expression, although the drug-induced Bcl-2 upregulation cannot prevent cell death. geldanamycin 15-17 H3 histone pseudogene 16 Homo sapiens 170-173 20493187-8 2010 Treatment with GA and 17-AAG led to growth arrests in G1 and S phases, increased sub-G1 hypodipoid cell population, induced apoptotic cell death, and upregulated P53 and P21 expression, although the drug-induced Bcl-2 upregulation cannot prevent cell death. tanespimycin 22-28 H3 histone pseudogene 16 Homo sapiens 170-173 20647331-8 2010 The importance of the p53 pathway to PIM1-driven cellular senescence was further shown by the observation that expression of dominant-negative p53 or shRNA targeting p21 blocked the PIM1-induced changes in the DNA damage response and increases in SA-beta-Gal activity. 2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid 247-258 H3 histone pseudogene 16 Homo sapiens 166-169 20559153-14 2010 CONCLUSIONS: Our results indicated that downregulation of TS and DHFR genes and upregulation of p21, p27, Lcn-2, and nm23-H1 genes may serve as new biomarkers for predicting responsiveness to pemetrexed. Pemetrexed 192-202 H3 histone pseudogene 16 Homo sapiens 96-99 19436953-4 2010 TMPP treatment effected a reduction in both cell cycle progression signals (FoxM1, KIS, Cdc25B, Cyclin D1, Cyclin A, and Aurora-B) and tumor cell survival (p27(Kip1) and p21(Cip1)), as well as induced the activation of caspase-3 and -9. 2,3,4-tribromo-3-methyl-1-phenylphospholane 1-oxide 0-4 H3 histone pseudogene 16 Homo sapiens 170-173 20623640-4 2010 Lower protein expression levels of p16, p21/Cip1, and p27/Kip1 were detected in the ethanol-treated E40 cells. Ethanol 84-91 H3 histone pseudogene 16 Homo sapiens 40-43 20673181-5 2010 Fractions P11 and P21 were found to be polyxyloses with molecular weight-averages of 469,171 and 157,665 Da, respectively. polyxyloses 39-50 H3 histone pseudogene 16 Homo sapiens 18-21 20642839-7 2010 SFN induced the expression of p21/CIP1 and p27/KIP1, and inhibited the expression of cyclin D1. sulforaphane 0-3 H3 histone pseudogene 16 Homo sapiens 30-33 20371239-7 2010 Western blot analysis indicated that BTZQ may up-regulate expression of cyclin B, p21, p53 and cytochrome c, but down-regulate cdk1 expression in a dose-dependent manner, leading to apoptosis of BC-M1 cells. btzq 37-41 H3 histone pseudogene 16 Homo sapiens 82-85 20657652-4 2010 METHODOLOGY/PRINCIPAL FINDINGS: In this study, we show that DCB-3503 suppresses the expression of pro-oncogenic or pro-survival proteins with short half-lives, including cyclin D1, survivin, beta-catenin, p53, and p21, without decreasing their mRNA levels. DCB 3503 60-68 H3 histone pseudogene 16 Homo sapiens 214-217 20403647-2 2010 Complex [Ni(DMBG)(2)](ClO(4))(2).2DMF (DMF: N,N-dimethylformamide) crystallizes in the monoclinic P2(1)/c space group while [Cu(DMBG)(2)](ClO(4))(2) adopt monoclinic P21/c space group as X-ray single crystal data indicate. [ni(dmbg)(2)](clo(4)) 8-29 H3 histone pseudogene 16 Homo sapiens 98-103 20453878-5 2010 We provide evidence that the antitumor effect on combination treatment is achieved by VPA-induced reactivation of p21, which is downregulated in aRMS cells by destabilization of the transcriptional regulator EGR1 by PAX3/FKHR. Valproic Acid 86-89 H3 histone pseudogene 16 Homo sapiens 114-117 20521794-5 2010 The trigonal prismatic cluster compound W(6)CCl(15) (P2(1)/c, Z = 4; a = 9.8830(4) A, b = 11.8945(4) A, c = 17.8670(7) A, beta = 107.883(2) degrees) is related to the already known compound W(6)CCl(16). Cefaclor 44-47 H3 histone pseudogene 16 Homo sapiens 53-60 20661724-5 2010 The cisplatin treatment significantly down-regulated the p53 and p21 expression level, while up-regulated the p27 expression in the YCC-3/R cells compared to the parental cells. Cisplatin 4-13 H3 histone pseudogene 16 Homo sapiens 65-68 20403647-2 2010 Complex [Ni(DMBG)(2)](ClO(4))(2).2DMF (DMF: N,N-dimethylformamide) crystallizes in the monoclinic P2(1)/c space group while [Cu(DMBG)(2)](ClO(4))(2) adopt monoclinic P21/c space group as X-ray single crystal data indicate. [ni(dmbg)(2)](clo(4)) 8-29 H3 histone pseudogene 16 Homo sapiens 166-171 20403647-2 2010 Complex [Ni(DMBG)(2)](ClO(4))(2).2DMF (DMF: N,N-dimethylformamide) crystallizes in the monoclinic P2(1)/c space group while [Cu(DMBG)(2)](ClO(4))(2) adopt monoclinic P21/c space group as X-ray single crystal data indicate. 2dmf 33-37 H3 histone pseudogene 16 Homo sapiens 98-103 20403647-2 2010 Complex [Ni(DMBG)(2)](ClO(4))(2).2DMF (DMF: N,N-dimethylformamide) crystallizes in the monoclinic P2(1)/c space group while [Cu(DMBG)(2)](ClO(4))(2) adopt monoclinic P21/c space group as X-ray single crystal data indicate. 2dmf 33-37 H3 histone pseudogene 16 Homo sapiens 166-171 20403647-2 2010 Complex [Ni(DMBG)(2)](ClO(4))(2).2DMF (DMF: N,N-dimethylformamide) crystallizes in the monoclinic P2(1)/c space group while [Cu(DMBG)(2)](ClO(4))(2) adopt monoclinic P21/c space group as X-ray single crystal data indicate. Dimethylformamide 34-37 H3 histone pseudogene 16 Homo sapiens 98-103 20403647-2 2010 Complex [Ni(DMBG)(2)](ClO(4))(2).2DMF (DMF: N,N-dimethylformamide) crystallizes in the monoclinic P2(1)/c space group while [Cu(DMBG)(2)](ClO(4))(2) adopt monoclinic P21/c space group as X-ray single crystal data indicate. Dimethylformamide 34-37 H3 histone pseudogene 16 Homo sapiens 166-171 20403647-2 2010 Complex [Ni(DMBG)(2)](ClO(4))(2).2DMF (DMF: N,N-dimethylformamide) crystallizes in the monoclinic P2(1)/c space group while [Cu(DMBG)(2)](ClO(4))(2) adopt monoclinic P21/c space group as X-ray single crystal data indicate. Dimethylformamide 44-65 H3 histone pseudogene 16 Homo sapiens 98-103 20514393-3 2010 Ceramide induced a selective arrest of MCF-7 cells in the G1-phase, which was associated with a decreased expression of cyclins D and E and increased expression of p53 and p21. Ceramides 0-8 H3 histone pseudogene 16 Homo sapiens 172-175 20397022-9 2010 Cell cycle inhibitors p21 and p27 are induced in the three cell lines by bortezomib and the combination treatment. Bortezomib 73-83 H3 histone pseudogene 16 Homo sapiens 22-25 20514393-6 2010 The increased sensitivity to ceramide, in the context of p53 inhibition, may be due to decreased expression of p21, as siRNA targeted to p21 also sensitized MCF-7 cells to ceramide-induced death. Ceramides 29-37 H3 histone pseudogene 16 Homo sapiens 111-114 20514393-6 2010 The increased sensitivity to ceramide, in the context of p53 inhibition, may be due to decreased expression of p21, as siRNA targeted to p21 also sensitized MCF-7 cells to ceramide-induced death. Ceramides 29-37 H3 histone pseudogene 16 Homo sapiens 137-140 20493172-5 2010 delta-T3-induced cell cycle arrest and proapoptotic gene/protein expression (e.g., p21, p27, and caspases) were abrogated by alpha-Toc. delta-t3 0-8 H3 histone pseudogene 16 Homo sapiens 83-86 20304059-4 2010 In TDEC, calcitriol induces G(0)/G(1) arrest, modulates p27 and p21, and induces apoptotic cell death and decreases P-Erk and P-Akt. Calcitriol 9-19 H3 histone pseudogene 16 Homo sapiens 64-67 20375080-5 2010 In arsenite-exposed cells, the levels of phospho-p53, p21, and mdm2 increase at early times after exposure. arsenite 3-11 H3 histone pseudogene 16 Homo sapiens 54-57 20501850-8 2010 In a phase I clinical trial of CDDO (RTA-401) in leukemia, CDDO induced an increase in PPARgamma mRNA expression in six of nine patient samples; of those, induction of differentiation was documented in four patients and that of p21 in three patients, all expressing DRIP205 protein. 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid 31-35 H3 histone pseudogene 16 Homo sapiens 228-231 21188109-2 2010 Temsirolimus (also known as CCI-779), a dihydroester of rapamycin, in MCL cell lines inhibited mTOR, downregulated p21 and v-Raf, and induced autophagy. temsirolimus 0-12 H3 histone pseudogene 16 Homo sapiens 115-118 21188109-2 2010 Temsirolimus (also known as CCI-779), a dihydroester of rapamycin, in MCL cell lines inhibited mTOR, downregulated p21 and v-Raf, and induced autophagy. CCI 28-31 H3 histone pseudogene 16 Homo sapiens 115-118 20501850-8 2010 In a phase I clinical trial of CDDO (RTA-401) in leukemia, CDDO induced an increase in PPARgamma mRNA expression in six of nine patient samples; of those, induction of differentiation was documented in four patients and that of p21 in three patients, all expressing DRIP205 protein. 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid 59-63 H3 histone pseudogene 16 Homo sapiens 228-231 21346872-3 2010 In the present insilico study, the inhibitory effect of different flavonoid compounds on mutant H Ras protein p21 has been assessed. Flavonoids 66-75 H3 histone pseudogene 16 Homo sapiens 110-113 20587334-6 2010 Transient transfection assays indicated that overexpression of LBH or alphaB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both alphaB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53. alphab-crystallin 180-197 H3 histone pseudogene 16 Homo sapiens 138-141 21346872-7 2010 Our study demonstrates that flavonoids (particularly Naringenin, Daidzein, and Hesperetin) are the effective drugs to inhibit function of mutant H-Ras P21 protein, which in turn arrests the process of cell growth and proliferation of the cancer cell. Flavonoids 28-38 H3 histone pseudogene 16 Homo sapiens 151-154 21346872-7 2010 Our study demonstrates that flavonoids (particularly Naringenin, Daidzein, and Hesperetin) are the effective drugs to inhibit function of mutant H-Ras P21 protein, which in turn arrests the process of cell growth and proliferation of the cancer cell. naringenin 53-63 H3 histone pseudogene 16 Homo sapiens 151-154 21346872-7 2010 Our study demonstrates that flavonoids (particularly Naringenin, Daidzein, and Hesperetin) are the effective drugs to inhibit function of mutant H-Ras P21 protein, which in turn arrests the process of cell growth and proliferation of the cancer cell. daidzein 65-73 H3 histone pseudogene 16 Homo sapiens 151-154 21346872-7 2010 Our study demonstrates that flavonoids (particularly Naringenin, Daidzein, and Hesperetin) are the effective drugs to inhibit function of mutant H-Ras P21 protein, which in turn arrests the process of cell growth and proliferation of the cancer cell. hesperetin 79-89 H3 histone pseudogene 16 Homo sapiens 151-154 19609669-7 2010 The additive effect of elesclomol on chemotherapy drug-induced apoptosis was associated with increases in cleaved caspase-3, p21(Cip1), and p27(Kip1) and decreases in the Inhibitor of Apoptosis Protein levels and NF-kappaB activity. elesclomol 23-33 H3 histone pseudogene 16 Homo sapiens 125-128 20171194-5 2010 Inhibition of p38 using SB202190 or SB203580 inhibited BEL-induced increases in P-p53 (ser15), p53 and p21, and altered the number of cells in G1 in LNCaP cells, and S-phase in PC-3 cells. SB 203580 36-44 H3 histone pseudogene 16 Homo sapiens 103-106 20587334-0 2010 Synergistic efficacy of LBH and alphaB-crystallin through inhibiting transcriptional activities of p53 and p21. alphab-crystallin 32-49 H3 histone pseudogene 16 Homo sapiens 107-110 20587334-6 2010 Transient transfection assays indicated that overexpression of LBH or alphaB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both alphaB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53. alphab-crystallin 70-87 H3 histone pseudogene 16 Homo sapiens 138-141 20587334-6 2010 Transient transfection assays indicated that overexpression of LBH or alphaB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both alphaB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53. alphab-crystallin 70-87 H3 histone pseudogene 16 Homo sapiens 286-289 20042273-0 2010 p21(Cip1) confers resistance to imatinib in human chronic myeloid leukemia cells. Imatinib Mesylate 32-40 H3 histone pseudogene 16 Homo sapiens 0-3 20042273-3 2010 We describe that imatinib down-regulates p21(Cip1) expression in CML cells. Imatinib Mesylate 17-25 H3 histone pseudogene 16 Homo sapiens 41-44 20587334-6 2010 Transient transfection assays indicated that overexpression of LBH or alphaB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both alphaB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53. alphab-crystallin 180-197 H3 histone pseudogene 16 Homo sapiens 286-289 20042273-4 2010 Using K562 cells with inducible p21 expression and transient transfections we found that p21 confers partial resistance to imatinib-induced apoptosis. Imatinib Mesylate 123-131 H3 histone pseudogene 16 Homo sapiens 32-35 20042273-4 2010 Using K562 cells with inducible p21 expression and transient transfections we found that p21 confers partial resistance to imatinib-induced apoptosis. Imatinib Mesylate 123-131 H3 histone pseudogene 16 Homo sapiens 89-92 20587334-7 2010 These results showed that the interaction of LBH and alphaB-crystallin may inhibit synergistically the transcriptional regulation of p53 and p21. alphab-crystallin 53-70 H3 histone pseudogene 16 Homo sapiens 141-144 20042273-6 2010 The results suggest an involvement of p21(Cip1) in the response to imatinib in CML. Imatinib Mesylate 67-75 H3 histone pseudogene 16 Homo sapiens 38-41 20404564-0 2010 The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21. romidepsin 61-66 H3 histone pseudogene 16 Homo sapiens 161-164 20235278-6 2010 Treatment Ki67p-GFP expressing HT1080 cells with mitomycin C, an antineoplastic agent, induces P21 and P27 expression, G(1)/S/G(2)M block and attenuates Ki67p activity. Mitomycin 49-60 H3 histone pseudogene 16 Homo sapiens 95-98 20404564-0 2010 The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21. Aspirin 84-91 H3 histone pseudogene 16 Homo sapiens 161-164 20404564-0 2010 The effects of the histone deacetylase inhibitor romidepsin (FK228) are enhanced by aspirin (ASA) in COX-1 positive ovarian cancer cells through augmentation of p21. Aspirin 93-96 H3 histone pseudogene 16 Homo sapiens 161-164 20404564-10 2010 Upregulation of the cell cycle control protein p21 was induced robustly by FK228 in both cell lines. romidepsin 75-80 H3 histone pseudogene 16 Homo sapiens 47-50 20404564-11 2010 In the COX-1 positive cells, p21 expression was augmented by the addition of ASA to FK228 treatment. Aspirin 77-80 H3 histone pseudogene 16 Homo sapiens 29-32 20456495-9 2010 Both curcuminoids induced G2/M block and inhibited keratinocyte growth, and THC increased cellular levels of p21, a known p53 transcriptional target. tetrahydrocurcumin 76-79 H3 histone pseudogene 16 Homo sapiens 109-112 20404564-11 2010 In the COX-1 positive cells, p21 expression was augmented by the addition of ASA to FK228 treatment. romidepsin 84-89 H3 histone pseudogene 16 Homo sapiens 29-32 20404564-12 2010 Furthermore, COX-1 siRNA attenuated the effects of combined ASA and FK228 on the levels of p21 expression and the amount of growth inhibition. Aspirin 60-63 H3 histone pseudogene 16 Homo sapiens 91-94 20404564-12 2010 Furthermore, COX-1 siRNA attenuated the effects of combined ASA and FK228 on the levels of p21 expression and the amount of growth inhibition. romidepsin 68-73 H3 histone pseudogene 16 Homo sapiens 91-94 20456495-10 2010 These data demonstrate that curcuminoids can differentially regulate MAP kinases to inhibit keratinocyte growth while inducing p21. curcuminoids 28-40 H3 histone pseudogene 16 Homo sapiens 127-130 20404564-13 2010 The additional increase in p21 by ASA in FK228-treated cells was not observed at the promoter or transcriptional levels. Aspirin 34-37 H3 histone pseudogene 16 Homo sapiens 27-30 20404564-13 2010 The additional increase in p21 by ASA in FK228-treated cells was not observed at the promoter or transcriptional levels. romidepsin 41-46 H3 histone pseudogene 16 Homo sapiens 27-30 20404564-14 2010 However, a significant delay in p21 protein degradation in the presence of ASA and FK228 in COX-1 positive cells was associated with inhibition of proteasome activity. Aspirin 75-78 H3 histone pseudogene 16 Homo sapiens 32-35 20404564-14 2010 However, a significant delay in p21 protein degradation in the presence of ASA and FK228 in COX-1 positive cells was associated with inhibition of proteasome activity. romidepsin 83-88 H3 histone pseudogene 16 Homo sapiens 32-35 20351180-6 2010 Our results thus suggest that p400 represses basal p21 gene expression through dual mechanisms that include the direct inhibition of TIP60 enzymatic activity described here and the previously described ATP-dependent positioning of H2A.Z at the promoter. Adenosine Triphosphate 202-205 H3 histone pseudogene 16 Homo sapiens 51-54 20429769-3 2010 Both azadirachtin and nimbolide significantly suppressed the viability of HeLa cells in a dose-dependent manner by inducing cell cycle arrest at G0/G1 phase accompanied by p53-dependent p21 accumulation and down-regulation of the cell cycle regulatory proteins cyclin B, cyclin D1 and PCNA. azadirachtin 5-17 H3 histone pseudogene 16 Homo sapiens 186-189 20429769-3 2010 Both azadirachtin and nimbolide significantly suppressed the viability of HeLa cells in a dose-dependent manner by inducing cell cycle arrest at G0/G1 phase accompanied by p53-dependent p21 accumulation and down-regulation of the cell cycle regulatory proteins cyclin B, cyclin D1 and PCNA. nimbolide 22-31 H3 histone pseudogene 16 Homo sapiens 186-189 20336762-7 2010 The results showed that DBDCT-mediated cell-cycle arrest might occur through the induction of p21 in a p53-dependent manner and that DBDCT induction of the mitochondrial apoptotic signaling pathway is perhaps mediated by increasing Bax/Bcl-2 ratios, which result in the loss of DeltaPsi(m), release of cytochrome c into the cytoplasm, activation of caspase-3 and -9, and increased reactive oxygen species (ROS) generation. dbdct 24-29 H3 histone pseudogene 16 Homo sapiens 94-97 20392637-2 2010 Multiple compounds bearing an N1-piperidine demonstrate EC(50)s of 20-100 nM in human A549, HL60, and PC3 cells, in vitro and in vivo hyperacetylation of histones H3 and H4, and induction of p21(waf). n1-piperidine 30-43 H3 histone pseudogene 16 Homo sapiens 191-194 20417621-8 2010 Furthermore, miR-1285 inhibits the transcription of p21, a master gene downstream of p53. mir-1285 13-21 H3 histone pseudogene 16 Homo sapiens 52-55 20346999-7 2010 Additionally, bolus (3h) doxorubicin incubation led to phosphorylation of p53 at serine 392, induction of p21, G2 arrest and increase of proapoptotic protein Bax. Tritium 21-23 H3 histone pseudogene 16 Homo sapiens 106-109 20346999-7 2010 Additionally, bolus (3h) doxorubicin incubation led to phosphorylation of p53 at serine 392, induction of p21, G2 arrest and increase of proapoptotic protein Bax. Doxorubicin 25-36 H3 histone pseudogene 16 Homo sapiens 106-109 20346999-9 2010 Continuous (24h) treatment with 5 microM doxorubicin resulted in cell cycle arrest in G0/G1 phase that was neither accompanied by phosphorylation and activation of p53 nor enhanced expression of p21. Doxorubicin 41-52 H3 histone pseudogene 16 Homo sapiens 195-198 20439741-0 2010 Small-molecule p21-activated kinase inhibitor PF-3758309 is a potent inhibitor of oncogenic signaling and tumor growth. PF 3758309 46-56 H3 histone pseudogene 16 Homo sapiens 15-18 20138958-0 2010 Iodine induces apoptosis via regulating MAPKs-related p53, p21, and Bcl-xL in thyroid cancer cells. Iodine 0-6 H3 histone pseudogene 16 Homo sapiens 59-62 20138958-6 2010 Iodine treatment decreased the level of mutant p53 including the R273H mutant that possesses anti-apoptotic features, but increased the p21 level. Iodine 0-6 H3 histone pseudogene 16 Homo sapiens 136-139 20138958-8 2010 Moreover, iodine transiently activated the subfamily members of mitogen activated protein kinases (MAPKs) (ERK1/2, p38 and JNK1/2) which contribute to modulate p53, p21 and Bcl-xL expression. Iodine 10-16 H3 histone pseudogene 16 Homo sapiens 165-168 20138958-10 2010 Collectively, iodine-induced apoptotic pathway is involved in the activation of MAPKs-related p21, Bcl-xL and mutant p53 regulation. Iodine 14-20 H3 histone pseudogene 16 Homo sapiens 94-97 20646592-5 2010 And the expressions of cell cycle protein P53, P21, CDK2 were detected by Western blot after the treatment of capsaicin. Capsaicin 110-119 H3 histone pseudogene 16 Homo sapiens 47-50 20646592-11 2010 After a 48-hour treatment with capsaicin, the expressions of P53 and P21 were up-regulated in contrary to the expression of CDK2. Capsaicin 31-40 H3 histone pseudogene 16 Homo sapiens 69-72 20646592-12 2010 CONCLUSION: Capsaicin induces the cell cycle arrest of bladder cancer RT4 cells G(0)/G(1) phase and growth inhibition via TRPV1 receptor by modulating the expression of P53, P21 and CDK2. Capsaicin 12-21 H3 histone pseudogene 16 Homo sapiens 174-177 20062073-0 2010 HSP72 depletion suppresses gammaH2AX activation by genotoxic stresses via p53/p21 signaling. gammah2ax 27-36 H3 histone pseudogene 16 Homo sapiens 78-81 20094798-6 2010 Imatinib did not significantly affect the nutlin-3-induced expression of p53 but abrogated that of p21. Imatinib Mesylate 0-8 H3 histone pseudogene 16 Homo sapiens 99-102 20094798-7 2010 Furthermore, activation of Bax as well as caspase-3 induced by combined treatment with imatinib and nutlin-3 was observed preferentially in cells expressing p21 at reduced levels. Imatinib Mesylate 87-95 H3 histone pseudogene 16 Homo sapiens 157-160 20094798-8 2010 The present study indicates that combined treatment with nutlin-3 and imatinib activates p53 without inducing p21 and synergistically activates Bax-mediated intrinsic mitochondrial pathway to induce apoptosis in BCR/ABL-expressing cells. Imatinib Mesylate 70-78 H3 histone pseudogene 16 Homo sapiens 110-113 19913353-13 2010 The p21 and p27 gene expressions increased markedly while cyclin B1 and D1 gene expression decreased markedly by treatment with marchantin A. marchantin A 128-140 H3 histone pseudogene 16 Homo sapiens 4-7 20423286-4 2010 MI-63 induced G1 phase arrest and increased p21 expression. 2-methyl-4-isothiazolin-3-one 0-2 H3 histone pseudogene 16 Homo sapiens 44-47 20377184-1 2010 The standard molar enthalpies of formation and sublimation of crystalline (monoclinic, space group P2(1)/c) nicotinic acid (NA), at 298.15 K, were determined as Delta(f)H(m)(o)(NA, cr) = -344.7 +/- 1.2 kJ x mol(-1) and Delta(sub)H(m)(o)(NA) = 112.1 +/- 0.5 kJ x mol(-1) by using combustion calorimetry, drop-sublimation Calvet microcalorimetry, and the Knudsen effusion method. Chromium 62-64 H3 histone pseudogene 16 Homo sapiens 99-104 20371965-6 2010 Moreover, it was shown that cotreatment with MDA-LDL and BaP markedly induced the expression of human cytochrome P4501A1 (hCYP1A1) messenger ribonucleic acid (mRNA) and significantly induced the expressions of p53 and p21 mRNAs. mda-ldl 45-52 H3 histone pseudogene 16 Homo sapiens 218-221 20371965-6 2010 Moreover, it was shown that cotreatment with MDA-LDL and BaP markedly induced the expression of human cytochrome P4501A1 (hCYP1A1) messenger ribonucleic acid (mRNA) and significantly induced the expressions of p53 and p21 mRNAs. Benzo(a)pyrene 57-60 H3 histone pseudogene 16 Homo sapiens 218-221 20424123-10 2010 In contrast, doxorubicin or nutlin-3 treatment-both leading to p53-p21 activation-or CDK2 inhibition had no effect on SKP2 regulation in MYCN-amplified cells. nutlin 28-34 H3 histone pseudogene 16 Homo sapiens 67-70 20082627-9 2010 In addition, HL-60 cells were arrested in the G(0)/G(1) phase via the induction of p53/p21 by pipoxolan. pipoxolan 94-103 H3 histone pseudogene 16 Homo sapiens 87-90 20931760-9 2010 The molecular senescence marker P21 increased significantly after boningmycin treatment at a dosage of 0.1 micromol x L(-1), whereas a higher concentration of it induced apoptosis. boningmycin 66-77 H3 histone pseudogene 16 Homo sapiens 32-35 20160501-7 2010 This inhibitory effect was not dependent on the status of p53 and p21 although GDP366 potently increased p53 and p21 levels. GDP 366 79-85 H3 histone pseudogene 16 Homo sapiens 113-116 20110807-2 2010 Cucurbitacin E at low concentrations (3-50 nmol/l) inhibited the growth of HL-60 cells, which was associated with G2/M cell-cycle arrest, decrease in the levels of cyclin-dependent kinase1, and increase in the levels of p21. cucurbitacin E 0-14 H3 histone pseudogene 16 Homo sapiens 220-223 19882681-6 2010 Expression of BRCA-1, p53, p21(WAF), and c-myc was increased by estradiol stimulation and subsequently decreased by melatonin treatment in both cell lines, except for p53 expression in the transfected cell line, thereby proving the antiestrogenic effect of melatonin at molecular level. Estradiol 64-73 H3 histone pseudogene 16 Homo sapiens 27-30 20100536-8 2010 Moreover, immunoblot analysis indicated that the co-activation of pro-apoptotic factors Bax and p21 were observed in the p73 alpha infected cells after cisplatin treatment. Cisplatin 152-161 H3 histone pseudogene 16 Homo sapiens 96-99 20450546-6 2010 The expression of p21 protein was significantly up-regulated and the expression of phosphorylation ERK was significantly down-regulated after A549 cells were treated with TSA. trichostatin A 171-174 H3 histone pseudogene 16 Homo sapiens 18-21 20088798-5 2010 Mechanistically, lenalidomide plus dexamethasone synergistically induced expression of the tumor suppressor genes Egr1, Egr2, Egr3, p15, p21, and p27 in MM cell lines and MM patient cells. Lenalidomide 17-29 H3 histone pseudogene 16 Homo sapiens 137-140 20022955-4 2010 In a promoter-specific context, inhibition of H3R17 methylation represses expression of p21, a p53-responsive gene, thus implicating a possible role for H3 Arg-17 methylation in tumor suppressor function. Arginine 156-159 H3 histone pseudogene 16 Homo sapiens 88-91 20450732-10 2010 Cells pretreated with higher concentrations of vitexicarpin expressed less c-Myc and Bcl-2 in Hs578T cells.In contrast, p21 decreased when cells were treated with the same conditions. casticin 47-59 H3 histone pseudogene 16 Homo sapiens 120-123 20450732-11 2010 When c-Myc transient transfection was performed in vitexicarpin-treated cells, the effect of p21 and Bcl-2 disappeared. casticin 51-63 H3 histone pseudogene 16 Homo sapiens 93-96 20088798-5 2010 Mechanistically, lenalidomide plus dexamethasone synergistically induced expression of the tumor suppressor genes Egr1, Egr2, Egr3, p15, p21, and p27 in MM cell lines and MM patient cells. Dexamethasone 35-48 H3 histone pseudogene 16 Homo sapiens 137-140 20122271-8 2010 Down-regulation of COX-2, EGFR, p-EGFR and up-regulation of p21 and p27 were found in Ist-Mes-2, after treatment with single agents and in combination. 2-(N-morpholino)ethanesulfonic acid 90-93 H3 histone pseudogene 16 Homo sapiens 60-63 21787594-7 2010 Taken together, these data suggested that cell injuries were triggered by the generation of oxidative stress; p53 and p21 mediated G1 phase arrest is a potential mechanistic pathway of silica nanoparticles induced damage in H9c2(2-1) cells. Silicon Dioxide 185-191 H3 histone pseudogene 16 Homo sapiens 118-121 20086099-8 2010 It has been known that p21 is required for a proper tamoxifen response in breast cancer. Tamoxifen 52-61 H3 histone pseudogene 16 Homo sapiens 23-26 20086099-9 2010 We show that the overexpression of 14-3-3tau inhibits tamoxifen-induced p21 induction and growth arrest in MCF7 cells. Tamoxifen 54-63 H3 histone pseudogene 16 Homo sapiens 72-75 20383943-7 2010 Besides, the NFkappaB pathway was not involved in bortezomib treatment in neuroblastoma CHP126 cells, bortezomib-driven apoptotic events were associated with promoting p21 and Bax expression and down-regulating Bcl-2 expression. Bortezomib 102-112 H3 histone pseudogene 16 Homo sapiens 168-171 19908243-4 2010 In mechanistic studies, silibinin (50-75 microM) modulated the protein levels of cyclin-dependent kinases (CDKs) (4, 6, and 2), cyclins (D1, D3, and E), CDKIs (p18/INK4C, p21/Cip1, and p27/Kip1) in a differential manner in these three cell lines. Silybin 24-33 H3 histone pseudogene 16 Homo sapiens 171-174 20067818-6 2010 Treatment of cells with the p38 inhibitor SB202190, but not the ERK1/2 inhibitor PD98059, partially reversed BrO(3)(-)-induced G2/M arrest and decreased BrO(3)(-)-induced p-p53, p21 and cyclin B1 expression. 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole 42-50 H3 histone pseudogene 16 Homo sapiens 178-181 20067818-8 2010 The antioxidant ascorbic acid inhibited BrO(3)(-)-induced p38 activation, G2/M arrest, p-p53, p21 and cyclin B1 expression; however, ascorbic acid had no effect on BrO(3)(-)-induced formation of 8-OHdG, a marker of DNA oxidative damage, whose increases preceded cell death by 24h. Ascorbic Acid 16-29 H3 histone pseudogene 16 Homo sapiens 94-97 20067818-8 2010 The antioxidant ascorbic acid inhibited BrO(3)(-)-induced p38 activation, G2/M arrest, p-p53, p21 and cyclin B1 expression; however, ascorbic acid had no effect on BrO(3)(-)-induced formation of 8-OHdG, a marker of DNA oxidative damage, whose increases preceded cell death by 24h. bro(3)(-) 40-49 H3 histone pseudogene 16 Homo sapiens 94-97 19895793-6 2010 Cell cycle regulatory gene analysis showed increased protein levels of cyclin A, cyclin B, Chk2, Cdk2, and P27 in hepatoma cells after time courses of emodin treatment, and Western blot analysis showed decreased protein levels of Cdc25c and P21. Emodin 151-157 H3 histone pseudogene 16 Homo sapiens 241-244 19788889-8 2010 Finally, p21 deletion also sensitized HCT116 cells to the Nutlin-3-induced DNA damage response, suggesting that cell cycle checkpoint abnormalities may promote this response. nutlin 3 58-66 H3 histone pseudogene 16 Homo sapiens 9-12 20028382-5 2010 Treatment with resveratrol led to G(1) phase cell cycle arrest in T24 cells by activation of p21 and downregulation of cyclin D1, cyclin-dependent kinase 4, and phosphorylated Rb. Resveratrol 15-26 H3 histone pseudogene 16 Homo sapiens 93-96 19621385-12 2010 The combination of Ki23057 and 5-FU decreased DPD expression and increased apoptosis rates and p21 expression level of SGC cells. Ki23057 19-26 H3 histone pseudogene 16 Homo sapiens 95-98 19621385-12 2010 The combination of Ki23057 and 5-FU decreased DPD expression and increased apoptosis rates and p21 expression level of SGC cells. Fluorouracil 31-35 H3 histone pseudogene 16 Homo sapiens 95-98 19583730-5 2010 Finally, the effect of p21 knockdown in the susceptibility to doxorubicin was examined with RT112 stable transfectants with short hairpin RNA (shRNA) of p21. Doxorubicin 62-73 H3 histone pseudogene 16 Homo sapiens 23-26 19583730-8 2010 The combined treatment with dicoumarol suppressed p53/p21 induction by doxorubicin and resulted in sequential p38 MAPK activation, myeloid cell leukaemia 1 suppression and caspase cleavage. Dicumarol 28-38 H3 histone pseudogene 16 Homo sapiens 54-57 19583730-8 2010 The combined treatment with dicoumarol suppressed p53/p21 induction by doxorubicin and resulted in sequential p38 MAPK activation, myeloid cell leukaemia 1 suppression and caspase cleavage. Doxorubicin 71-82 H3 histone pseudogene 16 Homo sapiens 54-57 19583730-9 2010 The synergistic effect of doxorubicin/dicoumarol was suppressed by the p38 MAPK inhibitor SB202190 and, furthermore, p21 knockdown with shRNA transfection made RT112 cells six times more susceptible to doxorubicin with p38 MAPK activation. Doxorubicin 26-37 H3 histone pseudogene 16 Homo sapiens 117-120 19583730-9 2010 The synergistic effect of doxorubicin/dicoumarol was suppressed by the p38 MAPK inhibitor SB202190 and, furthermore, p21 knockdown with shRNA transfection made RT112 cells six times more susceptible to doxorubicin with p38 MAPK activation. Doxorubicin 202-213 H3 histone pseudogene 16 Homo sapiens 117-120 19583730-10 2010 CONCLUSION: These results suggest that concomitant use of dicoumarol could enhance the cytotoxicity of doxorubicin in urothelial cancer cells with wt-p53 through the p53/p21/p38 MAPK pathways. Dicumarol 58-68 H3 histone pseudogene 16 Homo sapiens 170-173 19583730-10 2010 CONCLUSION: These results suggest that concomitant use of dicoumarol could enhance the cytotoxicity of doxorubicin in urothelial cancer cells with wt-p53 through the p53/p21/p38 MAPK pathways. Doxorubicin 103-114 H3 histone pseudogene 16 Homo sapiens 170-173 19922491-10 2010 In addition, 2HBZ caused a marked increase in p21, p53 and Bax protein expressions and these effects were associated with an increase in G1 and G2 arrest of the cell cycle and a reduction in S-phase. 2hbz 13-17 H3 histone pseudogene 16 Homo sapiens 46-49 21579708-1 2010 The crystal structure of the title compound, C(16)H(13)ClO(2) (II), (space group P2(1)/c,) is a polymorph of the structure, (I), reported by Harrison, Yathirajan, Sarojini, Narayana & Indira [Acta Cryst. c(16)h(13)clo(2) 45-61 H3 histone pseudogene 16 Homo sapiens 81-86 19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 44-57 H3 histone pseudogene 16 Homo sapiens 131-134 19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 59-61 H3 histone pseudogene 16 Homo sapiens 131-134 20103602-8 2010 Radiosensitization of PTEN-deficient U87MG cells by caffeine was significantly correlated with the activation of the G(1) DNA damage checkpoint that occurred independently of de novo synthesis of p53 and p21. Caffeine 52-60 H3 histone pseudogene 16 Homo sapiens 204-207 19588502-8 2010 Using Western blotting, we show that Bac-ELP1-p21 caused a decrease in Rb phosphorylation levels in cells treated at 42 degrees C. The polypeptide also induced caspase activation, PARP cleavage, and cell cycle arrest in S-phase and G2/M-phase. Rubidium 71-73 H3 histone pseudogene 16 Homo sapiens 46-49 19346318-8 2010 NNK promoted the nuclear p21, whereas troglitazone increased cytosolic p21. Troglitazone 38-50 H3 histone pseudogene 16 Homo sapiens 71-74 20574922-4 2010 Cell cycle check point proteins such as p21 and stratifin (14-3-3 sigma) increased at mRNA and protein level, whereas cell cycle progression proteins such as cell division cycle 25 homolog and cyclin-dependent kinase 1 decreased after DHA treatment. Docosahexaenoic Acids 235-238 H3 histone pseudogene 16 Homo sapiens 40-71 19329556-0 2010 Diesel particle-induced transcriptional expression of p21 involves activation of EGFR, Src, and Stat3. diesel 0-6 H3 histone pseudogene 16 Homo sapiens 54-57 19475409-0 2010 Treatment of K562 cells with 1,25-dihydroxyvitamin D3 induces distinct alterations in the expression of apoptosis-related genes BCL2, BAX, BCLXL, and p21. Calcitriol 29-53 H3 histone pseudogene 16 Homo sapiens 150-153 20332618-3 2010 Culturing cells in the 8 mM-Cl(-)-containing culture medium upregulated the protein expression level of p21 (a CDK inhibitor) inhibiting transition of G(1) to S phase, and diminished the incorporation of 5-ethynyl-2"-deoxyuridine (EdU; a thymidine analogue) into DNA. 5-ethynyl-2'-deoxyuridine 204-229 H3 histone pseudogene 16 Homo sapiens 104-107 20332618-3 2010 Culturing cells in the 8 mM-Cl(-)-containing culture medium upregulated the protein expression level of p21 (a CDK inhibitor) inhibiting transition of G(1) to S phase, and diminished the incorporation of 5-ethynyl-2"-deoxyuridine (EdU; a thymidine analogue) into DNA. 5-ethynyl-2'-deoxyuridine 231-234 H3 histone pseudogene 16 Homo sapiens 104-107 20332618-3 2010 Culturing cells in the 8 mM-Cl(-)-containing culture medium upregulated the protein expression level of p21 (a CDK inhibitor) inhibiting transition of G(1) to S phase, and diminished the incorporation of 5-ethynyl-2"-deoxyuridine (EdU; a thymidine analogue) into DNA. Thymidine 238-247 H3 histone pseudogene 16 Homo sapiens 104-107 19797611-2 2010 Treatment with 1,4-diamino-2,3-dicyano-1,4-bis(methylthio)butadiene (U0126) (an extracellular signal-regulated kinase inhibitor) suppressed the HGF-induced expression of UGT1A1 and CYP2B6, as well as p16, p21, and p27 in HepG2 cells. u0124 15-67 H3 histone pseudogene 16 Homo sapiens 205-208 19797611-2 2010 Treatment with 1,4-diamino-2,3-dicyano-1,4-bis(methylthio)butadiene (U0126) (an extracellular signal-regulated kinase inhibitor) suppressed the HGF-induced expression of UGT1A1 and CYP2B6, as well as p16, p21, and p27 in HepG2 cells. U 0126 69-74 H3 histone pseudogene 16 Homo sapiens 205-208 19889638-3 2010 Application of OSS (0.5 +/- 4 dynes/cm(2)) to MG63 cells induced sustained activation of phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR/p70S6K (p70S6 kinase) signaling cascades and hence cell proliferation, which was accompanied by increased expression of cyclins A and D1, cyclin-dependent protein kinases-2, -4, and -6, and bone formation-related genes (c-fos, Egr-1, and Cox-2) and decreased expression of p21(CIP1) and p27(KIP1). OSS 15-18 H3 histone pseudogene 16 Homo sapiens 408-411 19608275-7 2010 The enhanced cytotoxicity of ATO+bortezomib was associated with augmented STAT3 inhibition and JNK activation, up-regulation of Bim, p21, p27, p53 as well as down-regulation of Bcl-2. ato 29-32 H3 histone pseudogene 16 Homo sapiens 133-136 19608275-7 2010 The enhanced cytotoxicity of ATO+bortezomib was associated with augmented STAT3 inhibition and JNK activation, up-regulation of Bim, p21, p27, p53 as well as down-regulation of Bcl-2. Bortezomib 33-43 H3 histone pseudogene 16 Homo sapiens 133-136 19157829-6 2010 Lycopene prevented the arrest in G0/G1 phase of cell cycle induced by the oxysterol and counteracted the increased expression of p53 and p21. Lycopene 0-8 H3 histone pseudogene 16 Homo sapiens 137-140 20041160-5 2009 MiR-24 over expression in cells with wt-p53 upregulated TP53 and p21 protein; however, in p53-null cells miR-24 still induced cell cycle arrest without the involvement of p21. mir-24 0-6 H3 histone pseudogene 16 Homo sapiens 65-68 20524403-6 2010 Also, homozygous carriers of the p21 Ser allele showed a substantially increased risk of developing cervical adenocarcinoma (OR 2.07; 95% CI 1.13-3.79) compared to genotypes containing the Arg allele. Serine 37-40 H3 histone pseudogene 16 Homo sapiens 33-36 20524403-6 2010 Also, homozygous carriers of the p21 Ser allele showed a substantially increased risk of developing cervical adenocarcinoma (OR 2.07; 95% CI 1.13-3.79) compared to genotypes containing the Arg allele. Arginine 189-192 H3 histone pseudogene 16 Homo sapiens 33-36 20524403-7 2010 In addition, the combination of the Pro allele containing genotypes of p53 and the Ser homozygous genotype of p21 posed a remarkably increased risk (OR 5.22; 95% CI 2.24-12.16), although the interaction of the two genes could not be found. Serine 83-86 H3 histone pseudogene 16 Homo sapiens 110-113 20349730-8 2010 Western blot showed cryptotanshinone decreased expressions of HPV E6 and increased expressions of p53 and p21 proteins. cryptotanshinone 20-36 H3 histone pseudogene 16 Homo sapiens 106-109 20211058-8 2010 The results of flow cytometry showed that: after SW480 cells were treated with 0, 20, 40, 80 microg/ml genistein for 48 h, the FI values of PCNA were 1.49 +/- 0.02, 1.28 +/- 0.04, 1.14 +/- 0.03, and 0.93 +/- 0.08; the FI values of VEGF were 1.75 +/- 0.02, 1.34 +/- 0.06, 1.32 +/- 0.04, and 1.23 +/- 0.04; the fluorescence index (FI) values of p21 were 1.26 +/- 0.05, 1.36 +/- 0.06, 1.61 +/- 0.03, and 1.73 +/- 0.03, respectively. Genistein 103-112 H3 histone pseudogene 16 Homo sapiens 343-346 20095972-5 2009 Specific PAHAs (polyaminohydroxamic acids) and PABAs (polyaminobenzamides) polyamine analogues have demonstrated potent inhibition of the HDACs, re-expression of p21 and significant inhibition of tumour growth. pahas 9-14 H3 histone pseudogene 16 Homo sapiens 162-165 19947935-5 2009 Furthermore, adenosine was found to modulate the expression of some important proteins in the cell cycle, such as cyclin B and p21, and to inhibit the transition of metaphase to anaphase in mitosis. Adenosine 13-22 H3 histone pseudogene 16 Homo sapiens 127-130 19812222-6 2009 Based on the similarity of SFN metabolites and other phytochemicals to known HDAC inhibitors, we previously demonstrated that sulforaphane acted as an HDAC inhibitor in the prostate, causing enhanced histone acetylation, derepression of P21 and Bax, and induction of cell cycle arrest/apoptosis, leading to cancer prevention. sulforaphane 126-138 H3 histone pseudogene 16 Homo sapiens 237-240 19602434-8 2009 Moreover, upon sodium selenite treatment, there was a tendency for cells to accumulate at G2 phase which was accompanied by the increasing expression of cyclin B1, Cdc2 p34, p21 and the sub G1 fraction of the cell cycle. Sodium Selenite 15-30 H3 histone pseudogene 16 Homo sapiens 174-177 20095972-5 2009 Specific PAHAs (polyaminohydroxamic acids) and PABAs (polyaminobenzamides) polyamine analogues have demonstrated potent inhibition of the HDACs, re-expression of p21 and significant inhibition of tumour growth. Polyamines 75-84 H3 histone pseudogene 16 Homo sapiens 162-165 19735649-7 2009 Release of G2/M arrest by caffeine was accompanied by a decrease in the levels of p53/p21; however, gamma-H2AX levels were unchanged. Caffeine 26-34 H3 histone pseudogene 16 Homo sapiens 86-89 19862782-6 2009 The high-temperature solid phases of even carboxylic acids are all P2(1)/c with Z=4, the molecules are united into dimers via strong hydrogen bonds. Carboxylic Acids 42-58 H3 histone pseudogene 16 Homo sapiens 67-72 19544329-3 2009 It caused oxidative stress by early generation of nitric oxide and reactive oxygen species that robustly up regulated time-dependent expression of p53/p21/PUMA while conversely abrogating phosphatidylinositol-3-kinase (PI3K)/Akt pathways in parallel. Nitric Oxide 50-62 H3 histone pseudogene 16 Homo sapiens 151-154 19544329-3 2009 It caused oxidative stress by early generation of nitric oxide and reactive oxygen species that robustly up regulated time-dependent expression of p53/p21/PUMA while conversely abrogating phosphatidylinositol-3-kinase (PI3K)/Akt pathways in parallel. Reactive Oxygen Species 67-90 H3 histone pseudogene 16 Homo sapiens 151-154 20095972-5 2009 Specific PAHAs (polyaminohydroxamic acids) and PABAs (polyaminobenzamides) polyamine analogues have demonstrated potent inhibition of the HDACs, re-expression of p21 and significant inhibition of tumour growth. polyaminohydroxamic acids 16-41 H3 histone pseudogene 16 Homo sapiens 162-165 20095972-5 2009 Specific PAHAs (polyaminohydroxamic acids) and PABAs (polyaminobenzamides) polyamine analogues have demonstrated potent inhibition of the HDACs, re-expression of p21 and significant inhibition of tumour growth. pabas 47-52 H3 histone pseudogene 16 Homo sapiens 162-165 20095972-5 2009 Specific PAHAs (polyaminohydroxamic acids) and PABAs (polyaminobenzamides) polyamine analogues have demonstrated potent inhibition of the HDACs, re-expression of p21 and significant inhibition of tumour growth. polyaminobenzamides 54-73 H3 histone pseudogene 16 Homo sapiens 162-165 19693773-0 2009 Involvement of the JNK activation in terbinafine-induced p21 up-regulation and DNA synthesis inhibition in human vascular endothelial cells. Terbinafine 37-48 H3 histone pseudogene 16 Homo sapiens 57-60 19752719-5 2009 Simultaneous exposure to lapatinib and caelyx in SkBr3 cell line produced an additive cytotoxic effect with dephosphorylation of HER2 and EGFR, an upregulation of p21, and an induction of apoptosis through dephosphorylation of BAD and caspase cleavage. Lapatinib 25-34 H3 histone pseudogene 16 Homo sapiens 163-166 19752719-5 2009 Simultaneous exposure to lapatinib and caelyx in SkBr3 cell line produced an additive cytotoxic effect with dephosphorylation of HER2 and EGFR, an upregulation of p21, and an induction of apoptosis through dephosphorylation of BAD and caspase cleavage. liposomal doxorubicin 39-45 H3 histone pseudogene 16 Homo sapiens 163-166 19693773-7 2009 Taken together, our results suggest that JNK activation is involved in the TB-induced inhibition of ERK phosphorylation, p53 and p21 up-regulation and DNA synthesis inhibition in HUVEC. Terbinafine 75-77 H3 histone pseudogene 16 Homo sapiens 129-132 19693773-1 2009 Previously, we demonstrated that the extracellular signal-regulated kinase (ERK)-mediated pathway contributes to the terbinafine (TB)-induced increases of p21 and p53 protein level as well as decrease of DNA synthesis in human umbilical venous endothelial cells (HUVEC). Terbinafine 117-128 H3 histone pseudogene 16 Homo sapiens 155-158 19693773-1 2009 Previously, we demonstrated that the extracellular signal-regulated kinase (ERK)-mediated pathway contributes to the terbinafine (TB)-induced increases of p21 and p53 protein level as well as decrease of DNA synthesis in human umbilical venous endothelial cells (HUVEC). Terbinafine 130-132 H3 histone pseudogene 16 Homo sapiens 155-158 19693773-2 2009 The aim of this study is to examine the involvement of c-Jun NH2-terminal kinase (JNK) in the TB-induced increase of p21 protein level and DNA synthesis inhibition. Terbinafine 94-96 H3 histone pseudogene 16 Homo sapiens 117-120 19693773-4 2009 Transfection of HUVEC with JNK1 dominant negative (DN-JNK1) prevented the TB-induced increases of p21 and p53 protein level and decrease of DNA synthesis, suggesting that JNK1/2 activation is involved in the TB-induced cell cycle arrest in HUVEC. Terbinafine 74-76 H3 histone pseudogene 16 Homo sapiens 98-101 19620837-6 2009 We show that gefitinib reduces p-Akt levels, concomitant with elevation of p21 levels and suppression of cdk2/4 and cyclinE/D1 activities, which result in impaired cell cycle progression through G1 arrest only in parental PC-9 cells, in which it inhibits growth. Gefitinib 13-22 H3 histone pseudogene 16 Homo sapiens 75-78 21160963-4 2009 In both the BilIN and IPNB series, the expression of p21, p53, and cyclin D1 was upregulated with histological progression. Bile Pigments 12-17 H3 histone pseudogene 16 Homo sapiens 53-56 21160963-4 2009 In both the BilIN and IPNB series, the expression of p21, p53, and cyclin D1 was upregulated with histological progression. ipnb 22-26 H3 histone pseudogene 16 Homo sapiens 53-56 19233506-0 2009 Decitabine, differently from DNMT1 silencing, exerts its antiproliferative activity through p21 upregulation in malignant pleural mesothelioma (MPM) cells. Decitabine 0-10 H3 histone pseudogene 16 Homo sapiens 92-95 19233506-7 2009 Interestingly, both strategies substantially decrease cell survival of MPM cells but the antitumor activity of Decitabine, differently from DNMT1 silencing, is mediated, at least in part, by a p53-independent p21 upregulation, and is characterized by the arrest of MPM cells at the G2/M phase of the cell cycle. Decitabine 111-121 H3 histone pseudogene 16 Homo sapiens 209-212 19806015-0 2009 Nrf2 and p21 regulate the fine balance between life and death by controlling ROS levels. ros 77-80 H3 histone pseudogene 16 Homo sapiens 9-12 19669889-4 2009 Our results showed that EGCG treatment caused cell proliferation inhibition during I/R injury, and this effect was associated with increased p27 and p21 levels and reduced cyclin D1 level. epigallocatechin gallate 24-28 H3 histone pseudogene 16 Homo sapiens 149-152 19620837-7 2009 Our present data suggested that after long-term exposure to gefitinib, the survival of PC-9-ZD cells with heightened levels of p-Akt and reduced levels of p21 resisted further gefitinib-induced inhibition of cell growth. Gefitinib 60-69 H3 histone pseudogene 16 Homo sapiens 155-158 19620837-7 2009 Our present data suggested that after long-term exposure to gefitinib, the survival of PC-9-ZD cells with heightened levels of p-Akt and reduced levels of p21 resisted further gefitinib-induced inhibition of cell growth. Gefitinib 176-185 H3 histone pseudogene 16 Homo sapiens 155-158 19620837-9 2009 TNF-alpha treatment induced an elevated activated NFkappaB/p65, concomitant with induced p21 levels, which resulted in increased sensitivity to gefitinib in PC-9-ZD cells. Gefitinib 144-153 H3 histone pseudogene 16 Homo sapiens 89-92 19620837-10 2009 Consistent with our earlier observation that p21 is induced in an NFkappaB/p65-dependent manner, we conclude that p21 plays an important role in mediating cell growth inhibition by gefitinib. Gefitinib 181-190 H3 histone pseudogene 16 Homo sapiens 45-48 19846942-5 2009 Doxycycline consistently activated transcription of p53, p21 and Fas/FasL-cascade-related genes, while reducing the expression of Bcl-xL and Mcl-1. Doxycycline 0-11 H3 histone pseudogene 16 Homo sapiens 57-60 19620837-10 2009 Consistent with our earlier observation that p21 is induced in an NFkappaB/p65-dependent manner, we conclude that p21 plays an important role in mediating cell growth inhibition by gefitinib. Gefitinib 181-190 H3 histone pseudogene 16 Homo sapiens 114-117 19724892-6 2009 In HL-60 cells 50% proliferation inhibition was achieved by 1.7 microg dichloromethane extract/ml medium and correlated with the activation of Chk2, down-regulation of Cdc25A, suppression of cyclin D1 level, and transient induction of p21. Methylene Chloride 71-86 H3 histone pseudogene 16 Homo sapiens 235-238 19478553-4 2009 Treatment of synchronized leukemia cells with varying concentrations of SP600125 results in significant G2/M cell cycle arrest with elevated p21 levels, phosphorylation of histone H3 within 24 h, and endoreduplication with elevated Cdk2 protein levels after 48 h. SP600125 also induces significant abnormal microtubule dynamics in vivo. pyrazolanthrone 72-80 H3 histone pseudogene 16 Homo sapiens 141-144 19840446-0 2009 [Effect of tetrandrine combined with daunorubicin on expressions of P21 and P-gp in K562/A02 cells]. tetrandrine 11-22 H3 histone pseudogene 16 Homo sapiens 68-71 19840446-0 2009 [Effect of tetrandrine combined with daunorubicin on expressions of P21 and P-gp in K562/A02 cells]. Daunorubicin 37-49 H3 histone pseudogene 16 Homo sapiens 68-71 19840446-1 2009 This study was aimed to investigate the reversal effect of Tetrandrine (TET) combined with daunorubicin (DNR) on multidrug resistance (MDR) of K562/A02 cells and its relation to P21, P-gp and their genes so as to provide the new theoretic evidence for clinical use of TET. tetrandrine 59-70 H3 histone pseudogene 16 Homo sapiens 178-181 19840446-1 2009 This study was aimed to investigate the reversal effect of Tetrandrine (TET) combined with daunorubicin (DNR) on multidrug resistance (MDR) of K562/A02 cells and its relation to P21, P-gp and their genes so as to provide the new theoretic evidence for clinical use of TET. tet 72-75 H3 histone pseudogene 16 Homo sapiens 178-181 19840446-4 2009 The results showed that the expression of P21 was enhanced along with increasing of TET concentration, the expression of P-gp was reduced along with increasing of TET concentration and expression of mdr-1 gene was almost not observed in K562 cells, but the high expression of mdr-1 gene was seen in K562/A02 cells, furthermore, the expression of mdr-1 gene in K562/A02 cells increasingly was reduced along with increasing of TET concentration. tet 84-87 H3 histone pseudogene 16 Homo sapiens 42-45 19840446-4 2009 The results showed that the expression of P21 was enhanced along with increasing of TET concentration, the expression of P-gp was reduced along with increasing of TET concentration and expression of mdr-1 gene was almost not observed in K562 cells, but the high expression of mdr-1 gene was seen in K562/A02 cells, furthermore, the expression of mdr-1 gene in K562/A02 cells increasingly was reduced along with increasing of TET concentration. tet 163-166 H3 histone pseudogene 16 Homo sapiens 42-45 19840446-4 2009 The results showed that the expression of P21 was enhanced along with increasing of TET concentration, the expression of P-gp was reduced along with increasing of TET concentration and expression of mdr-1 gene was almost not observed in K562 cells, but the high expression of mdr-1 gene was seen in K562/A02 cells, furthermore, the expression of mdr-1 gene in K562/A02 cells increasingly was reduced along with increasing of TET concentration. tet 163-166 H3 histone pseudogene 16 Homo sapiens 42-45 19840446-5 2009 It is concluded that the TET possesses the reversal effect on multiple drug resistance of K562/A02 cells with concentration dependence, the reversal effect of TET may be related to up-regulation of P21 expression and down-regulation of P-gp and mdr-1 gene expressions in K562/A02 cells. tet 25-28 H3 histone pseudogene 16 Homo sapiens 198-201 19840446-5 2009 It is concluded that the TET possesses the reversal effect on multiple drug resistance of K562/A02 cells with concentration dependence, the reversal effect of TET may be related to up-regulation of P21 expression and down-regulation of P-gp and mdr-1 gene expressions in K562/A02 cells. tet 159-162 H3 histone pseudogene 16 Homo sapiens 198-201 20055131-0 2009 [Effect of p21-targeted shRNA on curcumin-induced apoptosis of human hepatoma Huh7 cells]. Curcumin 33-41 H3 histone pseudogene 16 Homo sapiens 11-14 20055131-1 2009 In the present study, shRNA plasmid of pSi-p21 targeting p21 mRNA was constructed and the effect of p21 shRNA on curcumin-induced apoptosis of human hepatoma Huh7 cells was investigated. Curcumin 113-121 H3 histone pseudogene 16 Homo sapiens 57-60 20055131-1 2009 In the present study, shRNA plasmid of pSi-p21 targeting p21 mRNA was constructed and the effect of p21 shRNA on curcumin-induced apoptosis of human hepatoma Huh7 cells was investigated. Curcumin 113-121 H3 histone pseudogene 16 Homo sapiens 57-60 20055131-2 2009 The effect of curcumin on the expression of p21 mRNA and protein and the silence efficiency of pSi-p21 were detected with RT-PCR and Western blotting. Curcumin 14-22 H3 histone pseudogene 16 Homo sapiens 44-47 20055131-3 2009 The effect of pSi-p21 on curcumin-induced apoptosis of Huh7 cells was evaluated with DAPI staining. Curcumin 25-33 H3 histone pseudogene 16 Homo sapiens 18-21 20055131-4 2009 The results showed that curcumin significantly upregulated p21 mRNA and protein expression, which was knocked down by pSi-p21 of Huh7 cells. Curcumin 24-32 H3 histone pseudogene 16 Homo sapiens 59-62 20055131-4 2009 The results showed that curcumin significantly upregulated p21 mRNA and protein expression, which was knocked down by pSi-p21 of Huh7 cells. Curcumin 24-32 H3 histone pseudogene 16 Homo sapiens 122-125 20055131-5 2009 DAPI staining results showed that pSi-p21 significantly decreased curcumin-induced apoptosis of Huh7 cells. DAPI 0-4 H3 histone pseudogene 16 Homo sapiens 38-41 20055131-5 2009 DAPI staining results showed that pSi-p21 significantly decreased curcumin-induced apoptosis of Huh7 cells. Curcumin 66-74 H3 histone pseudogene 16 Homo sapiens 38-41 20055131-6 2009 The data suggested that curcumin induced apoptosis of Huh7 cells via upregulation of p21 expression. Curcumin 24-32 H3 histone pseudogene 16 Homo sapiens 85-88 19777612-10 2009 CIE arrested the cell cycle in the S phase by increasing P21 and decreasing CDK4 protein expression. chlorimuron ethyl 0-3 H3 histone pseudogene 16 Homo sapiens 57-60 19638619-4 2009 DZNep treatment induced p16, p21, p27, and FBXO32 while depleting cyclin E and HOXA9 levels. 3-deazaneplanocin 0-5 H3 histone pseudogene 16 Homo sapiens 29-32 19477940-0 2009 Fibroblast growth factor 2 reactivates G1 checkpoint in SK-N-MC cells via regulation of p21, inhibitor of differentiation genes (Id1-3), and epithelium-mesenchyme transition-like events. sk-n-mc 56-63 H3 histone pseudogene 16 Homo sapiens 88-91 19450571-7 2009 We further investigated the effects of panaxydol on the expression of Id-1, Id-2, p21 and pRb by RT-PCR or immunoblotting analysis. panaxydol 39-48 H3 histone pseudogene 16 Homo sapiens 82-85 19450571-12 2009 Furthermore, panaxydol increased the mRNA content of p21 while reducing that of Id-1 and Id-2. panaxydol 13-22 H3 histone pseudogene 16 Homo sapiens 53-56 19450571-13 2009 Panaxydol also increased the protein levels of p21, pRb and the hypophosphorylated pRb in a dose-dependent manner. panaxydol 0-9 H3 histone pseudogene 16 Homo sapiens 47-50 19639184-3 2009 This MLH1-deficient subline selected for TSA resistance by stepwise exposures to increasing TSA concentrations exhibited failure in the accumulation of acetylated histones, in p21 induction, and in apoptosis activation. trichostatin A 92-95 H3 histone pseudogene 16 Homo sapiens 176-179 19553104-4 2009 At a low concentration SAHA decreases Ki-67 and cyclin A positive cells and increases p21 positive cells in the outer layer while it induces a ROS-dependent apoptosis in the central zone of the spheroid. Vorinostat 23-27 H3 histone pseudogene 16 Homo sapiens 86-89 19553104-5 2009 Coimmunostaining of p21 and apoptotic cells confirms that SAHA effects are different depending on the position of the cells within the spheroid. Vorinostat 58-62 H3 histone pseudogene 16 Homo sapiens 20-23 19706164-10 2009 Celecoxib induced G1-phase cell cycle arrest, accompanied with p21 activation in U87MG cells. Celecoxib 0-9 H3 histone pseudogene 16 Homo sapiens 63-66 19830854-6 2009 RESULT: The growth of RPMI 8226 cells was suppressed in a dose-dependent manner after treatment with BBM(P<0.05), and its IC(50) value was 3.83 microg/ml at 48 h. Both DNA ladder and FCM results showed that BBM induced apoptosis of RPMI 8226 cells with concomitant increase of activated p53, p21 and GADD45gamma mRNA. berbamine 101-104 H3 histone pseudogene 16 Homo sapiens 295-298 19662644-10 2009 In p53 positive Hep G2 cells, EGCG blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression. epigallocatechin gallate 30-34 H3 histone pseudogene 16 Homo sapiens 138-141 19157955-5 2009 Western blot analyses demonstrated that the expression of p21 protein was remarkably augmented and hyperacetylation of p53 was induced after SAHA treatment. Vorinostat 141-145 H3 histone pseudogene 16 Homo sapiens 58-61 19654295-10 2009 Both bax and p21, however, were required for zerumbone to stimulate TRAIL-induced apoptosis. zerumbone 45-54 H3 histone pseudogene 16 Homo sapiens 13-16 19667188-4 2009 We analyzed plasma plant sterol (PPS) levels, a surrogate measure of cholesterol absorption from the intestine, where previous studies have implicated 2p21 mutations in the ATP binding cassette subfamily G members 5 or 8 (ABCG5 or ABCG8) genes. Sterols 25-31 H3 histone pseudogene 16 Homo sapiens 152-155 19667188-4 2009 We analyzed plasma plant sterol (PPS) levels, a surrogate measure of cholesterol absorption from the intestine, where previous studies have implicated 2p21 mutations in the ATP binding cassette subfamily G members 5 or 8 (ABCG5 or ABCG8) genes. pps 33-36 H3 histone pseudogene 16 Homo sapiens 152-155 19661301-6 2009 Cytotoxicity in cell lines that differed in intrinsic sensitivity to bortezomib correlated with sustained inhibition of proteasome activity, survivin expression and induction of p21 expression. Bortezomib 69-79 H3 histone pseudogene 16 Homo sapiens 178-181 19672316-4 2009 Here, we report that Siomycin A and thiostrepton stabilize the expression of a variety of proteins, such as p21, Mcl-1, p53 and hdm-2 and also act as proteasome inhibitors in vitro. siomycin A 21-31 H3 histone pseudogene 16 Homo sapiens 108-111 19672316-4 2009 Here, we report that Siomycin A and thiostrepton stabilize the expression of a variety of proteins, such as p21, Mcl-1, p53 and hdm-2 and also act as proteasome inhibitors in vitro. Thiostrepton 36-48 H3 histone pseudogene 16 Homo sapiens 108-111 19491661-11 2009 In conclusion, YSL significantly inhibited the growth of human hepatocellular carcinoma BEL-7402 cells and its anti-tumor effects may result from the upregulation of cyclin P21 and P27, and downregulation of cyclin PCNA. H-Tyr-Ser-Leu-OH 15-18 H3 histone pseudogene 16 Homo sapiens 173-176 19723072-5 2009 Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites. Phenylbutyrates 52-67 H3 histone pseudogene 16 Homo sapiens 148-151 19723072-5 2009 Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites. Tretinoin 94-96 H3 histone pseudogene 16 Homo sapiens 148-151 19723072-5 2009 Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites. Niacinamide 101-111 H3 histone pseudogene 16 Homo sapiens 148-151 19515559-4 2009 The MTT correlates with clonogenic assays and most importantly compound 10 down regulates hypoxia induces genes (HIF-1alpha, P21 and VEGF) appropriately. monooxyethylene trimethylolpropane tristearate 4-7 H3 histone pseudogene 16 Homo sapiens 125-128 19586014-7 2009 In the second example, the room-temperature structure is determined to be K(4)Cd(3)(SO(4))(5) x 3 H(2)O, crystallizing in a monoclinic space group, P2(1)/n. k(4)cd(3) 74-83 H3 histone pseudogene 16 Homo sapiens 148-153 19193378-10 2009 Furthermore, mRNA expression of p21 was downregulated in a dose dependent manner, suggesting that growth inductive effects of telmisartan might be regulated by the PI3K/Akt and p21 signaling pathway. Telmisartan 126-137 H3 histone pseudogene 16 Homo sapiens 32-35 19193378-10 2009 Furthermore, mRNA expression of p21 was downregulated in a dose dependent manner, suggesting that growth inductive effects of telmisartan might be regulated by the PI3K/Akt and p21 signaling pathway. Telmisartan 126-137 H3 histone pseudogene 16 Homo sapiens 177-180 19402126-4 2009 As with other human cancer cell lines, LBH589 causes up-regulation of p21, G2/M cell cycle arrest, and cell death of human HNSCC cell lines, as measured using flow cytometry and cDNA microarrays. Panobinostat 39-45 H3 histone pseudogene 16 Homo sapiens 70-73 19220580-5 2009 Sorafenib-induced growth suppression and apoptosis were associated with inhibition of angiogenesis, down-regulation of phospho-platelet-derived growth factor receptor beta Tyr1021, phospho-eIF4E Ser209, phospho-c-Raf Ser259, c-Raf, Mcl-1, Bcl-2, Bcl-x and positive cell cycle regulators, up-regulation of apoptosis signalling kinase-1, p27 and p21. Sorafenib 0-9 H3 histone pseudogene 16 Homo sapiens 344-347 18657224-8 2009 In vivo, VPA significantly inhibited the growth of Caki-1 in subcutaneous xenografts, accompanied by a strong accumulation of p21 and bax in tissue specimens of VPA-treated animals. Valproic Acid 9-12 H3 histone pseudogene 16 Homo sapiens 126-129 19559722-6 2009 Differential expression of BRCA1, cyclin B1, pRb and p21 in U-2 OS and A549 cells indicates that resveratrol can engage various molecular mechanisms to arrest cell cycle progression. Resveratrol 97-108 H3 histone pseudogene 16 Homo sapiens 53-56 19507186-8 2009 Radiosensitization was achieved with a substantial elevation of cleaved PARP-1 in DETANONOate-HT-29-treated versus control cells, which was accompanied by elevation of p21, p27, and BAX, and a concomitant decrease in Bcl-2. 2,2'-(hydroxynitrosohydrazono)bis-ethanamine 82-93 H3 histone pseudogene 16 Homo sapiens 168-171 19581590-7 2009 Here, we show that shorter-tailed Ubs, such as UBB(+1), bind to the proteasome but because they cannot be efficiently degraded, they inhibit the degradation of other Ub system"s substrates such as Myc, p21, Mdm2, and MyoD. N-[(S)-({[(Benzyloxy)carbonyl]amino}methyl)(Hydroxy)phosphoryl]-L-Leucyl-L-Valine 34-37 H3 histone pseudogene 16 Homo sapiens 202-205 19125423-2 2009 CDODA-Me also induced p21 and p27 protein expression and downregulates cyclin D1; however, these responses were receptor-independent. methyl 2-cyano-3,11-dioxo-18beta-olean-1,12-dien-30-oate 0-8 H3 histone pseudogene 16 Homo sapiens 22-25 19638451-6 2009 Molecular analyses for cell cycle regulators showed that silibinin decreases the level of cyclins (D1, D3, A and B1) and cyclin-dependent kinases (1, 2, 4, and 6) and increases the level of cyclin-dependent kinase inhibitors (p21 and p27). Silybin 57-66 H3 histone pseudogene 16 Homo sapiens 226-229 19610135-10 2009 Recently, a pre-clinical study demonstrated that a less calcemic analog of 1alpha,25(OH)(2)D(3), 19-nor-1alpha,25(OH)(2)D(2) (Paricalcitol), is effective in inhibiting tumor growth in vitro and in vivo, via upregulation of p21 and p27 tumor suppressor genes. paricalcitol 126-138 H3 histone pseudogene 16 Homo sapiens 223-226 21828487-1 2009 Molecular dynamics (MD) simulation of calcium carbonate at high pressure was performed to understand the phase transition between calcite [Formula: see text] and CaCO(3)-II (P 2(1)/c). Calcium Carbonate 38-55 H3 histone pseudogene 16 Homo sapiens 174-180 21828487-7 2009 It can be suggested that the existence of the P 2(1)/c structure and the switching of its orientation just below the transition pressure are responsible for the change of the slope of the dP/dT curve at the boundary from negative to positive on an increase of temperature, because the switching increases entropy and results in an expansion of the stability field of calcite. Thymidine 191-193 H3 histone pseudogene 16 Homo sapiens 46-52 19497413-8 2009 Although both compounds are weakly but equally effective inhibitors of iNOS protein expression and activity, only Se-PBIT significantly enhanced the levels of p53, p38, p27 and p21 protein expression, reduced levels of phospholipase A2 (PLA2) but had no effect on cyclooxygenase-2 (COX-2) protein levels; such molecular targets are involved in cell growth inhibition, induction of apoptosis and cell cycle regulation. se-pbit 114-121 H3 histone pseudogene 16 Homo sapiens 177-180 21828487-7 2009 It can be suggested that the existence of the P 2(1)/c structure and the switching of its orientation just below the transition pressure are responsible for the change of the slope of the dP/dT curve at the boundary from negative to positive on an increase of temperature, because the switching increases entropy and results in an expansion of the stability field of calcite. dp 188-190 H3 histone pseudogene 16 Homo sapiens 46-52 19440035-7 2009 Treatment of MCL cells with vorinostat or 17-DMAG was associated with the inductionof p21 and p27, as well as with depletion of c-Myc, c-RAF, AKT and CDK4. Vorinostat 28-38 H3 histone pseudogene 16 Homo sapiens 86-89 19440035-7 2009 Treatment of MCL cells with vorinostat or 17-DMAG was associated with the inductionof p21 and p27, as well as with depletion of c-Myc, c-RAF, AKT and CDK4. 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin 42-49 H3 histone pseudogene 16 Homo sapiens 86-89 19557639-0 2009 Function of retinoid acid receptor alpha and p21 in all-trans-retinoic acid-induced acute T-lymphoblastic leukemia apoptosis. 2-octenal 56-62 H3 histone pseudogene 16 Homo sapiens 45-48 19513541-6 2009 Furthermore, p53, the tumor suppressor which transcriptionally regulates p21, was also upregulated with PI-103 treatment. PI103 104-110 H3 histone pseudogene 16 Homo sapiens 73-76 19233470-5 2009 It is shown that depsipeptide is effective at submicromolar concentrations and acts mainly by apoptosis induction, upregulation of p21 and cell cycle inhibition in G2/M. Depsipeptides 17-29 H3 histone pseudogene 16 Homo sapiens 131-134 19557639-0 2009 Function of retinoid acid receptor alpha and p21 in all-trans-retinoic acid-induced acute T-lymphoblastic leukemia apoptosis. Tretinoin 62-75 H3 histone pseudogene 16 Homo sapiens 45-48 19557639-7 2009 Consequently, it has been shown that, in RA-treated Molt3 cells, upregulation of p21 due to RA accompanies caspase 3/PARP activation which precedes the occurrence of apoptosis. Tretinoin 41-43 H3 histone pseudogene 16 Homo sapiens 81-84 19557639-7 2009 Consequently, it has been shown that, in RA-treated Molt3 cells, upregulation of p21 due to RA accompanies caspase 3/PARP activation which precedes the occurrence of apoptosis. Tretinoin 92-94 H3 histone pseudogene 16 Homo sapiens 81-84 19471117-3 2009 In human and rodent cell lines, rapamycin (an inhibitor of mTOR) dramatically decelerated loss of proliferative potential caused by ectopic p21, p16 and sodium butyrate-induced p21. Butyric Acid 153-168 H3 histone pseudogene 16 Homo sapiens 177-180 19584258-5 2009 Interactions of Nur77 with the p21 promoter in Panc1 cells treated with DIM-C-pPhOCH3 were also confirmed in chromatin immunoprecipitation assays. DIM-C-pPhOCH3 72-85 H3 histone pseudogene 16 Homo sapiens 31-34 19528459-4 2009 Moreover, activation of p53, p53-dependent expression of p21 and p21-dependent senescence were observed in sigma-KO, but not parental cells after a treatment with a low cisplatin dose. Cisplatin 169-178 H3 histone pseudogene 16 Homo sapiens 57-60 19509159-10 2009 Mixed tocopherols increased the expression of p21, p27, caspase-3, and peroxisome proliferator activated receptor-gamma, and inhibited AKT and estrogen signaling in mammary tumors. Tocopherols 6-17 H3 histone pseudogene 16 Homo sapiens 46-49 19528459-4 2009 Moreover, activation of p53, p53-dependent expression of p21 and p21-dependent senescence were observed in sigma-KO, but not parental cells after a treatment with a low cisplatin dose. Cisplatin 169-178 H3 histone pseudogene 16 Homo sapiens 65-68 19528459-5 2009 CONCLUSION: A 14-3-3sigma-dependent mechanism inhibits p53 activation in parental cells treated with a low cisplatin dose, thereby blocking p21 expression that is essential for senescence and consequently conferring to the parental cells a significant degree of resistance to cisplatin. Cisplatin 107-116 H3 histone pseudogene 16 Homo sapiens 140-143 19528459-5 2009 CONCLUSION: A 14-3-3sigma-dependent mechanism inhibits p53 activation in parental cells treated with a low cisplatin dose, thereby blocking p21 expression that is essential for senescence and consequently conferring to the parental cells a significant degree of resistance to cisplatin. Cisplatin 276-285 H3 histone pseudogene 16 Homo sapiens 140-143 19383849-3 2009 DHE suppresses the expression of cyclin D, cyclin A, cyclin-dependent kinase 2, and cdc25A and increases the amount of p53 and p21, resulting in G(0)/G(1)-S phase arrest in MCF-7 cells. dehydrocostus lactone 0-3 H3 histone pseudogene 16 Homo sapiens 127-130 19505915-0 2009 Association of genetic polymorphisms, mRNA expression of p53 and p21 with chronic benzene poisoning in a chinese occupational population. Benzene 82-89 H3 histone pseudogene 16 Homo sapiens 65-68 19627195-6 2009 Exposure of young HDFs to H(2)O(2) induced G2/M cell cycle arrest, positive senescence-associated (SA) beta-galactosidase (beta-gal) staining, and elevated p53, p21, and p16 protein levels. Hydrogen Peroxide 26-34 H3 histone pseudogene 16 Homo sapiens 161-164 19627195-7 2009 However, cotreatment with dropwort or Sedum ethanol extract significantly lowered p53, p21, and p16 levels and intracellular reactive oxygen species levels and attenuated the cell cycle arrest compared with H(2)O(2)-alone treatment. Ethanol 44-51 H3 histone pseudogene 16 Homo sapiens 87-90 19627195-10 2009 In conclusion, dropwort showed a potential anti-senescence activity in H(2)O(2)-treated HDFs, which might be mediated by reducing p16, p21, and p53 levels and oxidative stress. Hydrogen Peroxide 71-79 H3 histone pseudogene 16 Homo sapiens 135-138 19332559-6 2009 Phosphorylation at Thr18 enhances p53-dependent activation of not only p21 but also Lats2, two mediators of the postmitotic checkpoint. UNII-PYZ33YLR8A 19-24 H3 histone pseudogene 16 Homo sapiens 71-74 19624872-12 2009 Cleaved PARP appeared, along with an increased protein level of P21 and a decrease of survivin and CDK4 levels in U266 cells treated with MS-275. entinostat 138-144 H3 histone pseudogene 16 Homo sapiens 64-67 19289106-5 2009 Suppression of macroautophagy by bafilomycin A(1) induced G(0)/G(1) cell cycle arrest and apoptosis which were accompanied by the down-regulation of cyclin D(1) and cyclin E, the up-regulation of p21(Cip1) as well as cleavages of caspases-3, -7, -8, and -9 and PARP. bafilomycin A 33-46 H3 histone pseudogene 16 Homo sapiens 196-199 19127598-9 2009 In PCa patients ingesting isoflavones, we observed significant decreases in prostate COX-2 mRNA and increases in p21 mRNA. Isoflavones 26-37 H3 histone pseudogene 16 Homo sapiens 113-116 19127598-10 2009 There were significant correlations between COX-2 mRNA suppression, p21 mRNA stimulation and serum isoflavone levels. Isoflavones 99-109 H3 histone pseudogene 16 Homo sapiens 68-71 19177142-4 2009 Induction of cell-cycle arrest by ciglitazone is associated with changes in expression of key cell-cycle regulators such as p21, cyclin D1, and pRB hypophosphorylation. ciglitazone 34-45 H3 histone pseudogene 16 Homo sapiens 124-127 19505915-3 2009 To investigate whether benzene exposure may influence mRNA expression of p53 and p21 in benzene-exposed workers, we also chose 39 CBP workers, 38 occupationally benzene-exposure workers, and 37 nonexposure workers in the same region of China. Benzene 88-95 H3 histone pseudogene 16 Homo sapiens 81-84 19505915-3 2009 To investigate whether benzene exposure may influence mRNA expression of p53 and p21 in benzene-exposed workers, we also chose 39 CBP workers, 38 occupationally benzene-exposure workers, and 37 nonexposure workers in the same region of China. Benzene 88-95 H3 histone pseudogene 16 Homo sapiens 81-84 19550397-6 2009 Both doxorubicin- and cisplatin-resistant cells are characterized by the changes in the expression of several cell cycle regulators -- Ki-67, cyclin D1, pRb and p21). Doxorubicin 5-16 H3 histone pseudogene 16 Homo sapiens 161-164 19550397-6 2009 Both doxorubicin- and cisplatin-resistant cells are characterized by the changes in the expression of several cell cycle regulators -- Ki-67, cyclin D1, pRb and p21). Cisplatin 22-31 H3 histone pseudogene 16 Homo sapiens 161-164 19726333-10 2009 PTEN overexpression can efficiently inhibit the proliferation of HASMCs possibly through the PI3K/PKB/AKt and P21 pathways. hasmcs 65-71 H3 histone pseudogene 16 Homo sapiens 110-113 19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 29-42 H3 histone pseudogene 16 Homo sapiens 183-186 19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 44-46 H3 histone pseudogene 16 Homo sapiens 183-186 19951532-13 2009 The expression level of P21 was up-regulated after the NB4 cells treated with As2O3. Arsenic Trioxide 78-83 H3 histone pseudogene 16 Homo sapiens 24-27 19951532-16 2009 P21 is up-regulated after arsenic trioxide activated the JAK1 to inhibit the proliferation of NB4 cells. Arsenic Trioxide 26-42 H3 histone pseudogene 16 Homo sapiens 0-3 19323979-5 2009 Treatment of HUVEC with ATN-224 caused increased superoxide levels, phospho-ERK signalling, nuclear NRF1 expression, HO-1 expression and induction of the anti-apoptotic proteins P21, BCL2 and BCLXL. tetrathiomolybdate 24-31 H3 histone pseudogene 16 Homo sapiens 178-181 19383849-4 2009 In contrast, DHE caused S-G(2)/M arrest by increasing p21 expression and chk1 activation and inhibiting cyclin A, cyclin B, cdc25A, and cdc25C expression in MDA-MB-231 cells. dehydrocostus lactone 13-16 H3 histone pseudogene 16 Homo sapiens 54-57 19336515-10 2009 Further, Twist1 reduction in Adriamycin-treated cells promoted p53-dependent p21 induction and disrupted the association of p53 with Mdm2. Doxorubicin 29-39 H3 histone pseudogene 16 Homo sapiens 77-80 19475715-6 2009 In contrast, treatment with N-acetyl cysteine (NAC) can prevent cell cycle arrest and p21 up-regulation at early hours. Acetylcysteine 28-45 H3 histone pseudogene 16 Homo sapiens 86-89 19475715-6 2009 In contrast, treatment with N-acetyl cysteine (NAC) can prevent cell cycle arrest and p21 up-regulation at early hours. Acetylcysteine 47-50 H3 histone pseudogene 16 Homo sapiens 86-89 19288022-9 2009 Our results show that one molecular mechanism of curcumin inhibits the proliferation of MDA-MB-231 cells either through up-regulating p21 expression and then inducing apoptosis, or through up-regulating the Bax to Bcl-2 ratio and then inducing apoptosis. Curcumin 49-57 H3 histone pseudogene 16 Homo sapiens 134-137 19281788-3 2009 Treatment of AGS cells with eupatilin induced cell cycle arrest at the G(1) phase with the concomitant induction of p21(cip1), a cell cycle inhibitor. eupatilin 28-37 H3 histone pseudogene 16 Homo sapiens 116-119 19281788-9 2009 Blockade of ERK signaling by PD098059 or the dominant-negative ERK2 significantly reduced eupatilin-induced TFF1 and p21 expression as well as ZO-1 redistribution, indicating that ERK cascades may mediate eupatilin-induced AGS cell differentiation. eupatilin 90-99 H3 histone pseudogene 16 Homo sapiens 117-120 19505399-10 2009 Signaling through alpha7 and alpha3 nAChRs also significantly (p<0.05) altered expression of the cell state regulators p21 and Bcl-2, respectively, suggesting that downregulation of inflammation via nAChRs includes effects on the T cell cycle progression and apoptosis. nachrs 36-42 H3 histone pseudogene 16 Homo sapiens 122-125 19288022-8 2009 Curcumin increased the protein expressions of p21 and Bax, but decreased the protein expression of p53 and Bcl-2 in MDA-MB-231 cells. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 46-49 19139269-4 2009 Exposure to capsaicin or DHC caused induction of p53, p21, and G(0)/G(1) arrest. Capsaicin 12-21 H3 histone pseudogene 16 Homo sapiens 54-57 19139269-4 2009 Exposure to capsaicin or DHC caused induction of p53, p21, and G(0)/G(1) arrest. dihydrocapsaicin 25-28 H3 histone pseudogene 16 Homo sapiens 54-57 19344784-5 2009 Pretreatment of host cells with P21-His(6) inhibited cell invasion by extracellular amastigotes from G and CL strains. Histidine 36-39 H3 histone pseudogene 16 Homo sapiens 32-35 19468318-6 2009 Pretreatment with nitric oxide (NO) scavengers inhibited apoptotic biochemical changes induced by 5 microM MG/15 mM glucose, and increased the gene expression levels of p53 and p21 involved in apoptotic signaling. Nitric Oxide 18-30 H3 histone pseudogene 16 Homo sapiens 177-180 19468318-6 2009 Pretreatment with nitric oxide (NO) scavengers inhibited apoptotic biochemical changes induced by 5 microM MG/15 mM glucose, and increased the gene expression levels of p53 and p21 involved in apoptotic signaling. Glucose 116-123 H3 histone pseudogene 16 Homo sapiens 177-180 19124833-0 2009 p21-activated kinase regulates mast cell degranulation via effects on calcium mobilization and cytoskeletal dynamics. Calcium 70-77 H3 histone pseudogene 16 Homo sapiens 0-3 19161984-0 2009 p21 functions in a post-mitotic block checkpoint in the apoptotic response to vinblastine. Vinblastine 78-89 H3 histone pseudogene 16 Homo sapiens 0-3 19276356-1 2009 p21 loss has been implicated in conferring oncogenic activity to known tumor suppressor gene KLF4 and cancer drug tamoxifen. Tamoxifen 114-123 H3 histone pseudogene 16 Homo sapiens 0-3 19161984-1 2009 We have shown previously that in KB-3 (HeLa) cells vinblastine causes downregulation of the CDK inhibitor p21 through a c-Jun regulated pathway. Vinblastine 51-62 H3 histone pseudogene 16 Homo sapiens 106-109 19161984-4 2009 Moreover, p21 null HCT116 cells were more prone to vinblastine-induced apoptosis relative to wild-type cells. Vinblastine 51-62 H3 histone pseudogene 16 Homo sapiens 10-13 19266600-8 2009 Furthermore, DHA down- regulated mRNA of bcl-2 and up-regulated p21. Docosahexaenoic Acids 13-16 H3 histone pseudogene 16 Homo sapiens 64-67 19161984-5 2009 The results provide support for a model whereby p21 downregulation promotes vinblastine-induced apoptosis by alleviating its protective function following mitotic arrest. Vinblastine 76-87 H3 histone pseudogene 16 Homo sapiens 48-51 19067706-13 2009 We further found that bexarotene activates p53 by phosphorylation at Ser15, which influences the binding of p53 to promoters for cell cycle arrest, induces p73 upregulation, and, in concordance, also modulates some p53/p73 downstream target genes, such as p21, Bax, survivin and cdc2. Bexarotene 22-32 H3 histone pseudogene 16 Homo sapiens 256-259 19245907-9 2009 Importantly, TTY inhibited carcinoid cellular growth and induced the cell-cycle inhibitors p21 and p27. tautomycin 13-16 H3 histone pseudogene 16 Homo sapiens 91-94 18949013-8 2009 After treatment with TSA, expression of the cell cycle kinase inhibitor p21 was upregulated and the cell cycle was arrested at G1. trichostatin A 21-24 H3 histone pseudogene 16 Homo sapiens 72-75 18575867-4 2009 The H69 cells and resistant cell lines have a p53 mutation and consequently decrease expression of p21 in response to platinum drug treatment, promoting progression of the cell cycle instead of increasing p21 to maintain the arrest. Platinum 118-126 H3 histone pseudogene 16 Homo sapiens 99-102 19038232-5 2009 Genistein stimulates p21(waf1/cip1) and cyclin B1 expression, phosphorylation/activation of ATM and Chk2 kinases, and Tyr15-phosphorylation/inactivation of Cdc2 (Cdk1) kinase, and these effects are attenuated by MEK/ERK inhibitors, while LY294002 also attenuates ERK and ATM phosphorylation. Genistein 0-9 H3 histone pseudogene 16 Homo sapiens 21-24 19221487-1 2009 Human myeloid leukemia cells exposed to 1,25-dihydroxyvitamin D(3) (1,25D), a major cancer chemopreventive agent, acquire features of normal monocytes and arrest in the G(1) phase of the cell cycle, due to the upregulation of p27(Kip1) and p21(Cip1), but the mechanism is not clear. Calcitriol 40-66 H3 histone pseudogene 16 Homo sapiens 240-243 19196987-6 2009 Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle. Serine 17-20 H3 histone pseudogene 16 Homo sapiens 229-232 19196987-6 2009 Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle. Alanine 43-51 H3 histone pseudogene 16 Homo sapiens 229-232 19059205-3 2009 In this work, DU-145 cells were used to demonstrate that SPBE and its sterol components, beta-sitosterol and stigmasterol, inhibit prostate cancer growth by increasing p53 protein expression and also inhibit carcinoma development by decreasing p21 and p27 protein expression. gamma-sitosterol 89-104 H3 histone pseudogene 16 Homo sapiens 244-247 19059205-3 2009 In this work, DU-145 cells were used to demonstrate that SPBE and its sterol components, beta-sitosterol and stigmasterol, inhibit prostate cancer growth by increasing p53 protein expression and also inhibit carcinoma development by decreasing p21 and p27 protein expression. Stigmasterol 109-121 H3 histone pseudogene 16 Homo sapiens 244-247 18929442-6 2009 Western Blot showed that SN-38 down-regulated protein expression of p-Akt and increased protein expression of p53 and p21, but it had no effects on protein expression of Bax, Bcl-2 and Akt. Irinotecan 25-30 H3 histone pseudogene 16 Homo sapiens 118-121 19127998-4 2009 The complexes, C32H54Ir2O4 and C32H54O4Rh2, are isostructural: monoclinic, P2(1)/n, Z = 4. c32h54ir2o4 15-26 H3 histone pseudogene 16 Homo sapiens 75-80 19127998-4 2009 The complexes, C32H54Ir2O4 and C32H54O4Rh2, are isostructural: monoclinic, P2(1)/n, Z = 4. c32h54o4rh2 31-42 H3 histone pseudogene 16 Homo sapiens 75-80 19308266-6 2009 In addition, Western blot analysis revealed that 1alpha,25(OH)(2)D(3) and menthol cooperatively modulate the expression of bcl-2 and p21 which provides the insight into the molecular mechanisms underlying the enhanced 1alpha,25(OH)(2)D(3)-mediated growth inhibition by menthol. Menthol 74-81 H3 histone pseudogene 16 Homo sapiens 133-136 19308266-6 2009 In addition, Western blot analysis revealed that 1alpha,25(OH)(2)D(3) and menthol cooperatively modulate the expression of bcl-2 and p21 which provides the insight into the molecular mechanisms underlying the enhanced 1alpha,25(OH)(2)D(3)-mediated growth inhibition by menthol. Menthol 269-276 H3 histone pseudogene 16 Homo sapiens 133-136 19259937-6 2009 S-phase arrest and expression of p21 could be inhibited by 7-hydroxystaurosporine, suggesting that the ataxia-telangiectasia and Rad-3-related-checkpoint kinase 1 (ATR-CHK1), and p21 pathways might play a role in the IR-mediated S-phase checkpoint in EC cells. 7-hydroxystaurosporine 59-81 H3 histone pseudogene 16 Homo sapiens 33-36 19259937-6 2009 S-phase arrest and expression of p21 could be inhibited by 7-hydroxystaurosporine, suggesting that the ataxia-telangiectasia and Rad-3-related-checkpoint kinase 1 (ATR-CHK1), and p21 pathways might play a role in the IR-mediated S-phase checkpoint in EC cells. 7-hydroxystaurosporine 59-81 H3 histone pseudogene 16 Homo sapiens 179-182 19105734-4 2009 The ion-separated tetraphosphenediide [Na(18-crown-6)(thf)2]2[t-Bu3SiPPPPSi-t-Bu3] was analyzed using X-ray crystallography (monoclinic, space group P2(1)/n). tetraphosphenediide 18-37 H3 histone pseudogene 16 Homo sapiens 149-154 19105734-4 2009 The ion-separated tetraphosphenediide [Na(18-crown-6)(thf)2]2[t-Bu3SiPPPPSi-t-Bu3] was analyzed using X-ray crystallography (monoclinic, space group P2(1)/n). na(18-crown-6)(thf)2]2[t-bu3sippppsi-t-bu3 39-81 H3 histone pseudogene 16 Homo sapiens 149-154 18398612-4 2009 RESULTS: Treatment of all cell types with VA resulted in a dose-dependent increase in histone H3 acetylation and p21 expression, as well as dose-dependent cytostasis. Valproic Acid 42-44 H3 histone pseudogene 16 Homo sapiens 113-116 18450412-8 2009 Indirubin-3-oxime-induced growth inhibition was associated with induction of Cdk inhibitor p21, inhibition of cyclin D1 and activation of caspase-3. indirubin-3'-monoxime 0-17 H3 histone pseudogene 16 Homo sapiens 91-94 19091346-18 2009 CONCLUSIONS: Finasteride administered 30 days before surgery appears to decrease the apoptotic factors caspase-7 and IGFBP-3 in cancer cells, while having little to no effect on caspase-3, insulin growth factor-1, bcl-2, p53 and p21. Finasteride 13-24 H3 histone pseudogene 16 Homo sapiens 229-232 19378559-3 2009 The compound {[FeO(HCOO)5(HCOO)3]2-.H2O.2(alpha-CH3NC5H5)}, (1) crystallizes in the monoclinic space group P2(1)/m with charge assisted hydrogen bonds linking the alpha-picolinium cations to the trinuclear groups. feo(hcoo)5(hcoo)3]2 15-34 H3 histone pseudogene 16 Homo sapiens 107-112 19140230-5 2009 On day 7, Western blotting was used to determine the effects of troglitazone and ciglitazone on the expression of p21 and phosphorylated-ERK (pERK) genes. Troglitazone 64-76 H3 histone pseudogene 16 Homo sapiens 114-117 19140230-5 2009 On day 7, Western blotting was used to determine the effects of troglitazone and ciglitazone on the expression of p21 and phosphorylated-ERK (pERK) genes. ciglitazone 81-92 H3 histone pseudogene 16 Homo sapiens 114-117 19140230-11 2009 When troglitazone and ciglitazone were administered to stomach cancer cells, levels of p21 expression were increased, but ERK phosphorylation levels were reduced. Troglitazone 5-17 H3 histone pseudogene 16 Homo sapiens 87-90 19140230-11 2009 When troglitazone and ciglitazone were administered to stomach cancer cells, levels of p21 expression were increased, but ERK phosphorylation levels were reduced. ciglitazone 22-33 H3 histone pseudogene 16 Homo sapiens 87-90 19003963-6 2009 The levels of p21 and p27 increased after treatment with doxorubicin or seliciclib alone or in combination, compared to untreated controls. Doxorubicin 57-68 H3 histone pseudogene 16 Homo sapiens 14-17 19738389-7 2009 Treatment with cyclopamine inhibited the proliferation and colony formation of ONB cells, induced ONB cell cycle arrest and apoptosis, and down-regulated the expression of Pacthed1, Gli1 and cyclin D1, but up-regulated p21 expression in vitro. cyclopamine 15-26 H3 histone pseudogene 16 Homo sapiens 219-222 19000652-5 2009 Analysis of the expression of breast cancer related genes indicated that EGFR, HER2, bcl-2, and COX-2 were significantly downregulated, while IFN-beta and p21 were remarkably upregulated by berberine. Berberine 190-199 H3 histone pseudogene 16 Homo sapiens 155-158 19072620-2 2009 Secnidazole crystallizes as a hemihydrate, which belongs to a monoclinic system having space group P2(1)/c, with a = 12.424 A, b = 12.187 A, c = 6.662 A, and beta = 100.9 degrees. secnidazole 0-11 H3 histone pseudogene 16 Homo sapiens 99-104 19821999-10 2009 Incubation of MDA-MB-231 cells with BU-32 results in the accumulation of cell cycle inhibitor proteins p21 and p27 and stabilization of the tumor suppressor protein p53. Busulfan 36-38 H3 histone pseudogene 16 Homo sapiens 103-106 19593673-6 2009 The molecular changes in both cell lines due to DOX treatment could be classified into: (1) the basal level of p53, p21, BRCA1, GST and TOPOIIalpha mRNA was higher in MCF7/DOX than MCF7/WT. Doxorubicin 48-51 H3 histone pseudogene 16 Homo sapiens 116-119 19009557-5 2009 Quercetin induced p21 CDK inhibitor with a concomitant decrease of phosphorylation of pRb, which inhibits the G(1)/S cell cycle progression by trapping E2F1. Quercetin 0-9 H3 histone pseudogene 16 Homo sapiens 18-21 19009557-6 2009 A low dose of quercetin induced mild DNA damage and Chk2 activation, which is the main regulator of p21 expression by quercetin. Quercetin 14-23 H3 histone pseudogene 16 Homo sapiens 100-103 19009557-6 2009 A low dose of quercetin induced mild DNA damage and Chk2 activation, which is the main regulator of p21 expression by quercetin. Quercetin 118-127 H3 histone pseudogene 16 Homo sapiens 100-103 19275612-3 2009 Immunoblot assay showed that chalcones significantly decreased the expression of cyclin Bl, cyclin A and Cdc2 protein, as well as increased the expression of p21 and p27 in a p53-independent manner, contributing to cell cycle arrest. Chalcones 29-38 H3 histone pseudogene 16 Homo sapiens 158-161 18649995-4 2008 Western blot analysis revealed that the protein level of p21 in HUVEC increased after DPTH-N10 treatment. 5,5-diphenyl-2-thiohydantoin-N10 86-94 H3 histone pseudogene 16 Homo sapiens 57-60 19020764-3 2008 Concomitant with G0/G1 arrest, HCT-116 cells treated with DPI resulted in strong and sustained upregulation of p53 and p21. diphenyleneiodonium 58-61 H3 histone pseudogene 16 Homo sapiens 119-122 19020764-4 2008 p53- or p21-deficient HCT-116 cells using a small interfering RNA (siRNA) significantly increased the progression into S phase by stimulation of DPI, compared with DPI alone. diphenyleneiodonium 145-148 H3 histone pseudogene 16 Homo sapiens 8-11 19020764-4 2008 p53- or p21-deficient HCT-116 cells using a small interfering RNA (siRNA) significantly increased the progression into S phase by stimulation of DPI, compared with DPI alone. diphenyleneiodonium 164-167 H3 histone pseudogene 16 Homo sapiens 8-11 19020764-5 2008 However, the silencing of p53 resulted in more efficient transition into S phase than the silencing of p21 siRNA and significantly inhibited p21 upregulation by DPI stimulation. diphenyleneiodonium 161-164 H3 histone pseudogene 16 Homo sapiens 103-106 19020764-5 2008 However, the silencing of p53 resulted in more efficient transition into S phase than the silencing of p21 siRNA and significantly inhibited p21 upregulation by DPI stimulation. diphenyleneiodonium 161-164 H3 histone pseudogene 16 Homo sapiens 141-144 19020764-6 2008 Interestingly, brief exposure to DPI did not change p53 expression, but showed transient upregulation of p21 and G0/G1 arrest. diphenyleneiodonium 33-36 H3 histone pseudogene 16 Homo sapiens 105-108 19020764-7 2008 These results suggest that p53 upregulation sustains G0/G1 cell cycle arrest and p21 upregulation by DPI stimulation in HCT-116 cells. diphenyleneiodonium 101-104 H3 histone pseudogene 16 Homo sapiens 81-84 19020764-8 2008 In HL-60 cells, DPI also induced p21 upregulation in a p53-independent manner and the increase of p21 expression seems to be regulated by DPI-mediated ERK activation. diphenyleneiodonium 16-19 H3 histone pseudogene 16 Homo sapiens 33-36 19020764-8 2008 In HL-60 cells, DPI also induced p21 upregulation in a p53-independent manner and the increase of p21 expression seems to be regulated by DPI-mediated ERK activation. diphenyleneiodonium 138-141 H3 histone pseudogene 16 Homo sapiens 98-101 19141979-7 2008 CONCLUSION: Celecoxib inhibited cell proliferation and apoptosis of human gastric cancer cell line BGC-823, which may be related to blocking the cell cycle progress by increasing the expression of p21 and inducing the apoptosis of gastric cancer cells by increasing the expression of Fas. Celecoxib 12-21 H3 histone pseudogene 16 Homo sapiens 197-200 18823952-4 2008 Up regulation of bax and the increased nuclear accumulation of p21 upon benomyl treatment confirmed the activation of p53. Benomyl 72-79 H3 histone pseudogene 16 Homo sapiens 63-66 19007111-3 2008 The metabolically released formaldehyde from the prodrugs was the dominant factor affecting cell viability by a ROS-dependent mechanism and was responsible for rapid phosphorylation of H2AX, suppression of the cell survival protein c-myc, and transient elevation in the expression of p21. Formaldehyde 27-39 H3 histone pseudogene 16 Homo sapiens 284-287 19007111-3 2008 The metabolically released formaldehyde from the prodrugs was the dominant factor affecting cell viability by a ROS-dependent mechanism and was responsible for rapid phosphorylation of H2AX, suppression of the cell survival protein c-myc, and transient elevation in the expression of p21. ros 112-115 H3 histone pseudogene 16 Homo sapiens 284-287 18835080-6 2008 The Trp fluorescence intensities of mutated p21(141-164) peptides (F150W, Y151W and F159W) increased upon binding to Ca(2+)-saturated calmodulin and fluorescence maxima were blue shifted from 350 nm to 330 nm. Tryptophan 4-7 H3 histone pseudogene 16 Homo sapiens 44-47 18649995-9 2008 Taken together, these data suggest that DPTH-N10 inhibits HUVEC proliferation by increasing the level of p21 protein, which in turn inhibits CDK2 kinase activity, and finally interrupts the cell cycle. 5,5-diphenyl-2-thiohydantoin-N10 40-48 H3 histone pseudogene 16 Homo sapiens 105-108 18649995-6 2008 Immunoprecipitation showed that the formation of the CDK2-p21 complex, but not the CDK2-p27, CDK4-p21, and CDK4-p27 complex, was increased in the DPTH-N10-treated HUVEC. 5,5-diphenyl-2-thiohydantoin-N10 146-154 H3 histone pseudogene 16 Homo sapiens 58-61 18649995-8 2008 Pretreatment of HUVEC with a p21, but not p27, antisense oligonucleotide reversed the DPTH-N10-induced inhibition of [3H]thymidine incorporation into HUVEC. 5,5-diphenyl-2-thiohydantoin-N10 86-94 H3 histone pseudogene 16 Homo sapiens 29-32 18649995-8 2008 Pretreatment of HUVEC with a p21, but not p27, antisense oligonucleotide reversed the DPTH-N10-induced inhibition of [3H]thymidine incorporation into HUVEC. Tritium 118-120 H3 histone pseudogene 16 Homo sapiens 29-32 18064564-6 2008 Induction of the stress related kinases JNK and p38 and the up-regulation of p21 and p27 were also observed after co-treatment of cells with HDACi and MG-132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 151-157 H3 histone pseudogene 16 Homo sapiens 77-80 21581414-1 2008 The titile compound, C(18)H(20)Cl(2)N(2)O(2), crystallizes as a monoclinic form in the space group P2(1)/n, with Z" = 1/2. c(18)h(20)cl(2)n( 21-38 H3 histone pseudogene 16 Homo sapiens 99-104 19010882-8 2008 We found that miR-128 expression caused a decrease in histone methylation (H3K27me(3)) and Akt phosphorylation, and up-regulation of p21(CIP1) levels, consistent with Bmi-1 down-regulation. mir-128 14-21 H3 histone pseudogene 16 Homo sapiens 133-136 19138995-8 2008 We found that the inhibitory effect of Gemini 0097 was associated with an increased level of cyclin-dependent kinase inhibitor p21 and the insulin-like growth factor binding protein 3 in both ER-positive and ER-negative mammary tumors. Gemini0097 39-50 H3 histone pseudogene 16 Homo sapiens 127-130 18850315-4 2008 The formation of CDK2-p21 and CDK2-p27 were increased and the CDK2 activity was decreased in the progesterone-treated HUVEC. Progesterone 97-109 H3 histone pseudogene 16 Homo sapiens 22-25 18850315-5 2008 The progesterone-inhibited [3H]thymidine incorporation was completely blocked when the expressions of p21 and p27 were knocked-down together. Tritium 28-30 H3 histone pseudogene 16 Homo sapiens 102-105 18850315-6 2008 Transfection of HUVEC with dominant negative p53 cDNA prevented the progesterone-induced increases in p21 and p27 promoter activity and protein level, decreases in thymidine incorporation, and capillary-like tube formation. Progesterone 68-80 H3 histone pseudogene 16 Homo sapiens 102-105 18822454-8 2008 Nevirapine treated cells strongly accumulated SA-b-Gal activity and also expressed increased levels of p53 and p21 when analyzed via RT-PCR. Nevirapine 0-10 H3 histone pseudogene 16 Homo sapiens 111-114 18671724-11 2008 These results demonstrate that G(0)/G(1) phase arrest is due to increased expression of p21 in cells treated with norsolorinic acid (10 and 20 micromol/L) for 24 h. Moreover, enhanced Fas and membrane-bound Fas ligand (mFasL) may be responsible for the apoptotic effect of norsolorinic acid. norsolorinic acid 114-131 H3 histone pseudogene 16 Homo sapiens 88-91 18671724-11 2008 These results demonstrate that G(0)/G(1) phase arrest is due to increased expression of p21 in cells treated with norsolorinic acid (10 and 20 micromol/L) for 24 h. Moreover, enhanced Fas and membrane-bound Fas ligand (mFasL) may be responsible for the apoptotic effect of norsolorinic acid. ammonium ferrous sulfate 184-187 H3 histone pseudogene 16 Homo sapiens 88-91 18671724-11 2008 These results demonstrate that G(0)/G(1) phase arrest is due to increased expression of p21 in cells treated with norsolorinic acid (10 and 20 micromol/L) for 24 h. Moreover, enhanced Fas and membrane-bound Fas ligand (mFasL) may be responsible for the apoptotic effect of norsolorinic acid. norsolorinic acid 273-290 H3 histone pseudogene 16 Homo sapiens 88-91 18671724-12 2008 Thus, the present study reports, for the first time, that induction of p21 and the Fas/mFas ligand apoptotic system may participate in the antiproliferative action of norsolorinic acid in T24 human bladder cancer cells. norsolorinic acid 167-184 H3 histone pseudogene 16 Homo sapiens 71-74 19031317-2 2008 Previous treatment of H4 cells with DHEA for 18 h reduced the gamma-ray-induced phosphorylation of Akt, activated p21(waf1) synthesis and up-regulated phosphorylation of Rb independent of p53. Dehydroepiandrosterone 36-40 H3 histone pseudogene 16 Homo sapiens 114-117 18981469-3 2008 3024-3036), published in this issue of Genes & Development, now elucidates the role of the cyclin-dependent kinase inhibitors (CKIs), p21 and p57, in mammalian endocycle regulation. Adenosine Monophosphate 46-49 H3 histone pseudogene 16 Homo sapiens 138-141 18949380-9 2008 Overall, the TsA-activated ERK pathway plays an important role in cell cycle arrest and apoptosis through the ERK-dependent induction of p21 in Ras-related human cancer cells. trichostatin A 13-16 H3 histone pseudogene 16 Homo sapiens 137-140 18949381-6 2008 The expression of p53, p21, bax and caspase-3 increased in Tan-I-treated cells. tanshinone 59-64 H3 histone pseudogene 16 Homo sapiens 23-26 18949381-8 2008 These findings suggest that Tan-I induces apoptosis in Colo 205 cells through both mitochondrial-mediated intrinsic cell-death pathways and p21-mediated G0/G1cell cycle arrest. tanshinone 28-33 H3 histone pseudogene 16 Homo sapiens 140-143 18729080-0 2008 Helenalin-mediated post-transcriptional regulation of p21(Cip1) inhibits 3T3-L1 preadipocyte proliferation. helenalin 0-9 H3 histone pseudogene 16 Homo sapiens 54-57 18799615-3 2008 Only in Ret/PTC1-positive TPC-1 cells did cAMP markedly inhibit the Raf/ERK cascade, leading to mTOR pathway inhibition, repression of cyclin D1 and p21 and p27 accumulation. Cyclic AMP 42-46 H3 histone pseudogene 16 Homo sapiens 149-152 18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 H3 histone pseudogene 16 Homo sapiens 120-123 18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 H3 histone pseudogene 16 Homo sapiens 120-123 18615564-5 2008 Doc induced a transient increase in G2/M phase followed by the appearance of G0/1 hypo- and hyperdiploid cells and increased p21 expression. Docetaxel 0-3 H3 histone pseudogene 16 Homo sapiens 125-128 18615564-7 2008 In conclusion, Doc would seem to trigger apoptosis in hormone-refractory prostate cancer cells via mitotic catastrophe through two forms of mitotic exit, in concomitance with increased p21 expression and caspase-2 activation. Docetaxel 15-18 H3 histone pseudogene 16 Homo sapiens 185-188 18729080-5 2008 Our results demonstrate that helenalin markedly increased p21 protein accumulation in both density-arrested and proliferating preadipocytes in a dose-dependent manner. helenalin 29-38 H3 histone pseudogene 16 Homo sapiens 58-61 18729080-7 2008 This notion was further supported by the modest accumulation of polyubiquitylated p21 following treatment with helenalin suggesting that suppression of targeted p21 proteolysis by the 26S proteasome contributed to helenalin-mediated p21 accumulation. helenalin 111-120 H3 histone pseudogene 16 Homo sapiens 82-85 18729080-7 2008 This notion was further supported by the modest accumulation of polyubiquitylated p21 following treatment with helenalin suggesting that suppression of targeted p21 proteolysis by the 26S proteasome contributed to helenalin-mediated p21 accumulation. helenalin 111-120 H3 histone pseudogene 16 Homo sapiens 161-164 18729080-7 2008 This notion was further supported by the modest accumulation of polyubiquitylated p21 following treatment with helenalin suggesting that suppression of targeted p21 proteolysis by the 26S proteasome contributed to helenalin-mediated p21 accumulation. helenalin 111-120 H3 histone pseudogene 16 Homo sapiens 161-164 18729080-7 2008 This notion was further supported by the modest accumulation of polyubiquitylated p21 following treatment with helenalin suggesting that suppression of targeted p21 proteolysis by the 26S proteasome contributed to helenalin-mediated p21 accumulation. helenalin 214-223 H3 histone pseudogene 16 Homo sapiens 82-85 18640142-1 2008 INTRODUCTION: Polymorphisms in p53, p21 and CCND1 could regulate the progression of the cell cycle and might increase the susceptibility to inorganic arsenic-related cancer risk. Arsenic 150-157 H3 histone pseudogene 16 Homo sapiens 36-39 18729080-7 2008 This notion was further supported by the modest accumulation of polyubiquitylated p21 following treatment with helenalin suggesting that suppression of targeted p21 proteolysis by the 26S proteasome contributed to helenalin-mediated p21 accumulation. helenalin 214-223 H3 histone pseudogene 16 Homo sapiens 161-164 18640142-7 2008 RESULTS: Subjects carrying the p21 Arg/Arg genotype had an increased UC risk (age and gender adjusted OR=1.53; 95% CI, 1.02-2.29). Arginine 35-38 H3 histone pseudogene 16 Homo sapiens 31-34 18729080-7 2008 This notion was further supported by the modest accumulation of polyubiquitylated p21 following treatment with helenalin suggesting that suppression of targeted p21 proteolysis by the 26S proteasome contributed to helenalin-mediated p21 accumulation. helenalin 214-223 H3 histone pseudogene 16 Homo sapiens 161-164 18640142-7 2008 RESULTS: Subjects carrying the p21 Arg/Arg genotype had an increased UC risk (age and gender adjusted OR=1.53; 95% CI, 1.02-2.29). Arginine 39-42 H3 histone pseudogene 16 Homo sapiens 31-34 18640142-12 2008 CONCLUSIONS: The results showed that the variant genotype of p21 might be a predictor of inorganic arsenic-related UC risk. Arsenic 99-106 H3 histone pseudogene 16 Homo sapiens 61-64 18729080-9 2008 Finally, helenalin increased protein-protein interactions between p21 and cyclin-dependent kinase 2 (Cdk2) which may account in part for the anti-proliferative effect in 3T3-L1 preadipocytes. helenalin 9-18 H3 histone pseudogene 16 Homo sapiens 66-69 18294363-4 2008 The results were as follows: (1) At P21, GL increased significantly the spleen weight by 163.6% and spleen index by 118.8% compared with RL (P < 0.05). Methyl Green 41-43 H3 histone pseudogene 16 Homo sapiens 36-39 18294363-7 2008 (3) At P21, GL enhanced spleen lymphocytes proliferation in response to concanavalin A compared with RL by 50.0% (P < 0.05). Methyl Green 12-14 H3 histone pseudogene 16 Homo sapiens 7-10 18834353-8 2008 When cells were treated with 20 microM 5-fluorouracil and 200 microg/ml Bupleuri Radix simultaneously, Bax protein increased in HepG2 cells at 24 hr; however, p21 and p53 proteins were up-regulated in normal human lymphocytes. Fluorouracil 39-53 H3 histone pseudogene 16 Homo sapiens 159-162 18766003-8 2008 Celecoxib reduced p-Rb and DP1/E2F1 complex predominantly via upregulated p21/CDK4 complex in HuH7 xenograft, but p27/CDK4 complex in C2D-HuH7 xenografts. Celecoxib 0-9 H3 histone pseudogene 16 Homo sapiens 74-77 18509599-9 2008 In addition, lower (but not higher) doses of DDAP arrested 90% of S-phase 2008.C13 cells, which might be associated with up-regulation of p21 and maintenance of low cyclin A expression. diammine dicarboxylic acid platinum 45-49 H3 histone pseudogene 16 Homo sapiens 138-141 18842998-1 2008 This study explores the relationship between genetic polymorphisms of p53, p21, and CCND1, and the susceptibility of chromosomal damage induced by vinyl chloride monomer (CH(2)=CHCl, VCM). Vinyl Chloride 147-161 H3 histone pseudogene 16 Homo sapiens 75-78 18384530-7 2008 In this work, we also show that melatonin elevates p21 protein levels and increases antioxidant capacity of prostate cancer cells. Melatonin 32-41 H3 histone pseudogene 16 Homo sapiens 51-54 18632985-6 2008 p21 was likely a direct target of HDAC4, because HDAC4 down-regulation increased p21 mRNA when protein synthesis was inhibited by cycloheximide. Cycloheximide 130-143 H3 histone pseudogene 16 Homo sapiens 0-3 18632985-6 2008 p21 was likely a direct target of HDAC4, because HDAC4 down-regulation increased p21 mRNA when protein synthesis was inhibited by cycloheximide. Cycloheximide 130-143 H3 histone pseudogene 16 Homo sapiens 81-84 18653452-7 2008 (iv) The mutation of all four glutamates to alanine does debilitate Nef MHC-I downregulation, but this quadruple mutation also impairs the ability of Nef to regulate p21-activated protein kinase and enhance viral particle infectivity. Glutamates 30-40 H3 histone pseudogene 16 Homo sapiens 166-169 18653452-7 2008 (iv) The mutation of all four glutamates to alanine does debilitate Nef MHC-I downregulation, but this quadruple mutation also impairs the ability of Nef to regulate p21-activated protein kinase and enhance viral particle infectivity. Alanine 44-51 H3 histone pseudogene 16 Homo sapiens 166-169 18813348-6 2008 Suppression of Hsf1 in A1-5 cells with quercetin or an Hsf1 siRNA reduced p53 nuclear importation and inhibited p53-mediated activation of a p21 reporter. Quercetin 39-48 H3 histone pseudogene 16 Homo sapiens 141-144 18515856-6 2008 Our results show that with acute treatment, VPA can increase the expression of net histone H3 acetylation and up-regulate p21 expression with no effect on p53 expression. Valproic Acid 44-47 H3 histone pseudogene 16 Homo sapiens 122-125 18583539-3 2008 Also, selenium-treated ATSCs significantly downregulated p53 and p21 tumor suppressor gene products. Selenium 6-14 H3 histone pseudogene 16 Homo sapiens 65-68 21201166-6 2008 The triply substituted benzene ring and the phenyl ring form dihedral angles of 12.2 (2) and 53.7 (2) , respectively, with the pyrazolone ring; the corresponding values in the P2(1)/c polymorph are 7.5 (2) and 42.6 (2) . Benzene 23-30 H3 histone pseudogene 16 Homo sapiens 176-181 21201166-6 2008 The triply substituted benzene ring and the phenyl ring form dihedral angles of 12.2 (2) and 53.7 (2) , respectively, with the pyrazolone ring; the corresponding values in the P2(1)/c polymorph are 7.5 (2) and 42.6 (2) . pyrazolone 127-137 H3 histone pseudogene 16 Homo sapiens 176-181 18504430-0 2008 Geldanamycin promotes premature mitotic entry and micronucleation in irradiated p53/p21 deficient colon carcinoma cells. geldanamycin 0-12 H3 histone pseudogene 16 Homo sapiens 84-87 18504430-8 2008 Clonogenic survival studies demonstrated higher sensitivity to GA alone or combination IR plus GA treatment in p53 and p21-null cells. geldanamycin 63-65 H3 histone pseudogene 16 Homo sapiens 119-122 18806879-10 2008 CONCLUSIONS: These results indicate that mitomycin-induced cellular apoptosis in corneal endothelial cells may be mediated through caspase-8, caspase-9, and the mitochondrial regulated pathways as well as through upregulation of p53-dependent and p21-dependent signal transduction pathways. Mitomycin 41-50 H3 histone pseudogene 16 Homo sapiens 247-250 19035307-5 2008 RESULTS: Putrescine and spermidine at 0.5 mg/l significantly stimulated cell growth, whereas mepacrine treatment confirmed the enhanced p21 expression previously reported by a recent study and growth inhibition. Quinacrine 93-102 H3 histone pseudogene 16 Homo sapiens 136-139 18710213-4 2008 Compound 4 (C12H17[NCO]C10H7)3Y(C4H8O) crystallized in the monoclinic space group P2(1)/c with a = 13.7820(11) A, b = 33.598(3) A, c = 16.0575(12) A, alpha = 90 degrees, beta = 98.762(3) degrees, gamma = 90 degrees, Z = 4. methional 32-37 H3 histone pseudogene 16 Homo sapiens 82-87 18490008-3 2008 The two beta-CD monomers of form III are isostructural to that of form I in the monoclinic space group P2(1) [Steiner, T.; Mason, S. A.; Saenger, W. J. betadex 8-15 H3 histone pseudogene 16 Homo sapiens 103-108 18384098-4 2008 Curcumin can also activate apoptosis, down-regulate cell survival gene products, and up-regulate p53, p21, and p27. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 102-105 18385759-7 2008 Furthermore p21, a cyclin-dependent kinase inhibitor downstream of S100/A11, was required for calcium-mediated induction of HBD-3 and FLG. Calcium 94-101 H3 histone pseudogene 16 Homo sapiens 12-15 18622903-6 2008 The expression of p53 and p21 and mitochondrial cytochrome c release were increased in tanshinone IIA-treated cells. tanshinone 87-101 H3 histone pseudogene 16 Homo sapiens 26-29 18790751-4 2008 Xanthohumol inhibition of K562 cell viability was associated with induction of apoptosis, increased p21 and p53 expression, and decreased survivin levels. xanthohumol 0-11 H3 histone pseudogene 16 Homo sapiens 100-103 18446786-6 2008 Resveratrol also caused p53 binding to the p21 promoter and increased abundance of COX-2 protein in UMSCC-22B cell nuclei. Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 43-46 18548481-11 2008 CONCLUSIONS: The pADxsi-PSES-AdoMetDC-ODC-PolyA AV specifically inhibited the expression of ODC and AdoMetDC and the synthesis of polyamine, while it induced p21 expression, resulting in cell growth arrest in the G1 phase in prostate cancer cells but not in other cells. Polyamines 130-139 H3 histone pseudogene 16 Homo sapiens 158-161 18662759-6 2008 Thus, these results indicated that TOCP might induce potential neurodevelopmental toxicity, and a possible mechanism of this toxicity might be the disturbance of cell proliferation by disrupting cell cycle regulatory proteins cyclin D1 and p21 expression. tri-o-cresyl phosphate 35-39 H3 histone pseudogene 16 Homo sapiens 240-243 18474441-6 2008 Moreover, troglitazone treatment, applied in a dose-dependent manner, caused a marked decrease in pRb, cyclin D1, cyclin D2, cyclin D3, Cdk2, Cdk4 and Cdk6 expression as well as a significant increase in p21 and p27 expression. Troglitazone 10-22 H3 histone pseudogene 16 Homo sapiens 204-207 18541724-3 2008 In this study, we report that the HDAC inhibitor vorinostat induced p21 expression and decreased Bcl-xL levels causing cell-cycle arrest and apoptosis. Vorinostat 49-59 H3 histone pseudogene 16 Homo sapiens 68-71 18391982-4 2008 As the mechanism, triptolide suppressed CDDP-induced p53 transcriptional activity, leading to p21 attenuation, which promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and Bax. triptolide 18-28 H3 histone pseudogene 16 Homo sapiens 94-97 18384113-6 2008 The cell cycle arrest coincided with an increase in expression of the cell cycle markers p21, p27 and p53 proteins in 2-ME-treated osteosarcoma cells. 2-Methoxyestradiol 118-122 H3 histone pseudogene 16 Homo sapiens 89-92 18950011-4 2008 Antisense oligonucleotide which directed blocked up the translation site resulted in growth inhibition, downregulation of Stat3, p-Stat3, Cyclins and CDKs, and upregulation of p21 and p27. Oligonucleotides 10-25 H3 histone pseudogene 16 Homo sapiens 176-179 19102934-3 2008 Eukaryotic vector pEGFP-C2-p21 was transfected into HepG cells by lipofectamine and positive clones were screened out by G418. Lipofectamine 66-79 H3 histone pseudogene 16 Homo sapiens 27-30 19102934-6 2008 RESULTS: After treatment with DOX, the expression of p53 and p21 was increased, whereas that of survivin was reduced during 24 hours of the treatment. Doxorubicin 30-33 H3 histone pseudogene 16 Homo sapiens 61-64 18391982-4 2008 As the mechanism, triptolide suppressed CDDP-induced p53 transcriptional activity, leading to p21 attenuation, which promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and Bax. Cisplatin 40-44 H3 histone pseudogene 16 Homo sapiens 94-97 18391985-9 2008 Furthermore, Fbw7 expression regulates the p53-dependent induction of genes such as Lats2 and p21 in response to vinblastine. Vinblastine 113-124 H3 histone pseudogene 16 Homo sapiens 94-97 18486125-11 2008 These findings suggest that MC-4 and MR-4 may share a common mechanism whereby the perinucear mitochondrial clustering, rather than p53, p21, or microtubule depolymerization, is critical for their pro-apoptotic action. MC-4 28-32 H3 histone pseudogene 16 Homo sapiens 137-140 18561895-8 2008 Cucurbitacins induced the expression of p53 and p21 predominantly in HCT116 cells that harbor mutant Ras. Cucurbitacins 0-13 H3 histone pseudogene 16 Homo sapiens 48-51 18561895-9 2008 Using HCT116 cells with targeted deletion of p53 or p21 we confirmed that p53 and p21 protect cells from apoptosis induced by cucurbitacins. Cucurbitacins 126-139 H3 histone pseudogene 16 Homo sapiens 52-55 18561895-9 2008 Using HCT116 cells with targeted deletion of p53 or p21 we confirmed that p53 and p21 protect cells from apoptosis induced by cucurbitacins. Cucurbitacins 126-139 H3 histone pseudogene 16 Homo sapiens 82-85 18561895-10 2008 These results demonstrated that sensitivity of human colon cancer cell lines to cucurbitacins depends on the kRas and p53/p21 status, and established that cucurbitacins can exert antitumorigenic activity in the absence of activated STAT3. Cucurbitacins 80-93 H3 histone pseudogene 16 Homo sapiens 122-125 18935826-3 2008 Though the pyroxene retains its P21/c symmetry, changes in the Raman spectra are observed between 6.8 and 7.7 GPa, possibly due to the formation of an additional bond between Li and O3 or some other transition that retains the mineral"s P21/c space group. pyroxene 11-19 H3 histone pseudogene 16 Homo sapiens 32-37 18935826-5 2008 Comparison is made with the Raman spectra of LiAlSi2O6 and LiFeSi2O6 in the P21/c phase and the visible spectra of NaCrSi2O6 at high pressures. lifesi2o6 59-68 H3 histone pseudogene 16 Homo sapiens 76-81 18780655-1 2008 AIM: To examine by means of immunohistochemistry the expression of the tumor suppressing gene p53 and gene p21 in cells of malignant melanoma of the uvea from formalin-paraffin material from patients, who were during the period 2000 - 2006 surgically treated due to malignant melanoma of the uvea at the Department of Ophthalmology in the University Hospital in Brno (Brunn), Czech Republic, E.U., and to correlate the results of the immunohistochemical detection with clinical signs of the tumor of each patient. Formaldehyde 159-167 H3 histone pseudogene 16 Homo sapiens 107-110 21783897-0 2008 Suppression of zinc-induced p53 phosphorylation and p21 expression by wortmannin in A549 human pulmonary epithelial cells. Wortmannin 70-80 H3 histone pseudogene 16 Homo sapiens 52-55 21783897-3 2008 Expression of cyclin-dependent kinase inhibitor p21, one of the genes regulated by p53, was up-regulated following exposure to ZnSO(4), and suppressed by preincubation with wortmannin. znso 127-131 H3 histone pseudogene 16 Homo sapiens 48-51 21783897-3 2008 Expression of cyclin-dependent kinase inhibitor p21, one of the genes regulated by p53, was up-regulated following exposure to ZnSO(4), and suppressed by preincubation with wortmannin. Wortmannin 173-183 H3 histone pseudogene 16 Homo sapiens 48-51 18332866-4 2008 Conditional overexpression of p21 in p53-deficient cells revealed that hyperoxia also stimulates wortmannin-sensitive degradation of p21. Wortmannin 97-107 H3 histone pseudogene 16 Homo sapiens 30-33 18332866-4 2008 Conditional overexpression of p21 in p53-deficient cells revealed that hyperoxia also stimulates wortmannin-sensitive degradation of p21. Wortmannin 97-107 H3 histone pseudogene 16 Homo sapiens 133-136 18594007-14 2008 Moreover, moscatilin induces DNA damage, phosphorylation of H2AX and p53, and up-regulation of p21. dendrophenol 10-20 H3 histone pseudogene 16 Homo sapiens 95-98 18645003-1 2008 Previous studies comparing the effects of two histone deacetylase (HDAC) inhibitors, trichostatin A (TSA) and CG-1521, have shown that these compounds selectively inhibit HDAC and induce differentially acetylated p53 isoforms and assembly of mutually exclusive transcriptional complexes on the p21 promoter. trichostatin A 85-99 H3 histone pseudogene 16 Homo sapiens 294-297 18645003-1 2008 Previous studies comparing the effects of two histone deacetylase (HDAC) inhibitors, trichostatin A (TSA) and CG-1521, have shown that these compounds selectively inhibit HDAC and induce differentially acetylated p53 isoforms and assembly of mutually exclusive transcriptional complexes on the p21 promoter. trichostatin A 101-104 H3 histone pseudogene 16 Homo sapiens 294-297 18645003-1 2008 Previous studies comparing the effects of two histone deacetylase (HDAC) inhibitors, trichostatin A (TSA) and CG-1521, have shown that these compounds selectively inhibit HDAC and induce differentially acetylated p53 isoforms and assembly of mutually exclusive transcriptional complexes on the p21 promoter. cysteinylglycine 110-112 H3 histone pseudogene 16 Homo sapiens 294-297 18645003-2 2008 To determine whether the differential transcriptional regulation seen in p21 gene is unique or whether it is representative of the genome-wide effects of these two HDAC inhibitors, we have used microarray and Ingenuity pathway analysis to compare the effects of TSA and CG-1521 on gene expression on LNCaP cells. trichostatin A 262-265 H3 histone pseudogene 16 Homo sapiens 73-76 18645003-5 2008 These data show that the selective effects of CG-1521 and TSA on the assembly of transcription complexes are not unique to the p21 gene and suggest that selective inhibition of HDAC can lead to significant changes in gene expression through the acetylation of transcription factors including but not limited to p53. cysteinylglycine 46-48 H3 histone pseudogene 16 Homo sapiens 127-130 18468651-7 2008 Western blot analysis revealed that pouterin caused increased expression of p21, thus indicating cell cycle arrest. pouterin 36-44 H3 histone pseudogene 16 Homo sapiens 76-79 18353898-3 2008 Nuclear p21 protein and mRNA levels as well as promoter activity in ZS cells, but not in ZD cells, were markedly elevated to almost twofold compared with ZN control cells. Zinc 154-156 H3 histone pseudogene 16 Homo sapiens 8-11 18523653-5 2008 Palmitic acid, as well as stearic acid and myristic acid, compromised the induction of p21 and Bax expression in response to double stranded breaks and ssDNA, while inhibition or knockdown of FASN enhanced these cellular events. Myristic Acid 43-56 H3 histone pseudogene 16 Homo sapiens 87-90 18523653-5 2008 Palmitic acid, as well as stearic acid and myristic acid, compromised the induction of p21 and Bax expression in response to double stranded breaks and ssDNA, while inhibition or knockdown of FASN enhanced these cellular events. Palmitic Acid 0-13 H3 histone pseudogene 16 Homo sapiens 87-90 18523653-5 2008 Palmitic acid, as well as stearic acid and myristic acid, compromised the induction of p21 and Bax expression in response to double stranded breaks and ssDNA, while inhibition or knockdown of FASN enhanced these cellular events. stearic acid 26-38 H3 histone pseudogene 16 Homo sapiens 87-90 18353898-6 2008 Abolishment of the increase in p53 protein in ZS cells with transfection of p53 siRNA normalized the elevated p21 protein to a similar level as in ZN control cells, which demonstrated that the p21 induction is p53 dependent. Zinc 147-149 H3 histone pseudogene 16 Homo sapiens 110-113 18353898-6 2008 Abolishment of the increase in p53 protein in ZS cells with transfection of p53 siRNA normalized the elevated p21 protein to a similar level as in ZN control cells, which demonstrated that the p21 induction is p53 dependent. Zinc 147-149 H3 histone pseudogene 16 Homo sapiens 193-196 18483381-5 2008 HDIs up-regulate p21, which is blocked by concomitant administration of 2-deoxy-d-glucose. Deoxyglucose 72-89 H3 histone pseudogene 16 Homo sapiens 17-20 18445700-5 2008 LBH589 or bortezomib alone increased expression of the cell cycle regulators p21 and p27. Panobinostat 0-6 H3 histone pseudogene 16 Homo sapiens 77-80 18445700-5 2008 LBH589 or bortezomib alone increased expression of the cell cycle regulators p21 and p27. Bortezomib 10-20 H3 histone pseudogene 16 Homo sapiens 77-80 18371935-9 2008 Fluoxetine showed the potential to disrupt skp2-CKS1 assembly required for ubiquitination and proteasomal degradation of p27 and p21. Fluoxetine 0-10 H3 histone pseudogene 16 Homo sapiens 129-132 18371935-11 2008 We found that fluoxetine treatment could accumulate p27 and p21, an immediate outcome characteristic of functional inhibition of CKS1. Fluoxetine 14-24 H3 histone pseudogene 16 Homo sapiens 60-63 18423603-0 2008 Curcumin induces apoptosis in HCT-116 human colon cancer cells in a p21-independent manner. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 68-71 18423603-3 2008 Several studies report that curcumin inhibits cancer cell proliferation and induces apoptosis in cancer cells through p21-mediated cell cycle arrest. Curcumin 28-36 H3 histone pseudogene 16 Homo sapiens 118-121 18423603-5 2008 In this study, we determined whether curcumin-induced cytotoxicity in cultures of HCT-116 human colon cancer cells was dependent on p21 status. Curcumin 37-45 H3 histone pseudogene 16 Homo sapiens 132-135 18423603-7 2008 Moreover, an equivalent cytotoxic effect by curcumin was observed in both p21(+/+) and p21(-/-)HCT-116 cells, indicating that curcumin-induced cytotoxicity was p21-independent. Curcumin 44-52 H3 histone pseudogene 16 Homo sapiens 74-77 18423603-7 2008 Moreover, an equivalent cytotoxic effect by curcumin was observed in both p21(+/+) and p21(-/-)HCT-116 cells, indicating that curcumin-induced cytotoxicity was p21-independent. Curcumin 44-52 H3 histone pseudogene 16 Homo sapiens 87-90 18423603-7 2008 Moreover, an equivalent cytotoxic effect by curcumin was observed in both p21(+/+) and p21(-/-)HCT-116 cells, indicating that curcumin-induced cytotoxicity was p21-independent. Curcumin 44-52 H3 histone pseudogene 16 Homo sapiens 87-90 18423603-9 2008 Western blot analysis showed that cell death in curcumin-treated cultures of p21(+/+) and p21(-/-) HCT-116 cells was associated with a reduction in pro-caspase-3 and PARP-1 cleavage, which are indicative of apoptosis. Curcumin 48-56 H3 histone pseudogene 16 Homo sapiens 77-80 18423603-9 2008 Western blot analysis showed that cell death in curcumin-treated cultures of p21(+/+) and p21(-/-) HCT-116 cells was associated with a reduction in pro-caspase-3 and PARP-1 cleavage, which are indicative of apoptosis. Curcumin 48-56 H3 histone pseudogene 16 Homo sapiens 90-93 18324646-7 2008 Further, in both PC3 and LNCaP cell lines, 25-OH-PPD increased expression of p21, p27, and Bax, induced PARP cleavage and activated caspases. 25-hydroxyprotopanaxadiol 43-52 H3 histone pseudogene 16 Homo sapiens 77-80 18493594-0 2008 Antagomir-17-5p abolishes the growth of therapy-resistant neuroblastoma through p21 and BIM. antagomir-17-5p 0-15 H3 histone pseudogene 16 Homo sapiens 80-83 18272192-0 2008 Inhibition of the ERK phosphorylation plays a role in terbinafine-induced p21 up-regulation and DNA synthesis inhibition in human vascular endothelial cells. Terbinafine 54-65 H3 histone pseudogene 16 Homo sapiens 74-77 18272192-1 2008 Previously, we showed that terbinafine (TB) induces cell-cycle arrest in cultured human umbilical vein endothelial cells (HUVEC) through an up-regulation of the p21 protein. Terbinafine 27-38 H3 histone pseudogene 16 Homo sapiens 161-164 18272192-4 2008 The p21 promoter activity was also increased by TB treatment. Terbinafine 48-50 H3 histone pseudogene 16 Homo sapiens 4-7 18272192-1 2008 Previously, we showed that terbinafine (TB) induces cell-cycle arrest in cultured human umbilical vein endothelial cells (HUVEC) through an up-regulation of the p21 protein. Terbinafine 40-42 H3 histone pseudogene 16 Homo sapiens 161-164 18272192-5 2008 Transfection of HUVEC with p53 dominant negative (DN) abolished the TB-induced increases of p21 promoter activity and protein level, suggesting that the TB-induced increase of p21 is p53-dependent. Terbinafine 68-70 H3 histone pseudogene 16 Homo sapiens 92-95 18272192-2 2008 The aim of this study is to delineate the molecular mechanisms underlying TB-induced increase of p21 protein. Terbinafine 74-76 H3 histone pseudogene 16 Homo sapiens 97-100 18272192-5 2008 Transfection of HUVEC with p53 dominant negative (DN) abolished the TB-induced increases of p21 promoter activity and protein level, suggesting that the TB-induced increase of p21 is p53-dependent. Terbinafine 68-70 H3 histone pseudogene 16 Homo sapiens 176-179 18272192-5 2008 Transfection of HUVEC with p53 dominant negative (DN) abolished the TB-induced increases of p21 promoter activity and protein level, suggesting that the TB-induced increase of p21 is p53-dependent. Terbinafine 153-155 H3 histone pseudogene 16 Homo sapiens 92-95 18272192-3 2008 RT-PCR analysis demonstrated that the mRNA levels of p21 and p53 were increased in the TB-treated HUVEC. Terbinafine 87-89 H3 histone pseudogene 16 Homo sapiens 53-56 18272192-5 2008 Transfection of HUVEC with p53 dominant negative (DN) abolished the TB-induced increases of p21 promoter activity and protein level, suggesting that the TB-induced increase of p21 is p53-dependent. Terbinafine 153-155 H3 histone pseudogene 16 Homo sapiens 176-179 18373075-5 2008 However, at a low dose of etoposide (repairable damage), Bid activated the S phase checkpoint through the up-regulation of p21 and p27, which are both p53-independent. Etoposide 26-35 H3 histone pseudogene 16 Homo sapiens 123-126 18272192-7 2008 Over-expression of mitogen-activated protein kinase (MEK)-1, the immediate upstream activator kinase of ERK, abolished the TB-induced increases of p21 and p53 protein and decrease of thymidine incorporation. Terbinafine 123-125 H3 histone pseudogene 16 Homo sapiens 147-150 18272192-9 2008 Taken together, these data suggest that the decrease of ERK activity plays a role in the TB-induced up-regulation of p21 in HUVEC. Terbinafine 89-91 H3 histone pseudogene 16 Homo sapiens 117-120 18272192-11 2008 Taken together, our results suggest that TB might cause a decrease of MEK, which in turn up-regulates p53 through the inhibition of ERK phosphorylation, and finally causes an increase of p21 expression and cell-cycle arrest. Terbinafine 41-43 H3 histone pseudogene 16 Homo sapiens 187-190 18223318-5 2008 Bortezomib-induced apoptosis was associated with activation of caspase 3, cleavage of PARP and induction of p27 and p21 expression. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 116-119 18355800-3 2008 We demonstrated that p27/Kip1, p21/Cip1 and the keratinocyte differentiation marker, human involucrin (hINV), were induced (>25 microM) in TB-induced differentiated A431 cells. Terbium 142-144 H3 histone pseudogene 16 Homo sapiens 31-34 18418051-4 2008 Using reporter assays and Electrophoretic Mobility Shift Assays (EMSA), our findings suggest that TAp73-mediated activation of the p21(cip/waf), 14-3-3sigma and Bax gene promoters is abrogated by expressed PLK1 for which post-translational modification of TAp73 Thr-27 appears to be a key step in MCF7 cells. Threonine 262-265 H3 histone pseudogene 16 Homo sapiens 131-134 18269916-0 2008 Induction of p21 by p65 in p53 null cells treated with Doxorubicin. Doxorubicin 55-66 H3 histone pseudogene 16 Homo sapiens 13-16 18269916-2 2008 Here we show that knockdown of p65 by IkappaBSR or p65 siRNA decreased the cytotoxic effect of DOX on HCT116 (p53+/+) cells, correlating with increased induction of p21. Doxorubicin 95-98 H3 histone pseudogene 16 Homo sapiens 165-168 18269916-5 2008 In HCT116 (p53-/-) cells, downregulation of p65 expression enhanced the cytotoxic effect of DOX, due to decreased p21 expression levels. Doxorubicin 92-95 H3 histone pseudogene 16 Homo sapiens 114-117 18269916-6 2008 We present evidence that in p53-null tumor cells treated with DOX, p65 was involved in induction of p21 expression by directly binding to the p21 promoter. Doxorubicin 62-65 H3 histone pseudogene 16 Homo sapiens 100-103 18269916-6 2008 We present evidence that in p53-null tumor cells treated with DOX, p65 was involved in induction of p21 expression by directly binding to the p21 promoter. Doxorubicin 62-65 H3 histone pseudogene 16 Homo sapiens 142-145 18538108-10 2008 Immunoblotting showed that mucronulatol induced an up-regulation of p21(Cip1) and p27(Kip1) while down-regulating cyclin E and CDK4 in a drug concentration-dependent manner. mucronulatol 27-39 H3 histone pseudogene 16 Homo sapiens 68-71 18380477-4 2008 An aggregation of Fas-procaspase 8-procaspase 3 and p21-procaspase 3 proteins by coimmunoprecipitation, immunoblotting analysis, and MALDI-mass spectrometry indicated the involvement of Fas and p21 in 1-mediated cytotoxicity, and pretreatment of cells with antisense FasL oligonucleotides partially abolished apoptosis. Oligonucleotides 272-288 H3 histone pseudogene 16 Homo sapiens 52-55 17982489-7 2008 GA also produced a p53/ATM-independent increase in the levels of p21-a potent inducer of cell-cycle arrest. geldanamycin 0-2 H3 histone pseudogene 16 Homo sapiens 65-68 18358095-7 2008 RESULTS: Rapamycin inhibited the proliferation of Jurkat, induced G1 phase arrest, unregulated the protein level of p21 as well as p27, and downregulated cyclinD3, phospho-p70s6k, and phospho-s6, but had no effect on apoptosis. Sirolimus 9-18 H3 histone pseudogene 16 Homo sapiens 116-119 18480997-9 2008 Western blotting showed that cisplatin decreased protein expression of E6 and increased protein expression of p53, p21 and Bax. Cisplatin 29-38 H3 histone pseudogene 16 Homo sapiens 115-118 17376583-0 2008 Histone deacetylase inhibitors trichostatin A and valproic acid induce cell cycle arrest and p21 expression in immortalized human endometrial stromal cells. trichostatin A 31-45 H3 histone pseudogene 16 Homo sapiens 93-96 17376583-0 2008 Histone deacetylase inhibitors trichostatin A and valproic acid induce cell cycle arrest and p21 expression in immortalized human endometrial stromal cells. Valproic Acid 50-63 H3 histone pseudogene 16 Homo sapiens 93-96 17376583-1 2008 OBJECTIVE: Following our observation that histone deacetylase inhibitors (HDACIs) trichostatin A (TSA) and valproic acid (VPA) can suppress proliferation of endometrial stromal cells, we sought to determine whether TSA and VPA do so by inducing cell cycle arrest and p21 expression. trichostatin A 98-101 H3 histone pseudogene 16 Homo sapiens 267-270 17376583-1 2008 OBJECTIVE: Following our observation that histone deacetylase inhibitors (HDACIs) trichostatin A (TSA) and valproic acid (VPA) can suppress proliferation of endometrial stromal cells, we sought to determine whether TSA and VPA do so by inducing cell cycle arrest and p21 expression. Valproic Acid 107-120 H3 histone pseudogene 16 Homo sapiens 267-270 17376583-1 2008 OBJECTIVE: Following our observation that histone deacetylase inhibitors (HDACIs) trichostatin A (TSA) and valproic acid (VPA) can suppress proliferation of endometrial stromal cells, we sought to determine whether TSA and VPA do so by inducing cell cycle arrest and p21 expression. Valproic Acid 122-125 H3 histone pseudogene 16 Homo sapiens 267-270 17376583-4 2008 Treatment with ATRA alone also induced cell cycle arrest and moderate increase in p21 expression but joint treatment of ATRA and TSA/VPA did not further enhance cell cycle arrest as compared with TSA/VPA treatment alone. Tretinoin 15-19 H3 histone pseudogene 16 Homo sapiens 82-85 18414054-7 2008 P21 expression, for example, is under normal conditions not affected by p53/47 but is induced 18-fold after treatment of cells with the DNA damaging drug doxorubicin. Doxorubicin 154-165 H3 histone pseudogene 16 Homo sapiens 0-3 18343280-0 2008 Temsirolimus downregulates p21 without altering cyclin D1 expression and induces autophagy and synergizes with vorinostat in mantle cell lymphoma. temsirolimus 0-12 H3 histone pseudogene 16 Homo sapiens 27-30 18343280-7 2008 Mechanistically, temsirolimus inhibited mTOR, as evidenced by inhibition of ribosomal S6 phosphorylation, and induced cell-cycle arrest in the G(0)/G(1) phase and a decrease in p21 expression without altering p27 or cyclin D1 levels. temsirolimus 17-29 H3 histone pseudogene 16 Homo sapiens 177-180 18022818-0 2008 Molecular mechanisms of p21 and p27 induction by 3-methylcholanthrene, an aryl-hydrocarbon receptor agonist, involved in antiproliferation of human umbilical vascular endothelial cells. Methylcholanthrene 49-69 H3 histone pseudogene 16 Homo sapiens 24-27 18022818-2 2008 Herein, pretreatment of HUVECs with p21 or p27 small interfering (si)RNA reduced 3MC-induced elimination of [(3)H]thymidine incorporation, demonstrating their essential roles in the antiproliferation of HUVECs. Methylcholanthrene 81-84 H3 histone pseudogene 16 Homo sapiens 36-39 18022818-3 2008 The molecular mechanisms of p21 and p27 involved in the antiproliferative effects of 3MC were elucidated in this study. Methylcholanthrene 85-88 H3 histone pseudogene 16 Homo sapiens 28-31 18022818-5 2008 Interestingly, 3MC-mediated p21 and p27 inductions were eliminated by resveratrol, an AhR antagonist, suggesting their AhR dependency, further confirmed by AhR siRNA. Methylcholanthrene 15-18 H3 histone pseudogene 16 Homo sapiens 28-31 18022818-5 2008 Interestingly, 3MC-mediated p21 and p27 inductions were eliminated by resveratrol, an AhR antagonist, suggesting their AhR dependency, further confirmed by AhR siRNA. Resveratrol 70-81 H3 histone pseudogene 16 Homo sapiens 28-31 18022818-6 2008 Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant. Methylcholanthrene 95-98 H3 histone pseudogene 16 Homo sapiens 72-75 18022818-6 2008 Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant. Acetylcysteine 144-160 H3 histone pseudogene 16 Homo sapiens 72-75 18022818-6 2008 Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant. Acetylcysteine 162-165 H3 histone pseudogene 16 Homo sapiens 72-75 18022818-7 2008 3MC concentration-dependently enhanced not only the consensus dioxin-responsive element (DRE)-driven luciferase activity, but also the binding activity of the AhR to the putative DRE derived from the p21 and p27 promoters. Methylcholanthrene 0-3 H3 histone pseudogene 16 Homo sapiens 200-203 18022818-8 2008 A deletion of the DRE (-285/-270) in p21 (-2,300/+8) only partially alleviated the 3MC-induced luciferase activity unless NAC was added, suggesting that there may be a DRE-independent mechanism associated with oxidative stress. Methylcholanthrene 83-86 H3 histone pseudogene 16 Homo sapiens 37-40 18022818-8 2008 A deletion of the DRE (-285/-270) in p21 (-2,300/+8) only partially alleviated the 3MC-induced luciferase activity unless NAC was added, suggesting that there may be a DRE-independent mechanism associated with oxidative stress. Acetylcysteine 122-125 H3 histone pseudogene 16 Homo sapiens 37-40 18022818-10 2008 Our study demonstrated that both the functional DRE and the phosphorylation of p38MAPK are essential for the induction of p21 and p27, resulting in the antiproliferative action of 3MC in HUVECs. Methylcholanthrene 180-183 H3 histone pseudogene 16 Homo sapiens 122-125 18027850-10 2008 Belinostat also increased the expression of p21 and decreased the expression of potentially oncogenic proteins (mutant p53 and ERG). belinostat 0-10 H3 histone pseudogene 16 Homo sapiens 44-47 18201741-9 2008 Furthermore, arsenite and hyperthermia treatments activated a p53/p21 pathway associated with apoptosis induction, whereas vincristine did not activate this pathway. arsenite 13-21 H3 histone pseudogene 16 Homo sapiens 66-69 18337644-11 2008 Consistent with the cell cycle arrest, simvastatin caused an increase in the mRNA levels of p21 and p27 on G361 and MMAc cells. Simvastatin 39-50 H3 histone pseudogene 16 Homo sapiens 92-95 18276780-6 2008 Transcriptosome profiling demonstrated that redoxal and stavudine acted synergistically to induce CDKN2A and p21, indicating cell cycle arrest in G1, as well as genes involved in intrinsic and extrinsic apoptosis. Stavudine 56-65 H3 histone pseudogene 16 Homo sapiens 109-112 18077097-3 2008 In turn, LacCer activates an "oxygen-sensitive" signaling pathway involving superoxides, nitric oxide, p21 Ras GTP loading, kinase cascade, PI3kinase/Akt activation, nuclear factor up-regulation ultimately contributing to phenotypic changes such as cell proliferation, adhesion, migration and angiogenesis. Oxygen 30-36 H3 histone pseudogene 16 Homo sapiens 103-106 18181020-6 2008 In addition, ellipticine increased the nuclear localization of endogenous p53 in HCT116 colon cancer cells with a resultant increase in the transactivation of the p21 promoter. ellipticine 13-24 H3 histone pseudogene 16 Homo sapiens 163-166 17721990-8 2008 Pretreatment with nitric oxide (NO) scavengers could inhibit 5 microM MG/20 mM glucose-induced cytochrome c release, decrease activation of caspase-9 and caspase-3, and increase the gene expression and protein levels of p53 and p21, which are known to be involved in apoptotic signaling. Nitric Oxide 18-30 H3 histone pseudogene 16 Homo sapiens 228-231 18323654-6 2008 Consequently, quercetin stimulated p21 expression and suppressed cyclin D1 expression in favor of cell cycle arrest. Quercetin 14-23 H3 histone pseudogene 16 Homo sapiens 35-38 17721990-8 2008 Pretreatment with nitric oxide (NO) scavengers could inhibit 5 microM MG/20 mM glucose-induced cytochrome c release, decrease activation of caspase-9 and caspase-3, and increase the gene expression and protein levels of p53 and p21, which are known to be involved in apoptotic signaling. Glucose 79-86 H3 histone pseudogene 16 Homo sapiens 228-231 17721990-9 2008 Inhibition of p53 protein expression using small interfering RNA (siRNA) blocked the activation of p21 and the cell apoptosis induced by 5 microM MG/20 mM glucose. Glucose 155-162 H3 histone pseudogene 16 Homo sapiens 99-102 17996025-3 2008 Many gamma-secretase substrates are coupled to intracellular signaling events such as cAMP-response element binding protein and Rac1/p21-activated kinase pathways, which are associated with synaptic function. Cyclic AMP 86-90 H3 histone pseudogene 16 Homo sapiens 133-136 17724473-2 2008 P-TEFb (positive transcription elongation factor b) inhibitors such as flavopiridol or 4-amino-6-hydrazino-7-b-d-ribofuranosyl-7H-pyrrolo[2,3-d]-pyrimidine-5-carboxamide (ARC) upregulate p53 protein levels, but inhibit the expression of its targets p21 and hdm2. 4-amino-6-hydrazino-7-b-d-ribofuranosyl-7h-pyrrolo[2,3-d]-pyrimidine-5-carboxamide 87-169 H3 histone pseudogene 16 Homo sapiens 249-252 18375874-5 2008 Second, t-BHP treatment alone resulted in an increase in the protein levels of P16 and P21, and a decline in intracellular adenosine 5"-triphosphate (ATP) level and mitochondrial complex IV activity. tert-Butylhydroperoxide 8-13 H3 histone pseudogene 16 Homo sapiens 87-90 18067855-0 2008 Chloride ions control the G1/S cell-cycle checkpoint by regulating the expression of p21 through a p53-independent pathway in human gastric cancer cells. Chlorides 0-8 H3 histone pseudogene 16 Homo sapiens 85-88 18023527-8 2008 Treatment with D2O in combination with dFdC significantly (p<0.05) increased the induction of apoptosis in PANC-1 and AsPC-1 cells and led to an overexpression of p21 tumor suppressor gene compared to incubation with dFdC alone. Deuterium Oxide 15-18 H3 histone pseudogene 16 Homo sapiens 166-169 18023527-8 2008 Treatment with D2O in combination with dFdC significantly (p<0.05) increased the induction of apoptosis in PANC-1 and AsPC-1 cells and led to an overexpression of p21 tumor suppressor gene compared to incubation with dFdC alone. gemcitabine 39-43 H3 histone pseudogene 16 Homo sapiens 166-169 18023527-8 2008 Treatment with D2O in combination with dFdC significantly (p<0.05) increased the induction of apoptosis in PANC-1 and AsPC-1 cells and led to an overexpression of p21 tumor suppressor gene compared to incubation with dFdC alone. gemcitabine 220-224 H3 histone pseudogene 16 Homo sapiens 166-169 18067855-5 2008 These observations indicate that chloride ions play important roles in cell-cycle progression by regulating the expression of p21 through a p53-independent pathway in human gastric cancer cells, leading to a novel, unique therapeutic strategy for gastric cancer treatment via control of [Cl(-)](i). Chlorides 33-41 H3 histone pseudogene 16 Homo sapiens 126-129 17653574-0 2008 Bendamustine induces G2 cell cycle arrest and apoptosis in myeloma cells: the role of ATM-Chk2-Cdc25A and ATM-p53-p21-pathways. Bendamustine Hydrochloride 0-12 H3 histone pseudogene 16 Homo sapiens 114-117 17644301-0 2008 Romidepsin (depsipeptide) induced cell cycle arrest, apoptosis and histone hyperacetylation in lung carcinoma cells (A549) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. romidepsin 0-10 H3 histone pseudogene 16 Homo sapiens 155-158 17644301-0 2008 Romidepsin (depsipeptide) induced cell cycle arrest, apoptosis and histone hyperacetylation in lung carcinoma cells (A549) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. Depsipeptides 12-24 H3 histone pseudogene 16 Homo sapiens 155-158 18163657-7 2008 The O/W nanodroplets cause the formation of needlelike dihydrate crystals with monoclinic unit cell and P21/c space group. dihydrate 55-64 H3 histone pseudogene 16 Homo sapiens 104-109 17849419-4 2008 RNAi-induced reduction of HDAC3 in SW480 cells increased their constitutive, butyrate-, TSA-, and TNF-alpha-induced expression of p21, but did not cause all the gene expression changes induced upon general histone deacetylase (HDAC) inhibition. Butyrates 77-85 H3 histone pseudogene 16 Homo sapiens 130-133 18230104-6 2008 RESULTS: The mRNA expression of p21 was significantly higher in the cyclosporine A group than in the control group. Cyclosporine 68-82 H3 histone pseudogene 16 Homo sapiens 32-35 18230104-7 2008 A greater number of positive anti-p21-stained cells were observed in the gingival epithelium of the cyclosporine A group than in the control group. Cyclosporine 100-114 H3 histone pseudogene 16 Homo sapiens 34-37 18230104-8 2008 Significantly higher levels of p21 protein and activity were observed in OECM1 cells after cyclosporine A treatment than in cells without treatment. Cyclosporine 91-105 H3 histone pseudogene 16 Homo sapiens 31-34 18230104-10 2008 CONCLUSION: In the present study, higher p21 mRNA and protein expressions were observed after cyclosporine A treatment. Cyclosporine 94-108 H3 histone pseudogene 16 Homo sapiens 41-44 18230104-11 2008 Thus, an up-regulation of p21 expression, via a p53-independent pathway, by cyclosporine A in gingival and oral epithelial cells was suggested. Cyclosporine 76-90 H3 histone pseudogene 16 Homo sapiens 26-29 17849419-4 2008 RNAi-induced reduction of HDAC3 in SW480 cells increased their constitutive, butyrate-, TSA-, and TNF-alpha-induced expression of p21, but did not cause all the gene expression changes induced upon general histone deacetylase (HDAC) inhibition. trichostatin A 88-91 H3 histone pseudogene 16 Homo sapiens 130-133 18382329-8 2008 2-Aminobicyclo-(2,2,1)-heptane-2-carboxylic acid treatment not only suppressed deoxyribonucleic acid synthesis in association with the up-regulation of the cyclin-dependent kinase inhibitor p21 but also enhanced apoptosis with caspase activation, thereby exerting both cytostatic and cytocidal effects in glioma cells with high LAT1 expression levels. 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid 0-48 H3 histone pseudogene 16 Homo sapiens 190-193 17989348-3 2008 beta-CDODA-Me induced p21 and p27, down-regulated cyclin D1 protein expression, and induced two other proapoptotic proteins, namely nonsteroidal anti-inflammatory drug-activated gene-1 and activating transcription factor-3. beta-cdoda-me 0-13 H3 histone pseudogene 16 Homo sapiens 22-25 17918159-6 2008 Expressions of p27(kip1) and p21(cip1) were significantly increased in LNCaP cells treated with naftopidil. naftopidil 96-106 H3 histone pseudogene 16 Homo sapiens 29-32 18155142-8 2008 The expression of p53, p21 and Mdm2 in both cytotrophoblast and stromal cells was increased following culture in 1% O(2). Oxygen 116-120 H3 histone pseudogene 16 Homo sapiens 23-26 18154926-9 2008 In order to define the components through which NMDA or H(2)O(2) induce the final elements of these pathways, p21 and c-jun, we have performed a detailed functional analysis of c-jun and p21 promoters following plasmid transfection. N-Methylaspartate 48-52 H3 histone pseudogene 16 Homo sapiens 110-113 18154926-9 2008 In order to define the components through which NMDA or H(2)O(2) induce the final elements of these pathways, p21 and c-jun, we have performed a detailed functional analysis of c-jun and p21 promoters following plasmid transfection. N-Methylaspartate 48-52 H3 histone pseudogene 16 Homo sapiens 187-190 18154926-9 2008 In order to define the components through which NMDA or H(2)O(2) induce the final elements of these pathways, p21 and c-jun, we have performed a detailed functional analysis of c-jun and p21 promoters following plasmid transfection. Hydrogen Peroxide 56-64 H3 histone pseudogene 16 Homo sapiens 110-113 18154926-9 2008 In order to define the components through which NMDA or H(2)O(2) induce the final elements of these pathways, p21 and c-jun, we have performed a detailed functional analysis of c-jun and p21 promoters following plasmid transfection. Hydrogen Peroxide 56-64 H3 histone pseudogene 16 Homo sapiens 187-190 18154926-10 2008 Both p21 and c-jun were activated after NMDA treatment, but this activation was abolished after H(2)O(2) treatment. N-Methylaspartate 40-44 H3 histone pseudogene 16 Homo sapiens 5-8 18154926-11 2008 We conclude that NMDA induces an early effect that involves activation of p53, ERK, PAK1, p21 and c-jun. N-Methylaspartate 17-21 H3 histone pseudogene 16 Homo sapiens 90-93 17918159-7 2008 In PC-3 cells, naftopidil induced p21(cip1) but not p27(kip1). naftopidil 15-25 H3 histone pseudogene 16 Homo sapiens 34-37 18172270-14 2008 DP enhanced acetylation of histone H4, increased p21 expression in lung cancer cells, and seemed to shift global gene expression profiles in these cells toward those detected in normal bronchial epithelia. dp 0-2 H3 histone pseudogene 16 Homo sapiens 49-52 18223228-7 2008 Immunoblot and immunohistochemical analysis was used to assess the effect of flavopiridol on cyclin D1 and p21 expression in vitro and in vivo, respectively. alvocidib 77-89 H3 histone pseudogene 16 Homo sapiens 107-110 18223228-10 2008 Flavopiridol (at 7.5 mg/kg) significantly inhibited the growth of xenografted rhabdoid tumors, and its effect was correlated with the induction of p21 and down-modulation of cyclin D1. alvocidib 0-12 H3 histone pseudogene 16 Homo sapiens 147-150 18196959-0 2008 Effects of estradiol and medroxyprogesterone acetate on expression of the cell cycle proteins cyclin D1, p21 and p27 in cultured human breast tissues. Estradiol 11-20 H3 histone pseudogene 16 Homo sapiens 105-108 18196959-0 2008 Effects of estradiol and medroxyprogesterone acetate on expression of the cell cycle proteins cyclin D1, p21 and p27 in cultured human breast tissues. Medroxyprogesterone Acetate 25-52 H3 histone pseudogene 16 Homo sapiens 105-108 18196959-11 2008 The level of p21 was lower (p < 0.001) in pre-HBT than in postm-HBT, whereas p27 levels were higher (p < 0.05) in pre-HBT than in postm- and peritum-HBT. hbt 49-52 H3 histone pseudogene 16 Homo sapiens 13-16 18196959-11 2008 The level of p21 was lower (p < 0.001) in pre-HBT than in postm-HBT, whereas p27 levels were higher (p < 0.05) in pre-HBT than in postm- and peritum-HBT. hbt 67-70 H3 histone pseudogene 16 Homo sapiens 13-16 18196959-11 2008 The level of p21 was lower (p < 0.001) in pre-HBT than in postm-HBT, whereas p27 levels were higher (p < 0.05) in pre-HBT than in postm- and peritum-HBT. hbt 67-70 H3 histone pseudogene 16 Homo sapiens 13-16 18196959-11 2008 The level of p21 was lower (p < 0.001) in pre-HBT than in postm-HBT, whereas p27 levels were higher (p < 0.05) in pre-HBT than in postm- and peritum-HBT. hbt 67-70 H3 histone pseudogene 16 Homo sapiens 13-16 19005580-4 2008 The smenospongine treatment increased expression of p21 and inhibited phosphorylation of Rb in K562 cells, suggesting the p21-Rb pathway play an important role in G1 arrest in K562 cells. smenospongine 4-17 H3 histone pseudogene 16 Homo sapiens 52-55 17943175-3 2008 Here, we provide further evidence that ABT-869 treatment significantly downregulates cyclins D and E but increases the expression of p21 and p27. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 39-42 H3 histone pseudogene 16 Homo sapiens 133-136 19005580-4 2008 The smenospongine treatment increased expression of p21 and inhibited phosphorylation of Rb in K562 cells, suggesting the p21-Rb pathway play an important role in G1 arrest in K562 cells. smenospongine 4-17 H3 histone pseudogene 16 Homo sapiens 122-125 19005580-6 2008 Smenospongine might induce p21 expression via another mechanism than transactivation of p21 promoter. smenospongine 0-13 H3 histone pseudogene 16 Homo sapiens 27-30 19005580-6 2008 Smenospongine might induce p21 expression via another mechanism than transactivation of p21 promoter. smenospongine 0-13 H3 histone pseudogene 16 Homo sapiens 88-91 18725985-6 2008 15d-PGJ(2) induced the expression of CDK inhibitor p21 protein in human chondrosarcoma cells, which appears to be involved in the mechanism of inhibition of cell proliferation. 15d-pgj 0-7 H3 histone pseudogene 16 Homo sapiens 51-54 19112505-8 2008 The induction of p21 was mediated by increased level of phosphorylated p53 at ser-15. Serine 78-81 H3 histone pseudogene 16 Homo sapiens 17-20 18094076-7 2008 Chromatin immunoprecipitation revealed preferential association of c-Jun with the p21 (cyclin-dependent kinase inhibitor) gene promoter after vinblastine treatment. Vinblastine 142-153 H3 histone pseudogene 16 Homo sapiens 82-85 18094076-8 2008 In KB-3 cells, which have compromised p53 function, and in p53-null cells but not in p53 wild-type cells, vinblastine caused down-regulation of p21 expression concomitant with increased c-Jun expression, suggesting a role for c-Jun in negative regulation of the p21 promoter independent of p53. Vinblastine 106-117 H3 histone pseudogene 16 Homo sapiens 144-147 18094076-8 2008 In KB-3 cells, which have compromised p53 function, and in p53-null cells but not in p53 wild-type cells, vinblastine caused down-regulation of p21 expression concomitant with increased c-Jun expression, suggesting a role for c-Jun in negative regulation of the p21 promoter independent of p53. Vinblastine 106-117 H3 histone pseudogene 16 Homo sapiens 262-265 18094076-9 2008 These results provide strong evidence that c-Jun induction in response to vinblastine plays a proapoptotic role in part via down-regulation of p21, promoting cycling and subsequent cell death of mitotically impaired cells. Vinblastine 74-85 H3 histone pseudogene 16 Homo sapiens 143-146 18999881-9 2008 Radiosensitizing effect of VA is not caused by abrogation of G2/M cell cycle arrest, but VA induces p21 and leads to differentiation of HL-60 cells. Valproic Acid 27-29 H3 histone pseudogene 16 Homo sapiens 100-103 18999881-9 2008 Radiosensitizing effect of VA is not caused by abrogation of G2/M cell cycle arrest, but VA induces p21 and leads to differentiation of HL-60 cells. Valproic Acid 89-91 H3 histone pseudogene 16 Homo sapiens 100-103 18089808-3 2007 The protection was associated with suppression of the doxorubicin-induced senescence, where Hsp27 inhibited p53-mediated induction of p21, the major regulator of the senescence program. Doxorubicin 54-65 H3 histone pseudogene 16 Homo sapiens 134-137 18089834-6 2007 Using a human nontumorigenic mammary gland epithelial cell line, MCF10A, we confirm that in the absence of detectable DNA damage, chloroquine activates the tumor-suppressor p53 and the p53 downstream target gene p21, resulting in G(1) cell cycle arrest. Chloroquine 130-141 H3 histone pseudogene 16 Homo sapiens 212-215 18056187-14 2007 Baseline p21(waf) expression was associated with response to erlotinib and so might be useful as a tool to select patients for erlotinib therapy in this setting. Erlotinib Hydrochloride 61-70 H3 histone pseudogene 16 Homo sapiens 9-12 17916909-8 2007 Silibinin strongly increased phospho-extracellular signal-regulated kinase 1/2 (ERK1/2), Cip1/p21 and Kip1/p27 (cyclin-dependent kinase inhibitors) levels but moderately decreased Bcl-2 and survivin levels. Silybin 0-9 H3 histone pseudogene 16 Homo sapiens 94-97 17916909-11 2007 At molecular level, silibinin increased IGFBP-3, Cip1/p21, Kip1/p27 levels and ERK1/2 activation and decreased Bcl-2, survivin and VEGF levels in tumors. Silybin 20-29 H3 histone pseudogene 16 Homo sapiens 54-57 18031612-10 2007 The expressions of p21 and p53 was upregulated with PAB treatment, and cyclin B1 was upregulated and transported from the cytoplasm to nuclei, and sustained stable levels. pseudolaric acid B 52-55 H3 histone pseudogene 16 Homo sapiens 19-22 17904874-5 2007 Prolonged SP600125 treatment downregulated p21, Bax and Mdm2 expression, but increased the level of the cellular p53-Mdm2 complex. pyrazolanthrone 10-18 H3 histone pseudogene 16 Homo sapiens 43-46 17904874-6 2007 Taken together, we show that SP600125 could induce G2/M cell cycle arrest and endoreduplication in a p21 independent manner, and that SP600125 could also post-translationally modify p53 to modify its function. pyrazolanthrone 29-37 H3 histone pseudogene 16 Homo sapiens 101-104 18056187-14 2007 Baseline p21(waf) expression was associated with response to erlotinib and so might be useful as a tool to select patients for erlotinib therapy in this setting. Erlotinib Hydrochloride 127-136 H3 histone pseudogene 16 Homo sapiens 9-12 18006776-4 2007 RESULTS: PPARgamma is overexpressed in ACHN cells and barely detectable in 786-0 cells, and treatment with DIM-C-pPhtBu induces proteasome-dependent degradation of cyclin D1 and variable effects on p21 and p27 expression in both cell lines. 1,1-bis(3'-indolyl)-1-(4-t-butylphenyl)methane 107-119 H3 histone pseudogene 16 Homo sapiens 198-201 17945324-9 2007 In our present study, reduced p21 and Gadd45a expressions and increased centrosomal abnormality (atopic and multiple centrosomes) were observed in both arsenite-treated H1355 and p53-inhibited BEAS-2B cells as compared with similarly treated BEAS-2B cells. arsenite 152-160 H3 histone pseudogene 16 Homo sapiens 30-33 18088464-6 2007 The p21, survivin, cdc2 and Wee1Hu genes may be related to the differentiation and/or apoptosis of NB4 cells induced by As2O3. Arsenic Trioxide 120-125 H3 histone pseudogene 16 Homo sapiens 4-7 18088464-7 2007 It is concluded that p21, survivin, cdc2 and Wee1Hu may play an important role in the mechanism underling arsenic trioxide-mediated NB4 cell apoptosis. Arsenic Trioxide 106-122 H3 histone pseudogene 16 Homo sapiens 21-24 17888568-3 2007 Both POH and PA elicited dose-dependent cytotoxicity, induced cell cycle arrest and apoptosis with increasing expression of bax, p21 and caspase-3 activity in both the cell lines. perillyl alcohol 5-8 H3 histone pseudogene 16 Homo sapiens 129-132 17888568-3 2007 Both POH and PA elicited dose-dependent cytotoxicity, induced cell cycle arrest and apoptosis with increasing expression of bax, p21 and caspase-3 activity in both the cell lines. perillic acid 13-15 H3 histone pseudogene 16 Homo sapiens 129-132 18006756-7 2007 Although doxorubicin failed to induce TP53 expression or functional activity, quinacrine induced TP53 mRNA and protein expression, increased TP53 reporter activity and p21 protein expression, and induced growth inhibition in these wild-type TP53 cell lines. Quinacrine 78-88 H3 histone pseudogene 16 Homo sapiens 168-171 17884124-6 2007 CdCl(2) and the low-dose combined treatment inhibited mesenchymal proliferation at 12 h, which was associated with induction of p21(cip1) and inhibition of phospho-c-Jun. cdcl 0-4 H3 histone pseudogene 16 Homo sapiens 128-131 17893511-8 2007 p27 levels were slightly decreased, whereas p53 and p21 levels were significantly upregulated in doxorubicin-treated MCF-7 cells. Doxorubicin 97-108 H3 histone pseudogene 16 Homo sapiens 52-55 17996705-3 2007 Here we show that the acetylation of two lysine residues in p53 promotes recruitment of the TFIID subunit TAF1 to the p21 promoter through its bromodomains. Lysine 41-47 H3 histone pseudogene 16 Homo sapiens 118-121 17996705-4 2007 UV irradiation of cells diacetylates p53 at lysines 373 and 382, which in turn recruits TAF1 to a distal p53-binding site on the p21 promoter prior to looping to the core promoter. Lysine 44-51 H3 histone pseudogene 16 Homo sapiens 129-132 17959036-7 2007 IFNalpha markedly upregulated p53, Bax, Mdm2, and p21, downregulated Bcl-2, and activated caspase-3 and PARP cleavage in response to doxorubicin in U2OS cells. Doxorubicin 133-144 H3 histone pseudogene 16 Homo sapiens 50-53 18056950-4 2007 Maintenance of WI38 and IMR90 cells in 1.5% or 3% O(2) concentration significantly delayed the appearance of replicative senescence compared to cells grown in 20% O(2), induced the hypoxia-inducible factor-1alpha, and resulted in reduced expression levels of the key cell cycle modulators, namely p21 and p16. Oxygen 50-54 H3 histone pseudogene 16 Homo sapiens 297-300 17724373-6 2007 The results clearly demonstrated that both CN-BA and CN-BA-Me activated PPARgamma-dependent responses in colon (caveolin-1) and pancreatic (p21) cancer cells, whereas induction of KLF4 by these compounds in colon cancer cells was PPARgamma independent and also dependent on cell context. cn 43-45 H3 histone pseudogene 16 Homo sapiens 140-143 17516137-6 2007 Through interfering with the cell cycle of tumor cells, PS may induce apoptosis by downregulating the expression level of cyclin D1 and upregulating the level of p21 protein. Polysaccharides 56-58 H3 histone pseudogene 16 Homo sapiens 162-165 18226366-1 2007 OBJECTIVE: To explore the relationship between genetic polymorphism of P53, P21, CCND1 and susceptibility of chromosomal damage induced by vinyl chloride monomer (VCM). Vinyl Chloride 139-153 H3 histone pseudogene 16 Homo sapiens 76-79 17822515-6 2007 This article discusses three cellular regulators (p53, p21 and TRAIL) induced in synovial tissue that are important for iron metabolism. Iron 120-124 H3 histone pseudogene 16 Homo sapiens 55-58 17957141-6 2007 The CDK-inhibitor p21 was classified as a Class I gene, being significantly activated under cell cycle arrest conditions (i.e. doxorubicin and Nutlin-3) but not during UVC-induced apoptosis. Doxorubicin 127-138 H3 histone pseudogene 16 Homo sapiens 18-21 17957141-6 2007 The CDK-inhibitor p21 was classified as a Class I gene, being significantly activated under cell cycle arrest conditions (i.e. doxorubicin and Nutlin-3) but not during UVC-induced apoptosis. nutlin 3 143-151 H3 histone pseudogene 16 Homo sapiens 18-21 17914575-8 2007 To demonstrate the degree of loss of function, functional assays in yeast and bacteria with oligonucleotides for competitive electrophoretic mobility shift assays (EMSAs) were done proving that this mutation decreases TP53 ability to bind DNA of the TP53 response element from the human p21 gene. Oligonucleotides 92-108 H3 histone pseudogene 16 Homo sapiens 287-290 17595331-4 2007 Many attributes of primitive HSCs in the low-oxygenic osteoblastic niche, such as quiescence, and calcium receptor, N-cadherin, Notch1, and p21 are higher in the ROS(low) population. Reactive Oxygen Species 162-165 H3 histone pseudogene 16 Homo sapiens 140-143 17879397-5 2007 Silibinin-reduced HuH7 cell growth was associated with significantly up-regulated p21/CDK4 and p27/CDK4 complexes, down-regulated Rb-phosphorylation and E2F1/DP1 complex. Silybin 0-9 H3 histone pseudogene 16 Homo sapiens 82-85 17624594-8 2007 Western blot analyses showed that while pretreatment of TEA and Tet produced an increase in expressions of p53, p21, and Bax, pretreatment of these two agents led to a decrease in expressions of heat shock protein (hsp)90alpha, hsp90beta, and hsp70. Tetraethylammonium 56-59 H3 histone pseudogene 16 Homo sapiens 112-115 17624594-8 2007 Western blot analyses showed that while pretreatment of TEA and Tet produced an increase in expressions of p53, p21, and Bax, pretreatment of these two agents led to a decrease in expressions of heat shock protein (hsp)90alpha, hsp90beta, and hsp70. tetrandrine 64-67 H3 histone pseudogene 16 Homo sapiens 112-115 17845507-4 2007 Western blot assay showed that chalcone significantly increases the expression of p21 and p27 proteins, and decreases the levels of cyclin B1, cyclin A and Cdc2, thereby contributing to cell cycle arrest. Chalcone 31-39 H3 histone pseudogene 16 Homo sapiens 82-85 17803520-7 2007 Moreover, incubation with melatonin induces a decrease in p21 expression in these cells that is partially blocked by co-incubation with TPA. Melatonin 26-35 H3 histone pseudogene 16 Homo sapiens 58-61 17803520-7 2007 Moreover, incubation with melatonin induces a decrease in p21 expression in these cells that is partially blocked by co-incubation with TPA. Tetradecanoylphorbol Acetate 136-139 H3 histone pseudogene 16 Homo sapiens 58-61 17696482-10 2007 Pterostilbene increased the p53, p21, p27, and p16 proteins and decreased levels of cyclin A, cyclin E, cyclin-dependent kinase 2 (Cdk2), Cdk4, and Cdk6, but the expression of cyclin D1 was not affected. pterostilbene 0-13 H3 histone pseudogene 16 Homo sapiens 33-36 17397922-2 2007 Treatment of K562 cells with IQDMA resulted in G2/M phase cell cycle arrest, presumably involving the concomitant up-regulation of p21 and apoptosis through up-regulation of FasL and sequential activation of caspase-8 and caspase-3. N'-(11H-indolo(3,2-c)quinolin-6-yl)-N,N-dimethylethane-1,2-diamine 29-34 H3 histone pseudogene 16 Homo sapiens 131-134 17397922-5 2007 Further investigation showed that SP600125 reduced the activation of FasL, caspase-3, caspase-8, and led to a marked decline of p21. pyrazolanthrone 34-42 H3 histone pseudogene 16 Homo sapiens 128-131 17951408-5 2007 The p53-small interfering RNA transfection into the hOGG1-deficient GM00637 markedly inhibited the H(2)O(2)-induced activation of p53-downstream target proteins such as p21, Noxa, and caspase-3/7, which eventually resulted in the increased cell viability. gm00637 68-75 H3 histone pseudogene 16 Homo sapiens 169-172 17951408-5 2007 The p53-small interfering RNA transfection into the hOGG1-deficient GM00637 markedly inhibited the H(2)O(2)-induced activation of p53-downstream target proteins such as p21, Noxa, and caspase-3/7, which eventually resulted in the increased cell viability. Hydrogen Peroxide 99-107 H3 histone pseudogene 16 Homo sapiens 169-172 17938262-5 2007 Exposure of PC-3 and LNCaP cells to honokiol resulted in the induction of p21 (PC-3 and LNCaP) and p53 protein expression (LNCaP). honokiol 36-44 H3 histone pseudogene 16 Homo sapiens 74-77 17938263-0 2007 p21 and p27 induction by silibinin is essential for its cell cycle arrest effect in prostate carcinoma cells. Silybin 25-34 H3 histone pseudogene 16 Homo sapiens 0-3 17938263-1 2007 Recent studies have shown that silibinin induces p21/Cip1 and p27/Kip1 and G1 arrest in different prostate cancer cells irrespective of p53 status; however, biological significance and mechanism of such induction have not been studied. Silybin 31-40 H3 histone pseudogene 16 Homo sapiens 49-52 17938263-5 2007 Next, studies were done to examine mechanisms of their induction where cycloheximide-chase experiments showed that silibinin increases p21 and p27 protein half-life. Silybin 115-124 H3 histone pseudogene 16 Homo sapiens 135-138 17938263-8 2007 Further, silibinin caused a marked increase in p21 and p27 mRNA levels together with an increase in their promoter activity, also indicating a transcriptional mechanism. Silybin 9-18 H3 histone pseudogene 16 Homo sapiens 47-50 17938263-9 2007 Together, our results for the first time identify a central role of p21 and p27 induction and their regulatory mechanism in silibinin-mediated cell cycle arrest. Silybin 124-133 H3 histone pseudogene 16 Homo sapiens 68-71 17626009-7 2007 Molecular mediators on the way from increased ROS levels to the observed growth arrest include p38 MAPK, p53, and p21. Reactive Oxygen Species 46-49 H3 histone pseudogene 16 Homo sapiens 114-117 17875686-6 2007 We showed that the induction of p21 by HDACi was significantly impaired in HKe-3 cells with silenced STAT1 expression and showed that the ability of butyrate to activate p21 transcription was diminished in STAT1-deficient HKe-3 cells. Butyrates 149-157 H3 histone pseudogene 16 Homo sapiens 170-173 17875686-7 2007 Finally, we used cells with targeted deletion of p21 to confirm that p21 protects cells from butyrate-induced apoptosis, strongly suggesting that in these cells STAT1 deficiency promotes butyrate-induced apoptosis through impaired induction of p21. Butyrates 93-101 H3 histone pseudogene 16 Homo sapiens 69-72 17875686-7 2007 Finally, we used cells with targeted deletion of p21 to confirm that p21 protects cells from butyrate-induced apoptosis, strongly suggesting that in these cells STAT1 deficiency promotes butyrate-induced apoptosis through impaired induction of p21. Butyrates 93-101 H3 histone pseudogene 16 Homo sapiens 69-72 17875686-6 2007 We showed that the induction of p21 by HDACi was significantly impaired in HKe-3 cells with silenced STAT1 expression and showed that the ability of butyrate to activate p21 transcription was diminished in STAT1-deficient HKe-3 cells. Butyrates 149-157 H3 histone pseudogene 16 Homo sapiens 32-35 17458894-6 2007 The efficacy of docetaxel and Iressa differed in the three cell lines and an important synergistic interaction was observed with the sequence 1-h docetaxel --> 72-h Iressa during which Iressa doubled the fraction of docetaxel-induced apoptotic cells, amplifying a caspase-dependent apoptosis and inhibiting docetaxel-induced p21 hyperexpression. Docetaxel 16-25 H3 histone pseudogene 16 Homo sapiens 328-331 17404572-8 2007 The inability of overexpressed p18 Bax to locate to the nucleus, and the As(2)O(3)-induced reduction of p21 Bax in the cytosol, suggest an As(2)O(3)-induced mechanism where p18 Bax gets cleaved and "trapped" in the nucleus. (2)o(3) 75-82 H3 histone pseudogene 16 Homo sapiens 104-107 17404572-8 2007 The inability of overexpressed p18 Bax to locate to the nucleus, and the As(2)O(3)-induced reduction of p21 Bax in the cytosol, suggest an As(2)O(3)-induced mechanism where p18 Bax gets cleaved and "trapped" in the nucleus. Arsenic Trioxide 73-82 H3 histone pseudogene 16 Homo sapiens 104-107 17700259-10 2007 The carbon ions had a stronger effect on p53 and p21 expression than the gamma-ray irradiation. Carbon 4-10 H3 histone pseudogene 16 Homo sapiens 49-52 17458894-6 2007 The efficacy of docetaxel and Iressa differed in the three cell lines and an important synergistic interaction was observed with the sequence 1-h docetaxel --> 72-h Iressa during which Iressa doubled the fraction of docetaxel-induced apoptotic cells, amplifying a caspase-dependent apoptosis and inhibiting docetaxel-induced p21 hyperexpression. Docetaxel 146-155 H3 histone pseudogene 16 Homo sapiens 328-331 17458894-6 2007 The efficacy of docetaxel and Iressa differed in the three cell lines and an important synergistic interaction was observed with the sequence 1-h docetaxel --> 72-h Iressa during which Iressa doubled the fraction of docetaxel-induced apoptotic cells, amplifying a caspase-dependent apoptosis and inhibiting docetaxel-induced p21 hyperexpression. Docetaxel 146-155 H3 histone pseudogene 16 Homo sapiens 328-331 17458894-6 2007 The efficacy of docetaxel and Iressa differed in the three cell lines and an important synergistic interaction was observed with the sequence 1-h docetaxel --> 72-h Iressa during which Iressa doubled the fraction of docetaxel-induced apoptotic cells, amplifying a caspase-dependent apoptosis and inhibiting docetaxel-induced p21 hyperexpression. Docetaxel 146-155 H3 histone pseudogene 16 Homo sapiens 328-331 17390104-5 2007 We found that rapamysin inhibited ACNU-induced p21 induction, and knocking down of p21 protein by siRNA enhanced ACNU-induced apoptosis in U251MG cells. Nimustine 34-38 H3 histone pseudogene 16 Homo sapiens 47-50 17390104-5 2007 We found that rapamysin inhibited ACNU-induced p21 induction, and knocking down of p21 protein by siRNA enhanced ACNU-induced apoptosis in U251MG cells. Nimustine 113-117 H3 histone pseudogene 16 Homo sapiens 83-86 17655223-2 2007 K(UO2)(SO4)(OH)(H2O) (KUS1) crystallizes in space group P21/c, a = 8.0521(4) A, b = 7.9354(4) A, c = 11.3177(6) A, beta = 107.6780(10) degrees , V = 689.01(6) A3, and Z = 4. uo2 2-5 H3 histone pseudogene 16 Homo sapiens 56-61 17632540-8 2007 Furthermore, the inhibition of CaMKII decreased membrane-bound Tiam1 and GTP-bound Rac1, which are known to be involved in p21 expression and tumor growth in a variety of solid malignant neoplasms. Guanosine Triphosphate 73-76 H3 histone pseudogene 16 Homo sapiens 123-126 17609657-6 2007 We speculate that the higher rate of differentiation exhibited by the CD cells is due to the up-regulation of follistatin, peroxisome-proliferator-activated receptor-gamma co-activator-1alpha (PGC-1alpha), p21, and the myogenic genes, and the down-regulation of TGF-beta1 and myostatin. Cadmium 70-72 H3 histone pseudogene 16 Homo sapiens 206-209 17655223-2 2007 K(UO2)(SO4)(OH)(H2O) (KUS1) crystallizes in space group P21/c, a = 8.0521(4) A, b = 7.9354(4) A, c = 11.3177(6) A, beta = 107.6780(10) degrees , V = 689.01(6) A3, and Z = 4. Water 16-19 H3 histone pseudogene 16 Homo sapiens 56-61 17507429-6 2007 Testosterone reduced protein levels of cyclins D(1) and E and phosphorylation of retinoblastoma protein while elevating levels of p21(cip1) and p27(kip1). Testosterone 0-12 H3 histone pseudogene 16 Homo sapiens 130-133 17699787-5 2007 Relative to indole-3-carbinol, OSU-A9 displays a striking qualitative similarity in its effects on the phosphorylation or expression of multiple signaling targets, including Akt, mitogen-activated protein kinases, Bcl-2 family members, survivin, nuclear factor-kappaB, cyclin D1, p21, and p27. osu-a9 31-37 H3 histone pseudogene 16 Homo sapiens 280-283 17606321-10 2007 Treatment of the cells with either SPC or wortmannin increased the levels of p21, but decreased that of cyclin B1 and Cdc2. Wortmannin 42-52 H3 histone pseudogene 16 Homo sapiens 77-80 17766653-4 2007 Western blot analysis revealed degradation of cyclin D1 and an increase in cyclin-dependent kinases p21 and p27 with VPA treatment. Valproic Acid 117-120 H3 histone pseudogene 16 Homo sapiens 100-103 17559811-7 2007 The major role of the p53-p21 pathway in oxaliplatin sensitivity was confirmed in the p53 wild-type HCT116 cell line, using siRNA duplex, and knockdown of the TAp73 protein also enhanced resistance to oxaliplatin in this cell line. Oxaliplatin 41-52 H3 histone pseudogene 16 Homo sapiens 26-29 17256134-8 2007 PB + CRA induced p21 expression and cell-cycle arrest in G1 phase, while TX and DOXO induced G2/M arrest. Phenylbutyrates 0-2 H3 histone pseudogene 16 Homo sapiens 17-20 17611411-4 2007 This sensitization of cisplatin-induced apoptosis was associated with upregulation of p53, Bax and p21 in U2OS cells. Cisplatin 22-31 H3 histone pseudogene 16 Homo sapiens 99-102 17695552-3 2007 Western blot analysis was used to study celecoxib effects on the expression of mitogen-activated protein kinases (MAPKs), p53, p21, 14-3-4sigma, Bcl-2 and Bax. Celecoxib 40-49 H3 histone pseudogene 16 Homo sapiens 127-130 17762396-5 2007 Bortezomib produced significant growth inhibition in these cells (mean IC50 values: 1.26, 9.44 and 8.63 micromol/l, respectively) and was also observed to decrease the activity of the extracellular signal-regulated kinase 1/2 and Akt signal pathways, increasing the accumulation of p21. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 282-285 17389612-4 2007 In the studies examining changes in cell cycle and apoptosis regulators, isosilybin B and isosilybin A resulted in a decrease in the levels of both cyclins (D1, D3, E and A) and cyclin-dependent kinases (Cdk2, Cdk4 and cell division cycle 25A), but caused an increase in p21, p27 and p53 levels, except in 22Rv1 cells where isosilybin B caused a decrease in p21 protein level. isosilybin A 73-85 H3 histone pseudogene 16 Homo sapiens 271-274 17389612-4 2007 In the studies examining changes in cell cycle and apoptosis regulators, isosilybin B and isosilybin A resulted in a decrease in the levels of both cyclins (D1, D3, E and A) and cyclin-dependent kinases (Cdk2, Cdk4 and cell division cycle 25A), but caused an increase in p21, p27 and p53 levels, except in 22Rv1 cells where isosilybin B caused a decrease in p21 protein level. isosilybin A 73-85 H3 histone pseudogene 16 Homo sapiens 358-361 17389612-4 2007 In the studies examining changes in cell cycle and apoptosis regulators, isosilybin B and isosilybin A resulted in a decrease in the levels of both cyclins (D1, D3, E and A) and cyclin-dependent kinases (Cdk2, Cdk4 and cell division cycle 25A), but caused an increase in p21, p27 and p53 levels, except in 22Rv1 cells where isosilybin B caused a decrease in p21 protein level. isosilybin A 90-102 H3 histone pseudogene 16 Homo sapiens 271-274 17389612-4 2007 In the studies examining changes in cell cycle and apoptosis regulators, isosilybin B and isosilybin A resulted in a decrease in the levels of both cyclins (D1, D3, E and A) and cyclin-dependent kinases (Cdk2, Cdk4 and cell division cycle 25A), but caused an increase in p21, p27 and p53 levels, except in 22Rv1 cells where isosilybin B caused a decrease in p21 protein level. isosilybin A 90-102 H3 histone pseudogene 16 Homo sapiens 358-361 20535395-7 2007 Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest. Ascorbic Acid 139-152 H3 histone pseudogene 16 Homo sapiens 118-121 17185354-6 2007 Expression of p21 was determined by real-time PCR in Barrett"s oesophagus cell lines with or without LCA. Lithocholic Acid 101-104 H3 histone pseudogene 16 Homo sapiens 14-17 17185354-11 2007 LCA and ATRA caused a synergistic increase in RA signalling as shown by increased p21 (p<0.01). Lithocholic Acid 0-3 H3 histone pseudogene 16 Homo sapiens 82-85 17185354-11 2007 LCA and ATRA caused a synergistic increase in RA signalling as shown by increased p21 (p<0.01). Tretinoin 8-12 H3 histone pseudogene 16 Homo sapiens 82-85 17185354-11 2007 LCA and ATRA caused a synergistic increase in RA signalling as shown by increased p21 (p<0.01). Tretinoin 10-12 H3 histone pseudogene 16 Homo sapiens 82-85 20535395-7 2007 Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest. Ascorbic Acid 42-55 H3 histone pseudogene 16 Homo sapiens 118-121 17475222-5 2007 Guggulsterone suppressed the proliferation of cells through inhibition of DNA synthesis, producing cell cycle arrest in S-phase, and this arrest correlated with a decrease in the levels of cyclin D1 and cdc2 and a concomitant increase in the levels of cyclin-dependent kinase inhibitor p21 and p27. pregna-4,17-diene-3,16-dione 0-13 H3 histone pseudogene 16 Homo sapiens 286-289 17672346-3 2007 RESULT: ASMq flavonoids significantly inhibited growth of HepG2 cells in vitro, arrested HepG2 in the sub-G, phase, induced cell apoptosis and significantly down-regulated expression level of Bcl-2 mRNA, and up-regulated expression of p53, p21, Bax gene mRNA expressions. asmq flavonoids 8-23 H3 histone pseudogene 16 Homo sapiens 240-243 17477906-0 2007 Cytoplasmic localization and ubiquitination of p21(Cip1) by reactive oxygen species. Reactive Oxygen Species 60-83 H3 histone pseudogene 16 Homo sapiens 47-50 17477906-1 2007 Reactive oxygen species were previously shown to trigger p21(Cip1) protein degradation through a proteasome-dependent pathway, however the detailed mechanism of degradation remains to be elucidated. Reactive Oxygen Species 0-23 H3 histone pseudogene 16 Homo sapiens 57-60 17477906-2 2007 In this report, we showed that p21(Cip1) was degraded at an early phase after low dose H(2)O(2) treatment of a variety of cell types and that preincubation of cells with the antioxidant, N-acetylcysteine, prolonged p21(Cip1) half-life. Hydrogen Peroxide 87-95 H3 histone pseudogene 16 Homo sapiens 31-34 17477906-2 2007 In this report, we showed that p21(Cip1) was degraded at an early phase after low dose H(2)O(2) treatment of a variety of cell types and that preincubation of cells with the antioxidant, N-acetylcysteine, prolonged p21(Cip1) half-life. Acetylcysteine 187-203 H3 histone pseudogene 16 Homo sapiens 31-34 17477906-3 2007 A mutant p21(Cip1) in which all six lysines were changed to arginines was protected against H(2)O(2) treatment. Lysine 36-43 H3 histone pseudogene 16 Homo sapiens 9-12 17477906-3 2007 A mutant p21(Cip1) in which all six lysines were changed to arginines was protected against H(2)O(2) treatment. Arginine 60-69 H3 histone pseudogene 16 Homo sapiens 9-12 17477906-5 2007 Disruption of the two nuclear export signal (NES) sequences in p21(Cip1), or treatment with leptomycin B blocked H(2)O(2)-induced p21(Cip1) degradation. leptomycin B 92-104 H3 histone pseudogene 16 Homo sapiens 130-133 17477906-6 2007 Altogether, these results demonstrate that reactive oxygen species induce p21(Cip1) degradation through an NES-, Skp2-, and ubiquitin-dependent pathway. Reactive Oxygen Species 43-66 H3 histone pseudogene 16 Homo sapiens 74-77 17148504-4 2007 Our findings have shown that Astragalus saponins (AST) inhibit cell proliferation through accumulation in S phase and G2/M arrest, with concomitant suppression of p21 expression and inhibition of cyclin-dependent kinase activity. Saponins 40-48 H3 histone pseudogene 16 Homo sapiens 163-166 17314138-6 2007 Conversely, its interaction with a key cysteine residue on p21(ras), led to its activation, an obligatory activity for AS101-induced neuronal differentiation. Cysteine 39-47 H3 histone pseudogene 16 Homo sapiens 59-62 17314138-6 2007 Conversely, its interaction with a key cysteine residue on p21(ras), led to its activation, an obligatory activity for AS101-induced neuronal differentiation. ammonium trichloro(dioxoethylene-O,O'-)tellurate 119-124 H3 histone pseudogene 16 Homo sapiens 59-62 17371838-3 2007 Treatment of cells with doxorubicin causes phosphorylation and acetylation of p53, transcriptional upregulation of p21 and other target genes, and growth arrest. Doxorubicin 24-35 H3 histone pseudogene 16 Homo sapiens 115-118 17224908-6 2007 Proteasome inhibition by MG132 increases the occupancy of p53 protein at p53-responsive p21(waf1) promoter. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 25-30 H3 histone pseudogene 16 Homo sapiens 88-91 17428261-6 2007 The inhibitory effect of simvastatin on cell proliferation seemed to be associated with cell cycle arrest and increased expression of p21, p27, and activated caspase-3. Simvastatin 25-36 H3 histone pseudogene 16 Homo sapiens 134-137 17441809-0 2007 Vitamin K2 inhibits the proliferation of HepG2 cells by up-regulating the transcription of p21 gene. Vitamin K 2 0-10 H3 histone pseudogene 16 Homo sapiens 91-94 17464423-8 2007 The present results demonstrate that TIMP-1 may be one of the mediators that regulate the inhibitory effect of IL-6 on BEL-7402 proliferation in which STAT3 signal transduction and p21 up-regulation also play important roles. bel-7402 119-127 H3 histone pseudogene 16 Homo sapiens 181-184 17485089-5 2007 In addition, our immunoblot data revealed that DHMC treatment led to down-regulation of Bcl-xl, Bax, p21, Cox-2, p53 and upregulation of c-Myc. 7,8-dihydroxy-4-methylcoumarin 47-51 H3 histone pseudogene 16 Homo sapiens 101-104 17504227-6 2007 Moreover, while nutlin-3 up-regulated the expression of cyclin dependent kinase inhibitor p21, a p53-target gene mediating cell cycle block and showing anti-apoptotic activity, the simultaneous addition of TRAIL plus nutlin-3 induced the caspase-dependent cleavage of p21. nutlin 3 16-24 H3 histone pseudogene 16 Homo sapiens 90-93 17504227-6 2007 Moreover, while nutlin-3 up-regulated the expression of cyclin dependent kinase inhibitor p21, a p53-target gene mediating cell cycle block and showing anti-apoptotic activity, the simultaneous addition of TRAIL plus nutlin-3 induced the caspase-dependent cleavage of p21. nutlin 3 16-24 H3 histone pseudogene 16 Homo sapiens 268-271 17437483-3 2007 GSP-induced inhibition of cell proliferation was associated with an increase in G1-phase arrest at 24 h, which was mediated through the inhibition of cyclin-dependent kinases (Cdk) Cdk2, Cdk4, Cdk6 and cyclins D1, D2 and E and simultaneous increase in protein expression of cyclin-dependent kinase inhibitors (Cdki), Cip1/p21 and Kip1/p27, and enhanced binding of Cdki-Cdk. Grape Seed Proanthocyanidins 0-3 H3 histone pseudogene 16 Homo sapiens 322-325 17441809-6 2007 Whether vitamin K2 regulates the gene expression through action on the p21 promoter region was investigated by luciferase assay. Vitamin K 2 8-18 H3 histone pseudogene 16 Homo sapiens 71-74 17441809-10 2007 The expression of cell cycle regulatory protein p21 was induced by vitamin K2 treatment, but p27 was not. Vitamin K 2 67-77 H3 histone pseudogene 16 Homo sapiens 48-51 17441809-11 2007 By the luciferase assay, vitamin K2 significantly activated the promoter of p21. Vitamin K 2 25-35 H3 histone pseudogene 16 Homo sapiens 76-79 17441809-12 2007 Knock-down of p21 by siRNA reversed the growth inhibition of HepG2 cells by vitamin K2. Vitamin K 2 76-86 H3 histone pseudogene 16 Homo sapiens 14-17 17441809-13 2007 CONCLUSIONS: The findings suggest that vitamin K2 suppresses the proliferation of HCC cells by blocking the cell cycle G1/S progression through the transcriptional induction of p21. Vitamin K 2 39-49 H3 histone pseudogene 16 Homo sapiens 177-180 17513606-4 2007 We found that Tubocapsanolide A treatment led to up-regulation of cyclin E, p21, and p27, whereas other cyclins and cyclin-dependent kinases were not affected in A549 cells. tubocapsanolide 14-29 H3 histone pseudogene 16 Homo sapiens 76-79 17390014-8 2007 However, the apoptosis-related proteins such as p21 and Bax were overexpressed by As4O6. Arsenic Trioxide 82-87 H3 histone pseudogene 16 Homo sapiens 48-51 17388562-7 2007 25 GPa, there is a phase transition of ammonium cyanate (from tetragonal P4/nmm to monoclinic P21/m) involving a rearrangement of the ammonium cyanate molecules. ammonium cyanate 39-55 H3 histone pseudogene 16 Homo sapiens 94-99 17388562-7 2007 25 GPa, there is a phase transition of ammonium cyanate (from tetragonal P4/nmm to monoclinic P21/m) involving a rearrangement of the ammonium cyanate molecules. ammonium cyanate 134-150 H3 histone pseudogene 16 Homo sapiens 94-99 17388562-9 2007 The crystalline phase of urea obtained above 535 GPa also has P21/m symmetry (Z = 2). Urea 25-29 H3 histone pseudogene 16 Homo sapiens 62-67 17440101-0 2007 p53 and p21 determine the sensitivity of noscapine-induced apoptosis in colon cancer cells. Noscapine 41-50 H3 histone pseudogene 16 Homo sapiens 8-11 17440101-3 2007 In this study, we compared chemosensitivity, cell cycle distribution, and apoptosis on noscapine treatment in four cell lines derived from the colorectal carcinoma HCT116 cells: p53(+/+) (p53-wt), p53(-/-) (p53-null), p21(-/-) (p21-null), and BAX(-/-) (BAX-null). Noscapine 87-96 H3 histone pseudogene 16 Homo sapiens 218-221 17335275-6 2007 Crystals of trans-bis(2,2"-dioxybiphenyl)tetrachloro-cyclotetraphosphazene were obtained in two different space groups: Pnna (orthorhombic) and P21/n (monoclinic). trans-bis(2,2"-dioxybiphenyl)tetrachloro-cyclotetraphosphazene 12-74 H3 histone pseudogene 16 Homo sapiens 144-147 17440101-3 2007 In this study, we compared chemosensitivity, cell cycle distribution, and apoptosis on noscapine treatment in four cell lines derived from the colorectal carcinoma HCT116 cells: p53(+/+) (p53-wt), p53(-/-) (p53-null), p21(-/-) (p21-null), and BAX(-/-) (BAX-null). Noscapine 87-96 H3 histone pseudogene 16 Homo sapiens 228-231 17440101-4 2007 Using these isogenic variants, we investigated the roles of p53, BAX, and p21 in the cellular response to treatment with noscapine. Noscapine 121-130 H3 histone pseudogene 16 Homo sapiens 74-77 17440101-7 2007 Conversely, loss of p53 and p21 alleles had a counter effect on both BAX and Bcl-2 expression and the p53-null and p21-null cells were significantly resistant to the antiproliferative and apoptotic effects of noscapine. Noscapine 209-218 H3 histone pseudogene 16 Homo sapiens 28-31 17440101-7 2007 Conversely, loss of p53 and p21 alleles had a counter effect on both BAX and Bcl-2 expression and the p53-null and p21-null cells were significantly resistant to the antiproliferative and apoptotic effects of noscapine. Noscapine 209-218 H3 histone pseudogene 16 Homo sapiens 115-118 17440101-9 2007 Interestingly, despite increased levels of p53, p21-null cells were resistant to apoptosis, suggesting a proapoptotic role of p21 and implying that p53 is a necessary but not sufficient condition for noscapine-mediated apoptosis. Noscapine 200-209 H3 histone pseudogene 16 Homo sapiens 48-51 17230511-9 2007 p21 induction is closely associated with FK228 or TSA but not 5-Aza, which is mediated via p53-independent pathway. romidepsin 41-46 H3 histone pseudogene 16 Homo sapiens 0-3 17230511-9 2007 p21 induction is closely associated with FK228 or TSA but not 5-Aza, which is mediated via p53-independent pathway. trichostatin A 50-53 H3 histone pseudogene 16 Homo sapiens 0-3 17230511-12 2007 The elevated p21 level mediated via p53 independent pathway is a hallmark of FK228 mechanism of action. romidepsin 77-82 H3 histone pseudogene 16 Homo sapiens 13-16 17055654-7 2007 Increased levels of p21 can result in growth inhibition, reduced repair from the p21-PCNA interaction, and increased generation of reactive oxygen. Oxygen 140-146 H3 histone pseudogene 16 Homo sapiens 20-23 17326628-3 2007 In meso-2, the right/left-handed chirality of the originally formed chain is transferred oppositely to adjacent chains through the interchain hydrogen-bonding interactions of hexameric water clusters, leading to the formation of meso-2 with a central symmetrical space group, P21/n, in which the 1D helical chains are packed in an alternating right- and left-handed chirality. Water 185-190 H3 histone pseudogene 16 Homo sapiens 276-279 17409429-7 2007 PD98059 prevented p53-mediated induction of p21 at the transcriptional level. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 0-7 H3 histone pseudogene 16 Homo sapiens 44-47 17409429-8 2007 The repressed expression of antiapototic p21 also seemed to contribute to synergism between PD98059 and Nutlin-3a because (a) the synergistic apoptogenic effect was preserved in G(1) cells, (b) p53-mediated induction of p21 was preferentially seen in G(1) cells, (c) PD98059 strongly antagonized p21 induction by Nutlin-3a, and (d) cells with high p21 levels were resistant to apoptosis. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 92-99 H3 histone pseudogene 16 Homo sapiens 41-44 17409429-8 2007 The repressed expression of antiapototic p21 also seemed to contribute to synergism between PD98059 and Nutlin-3a because (a) the synergistic apoptogenic effect was preserved in G(1) cells, (b) p53-mediated induction of p21 was preferentially seen in G(1) cells, (c) PD98059 strongly antagonized p21 induction by Nutlin-3a, and (d) cells with high p21 levels were resistant to apoptosis. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 92-99 H3 histone pseudogene 16 Homo sapiens 220-223 17409429-8 2007 The repressed expression of antiapototic p21 also seemed to contribute to synergism between PD98059 and Nutlin-3a because (a) the synergistic apoptogenic effect was preserved in G(1) cells, (b) p53-mediated induction of p21 was preferentially seen in G(1) cells, (c) PD98059 strongly antagonized p21 induction by Nutlin-3a, and (d) cells with high p21 levels were resistant to apoptosis. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 92-99 H3 histone pseudogene 16 Homo sapiens 220-223 17409429-8 2007 The repressed expression of antiapototic p21 also seemed to contribute to synergism between PD98059 and Nutlin-3a because (a) the synergistic apoptogenic effect was preserved in G(1) cells, (b) p53-mediated induction of p21 was preferentially seen in G(1) cells, (c) PD98059 strongly antagonized p21 induction by Nutlin-3a, and (d) cells with high p21 levels were resistant to apoptosis. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 92-99 H3 histone pseudogene 16 Homo sapiens 220-223 17409429-8 2007 The repressed expression of antiapototic p21 also seemed to contribute to synergism between PD98059 and Nutlin-3a because (a) the synergistic apoptogenic effect was preserved in G(1) cells, (b) p53-mediated induction of p21 was preferentially seen in G(1) cells, (c) PD98059 strongly antagonized p21 induction by Nutlin-3a, and (d) cells with high p21 levels were resistant to apoptosis. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 267-274 H3 histone pseudogene 16 Homo sapiens 41-44 17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Tretinoin 40-44 H3 histone pseudogene 16 Homo sapiens 345-348 17179232-7 2007 Treatment with MS-275 induced increase in protein and histone H3/H4 acetylation, p21 expression, and caspase-3 activation in bone marrow mononuclear cells. entinostat 15-21 H3 histone pseudogene 16 Homo sapiens 81-84 17332940-8 2007 Following silencing of p53 or p21 we observed extensive apoptosis concomitant with extensive depolarization of mitochondrial membrane and depletion of reduced glutathione. Glutathione 159-170 H3 histone pseudogene 16 Homo sapiens 30-33 17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Minoxidil 13-22 H3 histone pseudogene 16 Homo sapiens 150-153 17520098-0 2007 Quercetin induces cell cycle G1 arrest through elevating Cdk inhibitors p21 and p27 in human hepatoma cell line (HepG2). Quercetin 0-9 H3 histone pseudogene 16 Homo sapiens 72-75 17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Tretinoin 28-32 H3 histone pseudogene 16 Homo sapiens 150-153 17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Minoxidil 25-34 H3 histone pseudogene 16 Homo sapiens 345-348 17315026-7 2007 Mechanistic studies indicated that Pemetrexed provoked this action by a combined effect that included cell cycle blockade, probably by p21 upregulation, and induction of apoptosis through caspase-dependent and -independent mechanisms. Pemetrexed 35-45 H3 histone pseudogene 16 Homo sapiens 135-138 17520098-6 2007 Furthermore, the results indicate that quercetin increased the content of Cdk inhibitor p21 protein, which was correlated with the elevation in p53 levels during 12 h of incubation. Quercetin 39-48 H3 histone pseudogene 16 Homo sapiens 88-91 17520098-8 2007 From our results it can be concluded that quercetin blocks cell cycle progression at G(1) phase and exerts its growth-inhibitory effect through the increase of Cdk inhibitors p21 and p27 and tumor suppressor p53 in HepG2. Quercetin 42-51 H3 histone pseudogene 16 Homo sapiens 175-178 17320764-1 2007 p21ras GTPase is the protein product of the most commonly mutated human oncogene and has been identified as a target for reactive oxygen and nitrogen species. reactive oxygen and nitrogen species 121-157 H3 histone pseudogene 16 Homo sapiens 0-3 17409683-7 2007 SAL activated the suppression system of cell proliferation, such as down-regulation of c-myc and cdk4, and up-regulation of p21 and p27, inducing G1 arrest of the cell cycle, and consequently inhibited cell proliferation of Raji cells. sal 0-3 H3 histone pseudogene 16 Homo sapiens 124-127 17275298-1 2007 A novel series of antiproliferative agents containing pyrazolo[1,5-a]pyrimidin-7-yl phenyl amides, selective for p21-deficient cells, were identified by high-throughput screening. pyrazolo[1,5-a]pyrimidin-7-yl phenyl amides 54-97 H3 histone pseudogene 16 Homo sapiens 113-116 16740359-5 2007 We concluded that PML and all-trans-retinoic acid cause cell death by different pathways: PML activates ERK1/2, p38 MAPK, and p21; arrests the cell cycle; and later causes cell death; and all-trans-retinoic acid activates proteasome function, caspase cleavage, and apoptosis. Tretinoin 26-49 H3 histone pseudogene 16 Homo sapiens 126-129 17320764-5 2007 The results of LC-MS/MS analysis of tryptic peptides of p21ras treated with ONOO(-) showed that ICAT labeling of Cys(118) was decreased by 47%, whereas Cys(80) was not significantly affected and was thereby shown to be less reactive. Peptides 44-52 H3 histone pseudogene 16 Homo sapiens 56-59 17320764-5 2007 The results of LC-MS/MS analysis of tryptic peptides of p21ras treated with ONOO(-) showed that ICAT labeling of Cys(118) was decreased by 47%, whereas Cys(80) was not significantly affected and was thereby shown to be less reactive. onoo 76-80 H3 histone pseudogene 16 Homo sapiens 56-59 17320764-5 2007 The results of LC-MS/MS analysis of tryptic peptides of p21ras treated with ONOO(-) showed that ICAT labeling of Cys(118) was decreased by 47%, whereas Cys(80) was not significantly affected and was thereby shown to be less reactive. Cysteine 113-116 H3 histone pseudogene 16 Homo sapiens 56-59 17320764-5 2007 The results of LC-MS/MS analysis of tryptic peptides of p21ras treated with ONOO(-) showed that ICAT labeling of Cys(118) was decreased by 47%, whereas Cys(80) was not significantly affected and was thereby shown to be less reactive. Cysteine 152-155 H3 histone pseudogene 16 Homo sapiens 56-59 17103031-0 2007 Lithium increases expression of p21(WAF/Cip1) and survivin in human glioblastoma cells. Lithium 0-7 H3 histone pseudogene 16 Homo sapiens 32-35 19690636-0 2007 BRCA1 Expression is an Important Biomarker for Chemosensitivity: Suppression of BRCA1 Increases the Apoptosis via Up-regulation of p53 and p21 During Cisplatin Treatment in Ovarian Cancer Cells. Cisplatin 150-159 H3 histone pseudogene 16 Homo sapiens 139-142 19690636-9 2007 However, cisplatin treatment under suppression of BRCA1 showed a significantly increased apoptosis along with up-regulation of p53 and p21 in A2780 cells. Cisplatin 9-18 H3 histone pseudogene 16 Homo sapiens 135-138 17103031-7 2007 The treatment with lithium did not alter the levels of Bcl-2 or procaspase-3 and did not cleave PARP, but increased the levels of p21(WAF/Cip1) and survivin. Lithium 19-26 H3 histone pseudogene 16 Homo sapiens 130-133 17103031-8 2007 Thus, increased expression of p21(WAF/Cip1) (a protein with antiapoptotic function), and survivin (a protein that supports the growth of cells by suppression of apoptosis and promotion of cell proliferation) may be the early events in the long-term cell response to lithium that are involved in the beneficial effects of this drug. Lithium 266-273 H3 histone pseudogene 16 Homo sapiens 30-33 17050787-10 2007 However, modulator proteins p53, p21, and p27 were increased by resveratrol only in LNCaP cells. Resveratrol 64-75 H3 histone pseudogene 16 Homo sapiens 33-36 17192405-2 2007 A detailed investigation of the Sp1-dependent agonistic activity of RU486 and R5020 on the folate receptor (FR) type alpha, p27, thymidine kinase 1 and p21 genes reveals a different mechanism. Mifepristone 68-73 H3 histone pseudogene 16 Homo sapiens 152-155 17229571-3 2007 Calcitriol increases the expression of insulin-like growth factor binding protein-3 (IGFBP-3), which plays a critical role in the inhibition of PCa cell growth by increasing the expression of the cell cycle inhibitor p21. Calcitriol 0-10 H3 histone pseudogene 16 Homo sapiens 217-220 17121856-6 2007 Furthermore, the co-activator complexes initiate the recruitment of the components of the basal transcription apparatus to the basal promoter with markedly different outcomes because only Ac-Lys-373 p53 promotes the assembly of the basal transcriptional apparatus on the p21 promoter. Lysine 191-194 H3 histone pseudogene 16 Homo sapiens 271-274 17172471-8 2007 Iron increases interactions of TAK1 and PI3K with p21ras as demonstrated by co-immunoprecipitation and co-localization of these proteins with caveolin-1 as shown by immunofluorescent microscopy. Iron 0-4 H3 histone pseudogene 16 Homo sapiens 50-53 17464209-5 2007 Suppression of p38 activation by SB203580 reduced the extent of apoptosis of the HeLa cells and also prevented induction of p21, release of cytochrome c, and cleavage of caspase-3 and PARP. SB 203580 33-41 H3 histone pseudogene 16 Homo sapiens 124-127 17190831-8 2007 Furthermore, expression of p21, which correlates with taxane sensitivity, is regulated by CAV1 phosphorylation in a p53-dependent manner. taxane 54-60 H3 histone pseudogene 16 Homo sapiens 27-30 17373752-8 2007 CONCLUSION: Our results support the hypothesis that cell cycle arrest induced by C2-ceramide may be mediated via accumulation of p21 and reduction of cyclinD1 and CDK7, at least partly, through PPARgamma activation. N-acetylsphingosine 81-92 H3 histone pseudogene 16 Homo sapiens 129-132 17121856-4 2007 Real-time PCR demonstrates that CG-1521 induces p21 transcription whereas trichostatin A does not alter the steady state level of p21 mRNA. cysteinylglycine 32-34 H3 histone pseudogene 16 Homo sapiens 48-51 16752155-3 2007 RA treatment resulted in an increase of p21, p27 and p53 protein levels and G1 arrest in UM cells, which correlated with significant down-modulation of surface Her2/neu proto-oncogene expression. Tretinoin 0-2 H3 histone pseudogene 16 Homo sapiens 40-43 17268597-5 2007 Mn(dca)(2)(pym)(H(2)O), , which crystallizes in the monoclinic space group P2(1)/c, has a unique interdigitated 2D network that consists of double-bridged [Mn(2)(dca)(2)(pym)(2)(H(2)O)(2)](2+)"dimers" that are connected via single-bridging dca ligands. Dichloroacetic Acid 3-6 H3 histone pseudogene 16 Homo sapiens 75-82 17268597-5 2007 Mn(dca)(2)(pym)(H(2)O), , which crystallizes in the monoclinic space group P2(1)/c, has a unique interdigitated 2D network that consists of double-bridged [Mn(2)(dca)(2)(pym)(2)(H(2)O)(2)](2+)"dimers" that are connected via single-bridging dca ligands. pyrimidine 11-14 H3 histone pseudogene 16 Homo sapiens 75-82 17169477-8 2007 At the same time, the expression level of p21 also was increased by 4-NQO exposure, leading to the cell cycle arrested in G(1) phase. 4-Nitroquinoline-1-oxide 68-73 H3 histone pseudogene 16 Homo sapiens 42-45 17235192-3 2007 Ab initio modeling with VASP in space groups P6(3)/m, P2(1)/m and Pm showed that both these angular parameters exhibited a linear dependence with the vanadium content. Vanadium 150-158 H3 histone pseudogene 16 Homo sapiens 54-59 17300726-5 2007 We then used this PTEN knockdown cell line to show that PTEN attenuation increases resistance to cisplatin-induced apoptosis, a finding associated with increased levels of the cyclin kinase inhibitor p21. Cisplatin 97-106 H3 histone pseudogene 16 Homo sapiens 200-203 17349212-8 2007 It was concluded that ATRA and HMBA played a role in the differentiation induction of HL-60 cells, which was mediated by the down-regulation of CD44, accompanied by down-regulation of cyclin E, and up-regulation of p27 and p21 mRNA. hexamethylene bisacetamide 31-35 H3 histone pseudogene 16 Homo sapiens 223-226 17174366-6 2007 We first established that resveratrol (10 microM), a pro-apoptotic agent in other cancer cells, induced p53-dependent apoptosis and c-fos, c-jun and p21 gene expression in both papillary and follicular thyroid cancer cells. Resveratrol 26-37 H3 histone pseudogene 16 Homo sapiens 149-152 17094109-0 2007 Mechanisms of guanosine triphosphate hydrolysis by Ras and Ras-GAP proteins as rationalized by ab initio QM/MM simulations. Guanosine Triphosphate 14-36 H3 histone pseudogene 16 Homo sapiens 51-54 17094109-0 2007 Mechanisms of guanosine triphosphate hydrolysis by Ras and Ras-GAP proteins as rationalized by ab initio QM/MM simulations. Guanosine Triphosphate 14-36 H3 histone pseudogene 16 Homo sapiens 59-62 17094109-1 2007 The hydrolysis reaction of guanosine triphosphate (GTP) by p21(ras) (Ras) has been modeled by using the ab initio type quantum mechanical-molecular mechanical simulations. Guanosine Triphosphate 27-49 H3 histone pseudogene 16 Homo sapiens 59-67 17094109-1 2007 The hydrolysis reaction of guanosine triphosphate (GTP) by p21(ras) (Ras) has been modeled by using the ab initio type quantum mechanical-molecular mechanical simulations. Guanosine Triphosphate 27-49 H3 histone pseudogene 16 Homo sapiens 69-72 17094109-1 2007 The hydrolysis reaction of guanosine triphosphate (GTP) by p21(ras) (Ras) has been modeled by using the ab initio type quantum mechanical-molecular mechanical simulations. Guanosine Triphosphate 51-54 H3 histone pseudogene 16 Homo sapiens 59-67 17094109-1 2007 The hydrolysis reaction of guanosine triphosphate (GTP) by p21(ras) (Ras) has been modeled by using the ab initio type quantum mechanical-molecular mechanical simulations. Guanosine Triphosphate 51-54 H3 histone pseudogene 16 Homo sapiens 69-72 17094109-2 2007 Initial geometry configurations have been prompted by atomic coordinates of the crystal structure (PDBID: 1QRA) corresponding to the prehydrolysis state of Ras in complex with GTP. Guanosine Triphosphate 176-179 H3 histone pseudogene 16 Homo sapiens 156-159 17094109-5 2007 At the first stage, a unified action of the nearest residues of Ras and the nearest water molecules results in a substantial spatial separation of the gamma-phosphate group of GTP from the rest of the molecule (GDP). Phosphates 157-166 H3 histone pseudogene 16 Homo sapiens 64-67 17094109-5 2007 At the first stage, a unified action of the nearest residues of Ras and the nearest water molecules results in a substantial spatial separation of the gamma-phosphate group of GTP from the rest of the molecule (GDP). Guanosine Triphosphate 176-179 H3 histone pseudogene 16 Homo sapiens 64-67 17094109-5 2007 At the first stage, a unified action of the nearest residues of Ras and the nearest water molecules results in a substantial spatial separation of the gamma-phosphate group of GTP from the rest of the molecule (GDP). Guanosine Diphosphate 211-214 H3 histone pseudogene 16 Homo sapiens 64-67 17188682-5 2007 FGF-10 prevented H2O2-induced upregulation of CDK inhibitor, p21. Hydrogen Peroxide 17-21 H3 histone pseudogene 16 Homo sapiens 61-64 17094109-7 2007 At the second stage, the inorganic phosphate is formed in consequence of proton transfers mediated by two water molecules and assisted by the Gln61 residue from Ras. inorganic 25-34 H3 histone pseudogene 16 Homo sapiens 161-164 17094109-7 2007 At the second stage, the inorganic phosphate is formed in consequence of proton transfers mediated by two water molecules and assisted by the Gln61 residue from Ras. Phosphates 35-44 H3 histone pseudogene 16 Homo sapiens 161-164 17094109-9 2007 The results of simulations are compared to the previous findings for the GTP hydrolysis in the Ras-GAP (p21(ras)-p120(GAP)) protein complex. Guanosine Triphosphate 73-76 H3 histone pseudogene 16 Homo sapiens 95-98 17094109-9 2007 The results of simulations are compared to the previous findings for the GTP hydrolysis in the Ras-GAP (p21(ras)-p120(GAP)) protein complex. Guanosine Triphosphate 73-76 H3 histone pseudogene 16 Homo sapiens 104-107 17094109-9 2007 The results of simulations are compared to the previous findings for the GTP hydrolysis in the Ras-GAP (p21(ras)-p120(GAP)) protein complex. Guanosine Triphosphate 73-76 H3 histone pseudogene 16 Homo sapiens 108-111 17404061-10 2007 Moreover, jaceosidin elevated the expression of p53 and p21, while the compound inhibited the activation of ERK1/2 that is an important component of cell survival signaling. jaceosidin 10-20 H3 histone pseudogene 16 Homo sapiens 56-59 17079232-4 2007 We then present evidence that Dox-mediated induction of cell cycle regulator p21 expression is differentially regulated by KAP1 sumoylation status. Doxorubicin 30-33 H3 histone pseudogene 16 Homo sapiens 77-80 17079232-8 2007 Hence, sumoylation of KAP1 represses p21 transcription via a chromatin-silencing process without affecting interaction between KAP1.ZBRK1 and DNA, thus providing a novel mechanistic basis for the understanding of Dox-induced de-repression of p21 transcription. Doxorubicin 213-216 H3 histone pseudogene 16 Homo sapiens 242-245 17079232-9 2007 Taken together, our results suggest that Dox-induced decrease in KAP1 sumoylation is essential for Dox to induce p21 expression and subsequent cell growth inhibition in MCF-7 cells. Doxorubicin 41-44 H3 histone pseudogene 16 Homo sapiens 113-116 17079232-9 2007 Taken together, our results suggest that Dox-induced decrease in KAP1 sumoylation is essential for Dox to induce p21 expression and subsequent cell growth inhibition in MCF-7 cells. Doxorubicin 99-102 H3 histone pseudogene 16 Homo sapiens 113-116 17311112-5 2007 The level of p21 transcript, encoding p21 protein involved in the cell cycle, was increased several-fold by I3C comparing to its level in cells incubated with estradiol or DDT. Estradiol 159-168 H3 histone pseudogene 16 Homo sapiens 13-16 17311112-5 2007 The level of p21 transcript, encoding p21 protein involved in the cell cycle, was increased several-fold by I3C comparing to its level in cells incubated with estradiol or DDT. Estradiol 159-168 H3 histone pseudogene 16 Homo sapiens 38-41 17311112-5 2007 The level of p21 transcript, encoding p21 protein involved in the cell cycle, was increased several-fold by I3C comparing to its level in cells incubated with estradiol or DDT. DDT 172-175 H3 histone pseudogene 16 Homo sapiens 13-16 17311112-5 2007 The level of p21 transcript, encoding p21 protein involved in the cell cycle, was increased several-fold by I3C comparing to its level in cells incubated with estradiol or DDT. DDT 172-175 H3 histone pseudogene 16 Homo sapiens 38-41 17662641-3 2007 We show that bleomycin-treated A549 cells exhibit: senescence-like cell morphology; a senescence-associated increase in SA-beta-galactosidase activity; cell cycle arrest; and upregulation of p53 and p21. Bleomycin 13-22 H3 histone pseudogene 16 Homo sapiens 199-202 17352246-6 2007 RESULTS: Ascorbic acid was found to reduce the proliferation of cells and induce apoptosis by the modulation of p53, p21, Bcl-2 and Bax. Ascorbic Acid 9-22 H3 histone pseudogene 16 Homo sapiens 117-120 17171453-6 2007 Rebamipide treatment inhibited AGS cell proliferation and increased p21, Smad2/3 phosphorylation, and Smad2/3-Smad4 complex formation. rebamipide 0-10 H3 histone pseudogene 16 Homo sapiens 68-71 17116745-6 2007 NaHS treatment also resulted in stabilization of p53 coupled with induction of downstream proteins such as p21, Bax, and cytochrome c, as well as translocation of Bax from the cytosol to the mitochondria and release of cytochrome c from mitochondria. sodium bisulfide 0-4 H3 histone pseudogene 16 Homo sapiens 107-110 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 59-63 H3 histone pseudogene 16 Homo sapiens 52-55 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 59-63 H3 histone pseudogene 16 Homo sapiens 68-71 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 59-63 H3 histone pseudogene 16 Homo sapiens 68-71 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 215-219 H3 histone pseudogene 16 Homo sapiens 52-55 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 215-219 H3 histone pseudogene 16 Homo sapiens 52-55 17200334-10 2007 Moreover, analysis of p21 distribution in COLO-357 cells revealed that SAHA induced the cytoplasmic localization of both p21 and phospho-p21. Vorinostat 71-75 H3 histone pseudogene 16 Homo sapiens 22-25 17200334-10 2007 Moreover, analysis of p21 distribution in COLO-357 cells revealed that SAHA induced the cytoplasmic localization of both p21 and phospho-p21. Vorinostat 71-75 H3 histone pseudogene 16 Homo sapiens 121-124 17200334-10 2007 Moreover, analysis of p21 distribution in COLO-357 cells revealed that SAHA induced the cytoplasmic localization of both p21 and phospho-p21. Vorinostat 71-75 H3 histone pseudogene 16 Homo sapiens 121-124 17200334-11 2007 CONCLUSIONS: These data indicate that SAHA exerts proapoptotic effects in pancreatic cancer cells, in part, by up-regulating p21 and sequestering it in the cytoplasm, raising the possibility that SAHA may have therapeutic potential in the treatment of pancreatic cancer. Vorinostat 38-42 H3 histone pseudogene 16 Homo sapiens 125-128 17171453-8 2007 Inactivation of ERK2 by PD98059 partly attenuated rebamipide-induced p21 expression. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 24-31 H3 histone pseudogene 16 Homo sapiens 69-72 17171453-8 2007 Inactivation of ERK2 by PD98059 partly attenuated rebamipide-induced p21 expression. rebamipide 50-60 H3 histone pseudogene 16 Homo sapiens 69-72 17171453-10 2007 Inactivation of ERK2 partly inhibited rebamipide-induced p21 expression, indicating a crosstalk between ERK and Smad signaling pathways. rebamipide 38-48 H3 histone pseudogene 16 Homo sapiens 57-60 17604209-6 2007 Flavone induces apoptosis which is accompanied by caspase activation and p16, p21 and TRAIL over-expression in human myeloid leukemia cells. flavone 0-7 H3 histone pseudogene 16 Homo sapiens 78-81 17662641-6 2007 Our results support the hypothesis that downregulation of caveolin-1 expression affects bleomycin-induced cell cycle arrest and subsequent cellular senescence that is driven by p53 and p21. Bleomycin 88-97 H3 histone pseudogene 16 Homo sapiens 185-188 16956884-8 2006 Additionally, we found that adaphostin treatment induced a decrease in the phosphorylation of nucleophosmin, a major nuclear phosphoprotein, and that this decreased phosphorylation was a result of the p21- and p27-mediated inactivation of cyclin E-cyclin-dependent kinase 2 complex kinase activity. NSC 680410 28-38 H3 histone pseudogene 16 Homo sapiens 201-204 17237267-9 2007 The biological effect of LAQ824 was associated with p21 induction in both cell lines but G(2) cell cycle arrest in A2058 and apoptosis in HMV-I cell line. LAQ824 25-31 H3 histone pseudogene 16 Homo sapiens 52-55 17088910-0 2006 Upregulation of p27 and its inhibition of CDK2/cyclin E activity following DNA damage by a novel platinum agent are dependent on the expression of p21. Platinum 97-105 H3 histone pseudogene 16 Homo sapiens 147-150 17056014-4 2006 KAP1 reduction markedly enhanced the induction of p21, a product of the p53 target gene, after treatment with actinomycin D or gamma-irradiation, but not with camptothecin. Dactinomycin 110-123 H3 histone pseudogene 16 Homo sapiens 50-53 17122440-6 2006 Transfection of dnTCF-4 in the ISS10 human VSMC line significantly lowered TCF and cyclin D1 reporter activity but significantly elevated p21 reporter activity, indicating regulation of these genes by beta-catenin/TCF signaling. dntcf 16-21 H3 histone pseudogene 16 Homo sapiens 138-141 17088910-6 2006 Moreover, DAP-induced p21 promoted the selective increase of p27 in the CDK2 complex, but not in CDK4 complex, and this selective increase contributed to inhibition of the CDK2 kinase activity. (diaminocyclohexane)(diacetato)(dichloro)platinum 10-13 H3 histone pseudogene 16 Homo sapiens 22-25 17049505-6 2006 l-Lysine up-regulated p53, p21, and Bax protein levels and a down-regulation of Bcl-2alpha in all the cell lines tested. Lysine 0-8 H3 histone pseudogene 16 Homo sapiens 27-30 17341630-7 2006 After 8 and 24 h after the beginning of cultivation with 2 mM VA we detect p21, which is not observed after exposure to 4 mM VA. Valproic Acid 62-64 H3 histone pseudogene 16 Homo sapiens 75-78 17341630-7 2006 After 8 and 24 h after the beginning of cultivation with 2 mM VA we detect p21, which is not observed after exposure to 4 mM VA. Valproic Acid 125-127 H3 histone pseudogene 16 Homo sapiens 75-78 17172433-3 2006 Gallic acid treatment of DU145 cells resulted in a strong cell growth inhibition, cell cycle arrest, and apoptotic death in a dose- and time-dependent manner, together with a decrease in cyclin-dependent kinases and cyclins but strong induction in Cip1/p21. Gallic Acid 0-11 H3 histone pseudogene 16 Homo sapiens 253-256 17119452-11 2006 The increased expressions of p53 and p21, and the decreased expressions of cyclin A, cyclin E, CDK2 and CDK4, indicated the cell cycle arrest at G1/S phase after the cells had been treated with sodium ascorbate. Ascorbic Acid 194-210 H3 histone pseudogene 16 Homo sapiens 37-40 17119452-12 2006 Induction of apoptosis involved an increase in the levels of p53, p21 and cellular Ca, and a decrease in mitochondrial membrane potential and activation of caspase 3 before culminating in apoptosis in sodium ascorbate-treated A375.S2 cells. Ascorbic Acid 201-217 H3 histone pseudogene 16 Homo sapiens 66-69 16841329-4 2006 beta-Cryptoxanthin suppressed the protein levels of cyclin D1 and cyclin E, up-regulated the cell cycle inhibitor p21, increased the number of lung cancer cells in the G1/G0 phase and decreased those in the S phase of the cell cycle. Beta-Cryptoxanthin 0-18 H3 histone pseudogene 16 Homo sapiens 114-117 17045763-5 2006 The phospho-p53 (Ser-15), total p53, and p21 proteins were elevated by oxaliplatin in RKO cells; conversely, oxaliplatin decreased the securin protein expression. Oxaliplatin 71-82 H3 histone pseudogene 16 Homo sapiens 41-44 17045927-6 2006 Scavengers of singlet oxygen or NO could attenuate PDT-induced cell viability loss, nucleus morphology changes, cytochrome c release, mitochondria swelling, and apo-apoptosis gene p53 and p21 mRNA levels. Singlet Oxygen 14-28 H3 histone pseudogene 16 Homo sapiens 188-191 16940187-0 2006 Bafilomycin induces the p21-mediated growth inhibition of cancer cells under hypoxic conditions by expressing hypoxia-inducible factor-1alpha. bafilomycin 0-11 H3 histone pseudogene 16 Homo sapiens 24-27 16940187-6 2006 Furthermore, the HIF-1alpha induction by bafilomycin was augmented by hypoxia, which caused a robust induction of p21 and cell cycle arrest in cancer cells. bafilomycin 41-52 H3 histone pseudogene 16 Homo sapiens 114-117 17201158-6 2006 Curcumin also promoted the expression of Bax, cytochrome C, p53 and p21 but inhibited the expression of Bcl-2. Curcumin 0-8 H3 histone pseudogene 16 Homo sapiens 68-71 17003493-3 2006 However, we discovered that genes associated with differentiation (GDF15 and ATF3) and suppression of proliferation (CDKNa1/p21) were up-regulated in highly invasive uveal melanoma cells forming vasculogenic mimicry patterns, and genes associated with promotion of invasive and metastatic behavior such as CD44, CCNE2 (cyclin E2), THBS1 (thrombospondin 1), and CSPG2 (chondroitin sulfate proteoglycan; versican) were down-regulated. Chondroitin Sulfates 368-387 H3 histone pseudogene 16 Homo sapiens 124-127 16633716-5 2006 MDDD treatment also triggers induction of p53 and p21 at the protein levels, suggesting the activation of DNA damage response. 4-methyl-2,7-diamino-5,10-diphenyl-4,9-diaz-apyrenium chloride 0-4 H3 histone pseudogene 16 Homo sapiens 50-53 16899068-8 2006 Conversely, in C6 glioma cells, characterized by a low level of intercellular communication, an increase in gap junctional communication reduces glucose uptake by releasing type I and type II hexokinases from the mitochondria and decreases the exacerbated rate of proliferation due to the up-regulation of the Cdk inhibitors p21 and p27. Glucose 145-152 H3 histone pseudogene 16 Homo sapiens 325-328 16942782-6 2006 Capsaicin induced G0-G1 phase arrest underwent the promotion of p53 and p21, which is an inhibitor of Cdk2 and cyclin E complex before leading to the inhibitions of both compounds. Capsaicin 0-9 H3 histone pseudogene 16 Homo sapiens 72-75 17029827-5 2006 Following DNA damage, the activation of p53 acts as a transcriptional regulator of several target genes, including, p21 protein; a gene that encodes the Cdk inhibitor and is induced by exposure to benzo[a]pyrene. Benzo(a)pyrene 197-211 H3 histone pseudogene 16 Homo sapiens 116-119 17029827-7 2006 The overall results suggest that benzo[a]pyrene leads to serious DNA damage, which leads to the transcription of the p53 gene; that the subsequent p53 protein accumulation up-regulates the cellular p21 protein. Benzo(a)pyrene 33-47 H3 histone pseudogene 16 Homo sapiens 198-201 17003443-15 2006 The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 244-249 H3 histone pseudogene 16 Homo sapiens 93-96 16624386-13 2006 CIZAR increased the expression of p21(waf1) which is a part of p53-independent pathway and induced reduction of telomerase activity. cizar 0-5 H3 histone pseudogene 16 Homo sapiens 34-37 17003443-14 2006 MG132 caused a significant increase in p21 and p27 protein and decrease in CDK2, but no change in p53, p57, CDK4, or CDK6 protein. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 H3 histone pseudogene 16 Homo sapiens 39-42 16621886-4 2006 Our western blot analysis showed that berberine-induced G(1) cell cycle arrest was mediated through the increased expression of Cdki proteins (Cip1/p21 and Kip1/p27), a simultaneous decrease in Cdk2, Cdk4, Cdk6 and cyclins D1, D2 and E and enhanced binding of Cdki-Cdk. Berberine 38-47 H3 histone pseudogene 16 Homo sapiens 148-151 17109072-8 2006 Moreover, Tau-Cl inhibited PDGF-triggered cell proliferation (IC(50) value approximately 250-300 microM), accompanied by characteristic modulation of p53 transcriptional targets: down-regulation of proliferating cell nuclear antigen (PCNA) and survivin, and concomitant up-regulation of p21 mitotic inhibitor. N-chlorotaurine 10-16 H3 histone pseudogene 16 Homo sapiens 287-290 17003443-15 2006 The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 32-37 H3 histone pseudogene 16 Homo sapiens 93-96 16857700-3 2006 TSA caused a dose-dependent increase of G1-arrested cells at 24 h that correlated with increasing levels of p21 and apoptosis. trichostatin A 0-3 H3 histone pseudogene 16 Homo sapiens 108-111 17003443-15 2006 The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 32-37 H3 histone pseudogene 16 Homo sapiens 126-129 16766008-7 2006 Finally, it was demonstrated that CAPE promoted the ATRA-mediated nuclear transcription activation of RARalpha assessed by EMSA assay and enhanced the expression of target genes including RARalpha, C/EBPepsilon, and p21 protein resulting in the differentiation development of leukemia. caffeic acid phenethyl ester 34-38 H3 histone pseudogene 16 Homo sapiens 216-219 16849420-8 2006 Bortezomib inhibited NF-kappaB activity; increased p53, p21, and jun expression; and induced caspase-dependent apoptosis. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 56-59 16636661-7 2006 Binding of a peptide derived from the C-terminus of p21(CIP1) to the C-terminal domain of E7 was characterized by monitoring chemical shift perturbations of the amide groups of E7. Amides 161-166 H3 histone pseudogene 16 Homo sapiens 52-55 17441071-4 2006 Furthermore, the reaction of 1 a with hexamolybdate in acetonitrile gives the helical coordination polymer {[(Fe3(mu3-O)L6(H2O))(MoO4)-(Fe3(mu3-O)L6(H2O)2)] x 2 CH3CN x H2O}infinity 2 (L: H2C=CHCOO), which crystallizes in the space group P2(1). hexamolybdate 38-51 H3 histone pseudogene 16 Homo sapiens 238-243 17441071-4 2006 Furthermore, the reaction of 1 a with hexamolybdate in acetonitrile gives the helical coordination polymer {[(Fe3(mu3-O)L6(H2O))(MoO4)-(Fe3(mu3-O)L6(H2O)2)] x 2 CH3CN x H2O}infinity 2 (L: H2C=CHCOO), which crystallizes in the space group P2(1). acetonitrile 55-67 H3 histone pseudogene 16 Homo sapiens 238-243 17441071-4 2006 Furthermore, the reaction of 1 a with hexamolybdate in acetonitrile gives the helical coordination polymer {[(Fe3(mu3-O)L6(H2O))(MoO4)-(Fe3(mu3-O)L6(H2O)2)] x 2 CH3CN x H2O}infinity 2 (L: H2C=CHCOO), which crystallizes in the space group P2(1). Polymers 99-106 H3 histone pseudogene 16 Homo sapiens 238-243 17441071-4 2006 Furthermore, the reaction of 1 a with hexamolybdate in acetonitrile gives the helical coordination polymer {[(Fe3(mu3-O)L6(H2O))(MoO4)-(Fe3(mu3-O)L6(H2O)2)] x 2 CH3CN x H2O}infinity 2 (L: H2C=CHCOO), which crystallizes in the space group P2(1). [(fe3(mu3-o)l6(h2o 108-126 H3 histone pseudogene 16 Homo sapiens 238-243 17441071-4 2006 Furthermore, the reaction of 1 a with hexamolybdate in acetonitrile gives the helical coordination polymer {[(Fe3(mu3-O)L6(H2O))(MoO4)-(Fe3(mu3-O)L6(H2O)2)] x 2 CH3CN x H2O}infinity 2 (L: H2C=CHCOO), which crystallizes in the space group P2(1). moo4 129-133 H3 histone pseudogene 16 Homo sapiens 238-243 17441071-4 2006 Furthermore, the reaction of 1 a with hexamolybdate in acetonitrile gives the helical coordination polymer {[(Fe3(mu3-O)L6(H2O))(MoO4)-(Fe3(mu3-O)L6(H2O)2)] x 2 CH3CN x H2O}infinity 2 (L: H2C=CHCOO), which crystallizes in the space group P2(1). fe3(mu3-o)l6(h2o)2) 136-155 H3 histone pseudogene 16 Homo sapiens 238-243 16849332-6 2006 The results obtained from the Western blot experiment showed that NER defects resulted in enhanced CHK1 phosphorylation and p21 induction after cisplatin treatment. Cisplatin 144-153 H3 histone pseudogene 16 Homo sapiens 124-127 17094491-9 2006 Furthermore, (-)-gossypol treatment down-regulated cyclin-D1, Rb, CDK4 and CDK6, and up-regulated p21 and TGF-beta1 at the mRNA and/or protein levels. Gossypol 13-25 H3 histone pseudogene 16 Homo sapiens 98-101 16954624-1 2006 Sodium trichloromethanesulfonate monohydrate, Na+.CCl3SO3-.H2O, crystallizes in P2(1)/a with all the atoms located in general positions. sodium trichloromethanesulfonate monohydrate 0-44 H3 histone pseudogene 16 Homo sapiens 80-85 16954624-1 2006 Sodium trichloromethanesulfonate monohydrate, Na+.CCl3SO3-.H2O, crystallizes in P2(1)/a with all the atoms located in general positions. ccl3so3 50-57 H3 histone pseudogene 16 Homo sapiens 80-85 16954624-1 2006 Sodium trichloromethanesulfonate monohydrate, Na+.CCl3SO3-.H2O, crystallizes in P2(1)/a with all the atoms located in general positions. Water 59-62 H3 histone pseudogene 16 Homo sapiens 80-85 16951169-8 2006 In TDEC, calcitriol resulted in induction of G(0)/G(1) arrest (10.75%) and reduction of S-phase cells (6.8%) with induction of p27 and down-regulation of p21 protein expression. Calcitriol 9-19 H3 histone pseudogene 16 Homo sapiens 154-157 16777971-6 2006 Rosiglitazone-induced growth inhibition was associated with cell cycle arrest and changes in cell cycle regulators, such as an increase of cyclin-dependent kinases inhibitors p21(cip1) and p27(kip1), a decrease of cyclin D1, and inactivation of Rb protein. Rosiglitazone 0-13 H3 histone pseudogene 16 Homo sapiens 175-178 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Lovastatin 19-29 H3 histone pseudogene 16 Homo sapiens 289-292 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Fluvastatin 31-42 H3 histone pseudogene 16 Homo sapiens 289-292 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Simvastatin 48-59 H3 histone pseudogene 16 Homo sapiens 289-292 16815847-2 2006 This response is due to activation of Cdc42, resulting in p21-activated kinase-dependent phosphorylation and activation of MEK1 Ser(298) and activation of ERK1/2. Serine 128-131 H3 histone pseudogene 16 Homo sapiens 58-61 16797759-3 2006 By Western blot, the expression of 14-3-3sigma, p53 and p21 was coordinately upregulated in astrocytes following exposure to hydrogen peroxide, 4-hydroxy-2-nonenal (4-HNE) or etoposide, a topoisomerase II inhibitor. Hydrogen Peroxide 125-142 H3 histone pseudogene 16 Homo sapiens 56-59 16797759-3 2006 By Western blot, the expression of 14-3-3sigma, p53 and p21 was coordinately upregulated in astrocytes following exposure to hydrogen peroxide, 4-hydroxy-2-nonenal (4-HNE) or etoposide, a topoisomerase II inhibitor. 4-hydroxy-2-nonenal 144-163 H3 histone pseudogene 16 Homo sapiens 56-59 16797759-3 2006 By Western blot, the expression of 14-3-3sigma, p53 and p21 was coordinately upregulated in astrocytes following exposure to hydrogen peroxide, 4-hydroxy-2-nonenal (4-HNE) or etoposide, a topoisomerase II inhibitor. 4-hydroxy-2-nonenal 165-170 H3 histone pseudogene 16 Homo sapiens 56-59 16797759-3 2006 By Western blot, the expression of 14-3-3sigma, p53 and p21 was coordinately upregulated in astrocytes following exposure to hydrogen peroxide, 4-hydroxy-2-nonenal (4-HNE) or etoposide, a topoisomerase II inhibitor. Etoposide 175-184 H3 histone pseudogene 16 Homo sapiens 56-59 16867250-8 2006 The expression of G-protein coupled receptor kinase, protein kinase C (PKC)-zeta, N-ras protein were decreased, while cycle related protein p21 was increased by ginsenoside Rg1 in TNF-alpha treated VSMC. Ginsenosides 161-172 H3 histone pseudogene 16 Homo sapiens 140-143 16867250-9 2006 CONCLUSION: PKC-zeta and p21 pathway might be the mechanism for inhibitory effects of ginsenoside Rg1 on proliferation of VSMC. Ginsenosides 86-97 H3 histone pseudogene 16 Homo sapiens 25-28 16867250-9 2006 CONCLUSION: PKC-zeta and p21 pathway might be the mechanism for inhibitory effects of ginsenoside Rg1 on proliferation of VSMC. vsmc 122-126 H3 histone pseudogene 16 Homo sapiens 25-28 16872361-4 2006 The results here demonstrate evidence for approximately 25% apoptosis after treatment with calcium salicylate, which up-regulatd the expression of p53, p21 and Bax, and down-regulated Bcl-2 in HT-1080 cells. calcium salicylate 91-109 H3 histone pseudogene 16 Homo sapiens 152-155 16698776-6 2006 As a biological model system, we have used H-Ras p21 with an artificially introduced photo-labile GTP precursor (caged GTP) and a covalently attached fluorophore (IANBD amide). Guanosine Triphosphate 98-101 H3 histone pseudogene 16 Homo sapiens 49-52 16855382-8 2006 Furthermore, treatment with the p38 MAPK inhibitor SB203580 reduced p38 MAPK activity and cell cycle arrest, and also partially restored cyclin A, cyclin B1, cyclin D1 and p21 protein levels. SB 203580 51-59 H3 histone pseudogene 16 Homo sapiens 172-175 16849572-5 2006 Our results show that acute treatment (3 days) VPA can increase net histone H3 acetylation and up-regulate p21, AR, and cytosolic PSA expression. Valproic Acid 47-50 H3 histone pseudogene 16 Homo sapiens 107-110 16718685-8 2006 In conclusion, tolbutamide and dbcAMP inhibit C6-glioma cell proliferation by increasing Cx43, which correlates with a reduction in pRb phosphorylation due to the up-regulation of the Cdk inhibitors p21 and p27. Tolbutamide 15-26 H3 histone pseudogene 16 Homo sapiens 199-202 16718685-8 2006 In conclusion, tolbutamide and dbcAMP inhibit C6-glioma cell proliferation by increasing Cx43, which correlates with a reduction in pRb phosphorylation due to the up-regulation of the Cdk inhibitors p21 and p27. Bucladesine 31-37 H3 histone pseudogene 16 Homo sapiens 199-202 16483558-8 2006 The oxygen-sensitive signaling pathways involved have been characterized and point towards a central role of p21, TGFbeta and p38MAPK. Oxygen 4-10 H3 histone pseudogene 16 Homo sapiens 109-112 16841939-6 2006 Additionally, "top-down" analysis was conducted on p21ras S-glutathiolated by oxidized glutathione and identified C118 as the major site of glutathiolation among the four surface cysteines. Glutathione 87-98 H3 histone pseudogene 16 Homo sapiens 51-54 16718685-0 2006 Tolbutamide reduces glioma cell proliferation by increasing connexin43, which promotes the up-regulation of p21 and p27 and subsequent changes in retinoblastoma phosphorylation. Tolbutamide 0-11 H3 histone pseudogene 16 Homo sapiens 108-111 16718685-6 2006 However, the Cdk inhibitors p21 and p27 were up-regulated after treatment with tolbutamide and dbcAMP, suggesting that they would be involved in the decrease in pRb phosphorylation. Tolbutamide 79-90 H3 histone pseudogene 16 Homo sapiens 28-31 16718685-6 2006 However, the Cdk inhibitors p21 and p27 were up-regulated after treatment with tolbutamide and dbcAMP, suggesting that they would be involved in the decrease in pRb phosphorylation. Bucladesine 95-101 H3 histone pseudogene 16 Homo sapiens 28-31 16880957-4 2006 Moreover, myriaporone 3/4 displays a very rapid, reversible and p21-independent activity to block S phase progression in mammalian cells. myriaporone 10-21 H3 histone pseudogene 16 Homo sapiens 64-67 16813416-6 2006 [(R)-C7H16N2]2[Mo8O26] and [(S)-C7H16N2]2[Mo8O26] both crystallize in the noncentrosymmetric space group P2(1) (No. (r)-c7h16n2]2 1-14 H3 histone pseudogene 16 Homo sapiens 105-110 16857792-12 2006 We showed that PPARgamma agonist 15d-PGJ2 inhibited cell proliferation and induced p21 mRNA of endometrial carcinoma cell lines. 15-deoxy-delta(12,14)-prostaglandin J2 33-41 H3 histone pseudogene 16 Homo sapiens 83-86 16886662-2 2006 Calcitriol induces G0/G1 arrest, modulates p27 and p21, the cyclin-dependent kinase (cdk) inhibitors implicated in G1 arrest, and induces cleavage of caspase 3, PARP and the mitogen-activated protein kinase (MEK) in a caspase-dependent manner. Calcitriol 0-10 H3 histone pseudogene 16 Homo sapiens 51-54 16729877-7 2006 Gene classification and biological pathway analyses of the genes differentially expressed between the two main subtypes revealed different molecular mechanisms descriptive of the two expression-based subtypes: Signature genes of the luminal A subtype were over-represented by genes involved in fatty acid metabolism and steroid hormone-mediated signaling pathways, in particular estrogen receptor signaling, while signature genes of the basal-like subtype were over-represented by genes involved in cell proliferation and differentiation, p21-mediated pathway, and G1-S checkpoint of cell cycle-signaling pathways. Fatty Acids 294-304 H3 histone pseudogene 16 Homo sapiens 539-542 16805953-6 2006 Sal A at 10 microM induced cell apoptosis in PDGF-BB-incubated HSCs, together with a reduction of Bcl-2 protein expression, induction of cell cycle inhibitory proteins p21 and p27, and down-regulation of cyclins D1 and E, suppression of Akt phosphorylation, reduction in PDGF receptor phosphorylation, and an increase in caspase-3 activity. salvianolic acid A 0-5 H3 histone pseudogene 16 Homo sapiens 168-171 16737765-7 2006 An elevation in p21 mRNA and protein level was noted in SAS cells by sodium butyrate. Butyric Acid 69-84 H3 histone pseudogene 16 Homo sapiens 16-19 16331344-10 2006 Furthermore, in TP53 72Pro carriers with p21 Ser/Ser genotype, the occurrence of acute toxicity was reduced in normal weight but not overweight patients. Serine 45-48 H3 histone pseudogene 16 Homo sapiens 41-44 16331344-10 2006 Furthermore, in TP53 72Pro carriers with p21 Ser/Ser genotype, the occurrence of acute toxicity was reduced in normal weight but not overweight patients. Serine 49-52 H3 histone pseudogene 16 Homo sapiens 41-44 16368780-11 2006 TGF-beta dependent induction of p21 and downregulation of minichromosome maintenance protein 2 was lost in >80% of BE and AC. Beryllium 118-120 H3 histone pseudogene 16 Homo sapiens 32-35 16800929-5 2006 NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone. nab 0-3 H3 histone pseudogene 16 Homo sapiens 146-149 16800929-5 2006 NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 40-47 H3 histone pseudogene 16 Homo sapiens 146-149 16800929-5 2006 NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone. nab 53-56 H3 histone pseudogene 16 Homo sapiens 146-149 16800929-5 2006 NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone. nab 53-56 H3 histone pseudogene 16 Homo sapiens 146-149 16800929-5 2006 NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone. nab 53-56 H3 histone pseudogene 16 Homo sapiens 146-149 16713693-7 2006 Premature senescence is also induced upon chronic exposure to oligomycin, irrespective of ROS production, and oligomycin treatment induced the up-regulation of the cdk inhibitors p16, p21 and p27, which are also up-regulated in replicative senescence. Oligomycins 110-120 H3 histone pseudogene 16 Homo sapiens 184-187 16824077-9 2006 The most sensitive cell line to 2-ME, SK-Hep1, showed an up-regulation of the p53 and p21 proteins. 2-Methoxyestradiol 32-36 H3 histone pseudogene 16 Homo sapiens 86-89 16765349-0 2006 Increased p21 expression and complex formation with cyclin E/CDK2 in retinoid-induced pre-B lymphoma cell apoptosis. Retinoids 69-77 H3 histone pseudogene 16 Homo sapiens 10-13 16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 101-114 H3 histone pseudogene 16 Homo sapiens 23-26 16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 131-133 H3 histone pseudogene 16 Homo sapiens 23-26 16765349-2 2006 Yet the role of p21 upregulation by RA in lymphoma cells remains unknown. Tretinoin 36-38 H3 histone pseudogene 16 Homo sapiens 16-19 16765349-4 2006 Upregulated p21 by RA accompanies caspase-3 activation and precedes the occurrence of apoptosis. Tretinoin 19-21 H3 histone pseudogene 16 Homo sapiens 12-15 16765349-7 2006 Data presented here suggest a novel RA-signaling, by which RA-induced p21 induction and complex formation with cyclin E/CDK2 diverts CDK2 function from normally driving proliferation to alternatively promoting apoptosis. Tretinoin 36-38 H3 histone pseudogene 16 Homo sapiens 70-73 16697980-7 2006 In real-time PCR, the expressions of p21(cip1), p27(kip1) and p57(kip2) mRNAs remained unaltered for 8 h after treatment with deferoxamine but were significantly elevated after 1 day. Deferoxamine 126-138 H3 histone pseudogene 16 Homo sapiens 37-40 16705314-2 2006 We have previously demonstrated that either Calphostin C (CC) (a protein kinase C (PKC) inhibitor) or Parthenolide (an NF-kappaB inhibitor) abrogates HDACI-induced transcriptional activation of NF-kappaB and p21, which is associated with profound potentiation of HDACI-mediated induction of apoptosis. parthenolide 102-114 H3 histone pseudogene 16 Homo sapiens 208-211 16638572-2 2006 In both cell types, MMG induced partial arrest in G2M and increased p14-3-3, HSP70, HSP60 and p21 expression. 4-(5-phenyl-1H-pyrrolo[2,3-b]pyridin-3-yl)benzoic acid 20-23 H3 histone pseudogene 16 Homo sapiens 94-97 16533812-8 2006 Concurrent with its effect on cell growth, overexpression of HDAC3 and other Class I HDACs inhibited basal and butyrate-induced p21 transcription in a Sp1/Sp3-dependent manner, whereas silencing of HDAC3 stimulated p21 promoter activity and expression. Butyrates 111-119 H3 histone pseudogene 16 Homo sapiens 128-131 16533812-8 2006 Concurrent with its effect on cell growth, overexpression of HDAC3 and other Class I HDACs inhibited basal and butyrate-induced p21 transcription in a Sp1/Sp3-dependent manner, whereas silencing of HDAC3 stimulated p21 promoter activity and expression. Butyrates 111-119 H3 histone pseudogene 16 Homo sapiens 215-218 16651717-0 2006 Synthetic peptide (P-21) derived from Asp-hemolysin inhibits the induction of apoptosis on HUVECs by lysophosphatidylcholine. Lysophosphatidylcholines 101-124 H3 histone pseudogene 16 Homo sapiens 19-23 16651717-3 2006 In this study, to clarify the interaction between P-21 and LPC as a typical lipid moiety of OxLDL, we examined the influence of P-21 on LPC-induced apoptosis in human umbilical vein endothelial cells (HUVECs). Lysophosphatidylcholines 136-139 H3 histone pseudogene 16 Homo sapiens 128-132 16651717-4 2006 Based on flow cytometric analysis, using annexin V-fluorescein isothiocyanate and propidium iodide as probes to assess apoptosis, LPC induced the apoptosis of HUVECs, and P-21 significantly inhibited this activity by 82.4%. annexin v-fluorescein isothiocyanate 41-77 H3 histone pseudogene 16 Homo sapiens 171-175 16651717-4 2006 Based on flow cytometric analysis, using annexin V-fluorescein isothiocyanate and propidium iodide as probes to assess apoptosis, LPC induced the apoptosis of HUVECs, and P-21 significantly inhibited this activity by 82.4%. Propidium 82-98 H3 histone pseudogene 16 Homo sapiens 171-175 16651717-5 2006 Furthermore, dissociation-enhanced lanthanide fluorometric immunoassay indicated that LPC inhibited the binding of P-21 to OxLDL in a dose-dependent manner. Lanthanoid Series Elements 35-45 H3 histone pseudogene 16 Homo sapiens 115-119 16679590-1 2006 The title compound (with the systematic name 2-{[(1S)-1-(methoxycarbonyl)-3-methylbutyl]aminocarbonyl}benzoic acid), C15H19NO5, crystallizes in the monoclinic space group P2(1), with two independent molecules per asymmetric unit. N-(o-Carboxybenzoyl)-L-leucine methyl ester 45-114 H3 histone pseudogene 16 Homo sapiens 171-176 16675591-9 2006 These effects did not depend on the level of expression of EGFR but they were associated with the down-regulation of MAPK and Akt activity; in 1207 cells, gefitinib activity was associated with p27 up-regulation and p21 and matrix metalloproteinase-9 down-regulation. Gefitinib 155-164 H3 histone pseudogene 16 Homo sapiens 216-219 16697770-9 2006 Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033]. Arginine 88-91 H3 histone pseudogene 16 Homo sapiens 150-153 16697770-9 2006 Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033]. Arginine 88-91 H3 histone pseudogene 16 Homo sapiens 150-153 16697770-9 2006 Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033]. Arginine 88-91 H3 histone pseudogene 16 Homo sapiens 150-153 16697770-9 2006 Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033]. Arginine 88-91 H3 histone pseudogene 16 Homo sapiens 150-153 16697770-9 2006 Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033]. Arginine 88-91 H3 histone pseudogene 16 Homo sapiens 150-153 21144291-9 2006 (4)The expression levels of P53, P21, Fas, FasL and Bax were remarkably up-regulated after treatment with MSA. methylselenic acid 106-109 H3 histone pseudogene 16 Homo sapiens 33-36 16518417-5 2006 In RT112 and LNCap, CDDP induced p53 and p21 expression, while pretreatment of dicoumarol suppressed induction of p53/p21 and resulted in sequential activation of c-Jun N-terminal kinase (JNK) in a time-dependent manner. Cisplatin 20-24 H3 histone pseudogene 16 Homo sapiens 41-44 16518417-5 2006 In RT112 and LNCap, CDDP induced p53 and p21 expression, while pretreatment of dicoumarol suppressed induction of p53/p21 and resulted in sequential activation of c-Jun N-terminal kinase (JNK) in a time-dependent manner. Dicumarol 79-89 H3 histone pseudogene 16 Homo sapiens 118-121 16518417-7 2006 These results suggested that dicoumarol could enhance cytotoxicity of CDDP in urogenital cancer cells with wild-type p53 through the p53/p21/JNK pathways. Dicumarol 29-39 H3 histone pseudogene 16 Homo sapiens 137-140 16518417-7 2006 These results suggested that dicoumarol could enhance cytotoxicity of CDDP in urogenital cancer cells with wild-type p53 through the p53/p21/JNK pathways. Cisplatin 70-74 H3 histone pseudogene 16 Homo sapiens 137-140 16770740-4 2006 The levels of CDK2, CDC2, Cyclin A and Cyclin B proteins decreased, while the levels of CDK inhibitors viz., p21 and p27 were found to increase on staurosporine treatment. Staurosporine 147-160 H3 histone pseudogene 16 Homo sapiens 109-112 16525652-11 2006 Interestingly, DPA-induced elevation of p21/Cip1 was independent of the induction of p53 in Colo 205 cells. dpa 15-18 H3 histone pseudogene 16 Homo sapiens 40-43 16616141-0 2006 Evidence that low doses of Taxol enhance the functional transactivatory properties of p53 on p21 waf promoter in MCF-7 breast cancer cells. Paclitaxel 27-32 H3 histone pseudogene 16 Homo sapiens 93-96 16616141-1 2006 In the present study, we evidence how in breast cancer cells low doses of Taxol for 18 h determined the upregulation of p53 and p21 waf expression concomitantly with a decrease of the anti-apoptotic Bcl-2. Paclitaxel 74-79 H3 histone pseudogene 16 Homo sapiens 128-131 16616141-3 2006 Indeed, the most important finding of this study consists with the evidence that Taxol at lower concentrations is able to produce the activation of p21 promoter via p53. Paclitaxel 81-86 H3 histone pseudogene 16 Homo sapiens 148-151 16616141-4 2006 Prolonged exposure of MCF-7 cells to Taxol (48 h) resulted in an increased co-association between p21 and PCNA compared to control and this well fits with the simultaneous block of cell cycle into the G2/M phase. Paclitaxel 37-42 H3 histone pseudogene 16 Homo sapiens 98-101 16288207-10 2006 Moreover, ODQ-induced upregulation of p21 and Bax and ODQ-induced apoptosis were significantly reduced in a p53 mutant cell line relative to the wild-type parental cell line. 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one 10-13 H3 histone pseudogene 16 Homo sapiens 38-41 16562962-7 2006 Crystal data for C21H19BrN5O3Re (1): monoclinic, P2(1)/c, a = 13.1851(5) A, b = 16.1292(7) A, c = 10.2689(4) A, beta = 99.353(1) degrees , V = 2154.8(2) A3, Z = 4. c21h19brn5o3re 17-31 H3 histone pseudogene 16 Homo sapiens 49-56 16562962-10 2006 Crystal data for C26H21BrN3O5Re (4): monoclinic, P2(1)/c, a = 16.6504(6) A, b = 10.1564(4) A, c = 14.6954(5) A, beta = 96.739(1) degrees , V = 2467.9(2) A3, Z = 4. c26h21brn3o5re 17-31 H3 histone pseudogene 16 Homo sapiens 49-56 16562962-11 2006 Crystal data for C27H24BrN4O5Re (6): monoclinic, P2(1), a = 8.7791(9) A, b = 16.312(2) A, c = 8.9231(9) A, beta = 90.030(1) degrees , V = 1277.8(2) A3, Z = 2. c27h24brn4o5re 17-31 H3 histone pseudogene 16 Homo sapiens 49-54 16310807-6 2006 These results suggest that squamocin inhibits the proliferation of K562 cells via G2/M arrest in association with the induction of p21, p27 and the reduction of Cdk1 and Cdc25C kinase activities. squamocin 27-36 H3 histone pseudogene 16 Homo sapiens 131-134 16525652-10 2006 Further studies showed the induction of p21/Cip1, p27/Kip1, E-cadherin and dephosphorylated p120ctn expression was involved in DPA-induced anticancer effects. dpa 127-130 H3 histone pseudogene 16 Homo sapiens 40-43 16525652-12 2006 in vivo results demonstrated that DPA enhanced the in vivo anticancer activity of the chemotherapeutic agent, CPT-11, by elevation of p53-independent p21/Cip1 and p27/Kip1 expression. dpa 34-37 H3 histone pseudogene 16 Homo sapiens 150-153 16525652-12 2006 in vivo results demonstrated that DPA enhanced the in vivo anticancer activity of the chemotherapeutic agent, CPT-11, by elevation of p53-independent p21/Cip1 and p27/Kip1 expression. Irinotecan 110-116 H3 histone pseudogene 16 Homo sapiens 150-153 16480688-0 2006 Aaptamine, a spongean alkaloid, activates p21 promoter in a p53-independent manner. aaptamine 0-9 H3 histone pseudogene 16 Homo sapiens 42-45 16480688-6 2006 The activation of p21 promoter by aaptamine was led through acting Sp1 sites between -82 and -50bp in a p53-independent manner. aaptamine 34-43 H3 histone pseudogene 16 Homo sapiens 18-21 16480688-0 2006 Aaptamine, a spongean alkaloid, activates p21 promoter in a p53-independent manner. spongean alkaloid 13-30 H3 histone pseudogene 16 Homo sapiens 42-45 16480688-2 2006 Aaptamine activated p21 promoter stably transfected in MG63 cells dose-dependently at the concentrations of 20-50microM. aaptamine 0-9 H3 histone pseudogene 16 Homo sapiens 20-23 16480688-3 2006 Expression of p21 and its mRNA in the wild-type MG63 cells also increased by aaptamine-treatment. aaptamine 77-86 H3 histone pseudogene 16 Homo sapiens 14-17 16480688-5 2006 To analyze a responsive element of p21 promoter in the up-regulation of p21 by aaptamine, MG63 cells were transiently transfected with a series of the deleted or mutated promoter segments, and induction of luciferase with aaptamine treatment was examined by using these corresponding transfected cells. aaptamine 79-88 H3 histone pseudogene 16 Homo sapiens 35-38 16480688-5 2006 To analyze a responsive element of p21 promoter in the up-regulation of p21 by aaptamine, MG63 cells were transiently transfected with a series of the deleted or mutated promoter segments, and induction of luciferase with aaptamine treatment was examined by using these corresponding transfected cells. aaptamine 79-88 H3 histone pseudogene 16 Homo sapiens 72-75 16508959-11 2006 Caveolin 1 induction and stresses with both IL-1beta and H2O2 up-regulated p53 and p21 and down-regulated phosphorylated retinoblastoma (Rb), suggesting that the p53/p21/Rb phosphorylation pathway, as well as prolonged p38 MAPK activation, may mediate the features of chondrocyte senescence induced by stress. Hydrogen Peroxide 57-61 H3 histone pseudogene 16 Homo sapiens 83-86 16413651-6 2006 Western blot analysis revealed that arecoline induced cyclin Bl, Wee 1, and phosphorylated cdc2 protein levels whereas it declined p21 protein expression in KB cancer cells. Arecoline 36-45 H3 histone pseudogene 16 Homo sapiens 131-134 16413651-7 2006 Nevertheless, arecoline induced p21, but decreased cdc2 and cyclin B1 protein levels in GK. Arecoline 14-23 H3 histone pseudogene 16 Homo sapiens 32-35 16518044-1 2006 At 120 K, 2,4-difluorobenzaldehyde benzoylhydrazone, C14H10F2N2O, (I), and 2,4-dichlorobenzaldehyde benzoylhydrazone, C14H10Cl2N2O, (II), are isomorphous and isostructural in P2(1)/n with Z" = 2. c14h10cl2n2o 118-130 H3 histone pseudogene 16 Homo sapiens 175-180 16282343-4 2006 Rapamycin induced an inhibition in the G1/S transition and a decrease in the mean MK ploidy via a diminution of p21 and cyclin D3 occurring at a transcriptional level. Sirolimus 0-9 H3 histone pseudogene 16 Homo sapiens 112-115 16508959-11 2006 Caveolin 1 induction and stresses with both IL-1beta and H2O2 up-regulated p53 and p21 and down-regulated phosphorylated retinoblastoma (Rb), suggesting that the p53/p21/Rb phosphorylation pathway, as well as prolonged p38 MAPK activation, may mediate the features of chondrocyte senescence induced by stress. Hydrogen Peroxide 57-61 H3 histone pseudogene 16 Homo sapiens 166-169 16549753-8 2006 RESULTS: There was increased expression of p16, p21, p53, BCLxL, and BCLxS genes with cisplatin treatment in the CCL23 and CCL23AS cells. Cisplatin 86-95 H3 histone pseudogene 16 Homo sapiens 48-51 16549753-14 2006 However, CAL27 cells still exhibited increased expression of p21 after treatment with cisplatin. Cisplatin 86-95 H3 histone pseudogene 16 Homo sapiens 61-64 16344270-9 2006 Violacein causes cell cycle block at G(1), upregulates p53, p27 and p21 levels and decreases the expression of cyclin D1. violacein 0-9 H3 histone pseudogene 16 Homo sapiens 68-71 16549753-15 2006 CONCLUSIONS: These results, in combination with increased expression of the p53 downstream effecter p21, indicate that the cisplatin-induced cell cycle arrest operates through the p16/p53-dependent pathway, and a caspase-independent pathway may be involved. Cisplatin 123-132 H3 histone pseudogene 16 Homo sapiens 100-103 16601291-9 2006 15d-PGJ(2) significantly inhibited estrogen-mediated proliferation of MCF-7 cells, and caused accumulation of p21 and p27 protein. 15d-pgj 0-7 H3 histone pseudogene 16 Homo sapiens 110-113 16382479-2 2006 Hexahalogenated benzenes (C6Cl(6-n)Br(n), C6Cl(6-n)I(n), C6Br(6-n)I(n)) crystallise in two main packing modes, which take the monoclinic space group P2(1)/n and the triclinic space group P1. Benzene 16-24 H3 histone pseudogene 16 Homo sapiens 149-154 16229013-8 2006 Gefitinib promoted the cleavage of full-length p21 Bax into p18 Bax in mitochondrial-enriched fraction, a characteristic feature of Bax activation toward apoptosis. Gefitinib 0-9 H3 histone pseudogene 16 Homo sapiens 47-50 16415107-3 2006 The activation is not dependent on upstream elements but rather is due to direct targeting of p21ras by reversible S-glutathiolation of cysteine thiols as demonstrated by biotin-labeling techniques. cysteine thiols 136-151 H3 histone pseudogene 16 Homo sapiens 94-97 16415107-3 2006 The activation is not dependent on upstream elements but rather is due to direct targeting of p21ras by reversible S-glutathiolation of cysteine thiols as demonstrated by biotin-labeling techniques. Biotin 171-177 H3 histone pseudogene 16 Homo sapiens 94-97 16415107-4 2006 The time course of p21ras S-glutathiolation following peroxynitrite corresponds to the increase in its Raf-1 binding activity and translocation to the membrane. Peroxynitrous Acid 54-67 H3 histone pseudogene 16 Homo sapiens 19-22 16415107-5 2006 Moreover, p21ras S-glutathiolation and activation can be reversed by dithiothreitol, confirming the importance of a disulfide bond. Dithiothreitol 69-83 H3 histone pseudogene 16 Homo sapiens 10-13 16415107-5 2006 Moreover, p21ras S-glutathiolation and activation can be reversed by dithiothreitol, confirming the importance of a disulfide bond. Disulfides 116-125 H3 histone pseudogene 16 Homo sapiens 10-13 16415107-8 2006 These results indicate that peroxynitrite arising from NO donors or pathological stimuli such as oxLDL triggers direct S-glutathiolation of p21ras Cys-118, which increases p21ras activity and mediates downstream signaling. Peroxynitrous Acid 28-41 H3 histone pseudogene 16 Homo sapiens 140-143 16415107-8 2006 These results indicate that peroxynitrite arising from NO donors or pathological stimuli such as oxLDL triggers direct S-glutathiolation of p21ras Cys-118, which increases p21ras activity and mediates downstream signaling. Cysteine 147-150 H3 histone pseudogene 16 Homo sapiens 140-143 16229013-4 2006 Following 2-h treatment, gefitinib significantly inhibited EGFR autophosphorylation and subsequent downstream signaling pathway through Erk and Akt, and induced accumulation of cells in the G0/G1 phase of the cell cycle at 24-h, accompanied by a concomitant increase in p21 transcript and increased expression of p27. Gefitinib 25-34 H3 histone pseudogene 16 Homo sapiens 270-273 16546993-8 2006 In contrast, low-dose CDDP killed cells in S phase, thereby causing an accumulation of G0-G1 cells (and increased p21 expression). Cisplatin 22-26 H3 histone pseudogene 16 Homo sapiens 114-117 16061352-5 2006 Flow cytometry analysis showed that diazene JK-279 induces G(2)/M phase arrest, mediated by the increase in p21 expression, and accompanied by an alteration in the expression of survivin. diazene 36-43 H3 histone pseudogene 16 Homo sapiens 108-111 16364249-0 2006 TP53 and P21 polymorphisms: response to cisplatinum/paclitaxel-based chemotherapy in ovarian cancer. Cisplatin 40-51 H3 histone pseudogene 16 Homo sapiens 9-12 16152627-9 2006 The p53-MDM2 interaction and absence of p21 production were restored in cells treated with I3C and the ATM inhibitor wortmannin. Wortmannin 117-127 H3 histone pseudogene 16 Homo sapiens 40-43 16364249-0 2006 TP53 and P21 polymorphisms: response to cisplatinum/paclitaxel-based chemotherapy in ovarian cancer. Paclitaxel 52-62 H3 histone pseudogene 16 Homo sapiens 9-12 16480579-19 2006 CONCLUSIONS: Exogenous WTA gene could inhibit the proliferation and colony forming ability of leukemia cells through up-regulating the expression of p21 and Cyclin A1 and arresting cell cycle at S phase. 5'-O-[(S)-ethoxy(hydroxy)phosphoryl]adenosine 23-26 H3 histone pseudogene 16 Homo sapiens 149-152 16267097-2 2006 Competitive HDAC inhibitors disrupt the cell cycle and/or induce apoptosis via de-repression of genes such as P21 and BAX, and cancer cells appear to be more sensitive than non-transformed cells to trichostatin A and related HDAC inhibitory compounds. trichostatin A 198-212 H3 histone pseudogene 16 Homo sapiens 110-113 16467108-10 2006 Lovastatin affected various IR-induced stress responses in HUVEC: It attenuated the increase in p53/p21 protein level and impaired the activation of nuclear factor-kappaB, Chk-1, and Akt kinase but did not inhibit extracellular signal-regulated kinase activation. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 100-103 16479163-8 2006 It was also shown that the association of p21 with p50 and other components of the pol delta complex increased in MCF7 cells treated with adriamycin. Doxorubicin 138-148 H3 histone pseudogene 16 Homo sapiens 42-45 16479163-9 2006 Our results suggested that p50 might target or anchor p21 to pol delta complex upon certain DNA damage such as adriamycin treatment. Doxorubicin 111-121 H3 histone pseudogene 16 Homo sapiens 54-57 17080554-7 2006 These results suggest that EGCG may have an inhibitory effect on UVB-induced photo-damage and apoptosis by blocking the cytokine secretion and the mRNA expressions of p53, p21 and c-fos genes. epigallocatechin gallate 27-31 H3 histone pseudogene 16 Homo sapiens 172-175 16513842-6 2006 In addition, we found that doxorubicin inhibited AR expression, and p21 protein completely disappeared after simultaneous treatment with trichostatin A and doxorubicin. trichostatin A 137-151 H3 histone pseudogene 16 Homo sapiens 68-71 16513842-6 2006 In addition, we found that doxorubicin inhibited AR expression, and p21 protein completely disappeared after simultaneous treatment with trichostatin A and doxorubicin. Doxorubicin 156-167 H3 histone pseudogene 16 Homo sapiens 68-71 16513842-9 2006 The protease/proteasome inhibitor MG132 protected AR and p21 from the effects of trichostatin A and doxorubicin and inhibited trichostatin A-induced cell death in AR-positive prostate cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 34-39 H3 histone pseudogene 16 Homo sapiens 57-60 16513842-11 2006 The synergistic effect of simultaneous treatment with trichostatin A and doxorubicin is mediated via inhibition of AR expression, induction of protease activity, increased expression of p53, and proteolysis of p21. trichostatin A 54-68 H3 histone pseudogene 16 Homo sapiens 210-213 16513842-11 2006 The synergistic effect of simultaneous treatment with trichostatin A and doxorubicin is mediated via inhibition of AR expression, induction of protease activity, increased expression of p53, and proteolysis of p21. Doxorubicin 73-84 H3 histone pseudogene 16 Homo sapiens 210-213 16413407-4 2006 As for the positive controls adozelesin and cisplatin, arrest was accompanied by phosphorylation of ATM kinase; dephosphorylation of pRB; decreases in RF-C, cyclin D1, Cdc25A, and Cdc6; and increases in p21. Cisplatin 44-53 H3 histone pseudogene 16 Homo sapiens 203-206 16112786-0 2006 Molecular mechanism of cell cycle blockage of hepatoma SK-Hep-1 cells by Epimedin C through suppression of mitogen-activated protein kinase activation and increased expression of CDK inhibitors p21(Cip1) and p27(Kip1). epimedin C 73-83 H3 histone pseudogene 16 Homo sapiens 194-197 16112786-6 2006 These data suggested that Epimedin C arrested the proliferation of these cells at G0/G1 phase through inhibition of CDK2 and CDK4 activities via an increased induction of p21(Cip1) and p27(Kip1). epimedin C 26-36 H3 histone pseudogene 16 Homo sapiens 171-174 16505103-4 2006 The berberine-induced inhibition of proliferation of DU145, PC-3, and LNCaP cells was associated with G1-phase arrest, which in DU145 cells was associated with inhibition of expression of cyclins D1, D2, and E and cyclin-dependent kinase (Cdk) 2, Cdk4, and Cdk6 proteins, increased expression of the Cdk inhibitory proteins (Cip1/p21 and Kip1/p27), and enhanced binding of Cdk inhibitors to Cdk. Berberine 4-13 H3 histone pseudogene 16 Homo sapiens 330-333 16052517-0 2006 Oh8dG induces G1 arrest in a human acute leukemia cell line by upregulating P21 and blocking the RAS to ERK signaling pathway. 8-ohdg 0-5 H3 histone pseudogene 16 Homo sapiens 76-79 16052517-3 2006 Simultaneously, oh8dG-treated KG-1 showed an increase in the oh8Gua content of DNA, upregulation of p21 (an inhibitor of cdk), and Ras inactivation. 8-ohdg 16-21 H3 histone pseudogene 16 Homo sapiens 100-103 16052517-9 2006 We report that oh8dG induces the arrest of KG-1 growth at the G1 phase mainly by upregulating p21 and inactivating Ras. 8-ohdg 15-20 H3 histone pseudogene 16 Homo sapiens 94-97 16550965-0 2006 Medroxyprogesterone acetate stimulates cdk inhibitors, p21 and p27, in endometrial carcinoma cells transfected with progesterone receptor-B cDNA. Medroxyprogesterone Acetate 0-27 H3 histone pseudogene 16 Homo sapiens 55-58 31394639-2 2006 Phosphorylation at Thr-145 and/or Ser-146 was reported to target p21 to the cytoplasm. Threonine 19-22 H3 histone pseudogene 16 Homo sapiens 65-68 31394639-2 2006 Phosphorylation at Thr-145 and/or Ser-146 was reported to target p21 to the cytoplasm. Serine 34-37 H3 histone pseudogene 16 Homo sapiens 65-68 31394639-7 2006 Further, lactacystin treatment enhanced T145A and S146A, but not T145D and S146D, which is consistent with the degradation of p21 by proteasome in the nucleus. lactacystin 9-20 H3 histone pseudogene 16 Homo sapiens 126-129 16343270-9 2006 SAHA lead to an upregulation of p21 in all cell lines and an upregulation of p27 in JeKo-1 and Granta-519 cells, while expression of p27 in Hbl-2 was not altered. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 32-35 16343270-11 2006 Treatment with NaB increased the expression of p21 in JeKo-1 and Hbl-2 cells, while in Granta 519 cells no effect was noted. nab 15-18 H3 histone pseudogene 16 Homo sapiens 47-50 16426974-2 2006 Here, we report small molecules that block lysine 382-acetylated p53 association with the bromodomain of the coactivator CBP, an interaction essential for p53-induced transcription of the cell cycle inhibitor p21 in response to DNA damage. Lysine 43-49 H3 histone pseudogene 16 Homo sapiens 209-212 16550965-7 2006 CONCLUSION: p21 and p27 may be related to progesterone-induced growth suppression in human endometrial adenocarcinoma. Progesterone 42-54 H3 histone pseudogene 16 Homo sapiens 12-15 16327987-5 2006 Cisplatin induced the accumulation of p53 and p21 proteins in A172 cells, but not in T98G cells. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 46-49 16280359-7 2006 p21 is normally induced only late after thymidine treatment. Thymidine 40-49 H3 histone pseudogene 16 Homo sapiens 0-3 16330856-1 2005 The title compound, C15H19NO5, crystallizes in the monoclinic space group P2(1)/c with four molecules in the asymmetric unit, which differ from each other in the orientation of their methoxy groups. c15h19no5 20-29 H3 histone pseudogene 16 Homo sapiens 74-79 16838851-3 2006 In addition to the GCV-induced cytotoxicity, apoptosis via caspase-7/8, cleavage of poly(ADP-ribose) polymerase, and accumulation of p53 and p21 were induced by GCV treatment. Ganciclovir 19-22 H3 histone pseudogene 16 Homo sapiens 141-144 16838851-3 2006 In addition to the GCV-induced cytotoxicity, apoptosis via caspase-7/8, cleavage of poly(ADP-ribose) polymerase, and accumulation of p53 and p21 were induced by GCV treatment. Ganciclovir 161-164 H3 histone pseudogene 16 Homo sapiens 141-144 16298082-3 2006 Neurofibrinomin, the protein product of the NF1 gene (neurofibromin gene (human)), is a guanosine triphosphate activating protein for p21(ras). Guanosine Triphosphate 88-110 H3 histone pseudogene 16 Homo sapiens 134-137 16328040-8 2006 Following dFdC + RT in OMS (% of cases), apoptosis and p21 expression increased (50%), p53 expression increased (75%) and cell proliferation decreased (75%). dfdc + rt 10-19 H3 histone pseudogene 16 Homo sapiens 55-58 16275167-4 2005 Cilostazol decreases the activity of phosphodiesterase type 3, leading to the accumulation of cyclic adenosine monophosphate, which initiates a cascade of events including upregulation of anti-oncogenes p53 and p21 and upregulation of hepatocyte growth factor (HGF). Cilostazol 0-10 H3 histone pseudogene 16 Homo sapiens 211-214 16275167-4 2005 Cilostazol decreases the activity of phosphodiesterase type 3, leading to the accumulation of cyclic adenosine monophosphate, which initiates a cascade of events including upregulation of anti-oncogenes p53 and p21 and upregulation of hepatocyte growth factor (HGF). Cyclic AMP 94-124 H3 histone pseudogene 16 Homo sapiens 211-214 16306677-1 2005 Crystals of m-carboxyphenylammonium monohydrogenphosphite, C7H8NO2+.H2PO3- (m-CPAMP), space group P2(1)/c, grown from aqueous solution undergo a reversible first-order single-crystal phase transition at Tc = 246 (2) K with a hysteresis of 3.6 K. The thermal behaviour of the sample was characterized by differential scanning calorimetry (DSC) experiments. m-carboxyphenylammonium monohydrogenphosphite 12-57 H3 histone pseudogene 16 Homo sapiens 98-105 16178003-3 2005 Proteasome inhibition with bortezomib has specifically promoted apoptosis of tumor cells through the stabilization of p53, p21, p27, Bax, and IkappaBalpha, resulting in nuclear factor kappaB inhibition. Bortezomib 27-37 H3 histone pseudogene 16 Homo sapiens 123-126 16193303-6 2005 Decitabine induced expression of the cell cycle inhibitor p21, arresting AML cell lines in G1 of the cell cycle. Decitabine 0-10 H3 histone pseudogene 16 Homo sapiens 58-61 16143523-0 2005 Parallel synthesis and biological evaluation of 5,6,7,8-tetrahydrobenzothieno[2,3-d]pyrimidin-4(3H)-one cytotoxic agents selective for p21-deficient cells. 5,6,7,8-Tetrahydro[1]benzothieno[2,3-d]pyrimidin-4(3H)-one 48-103 H3 histone pseudogene 16 Homo sapiens 135-138 16143523-3 2005 The 2-(1,4-dibenzodioxane)-substituted derivative 14 was identified as a highly selective and potent agent displaying an IC50 of 91 nM in the p21-deficient cell line. 2-(1,4-dibenzodioxane 4-25 H3 histone pseudogene 16 Homo sapiens 142-145 16149052-0 2005 Genistein-induced neuronal differentiation is associated with activation of extracellular signal-regulated kinases and upregulation of p21 and N-cadherin. Genistein 0-9 H3 histone pseudogene 16 Homo sapiens 135-138 16149052-5 2005 Meanwhile, genistein also upregulated N-cadherin and p21 (a Cdk inhibitor), but downregulated proliferating cell nuclear antigen protein (PCNA). Genistein 11-20 H3 histone pseudogene 16 Homo sapiens 53-56 16007142-6 2005 Furthermore, the kinase activities of Cdc2 and Cdk2 were significantly decreased following sodium butyrate treatment, accompanying downregulation of cyclin A and cyclin B, as well as upregulation of p21. Butyric Acid 91-106 H3 histone pseudogene 16 Homo sapiens 199-202 16049707-0 2005 Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. Quercetin 0-9 H3 histone pseudogene 16 Homo sapiens 119-122 16049707-6 2005 Addition of quercetin led to substantial decrease in the expression of Cdc2/Cdk-1, cyclin B1 and phosphorylated pRb and increase in p21. Quercetin 12-21 H3 histone pseudogene 16 Homo sapiens 132-135 16390854-8 2005 The down-regulation of the cyclin A, Bcl-2, and Bcl-X(L) expression with the simultaneous up-regulation of the p21 and Bax expression, and caspase-9 activation was observed in ECSC after bufalin treatment. bufalin 187-194 H3 histone pseudogene 16 Homo sapiens 111-114 16096850-7 2005 In OMS, apoptosis increased, cell proliferation decreased, and p53/p21 expression increased more pronounced following CDDP+RT. Cisplatin 118-122 H3 histone pseudogene 16 Homo sapiens 67-70 16049137-5 2005 Interestingly, EC overexpressing a mutant form of dynamin deficient in GTP binding (K44A) caused a selective inhibition in KDR protein level and endosomal vesicle formation and induced cell cycle arrest by inducing p21. Guanosine Triphosphate 71-74 H3 histone pseudogene 16 Homo sapiens 215-218 16054204-6 2005 Significant independent association was evident between the p21 arginine allele (rare allele with frequency of 0.1) at codon 31 and CaCx, compared to HPV-negative cytologically normal controls (OR(age-adjusted) = 2.01; 95% CI = 1.00-4.06; P = 0.05). Arginine 64-72 H3 histone pseudogene 16 Homo sapiens 60-63 16054204-8 2005 The p21 arginine allele was significantly associated with CaCx in the p53 proline non-homozygous group of subjects (OR(age-adjusted) = 2.68; 95% CI: 1.21-5.91; P = 0.01), and specifically in the p53 heterozygous group (OR(age-adjusted) = 2.91; 95% CI = 1.12-7.56; P = 0.03). Arginine 8-16 H3 histone pseudogene 16 Homo sapiens 4-7 16054204-8 2005 The p21 arginine allele was significantly associated with CaCx in the p53 proline non-homozygous group of subjects (OR(age-adjusted) = 2.68; 95% CI: 1.21-5.91; P = 0.01), and specifically in the p53 heterozygous group (OR(age-adjusted) = 2.91; 95% CI = 1.12-7.56; P = 0.03). cacx 58-62 H3 histone pseudogene 16 Homo sapiens 4-7 16054204-8 2005 The p21 arginine allele was significantly associated with CaCx in the p53 proline non-homozygous group of subjects (OR(age-adjusted) = 2.68; 95% CI: 1.21-5.91; P = 0.01), and specifically in the p53 heterozygous group (OR(age-adjusted) = 2.91; 95% CI = 1.12-7.56; P = 0.03). Proline 74-81 H3 histone pseudogene 16 Homo sapiens 4-7 16054204-10 2005 However, the two risk factors, p53 proline homozygosity and p21 arginine allele, although part of a common causal pathway, appear to act in a mutually exclusive manner. Arginine 64-72 H3 histone pseudogene 16 Homo sapiens 60-63 16142311-7 2005 APC protein and p21 were also expressed at a higher frequency in HP (100%, 100%), and SA (67%, 83%), than in TA (29%, p<0.03; 46%, p<0.05). sa 86-88 H3 histone pseudogene 16 Homo sapiens 16-19 16142311-8 2005 MC (68%, 100%) showed a higher frequency of expression of APC protein and p21 than NMC (19%, p<0.001; 45%, p<0.01). Methylcholanthrene 0-2 H3 histone pseudogene 16 Homo sapiens 74-77 16027227-3 2005 Minerval is a derivative of oleic acid (OA) with an enhanced antiproliferative activity in human cancer cells and animal models of cancer, which is associated with PKCalpha activation and p21(CIP) overexpression. Oleic Acid 28-38 H3 histone pseudogene 16 Homo sapiens 188-191 15976015-2 2005 Inhibition of proliferation by TPA in PANC-1 cells was associated with an increase in the level of p21, but this was not observed in MIA PaCa-2 or BxPC-3 cells. Tetradecanoylphorbol Acetate 31-34 H3 histone pseudogene 16 Homo sapiens 99-102 16096427-4 2005 In MCF7 cells treated with usnic acid, although there was an accumulation of p53 and p21 proteins, the transcriptional activity of p53 remained unaffected. usnic acid 27-37 H3 histone pseudogene 16 Homo sapiens 85-88 15976015-3 2005 The TPA-induced increase of p21 in PANC-1 cells was blocked by bisindolylmaleimide or rottlerin (inhibitors of protein kinase C). Tetradecanoylphorbol Acetate 4-7 H3 histone pseudogene 16 Homo sapiens 28-31 15976015-3 2005 The TPA-induced increase of p21 in PANC-1 cells was blocked by bisindolylmaleimide or rottlerin (inhibitors of protein kinase C). bisindolylmaleimide 63-82 H3 histone pseudogene 16 Homo sapiens 28-31 15976015-3 2005 The TPA-induced increase of p21 in PANC-1 cells was blocked by bisindolylmaleimide or rottlerin (inhibitors of protein kinase C). rottlerin 86-95 H3 histone pseudogene 16 Homo sapiens 28-31 32397049-1 2005 The SIESTA approach based on pseudopotentials and a localized basis set is used to calculate the electronic, elastic and equilibrium properties of P 21/c, Pbca, Pnma, Fm3m, P42nmc and Pa3 phases of HfO2. hafnium oxide 198-202 H3 histone pseudogene 16 Homo sapiens 147-153 16052566-7 2005 Our data also indicated that ERK activation and the potentiation of ATP calcium responses were sensitive to the src-like kinase inhibitor herbimycin A, p21(ras) farnesyltransferase inhibitor peptide, and some PKC inhibitors. atp calcium 68-79 H3 histone pseudogene 16 Homo sapiens 152-155 16171389-8 2005 We also show that p21 Max has an apparent KD (37 degrees C) of 7 x 10(-6), a value 10-100 times smaller than the b-HLH-LZ itself. b-hlh-lz 113-121 H3 histone pseudogene 16 Homo sapiens 18-21 16143778-1 2005 The racemic title compound, C20H20N4O4, crystallizes with Z"=2 in the space group P2(1)/c. c20h20n4o4 28-38 H3 histone pseudogene 16 Homo sapiens 82-87 16054119-3 2005 We showed that Cav3.1 activation resulted in the level of p21(ras)-GTP in the cells being rapidly decreased during the first 2 min, and then recovering between 2 min and 15 min. Guanosine Triphosphate 67-70 H3 histone pseudogene 16 Homo sapiens 58-61 16084079-8 2005 Further, silibinin modulates mitogenic and survival signalling, p53, Cip1/p21 and other cell cycle regulatory molecules to prevent UVB-induced skin carcinogenesis. Silybin 9-18 H3 histone pseudogene 16 Homo sapiens 74-77 16005212-1 2005 On the basis of a screening lead from an assay using a pair of p21 isogenic cell lines (p21-proficient cells and p21-deficient cells) to identify chemoselective agents, a series of novel thieno[2,3-d]pyrimidin-4(1H)-one-based analogs was prepared. thieno(2,3-d)pyrimidin-4-one 187-219 H3 histone pseudogene 16 Homo sapiens 88-91 16005212-1 2005 On the basis of a screening lead from an assay using a pair of p21 isogenic cell lines (p21-proficient cells and p21-deficient cells) to identify chemoselective agents, a series of novel thieno[2,3-d]pyrimidin-4(1H)-one-based analogs was prepared. thieno(2,3-d)pyrimidin-4-one 187-219 H3 histone pseudogene 16 Homo sapiens 88-91 16323045-1 2005 We have previously computed the structures of three loops, residues 591-596, 654-675 and 742-751, in the ras-p21 protein-binding domain (residues 568-1044) of the guanine nucleotide-exchange-promoting SOS protein that were crystallographically undefined when one molecule of ras-p21 (unbound to nucleotide) binds to SOS. Guanine Nucleotides 163-181 H3 histone pseudogene 16 Homo sapiens 279-282 15880691-6 2005 Furthermore, inhibition of ERK through addition of PD98059 stimulated p53 activation in MCF7 cells and also led to upregulation of p53 downstream targets, p21 and Bax, which is a proapototic member of Bcl-2 family triggering mitochondrial pore opening. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 51-58 H3 histone pseudogene 16 Homo sapiens 155-158 15906320-1 2005 The mechanism of the hydrolysis reaction of guanosine triphosphate (GTP) by the protein complex Ras-GAP (p21(ras) - p120(GAP)) has been modeled by the quantum mechanical-molecular mechanical (QM/MM) and ab initio quantum calculations. Guanosine Triphosphate 44-66 H3 histone pseudogene 16 Homo sapiens 105-113 15906320-1 2005 The mechanism of the hydrolysis reaction of guanosine triphosphate (GTP) by the protein complex Ras-GAP (p21(ras) - p120(GAP)) has been modeled by the quantum mechanical-molecular mechanical (QM/MM) and ab initio quantum calculations. Guanosine Triphosphate 68-71 H3 histone pseudogene 16 Homo sapiens 105-113 15906320-4 2005 At the first stage, a unified motion of Arg789 of GAP, Gln61, Thr35 of Ras, and the lytic water molecule results in a substantial spatial separation of the gamma-phosphate group of GTP from the rest of the molecule (GDP). Phosphates 162-171 H3 histone pseudogene 16 Homo sapiens 71-74 15906320-4 2005 At the first stage, a unified motion of Arg789 of GAP, Gln61, Thr35 of Ras, and the lytic water molecule results in a substantial spatial separation of the gamma-phosphate group of GTP from the rest of the molecule (GDP). Guanosine Triphosphate 181-184 H3 histone pseudogene 16 Homo sapiens 71-74 15906320-4 2005 At the first stage, a unified motion of Arg789 of GAP, Gln61, Thr35 of Ras, and the lytic water molecule results in a substantial spatial separation of the gamma-phosphate group of GTP from the rest of the molecule (GDP). Guanosine Diphosphate 216-219 H3 histone pseudogene 16 Homo sapiens 71-74 16041086-0 2005 Structure of the clinopyroxene-type compound CaCuGe2O6 between 15 and 800 K. CaCuGe2O6 shows a strongly distorted clinopyroxene-type structure with P2(1)/c symmetry at 298 K. The Cu2+ ion at the M1 site is coordinated by six O atoms forming an octahedron, which deviates significantly from ideal geometry. clinopyroxene 17-30 H3 histone pseudogene 16 Homo sapiens 148-153 16041086-0 2005 Structure of the clinopyroxene-type compound CaCuGe2O6 between 15 and 800 K. CaCuGe2O6 shows a strongly distorted clinopyroxene-type structure with P2(1)/c symmetry at 298 K. The Cu2+ ion at the M1 site is coordinated by six O atoms forming an octahedron, which deviates significantly from ideal geometry. cacuge2o6 77-86 H3 histone pseudogene 16 Homo sapiens 148-153 16098148-5 2005 Doxycycline-induced expression of SEI proteins results in activation of the p21 gene and inhibition of cell growth, but the growth arrest was not suppressed by the siRNA-mediated knockdown of the endogenous p53 protein. Doxycycline 0-11 H3 histone pseudogene 16 Homo sapiens 76-79 16093429-4 2005 Transient transfection of H460 lung cancer cells and human umbilical vascular endothelial cells (HUVEC) with antisense oligonucleotides (ASODN) against MDM2 resulted in a reduced level of MDM2 and increased levels of p21 and p53. Oligonucleotides 119-135 H3 histone pseudogene 16 Homo sapiens 217-220 16093429-4 2005 Transient transfection of H460 lung cancer cells and human umbilical vascular endothelial cells (HUVEC) with antisense oligonucleotides (ASODN) against MDM2 resulted in a reduced level of MDM2 and increased levels of p21 and p53. asodn 137-142 H3 histone pseudogene 16 Homo sapiens 217-220 16323045-1 2005 We have previously computed the structures of three loops, residues 591-596, 654-675 and 742-751, in the ras-p21 protein-binding domain (residues 568-1044) of the guanine nucleotide-exchange-promoting SOS protein that were crystallographically undefined when one molecule of ras-p21 (unbound to nucleotide) binds to SOS. Guanine Nucleotides 163-181 H3 histone pseudogene 16 Homo sapiens 109-112 16323045-3 2005 More recently, a new crystal structure of SOS has been determined in which this protein binds to two molecules of ras-p21, one unbound to GTP and one bound to GTP. Guanosine Triphosphate 159-162 H3 histone pseudogene 16 Homo sapiens 118-121 15997071-0 2005 L-alanylglycyl-L-alanine monohydrate at 20 K. The X-ray crystal structure of the title compound, C8H15N3O4.H2O, at 20 K (space group P2(1)) reveals that the molecular conformation of the tripeptide is remarkably different from the water-free form (space group P2(1)2(1)2(1)) reported previously [Padiyar & Seshadri (1996), Acta Cryst. alanylglutamine 97-106 H3 histone pseudogene 16 Homo sapiens 133-138 15855057-5 2005 Because several *NO-stimulated genes are transcription factors, we analyzed the mRNA expression profile in U937 cells exposed to DPTA-NO for 14 h. We found that long-term *NO treatment influenced transcription rates of a rather limited set of genes, including CIDE-B, BNIP3, p21/Cip1, molybdopterin synthase, and TRAF4-associated factor 1. dpta-no 129-136 H3 histone pseudogene 16 Homo sapiens 275-278 16080505-8 2005 RESULTS: D-allose had a significant inhibitory effect on ovarian cancer cell proliferation in a dose-dependent manner, and caused a moderate G2/M arrest in the cell cycle, up-regulation of Cdk inhibitors p21 and p27 levels, and the induction of apoptosis in OVCAR-3 cells. allose 9-17 H3 histone pseudogene 16 Homo sapiens 204-207 15755852-6 2005 Using cultured rhesus OSE cells in vitro, we show that these levels of estradiol (1 mug/ml; approximately 3 mum) block the actions of serum growth factors, activate the G(1) phase retinoblastoma checkpoint, and induce p21, an inhibitor of kinases that normally inactivate the retinoblastoma checkpoint. Estradiol 71-80 H3 histone pseudogene 16 Homo sapiens 218-221 15755852-7 2005 We also show that estradiol increases p53 levels, which may contribute to p21 induction. Estradiol 18-27 H3 histone pseudogene 16 Homo sapiens 74-77 15956248-7 2005 Furthermore, treatment with ZM336372 led to a marked suppression of cellular proliferation and induction of the cell cycle inhibitors p21 and p18. N-(5-(3-dimethylaminobenzamido)-2-methylphenyl)-4-hydroxybenzamide 28-36 H3 histone pseudogene 16 Homo sapiens 134-137 15897584-1 2005 PURPOSE: Flavopiridol potently enhances the effect of irinotecan with cures in colorectal cancer xenografts, and is associated with modulation of several molecular targets, including p21, Differentiation-related gene 1 (Drg1), and p53. alvocidib 9-21 H3 histone pseudogene 16 Homo sapiens 183-186 15896711-7 2005 These appear to be followed by the specific activation of AMPK and the up-regulation of p53, p21, and Bax by genistein. Genistein 109-118 H3 histone pseudogene 16 Homo sapiens 93-96 15958577-8 2005 Although cisplatin treatment results in significant elevation in the expression of Fas ligand and intracellular p21 levels, expression of Siva-1 has no additional benefit. Cisplatin 9-18 H3 histone pseudogene 16 Homo sapiens 112-115 15750619-6 2005 However, lack of functional p21 resulted in the accumulation of cells in G2/M phase of the cell cycle and markedly enhanced p14 ARF-induced apoptosis that was, nevertheless, efficiently inhibited by the cell permeable broad-spectrum caspase inhibitor zVAD-fmk (valyl-alanyl-aspartyl-(O)-methyl)-fluoromethylketone). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 251-259 H3 histone pseudogene 16 Homo sapiens 28-31 15750619-6 2005 However, lack of functional p21 resulted in the accumulation of cells in G2/M phase of the cell cycle and markedly enhanced p14 ARF-induced apoptosis that was, nevertheless, efficiently inhibited by the cell permeable broad-spectrum caspase inhibitor zVAD-fmk (valyl-alanyl-aspartyl-(O)-methyl)-fluoromethylketone). valyl-alanyl-aspartyl-(o)-methyl)-fluoromethylketone 261-313 H3 histone pseudogene 16 Homo sapiens 28-31 15914890-2 2005 A new investigation establishes that Sr(2)YTaO(6) and the isostructural Sr(2)YNbO(6), distrontium yttrium niobium hexaoxide, in fact both adopt the commonly occurring monoclinic structure, with the space-group symmetry P2(1)/n. sr(2)ytao 37-46 H3 histone pseudogene 16 Homo sapiens 219-224 15914890-2 2005 A new investigation establishes that Sr(2)YTaO(6) and the isostructural Sr(2)YNbO(6), distrontium yttrium niobium hexaoxide, in fact both adopt the commonly occurring monoclinic structure, with the space-group symmetry P2(1)/n. sr(2)ynbo 72-81 H3 histone pseudogene 16 Homo sapiens 219-224 15914890-2 2005 A new investigation establishes that Sr(2)YTaO(6) and the isostructural Sr(2)YNbO(6), distrontium yttrium niobium hexaoxide, in fact both adopt the commonly occurring monoclinic structure, with the space-group symmetry P2(1)/n. distrontium yttrium niobium hexaoxide 86-123 H3 histone pseudogene 16 Homo sapiens 219-224 15605368-3 2005 Benzyl isothiocyanate (BITC) treatment down-regulates cyclins and CDKs and up-regulates the expression of the CDK inhibitor p21, but up-regulation of p27 or p53 was not detected. benzyl isothiocyanate 0-21 H3 histone pseudogene 16 Homo sapiens 124-127 15605368-3 2005 Benzyl isothiocyanate (BITC) treatment down-regulates cyclins and CDKs and up-regulates the expression of the CDK inhibitor p21, but up-regulation of p27 or p53 was not detected. benzyl isothiocyanate 23-27 H3 histone pseudogene 16 Homo sapiens 124-127 15897598-4 2005 In these models, both SAHA and m-carboxycinnamic acid bis-hydroxamide induced growth arrest and caspase-mediated apoptosis and increased p21 protein levels, retinoblastoma hypophosphorylation, BH3-interacting domain death agonist cleavage, Bax up-regulation, down-regulation of Bcl-2, A1, and Bcl-x(L) expression, and cleavage of poly(ADP-ribose) polymerase and caspase-8, -9, -3, -7, and -2. Vorinostat 22-26 H3 histone pseudogene 16 Homo sapiens 137-140 15897598-4 2005 In these models, both SAHA and m-carboxycinnamic acid bis-hydroxamide induced growth arrest and caspase-mediated apoptosis and increased p21 protein levels, retinoblastoma hypophosphorylation, BH3-interacting domain death agonist cleavage, Bax up-regulation, down-regulation of Bcl-2, A1, and Bcl-x(L) expression, and cleavage of poly(ADP-ribose) polymerase and caspase-8, -9, -3, -7, and -2. carboxycinnamic acid bishydroxamide 31-69 H3 histone pseudogene 16 Homo sapiens 137-140 15735718-5 2005 Here we demonstrate that DAP treatment of human cancer cells activates the p53-p21 pathway without activating other known mechanisms that inhibit Cdk4 and Cdk2 activities. dap 25-28 H3 histone pseudogene 16 Homo sapiens 79-82 15753078-5 2005 Accordingly, SP600125, the inhibitor of JNK, and wortmannin, the inhibitor of phosphatidylinositol 3-kinase, which is the upstream activator of PKB, inhibited the increase in the cellular content of p21. pyrazolanthrone 13-21 H3 histone pseudogene 16 Homo sapiens 199-202 15753078-5 2005 Accordingly, SP600125, the inhibitor of JNK, and wortmannin, the inhibitor of phosphatidylinositol 3-kinase, which is the upstream activator of PKB, inhibited the increase in the cellular content of p21. Wortmannin 49-59 H3 histone pseudogene 16 Homo sapiens 199-202 15753078-7 2005 When p21 expression was inhibited by cycloheximide, galectin-8 directed the cells toward apoptosis, which involves induction of poly(ADP-ribose) polymerase cleavage. Cycloheximide 37-50 H3 histone pseudogene 16 Homo sapiens 5-8 15897421-11 2005 Supradose levels of docetaxel produced distinct protein expression patterns for regulators of the cell cycle (cyclins A and B, p21, and p27), apoptosis (cleaved caspase-3 and cleaved PARP), and signal transduction (EGFR, pEGFR, pc-Jun, and pERK) in HNSCC, which supports a distinctive mechanism of action for supradose docetaxel levels. Docetaxel 20-29 H3 histone pseudogene 16 Homo sapiens 127-130 15846088-5 2005 The cell line that showed greatest reduction (85-90%) of p53 expression showed decreased p21 promoter activation after DNA damage with camptothecin, etoposide and MMS. Camptothecin 135-147 H3 histone pseudogene 16 Homo sapiens 89-92 15846088-5 2005 The cell line that showed greatest reduction (85-90%) of p53 expression showed decreased p21 promoter activation after DNA damage with camptothecin, etoposide and MMS. Etoposide 149-158 H3 histone pseudogene 16 Homo sapiens 89-92 15846088-5 2005 The cell line that showed greatest reduction (85-90%) of p53 expression showed decreased p21 promoter activation after DNA damage with camptothecin, etoposide and MMS. Methyl Methanesulfonate 163-166 H3 histone pseudogene 16 Homo sapiens 89-92 15735718-7 2005 Conversely, inhibition of p21 induction by cycloheximide or by p21 gene deletion prevents DAP-induced inhibition of Cdk4 and Cdk2 activities. dap 90-93 H3 histone pseudogene 16 Homo sapiens 63-66 15735718-8 2005 Attenuated p53 expression and p21 induction also eliminates DAP-induced G(1)-phase arrest and inhibition of Cdk4 and Cdk2 activities. dap 60-63 H3 histone pseudogene 16 Homo sapiens 30-33 15746940-2 2005 While p53 is constitutively acetylated at Lys320 in LNCaP cells, treatment with CG-1521, stabilizes the acetylation of p53 at Lys373, elevating p21 (and inducing cell cycle arrest). cysteinylglycine 80-82 H3 histone pseudogene 16 Homo sapiens 144-147 15746940-4 2005 TSA stabilizes the acetylation of p53 at Lys382, elevating p21 levels and inducing cell cycle arrest, but does not induce Bax translocation or apoptosis. trichostatin A 0-3 H3 histone pseudogene 16 Homo sapiens 59-62 15688362-10 2005 Increased nuclear localization of both p53 and p21(cip1) was observed in BDO2-treated cells, suggesting that the cell cycle arrest was p21(cip1)-mediated. bdo2 73-77 H3 histone pseudogene 16 Homo sapiens 47-50 15688362-10 2005 Increased nuclear localization of both p53 and p21(cip1) was observed in BDO2-treated cells, suggesting that the cell cycle arrest was p21(cip1)-mediated. bdo2 73-77 H3 histone pseudogene 16 Homo sapiens 135-138 15764647-0 2005 Ablation of either p21 or Bax prevents p53-dependent apoptosis induced by green tea polyphenol epigallocatechin-3-gallate. polyphenol epigallocatechin-3-gallate 84-121 H3 histone pseudogene 16 Homo sapiens 19-22 15764647-13 2005 In summary, using isogenic cell lines and siRNA, we have clearly demonstrated that EGCG activates growth arrest and apoptosis primarily via p53-dependent pathway that involves the function of both p21 and Bax such that down-regulation of either molecule confers a growth advantage to the cells. epigallocatechin gallate 83-87 H3 histone pseudogene 16 Homo sapiens 197-200 16283548-1 2005 In previous studies, involving molecular modeling of wild-type and oncogenic forms of the ras-p21 protein bound to GTPase activating protein GAP and the ras-specific guanine nucleotide exchange-promoting protein, SOS, we identified specific domains of GAP and SOS proteins that differ in conformation when the computed average structures of the corresponding wild-type and oncogenic complexes are superimposed. Guanine Nucleotides 166-184 H3 histone pseudogene 16 Homo sapiens 94-97 16283548-2 2005 Additionally, in these previous studies, we have synthesized peptides corresponding to these domains and found that all of them inhibit either or both oncogenic (Val 12-containing) p21- and insulin-activated wild-type p21-induced oocyte maturation. val 12 162-168 H3 histone pseudogene 16 Homo sapiens 181-184 16283548-2 2005 Additionally, in these previous studies, we have synthesized peptides corresponding to these domains and found that all of them inhibit either or both oncogenic (Val 12-containing) p21- and insulin-activated wild-type p21-induced oocyte maturation. val 12 162-168 H3 histone pseudogene 16 Homo sapiens 218-221 15735718-9 2005 Together, these findings establish that activation of the p53-p21 pathway is responsible for the DAP-induced G(1)-phase checkpoint response and provide the first solid evidence that p21 induction by p53 during a DNA damage-induced G(1)-phase checkpoint response inhibits both Cdk4 and Cdk2 activities. dap 97-100 H3 histone pseudogene 16 Homo sapiens 62-65 15735718-9 2005 Together, these findings establish that activation of the p53-p21 pathway is responsible for the DAP-induced G(1)-phase checkpoint response and provide the first solid evidence that p21 induction by p53 during a DNA damage-induced G(1)-phase checkpoint response inhibits both Cdk4 and Cdk2 activities. dap 97-100 H3 histone pseudogene 16 Homo sapiens 182-185 15735718-7 2005 Conversely, inhibition of p21 induction by cycloheximide or by p21 gene deletion prevents DAP-induced inhibition of Cdk4 and Cdk2 activities. Cycloheximide 43-56 H3 histone pseudogene 16 Homo sapiens 26-29 15735718-7 2005 Conversely, inhibition of p21 induction by cycloheximide or by p21 gene deletion prevents DAP-induced inhibition of Cdk4 and Cdk2 activities. dap 90-93 H3 histone pseudogene 16 Homo sapiens 26-29 15792451-4 2005 [Co(dca)2(H2O)2].2(2,3,5,6-tmpdo) (3) is in the monoclinic space group P2(1)/c with a = 9.4739(3), b = 11.3876(3), c = 12.1778(3) A, beta = 98.967(1) degrees , V = 1297.74(6) A(3), Z = 4, and R1 = 0.0481. ,3,5,6-tmpdo 20-32 H3 histone pseudogene 16 Homo sapiens 71-76 15819548-2 2005 All three oxides crystallize in the monoclinic space group P2(1)/n (Glazer tilt system #10, a(-)a(-)b(+)), forming a 1:1 ordered rock salt lattice of the Na(+) and Os(5+) cations. Oxides 10-16 H3 histone pseudogene 16 Homo sapiens 59-64 15708847-5 2005 Additionally, compared with the full-length cyclin E-CDK2 complexes, the LMW cyclin E-CDK2 complexes are significantly more resistant to inhibition by p21 and p27, despite equal binding of the CKIs to the LMW complexes. 2-(4-Amino-N-ethylanilino)ethanol 73-76 H3 histone pseudogene 16 Homo sapiens 151-154 15807891-9 2005 Patients and controls were genotyped for a single nucleotide polymorphism (C/A transversion) in the third base of codon 31 of p21, which leads to a serine (Ser)/arginine (Arg) substitution. Serine 148-154 H3 histone pseudogene 16 Homo sapiens 126-129 15725471-2 2005 We have previously reported that patients with T-LGL leukemia were seroreactive against BA21, a 34 amino acid peptide derived from HTLV-I envelope protein p21. D-Glucurono-6,3-lactonide 88-92 H3 histone pseudogene 16 Homo sapiens 155-158 15807891-9 2005 Patients and controls were genotyped for a single nucleotide polymorphism (C/A transversion) in the third base of codon 31 of p21, which leads to a serine (Ser)/arginine (Arg) substitution. Serine 156-159 H3 histone pseudogene 16 Homo sapiens 126-129 15807891-9 2005 Patients and controls were genotyped for a single nucleotide polymorphism (C/A transversion) in the third base of codon 31 of p21, which leads to a serine (Ser)/arginine (Arg) substitution. Arginine 161-169 H3 histone pseudogene 16 Homo sapiens 126-129 15807891-9 2005 Patients and controls were genotyped for a single nucleotide polymorphism (C/A transversion) in the third base of codon 31 of p21, which leads to a serine (Ser)/arginine (Arg) substitution. Arginine 171-174 H3 histone pseudogene 16 Homo sapiens 126-129 15805626-3 2005 In 2-chloro-N-(4-nitrophenyl)nicotinamide, C12H8ClN3O3, which crystallizes with Z" = 2 in space group P2(1)/n, the molecules are linked by two N-H...N hydrogen bonds into simple C(2)(2) (12) chains. 2-chloro-N-(4-nitrophenyl)pyridine-3-carboxamide 3-41 H3 histone pseudogene 16 Homo sapiens 102-107 15805626-3 2005 In 2-chloro-N-(4-nitrophenyl)nicotinamide, C12H8ClN3O3, which crystallizes with Z" = 2 in space group P2(1)/n, the molecules are linked by two N-H...N hydrogen bonds into simple C(2)(2) (12) chains. c12h8cln3o3 43-54 H3 histone pseudogene 16 Homo sapiens 102-107 15763342-7 2005 Both albumin synthesis rate and ammonia removal rate improved for HepG2/tk incubated with FR228 and pioglitazone for 3 days, which induced nuclear transport of p21. Ammonia 32-39 H3 histone pseudogene 16 Homo sapiens 160-163 15763342-7 2005 Both albumin synthesis rate and ammonia removal rate improved for HepG2/tk incubated with FR228 and pioglitazone for 3 days, which induced nuclear transport of p21. fr228 90-95 H3 histone pseudogene 16 Homo sapiens 160-163 15763342-7 2005 Both albumin synthesis rate and ammonia removal rate improved for HepG2/tk incubated with FR228 and pioglitazone for 3 days, which induced nuclear transport of p21. Pioglitazone 100-112 H3 histone pseudogene 16 Homo sapiens 160-163 15821341-2 2005 After treatment with evodiamine for the indicated time periods, anti-apoptotic protein SIRT1 expression was decreased; p53 expression and its phosphorylation were both enhanced, whereas transient induction of downstream p21 was not enough to promote cell cycle arrest. evodiamine 21-31 H3 histone pseudogene 16 Homo sapiens 220-223 15797377-4 2005 We further show that RAD001 sensitizes cells to cisplatin by inhibiting p53-induced p21 expression. Cisplatin 48-57 H3 histone pseudogene 16 Homo sapiens 84-87 15745803-1 2005 A novel series of p21 chemoselective agents containing a pyrazolo[1,5-a]pyrimidin-7-yl phenyl amides were identified by high throughput screening. pyrazolo[1,5-a]pyrimidin-7-yl phenyl amides 57-100 H3 histone pseudogene 16 Homo sapiens 18-21 15745803-3 2005 The isopropyl carbamate derivative 34 was identified as a highly chemoselective agent displaying a potency of 51 nM in the p21 deficient cell line. ISOPROPYL CARBAMATE 4-23 H3 histone pseudogene 16 Homo sapiens 123-126 15752352-0 2005 Dehydroepiandrosterone inhibits the proliferation of human umbilical vein endothelial cells by enhancing the expression of p53 and p21, restricting the phosphorylation of retinoblastoma protein, and is androgen- and estrogen-receptor independent. Dehydroepiandrosterone 0-22 H3 histone pseudogene 16 Homo sapiens 131-134 15694358-0 2005 Suppression of chondrosarcoma cells by 15-deoxy-Delta 12,14-prostaglandin J2 is associated with altered expression of Bax/Bcl-xL and p21. 15-deoxy-delta(12,14)-prostaglandin J2 39-76 H3 histone pseudogene 16 Homo sapiens 133-136 15694358-5 2005 Among cyclin-dependent kinase inhibitors, p21 was induced and up-regulated by 15d-PGJ(2), but p16 and p27 were not changed, suggesting that the involvement of p21 in inhibition of cell proliferation. 15d-pgj 78-85 H3 histone pseudogene 16 Homo sapiens 42-45 15755327-8 2005 We further demonstrated that p53 and p21 protein expression were induced following the E/P and retinoid treatments. Retinoids 95-103 H3 histone pseudogene 16 Homo sapiens 37-40 15732961-5 2005 [(Pt(pip2NCN))2(mu-bpe)](CF3SO3)2 x 2CH2Cl2: monoclinic, P21/c, a = 10.1288(6) A, b = 16.3346(9) A, c = 17.4764(10) A, beta = 90.882(2) degrees , V = 2891.1(3) A3, Z = 2. [(pt(pip2ncn))2(mu-bpe)](cf3so3)2 x 2ch2cl2 0-43 H3 histone pseudogene 16 Homo sapiens 57-62 15868936-0 2005 Ellagic acid induced p53/p21 expression, G1 arrest and apoptosis in human bladder cancer T24 cells. Ellagic Acid 0-12 H3 histone pseudogene 16 Homo sapiens 25-28 15868936-6 2005 Ellagic acid also increased p53 and p21 and decreased CDK2 gene expression, that may lead to the G0/G1 arrest of T24 cells. Ellagic Acid 0-12 H3 histone pseudogene 16 Homo sapiens 36-39 15752352-5 2005 DHEA diminished the levels of phosphorylated retinoblastoma protein and increased the expression of p53 and p21 mRNAs. Dehydroepiandrosterone 0-4 H3 histone pseudogene 16 Homo sapiens 108-111 15784690-12 2005 In addition, AZT induced an upregulation of cyclin D1 accompanied by a downregulation of the cyclin D1-associated inhibitors P18 and P57, and the G(1)-S check point gene P21, the net effect of which would be to foster a cell progression into S phase. Zidovudine 13-16 H3 histone pseudogene 16 Homo sapiens 170-173 15670932-3 2005 The crystal structure of a 3",5"-di-O-acetyl-protected derivative (monoclinic, P21, a/b/c= 6.666(1)/12.225(1)/24.676(2) A, beta=90.24(1) degrees , Z=4) shows exclusively C2"-endo deoxyribose puckering. 3",5"-di-o-acetyl 27-44 H3 histone pseudogene 16 Homo sapiens 79-82 15514006-1 2005 Present studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, induces acetylation of histone H3 and H4 and of heat shock protein 90 (hsp90), increases p21 levels, as well as induces cell-cycle G(1) phase accumulation and apoptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the activating length mutation of FLT-3. Panobinostat 26-32 H3 histone pseudogene 16 Homo sapiens 194-197 15715472-10 2005 The butyric acid and formaldehyde induced cell differentiation and increased p53 and p21 levels, suggesting that both affect cancer cells, the acid by inhibiting HDAC and the aldehyde by an as yet unknown mechanism. Butyric Acid 4-16 H3 histone pseudogene 16 Homo sapiens 85-88 15715472-10 2005 The butyric acid and formaldehyde induced cell differentiation and increased p53 and p21 levels, suggesting that both affect cancer cells, the acid by inhibiting HDAC and the aldehyde by an as yet unknown mechanism. Formaldehyde 21-33 H3 histone pseudogene 16 Homo sapiens 85-88 15715472-10 2005 The butyric acid and formaldehyde induced cell differentiation and increased p53 and p21 levels, suggesting that both affect cancer cells, the acid by inhibiting HDAC and the aldehyde by an as yet unknown mechanism. Aldehydes 25-33 H3 histone pseudogene 16 Homo sapiens 85-88 15859265-11 2005 Cu(3-apy)4NbOF5: monoclinic, space group P2(1)/n (No. cu(3-apy)4nbof5 0-15 H3 histone pseudogene 16 Homo sapiens 41-46 15711927-2 2005 Exposure of copper (10 and 25 microM) and zinc (10 and 25 microM) caused activation of p53 in ER+/p53+ human epithelial breast cancer MCF7 cells and resulted in up-regulation of p21. Copper 12-18 H3 histone pseudogene 16 Homo sapiens 178-181 15496615-6 2005 Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC. Cisplatin 114-123 H3 histone pseudogene 16 Homo sapiens 73-76 15496615-6 2005 Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC. Acetylcysteine 209-212 H3 histone pseudogene 16 Homo sapiens 73-76 15620706-3 2005 However, the induction of Chk2 (Thr68) phosphorylation and p21 expression by RPA1 siRNA transfection can be completely blocked by the ATM inhibitor caffeine. Caffeine 148-156 H3 histone pseudogene 16 Homo sapiens 59-62 15661398-8 2005 SAHA downregulated cyclin D1 and D2, and upregulated p53, p21, and p27. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 58-61 15662128-5 2005 Apoptosis induced by Bortezomib was associated with inhibition of the classical and alternative NF-kappaB pathways, upregulation of p53, p21 and p27 and activation of caspase cascade. Bortezomib 21-31 H3 histone pseudogene 16 Homo sapiens 137-140 15642166-12 2005 The p21 protein increased from 0.5 microM AZ-1, with the highest at 2 microM AZ-1. 2-aziridin-1-yl-3-((2-((2-(3-aziridin-1-yl-1,4-dioxo-1,4-dihydronaphthalen-2-yl)thio)ethoxy)ethyl)thio)naphthoquinone 42-46 H3 histone pseudogene 16 Homo sapiens 4-7 15642166-12 2005 The p21 protein increased from 0.5 microM AZ-1, with the highest at 2 microM AZ-1. 2-aziridin-1-yl-3-((2-((2-(3-aziridin-1-yl-1,4-dioxo-1,4-dihydronaphthalen-2-yl)thio)ethoxy)ethyl)thio)naphthoquinone 77-81 H3 histone pseudogene 16 Homo sapiens 4-7 15661398-9 2005 Chromatin immunoprecipitation analysis revealed a remarkable increase in the level of acetylated histones associated with the p21 promoter after SAHA treatment. Vorinostat 145-149 H3 histone pseudogene 16 Homo sapiens 126-129 15548565-5 2005 Using the ras activation assay, farnesylthiosalicylic acid inhibits p21(ras) binding to its substrate at comparable concentrations to those seen for superoxide inhibition. farnesylthiosalicylic acid 32-58 H3 histone pseudogene 16 Homo sapiens 68-71 15632825-3 2005 This study aimed to evaluate the effect of calphostin C (a protein kinase C inhibitor) on trichostatin A (a histone deacetylase inhibitor)-mediated upregulation of nuclear factor kappaB and p21 promotor transcriptional activity, as well as induction of apoptosis in lung and esophageal cancer cells. calphostin C 43-55 H3 histone pseudogene 16 Homo sapiens 190-193 15536518-2 2005 Therefore we are interested to improve the proliferation of primary myoblasts of DMD patients by a reduction in p21 using either antisense oligonucleotides (ASO) or short interfering RNAs (siRNA). Oligonucleotides 139-155 H3 histone pseudogene 16 Homo sapiens 112-115 15536518-2 2005 Therefore we are interested to improve the proliferation of primary myoblasts of DMD patients by a reduction in p21 using either antisense oligonucleotides (ASO) or short interfering RNAs (siRNA). Oligonucleotides, Antisense 157-160 H3 histone pseudogene 16 Homo sapiens 112-115 15632825-3 2005 This study aimed to evaluate the effect of calphostin C (a protein kinase C inhibitor) on trichostatin A (a histone deacetylase inhibitor)-mediated upregulation of nuclear factor kappaB and p21 promotor transcriptional activity, as well as induction of apoptosis in lung and esophageal cancer cells. trichostatin A 90-104 H3 histone pseudogene 16 Homo sapiens 190-193 15632825-9 2005 RESULTS: Exposure of lung or esophageal cancer cells to trichostatin A resulted in a dose- and cell-dependent 2-fold to greater than 20-fold increase of nuclear factor kappaB and p21 transcriptional activity. trichostatin A 56-70 H3 histone pseudogene 16 Homo sapiens 179-182 15632825-10 2005 Treatment with trichostatin A and calphostin C led to a 50% to 90% decrease of trichostatin A- mediated upregulation of nuclear factor kappaB and p21 activation. trichostatin A 15-29 H3 histone pseudogene 16 Homo sapiens 146-149 15632825-10 2005 Treatment with trichostatin A and calphostin C led to a 50% to 90% decrease of trichostatin A- mediated upregulation of nuclear factor kappaB and p21 activation. calphostin C 34-46 H3 histone pseudogene 16 Homo sapiens 146-149 15632825-10 2005 Treatment with trichostatin A and calphostin C led to a 50% to 90% decrease of trichostatin A- mediated upregulation of nuclear factor kappaB and p21 activation. trichostatin A 79-93 H3 histone pseudogene 16 Homo sapiens 146-149 15632825-11 2005 Inhibition of nuclear factor kappaB activity resulted in significant reduction (30% to >99%) of trichostatin A- mediated activation of not only nuclear factor kappaB transcription but also p21 promotor activity. trichostatin A 99-113 H3 histone pseudogene 16 Homo sapiens 192-195 15632825-13 2005 CONCLUSION: Inhibition of protein kinase C abrogates trichostatin A-mediated upregulation of nuclear factor kappaB transcriptional activity and p21 expression that is associated with profound induction of apoptosis in lung or esophageal cancer cells. trichostatin A 53-67 H3 histone pseudogene 16 Homo sapiens 144-147 16391388-7 2005 Copper treatment resulted in the upregulation of p21, reprimo, stathmin, and Tp53INP1, all known to participate in cell cycle arrest. Copper 0-6 H3 histone pseudogene 16 Homo sapiens 49-52 15533642-19 2005 Phenylacetate activates p53 and p21 through inhibition of methyltransferase and farnesylation of the RAS protein. phenylacetate 0-13 H3 histone pseudogene 16 Homo sapiens 32-35 15456784-9 2004 Subsequently, quercetin increased the levels of total p53 (DO-1), phospho-p53 (serine 15), and p21 proteins, which were translocated to the nuclei in A549 cells. Quercetin 14-23 H3 histone pseudogene 16 Homo sapiens 95-98 15483186-8 2005 The indole-mediated cell-cycle arrest may be related to the increased levels of the CDK-inhibitors p21 and p27 (only induced by NI3C). indole 4-10 H3 histone pseudogene 16 Homo sapiens 99-102 15483186-8 2005 The indole-mediated cell-cycle arrest may be related to the increased levels of the CDK-inhibitors p21 and p27 (only induced by NI3C). N-methoxyindole-3-carbinol 128-132 H3 histone pseudogene 16 Homo sapiens 99-102 15456784-11 2004 Furthermore, transfection of a small interfering RNA of p21 enhanced the quercetin-induced cell death in A549 cells. Quercetin 73-82 H3 histone pseudogene 16 Homo sapiens 56-59 15456784-12 2004 Together, our results suggest that survivin can reduce the cell growth inhibition and apoptosis, and p53 elevates the p21 level, which may attenuate the cell death in the quercetin-treated human lung carcinoma cells. Quercetin 171-180 H3 histone pseudogene 16 Homo sapiens 118-121 15536623-8 2004 Chromatin immunoprecipitation analysis revealed a notable increase in levels of acetylated histones associated with the p21 promoter after treatment with suberoylanilide bishydroxamine. suberoylanilide bishydroxamine 154-184 H3 histone pseudogene 16 Homo sapiens 120-123 15530866-0 2004 MIBG, an inhibitor of arginine-dependent mono(ADP-ribosyl)ation, prevents differentiation of L6 skeletal myoblasts by inhibiting expression of myogenin and p21(cip1). 3-Iodobenzylguanidine 0-4 H3 histone pseudogene 16 Homo sapiens 156-159 15601469-11 2004 RESULTS: Our results indicate that, in the colon carcinoma cell lines tested, sensitivity to DOX is associated with p21 upregulation upon drug exposure, and DOX cytotoxicity is potentiated by pre-treatment with TPL, but only in those cell lines in which p21 can be upregulated. tempol 211-214 H3 histone pseudogene 16 Homo sapiens 254-257 15601469-12 2004 CONCLUSIONS: p21 induction may significantly contribute to the response of colon adenocarcinomas cells to DOX treatment; and small molecules that can exploit p53-independent pathways for p21 induction, such as TPL, may find a place in chemotherapeutic protocols for the clinical management of colorectal cancer, where p53 function is often lost, due to genetic or epigenetic defects or to post-transcriptional inactivating mechanisms. Doxorubicin 106-109 H3 histone pseudogene 16 Homo sapiens 13-16 15601469-12 2004 CONCLUSIONS: p21 induction may significantly contribute to the response of colon adenocarcinomas cells to DOX treatment; and small molecules that can exploit p53-independent pathways for p21 induction, such as TPL, may find a place in chemotherapeutic protocols for the clinical management of colorectal cancer, where p53 function is often lost, due to genetic or epigenetic defects or to post-transcriptional inactivating mechanisms. Doxorubicin 106-109 H3 histone pseudogene 16 Homo sapiens 187-190 15601469-0 2004 Role of the p53/p21 system in the response of human colon carcinoma cells to Doxorubicin. Doxorubicin 77-88 H3 histone pseudogene 16 Homo sapiens 16-19 15601469-4 2004 The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels. Doxorubicin 147-158 H3 histone pseudogene 16 Homo sapiens 51-54 15601469-4 2004 The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels. Doxorubicin 147-158 H3 histone pseudogene 16 Homo sapiens 252-255 15601469-4 2004 The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels. Doxorubicin 160-163 H3 histone pseudogene 16 Homo sapiens 51-54 15601469-4 2004 The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels. Doxorubicin 220-223 H3 histone pseudogene 16 Homo sapiens 51-54 15601469-4 2004 The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels. Doxorubicin 220-223 H3 histone pseudogene 16 Homo sapiens 252-255 15601469-5 2004 METHODS: The relationship between p53 and p21 protein levels and the cytotoxic effect of DOX was investigated, by MTT assay and western blot analysis, in HCT116 (p53-positive) and HT29 (p53-negative) colon cancer cells. Doxorubicin 89-92 H3 histone pseudogene 16 Homo sapiens 42-45 15601469-7 2004 Finally, we evaluated the effect of pre-treatment with the piperidine nitroxide Tempol (TPL), an agent that was reported to induce p21 expression irrespective of p53 status, on the cytotoxicity of DOX in the four cell lines. piperidine nitroxide tempol 59-86 H3 histone pseudogene 16 Homo sapiens 131-134 15601469-7 2004 Finally, we evaluated the effect of pre-treatment with the piperidine nitroxide Tempol (TPL), an agent that was reported to induce p21 expression irrespective of p53 status, on the cytotoxicity of DOX in the four cell lines. tempol 88-91 H3 histone pseudogene 16 Homo sapiens 131-134 15601469-11 2004 RESULTS: Our results indicate that, in the colon carcinoma cell lines tested, sensitivity to DOX is associated with p21 upregulation upon drug exposure, and DOX cytotoxicity is potentiated by pre-treatment with TPL, but only in those cell lines in which p21 can be upregulated. Doxorubicin 93-96 H3 histone pseudogene 16 Homo sapiens 116-119 15530866-0 2004 MIBG, an inhibitor of arginine-dependent mono(ADP-ribosyl)ation, prevents differentiation of L6 skeletal myoblasts by inhibiting expression of myogenin and p21(cip1). Arginine 22-30 H3 histone pseudogene 16 Homo sapiens 156-159 15659824-9 2004 In the presence of estrogen, p21 and p53 protein expression were upregulated by high concentrations of genistein. Genistein 103-112 H3 histone pseudogene 16 Homo sapiens 29-32 15598783-6 2004 However, for p21 polymorphism, the frequencies of p21 Ser/Ser, Ser/Arg and Arg/Arg were 52 (26.0%), 85 (42.5%), 63 (31.5%) in case patients, 48 (26.5%), 82 (45.3%), 51 (28.2%) in BPH patients, and 76 (30.8%), 119 (48.2%), 52 (21.1%) in controls, respectively. Serine 54-57 H3 histone pseudogene 16 Homo sapiens 13-16 15548818-5 2004 The effects of trypan blue on the expression of apoptosis related and cell cycle arrest gene expressions including c-fos, c-jun, p53, and p21 were performed using reverse transcription-polymerase chain reaction and immunostaining. Trypan Blue 15-26 H3 histone pseudogene 16 Homo sapiens 138-141 15598783-6 2004 However, for p21 polymorphism, the frequencies of p21 Ser/Ser, Ser/Arg and Arg/Arg were 52 (26.0%), 85 (42.5%), 63 (31.5%) in case patients, 48 (26.5%), 82 (45.3%), 51 (28.2%) in BPH patients, and 76 (30.8%), 119 (48.2%), 52 (21.1%) in controls, respectively. Arginine 75-78 H3 histone pseudogene 16 Homo sapiens 13-16 15598783-6 2004 However, for p21 polymorphism, the frequencies of p21 Ser/Ser, Ser/Arg and Arg/Arg were 52 (26.0%), 85 (42.5%), 63 (31.5%) in case patients, 48 (26.5%), 82 (45.3%), 51 (28.2%) in BPH patients, and 76 (30.8%), 119 (48.2%), 52 (21.1%) in controls, respectively. Arginine 75-78 H3 histone pseudogene 16 Homo sapiens 13-16 15554637-9 2004 The neutral complex is isomorphous with the Ni(II) complex and crystallizes in the monoclinic space group P2(1)/c with cell dimensions a=13.8465(4) A, b=7.6453(2) A, c=15.0165(6) A, angles alpha=gamma=90 degrees , beta=103.2140(11) degrees , and Z=4. Nickel(2+) 44-50 H3 histone pseudogene 16 Homo sapiens 106-111 15589127-5 2004 A comparison of the amino acid sequences of these clones revealed greater production of p21 core protein among clones which contained alanine, rather than valine, at amino acid residue 189. Alanine 134-141 H3 histone pseudogene 16 Homo sapiens 88-91 15589127-6 2004 An exploration of Hepatitis Virus Database revealed that efficient p21 production related alanine at amino acid position 189 was observed in most clones of genotype 1 and in rare clones of genotype 2. Alanine 90-97 H3 histone pseudogene 16 Homo sapiens 67-70 15579018-8 2004 Furthermore apoptosis mechanisms in mesothelioma cells are under the control of the cholinergic system (nicotine antiapoptotic via induction of NF-kappaB complexes and phosphorilation of Bad at Serine(112), curare proapoptotic via G(0)-G(1) arrest p21(waf-1)-dependent, but p53-independent). Nicotine 104-112 H3 histone pseudogene 16 Homo sapiens 248-251 15520195-12 2004 The morphologic change and p21 up-regulation still were observed after Pg treatment. Progesterone 71-73 H3 histone pseudogene 16 Homo sapiens 27-30 15514285-4 2004 Both benzyl and phenethyl isothiocyanate increased DNA strand breakage, increased phosphorylation of the G(2)/M checkpoint enforcer Chk2, and induced p21 expression. benzyl and phenethyl isothiocyanate 5-40 H3 histone pseudogene 16 Homo sapiens 150-153 15514285-5 2004 These results suggest that the antiproliferative effects of benzyl and phenethyl isothiocyanates toward Caco-2 cells are due at least in part to the activation of the G(2)/M DNA damage checkpoint, and that sustained G(2)/M phase cell cycle arrest in response to benzyl and phenethyl isothiocyanates may be maintained through upregulation of p21. benzyl and phenethyl isothiocyanates 60-96 H3 histone pseudogene 16 Homo sapiens 341-344 15467202-6 2004 The protein and mRNA expression levels of p21 were up-regulated during saucernetin-8-dependent HL-60 cell differentiation, whereas the level of c-myc was down-regulated. saucernetin-8 71-84 H3 histone pseudogene 16 Homo sapiens 42-45 15492278-6 2004 In addition, some of the changes observed in SWB77 were opposite to those seen in methionine-dependent tumors, including expression of p21, TRAIL-R2, and TIEG. Methionine 82-92 H3 histone pseudogene 16 Homo sapiens 135-138 15492278-8 2004 Western blot analysis confirmed that methionine stress caused the following: (a) a marked increase of GADD45alpha and gamma in the wt-p53 cell lines SWB61 and 40; (b) an increase in GADD34 and p21 protein in all of the methionine-dependent lines; and (c) the induction of MDA7 and phospho-p38 in DAOY and SWB39, consistent with marked transcriptional activation of the former under methionine stress. Methionine 37-47 H3 histone pseudogene 16 Homo sapiens 193-196 15464472-13 2004 Combined gemcitabine and bortezomib enhanced p21 and p53 expression and induced S-phase and G2/M cell-cycle arrests, respectively. gemcitabine 9-20 H3 histone pseudogene 16 Homo sapiens 45-48 15464472-13 2004 Combined gemcitabine and bortezomib enhanced p21 and p53 expression and induced S-phase and G2/M cell-cycle arrests, respectively. Bortezomib 25-35 H3 histone pseudogene 16 Homo sapiens 45-48 15477762-6 2004 Whereas inhibition of HDACs by valproic acid or trichostatin A increases p21 expression, selective interference with HDAC2 by siRNA transfection or reconstitution of wildtype APC does not affect p21 expression. trichostatin A 48-62 H3 histone pseudogene 16 Homo sapiens 73-76 15475462-8 2004 OSI-461 enhanced the G0-G1 arrest caused by acyclic retinoid, and the combination of these agents caused a synergistic decrease in the levels of expression of cyclin D1 protein and mRNA, inhibited cyclin D1 promoter activity, decreased the level of hyperphosphorylated forms of the Rb protein, induced increased cellular levels of the p21(CIP1) protein and mRNA, and stimulated p21(CIP1) promoter activity. (5-fluoro-2-methyl-1-(4-pyridyl)methylene-3-(N-benzyl)-indene)-acetamide hydrochloride 0-7 H3 histone pseudogene 16 Homo sapiens 335-338 20368822-8 2004 EGCG differentially regulated the expression of genes and proteins (Bax, p21, Retinoblastoma, cyclin D1, CDK4 and Bcl-X(L)) more than 2 fold, showing a possible gene regulatory role for EGCG. epigallocatechin gallate 0-4 H3 histone pseudogene 16 Homo sapiens 73-76 20368823-9 2004 Reduced phosphorylation of the pRb and the increased expression of p21(Cip1) were observed subsequent to treatment with phenylacetate. phenylacetic acid 120-133 H3 histone pseudogene 16 Homo sapiens 67-70 15475462-8 2004 OSI-461 enhanced the G0-G1 arrest caused by acyclic retinoid, and the combination of these agents caused a synergistic decrease in the levels of expression of cyclin D1 protein and mRNA, inhibited cyclin D1 promoter activity, decreased the level of hyperphosphorylated forms of the Rb protein, induced increased cellular levels of the p21(CIP1) protein and mRNA, and stimulated p21(CIP1) promoter activity. (5-fluoro-2-methyl-1-(4-pyridyl)methylene-3-(N-benzyl)-indene)-acetamide hydrochloride 0-7 H3 histone pseudogene 16 Homo sapiens 378-381 15498118-4 2004 It is concluded that the NaB effect on cell proliferation/differentiation may be linked to its ability to induce expression of p21 mRNA and inhibit the cyclin D-CDK complexes. nab 25-28 H3 histone pseudogene 16 Homo sapiens 127-130 15354323-0 2004 Induction of apoptosis in a non-small cell human lung cancer cell line by isothiocyanates is associated with P53 and P21. Isothiocyanates 74-89 H3 histone pseudogene 16 Homo sapiens 117-120 15380677-8 2004 When p21 was knocked out, cell cycle of VSMC was not arrested by radiation, leading to increased proliferation. vsmc 40-44 H3 histone pseudogene 16 Homo sapiens 5-8 15258255-10 2004 In marked contrast, disruption of p53 and p21 was associated with increased sensitivity to C-1305. C 1305 91-97 H3 histone pseudogene 16 Homo sapiens 42-45 15326376-4 2004 We here show that inhibition of Chk1 but not of Chk2 in p21(-/-) and p53(-/-) cells caused a greater abrogation of G(2) block induced by ionizing radiation and cis-diamine-dichloroplatinum treatments and a greater sensitization to the same treatments than in the parental cell line with p53 and p21 wild type proteins. cis-diamine 160-171 H3 histone pseudogene 16 Homo sapiens 56-59 15360241-3 2004 Complex 1 x 6MeCN crystallizes in the triclinic space group P, and complex 2 x 2CH2Cl2 crystallizes in the monoclinic space group P2(1)/m. 2ch2cl2 79-86 H3 histone pseudogene 16 Homo sapiens 130-135 15326376-4 2004 We here show that inhibition of Chk1 but not of Chk2 in p21(-/-) and p53(-/-) cells caused a greater abrogation of G(2) block induced by ionizing radiation and cis-diamine-dichloroplatinum treatments and a greater sensitization to the same treatments than in the parental cell line with p53 and p21 wild type proteins. Platinum(II) chloride 172-188 H3 histone pseudogene 16 Homo sapiens 56-59 15289867-7 2004 Elevation of p21 but no p53 protein was observed in flavone-treated cells. flavone 52-59 H3 histone pseudogene 16 Homo sapiens 13-16 15231731-3 2004 Based on cDNA microarrays and protein analysis, we found that FUS at the intermediate peak pressure of 1.5 MPa induced a complex signaling cascade with upregulation of proapoptotic genes [e.g., p53, p21, Thy1 (CD 90)]. fusarubin 62-65 H3 histone pseudogene 16 Homo sapiens 199-202 15289856-3 2004 Our results demonstrated that diosgenin induced G2/M arrest of cell cycle progression through p21 up-regulation in a p53-independent pathway and strong induction of apoptosis in HEL cells. Diosgenin 30-39 H3 histone pseudogene 16 Homo sapiens 94-97 15289867-10 2004 Additionally, flavone induced apoptosis in primary colon carcinoma cells COLO205-X with appearance of DNA ladders, caspase 3 protein procession, PARP protein cleavage, and an increase in p21 (not p53) protein. flavone 14-21 H3 histone pseudogene 16 Homo sapiens 187-190 15289867-11 2004 These data provide evidence to suggest that flavone is an effective agent to induce apoptosis in colorectal carcinoma cells in vitro and in vivo; activation of caspase 3, ROS production, and increasing p21 protein are involved. flavone 44-51 H3 histone pseudogene 16 Homo sapiens 202-205 15242777-4 2004 Here, we have found that treatment of pyrrolidine dithiocarbamate (PDTC), a zinc ionophore, resulted in the accumulation of several proteasome substrates including p53 and p21 in HeLa cells. pyrrolidine dithiocarbamic acid 38-65 H3 histone pseudogene 16 Homo sapiens 172-175 15548374-6 2004 In mechanistic studies, IP6 resulted in an increase in cyclin-dependent kinase inhibitors (CDKIs) Cip1/p21 and Kip1/p27 levels, together with a decrease in cyclin-dependent kinase (CDK) 4 and cyclin D1 protein levels. Phytic Acid 24-27 H3 histone pseudogene 16 Homo sapiens 103-106 15185342-7 2004 The TB-induced cell-cycle arrest in HUVEC occurred when the cyclin-dependent kinase 2 (CDK2) activity was inhibited just as the protein level of p21 was increased and cyclin A was decreased. Terbinafine 4-6 H3 histone pseudogene 16 Homo sapiens 145-148 15185342-8 2004 Pretreatment of HUVEC with a p21 specific antisense oligonucleotide reversed the TB-induced inhibition of [(3)H]thymidine incorporation. Oligonucleotides 52-67 H3 histone pseudogene 16 Homo sapiens 29-32 15185342-8 2004 Pretreatment of HUVEC with a p21 specific antisense oligonucleotide reversed the TB-induced inhibition of [(3)H]thymidine incorporation. Terbinafine 81-83 H3 histone pseudogene 16 Homo sapiens 29-32 15185342-9 2004 Taken together, these results suggest an involvement of the p21-associated signaling pathway in the TB-induced antiproliferation in HUVEC. Terbinafine 100-102 H3 histone pseudogene 16 Homo sapiens 60-63 15016620-3 2004 Both S-nitroso-N-acetyl penicillamine and diethylenetriaminelNONOate dose-dependently suppressed [3H]-thymidine incorporation in cultured HPASMC, and induced the expression of p53 and p21 protein. S-Nitroso-N-Acetylpenicillamine 5-37 H3 histone pseudogene 16 Homo sapiens 184-187 15016620-3 2004 Both S-nitroso-N-acetyl penicillamine and diethylenetriaminelNONOate dose-dependently suppressed [3H]-thymidine incorporation in cultured HPASMC, and induced the expression of p53 and p21 protein. diethylenetriaminelnonoate 42-68 H3 histone pseudogene 16 Homo sapiens 184-187 15242777-4 2004 Here, we have found that treatment of pyrrolidine dithiocarbamate (PDTC), a zinc ionophore, resulted in the accumulation of several proteasome substrates including p53 and p21 in HeLa cells. pyrrolidine dithiocarbamic acid 67-71 H3 histone pseudogene 16 Homo sapiens 172-175 15276867-9 2004 DCQ treatment also induced an upregulation of p53 and p21 protein levels, key mediators of cell cycle arrest and apoptosis. 2-benzoyl-3-phenyl-6,7-dichloroquinoxaline-1,4-dioxide 0-3 H3 histone pseudogene 16 Homo sapiens 54-57 15254726-5 2004 Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time. Tretinoin 106-110 H3 histone pseudogene 16 Homo sapiens 19-22 15254726-8 2004 These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells. Tretinoin 75-79 H3 histone pseudogene 16 Homo sapiens 30-33 15159397-7 2004 Phosphorylation of p53(Ser-15) is necessary for an IR-induced G(1)/S arrest via transcriptional induction of the cyclin-dependent kinase inhibitor p21. Serine 23-26 H3 histone pseudogene 16 Homo sapiens 147-150 15159397-8 2004 Consistent with these data, repressing p53(Ser-15) phosphorylation by BRCA1-BARD1 depletion compromises p21 induction and the G(1)/S checkpoint arrest in response to IR but not UV radia-tion. Serine 43-46 H3 histone pseudogene 16 Homo sapiens 104-107 15254743-4 2004 Here, we show that SU5416 inhibited the expression of G1 cell cycle checkpoint regulators, p53, p21, p27 and MDM2 in ovarian carcinoma cells. Semaxinib 19-25 H3 histone pseudogene 16 Homo sapiens 96-99 15276867-11 2004 These findings indicate that DCQ inhibits the growth of ATL cell lines, at least in part, by inducing apoptosis mediated by the modulation of TGF expression, the upregulation in p53 and p21 proteins and downregulation in Bcl-2alpha expression. 2-benzoyl-3-phenyl-6,7-dichloroquinoxaline-1,4-dioxide 29-32 H3 histone pseudogene 16 Homo sapiens 186-189 15207728-7 2004 Molecular analysis indicates that induction of p53 and p21, and suppression of pRB are associated with apoptosis induced by 5-FUdR and may partly explain the hypersensitivity of E6E7/OSE cells to low-dose 5-FUdR. Floxuridine 124-130 H3 histone pseudogene 16 Homo sapiens 55-58 15188005-7 2004 Electrophoretic mobility studies of p53 binding to DNA and of p21 expression indicated that E(2) inhibited resveratrol-induced, p53-directed transcriptional activity. Resveratrol 107-118 H3 histone pseudogene 16 Homo sapiens 62-65 15236515-2 2004 At room temperature, (SPh(3))Mn(dca)(3) (1) crystallizes in the monoclinic space group P2(1)/c, with a = 11.7079(5) A, b = 12.8554(5) A, c = 16.8605(6) A, beta = 100.666(2) degrees, and V = 2493.8(3) A(3). Dichloroacetic Acid 32-35 H3 histone pseudogene 16 Homo sapiens 87-92 15226418-6 2004 We found that large N-terminal tags also stabilize the expression of the cell cycle inhibitor p21 but not that of substrates ubiquitinated on internal lysine residues. Nitrogen 20-21 H3 histone pseudogene 16 Homo sapiens 94-97 15330179-3 2004 The expression of p21 was detected after 24-h treatment with crambescidin 800, and an increase of the expression was observed after 48-h treatment, but there was no remarkable change in the expression level of p27. crambescidin 800 61-77 H3 histone pseudogene 16 Homo sapiens 18-21 15122344-0 2004 Induction of S-phase arrest and p21 overexpression by a small molecule 2[[3-(2,3-dichlorophenoxy)propyl] amino]ethanol in correlation with activation of ERK. [[3-(2,3-dichlorophenoxy)propyl] amino]ethanol 72-118 H3 histone pseudogene 16 Homo sapiens 32-35 15226418-7 2004 Consistent with this observation, lysineless p21 is ubiquitinated and degraded in a ubiquitin-dependent manner in intact cells. lysineless 34-44 H3 histone pseudogene 16 Homo sapiens 45-48 15226429-3 2004 CDK2 inhibition triggers a p53-p21 response via ATM- and ATR-dependent p53 phosphorylation at serine 15. Serine 94-100 H3 histone pseudogene 16 Homo sapiens 31-34 15122344-3 2004 Subsequently, we found that 2,3-DCPE could induce S-phase arrest and upregulate p21 but not p27 at a time- and dose-dependent but p53-dispensable manner in DLD-1 human colon cancer cells. 2-((3-(2,3-dichlorophenoxy)propyl)amino)ethanol 28-36 H3 histone pseudogene 16 Homo sapiens 80-83 15122344-5 2004 Moreover, p21 induction was dramatically attenuated by ERK inhibitors PD98059 and U0126. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 70-77 H3 histone pseudogene 16 Homo sapiens 10-13 15122344-5 2004 Moreover, p21 induction was dramatically attenuated by ERK inhibitors PD98059 and U0126. U 0126 82-87 H3 histone pseudogene 16 Homo sapiens 10-13 15122344-6 2004 Induction of p21 and S-phase arrest and corresponding activation of ERK were also observed in ATM-defective cells, suggesting that 2,3-DCPE-induced these events were ATM-dispensable. 2-((3-(2,3-dichlorophenoxy)propyl)amino)ethanol 131-139 H3 histone pseudogene 16 Homo sapiens 13-16 15122333-3 2004 Inhibition of the proteasome complex with MG-132 increased p21 protein levels in TGCT cells but much more in A2780 cells, whereas cisplatin had no additional effect on p21 protein levels. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 42-48 H3 histone pseudogene 16 Homo sapiens 59-62 15122333-5 2004 A similar induction of p53 irradiation, in contrast to cisplatin, substantially increased both p21 mRNA and protein expression in Tera cells. Cisplatin 55-64 H3 histone pseudogene 16 Homo sapiens 95-98 15122333-6 2004 Cisplatin-treated Tera cells expressing low p21 protein levels were Fas-sensitive, while irradiation-induced p21, which was mainly localized in the cytosol, rendered irradiated Tera cells resistant to Fas-induced apoptosis. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 44-47 15122333-6 2004 Cisplatin-treated Tera cells expressing low p21 protein levels were Fas-sensitive, while irradiation-induced p21, which was mainly localized in the cytosol, rendered irradiated Tera cells resistant to Fas-induced apoptosis. ammonium ferrous sulfate 68-71 H3 histone pseudogene 16 Homo sapiens 44-47 15122333-6 2004 Cisplatin-treated Tera cells expressing low p21 protein levels were Fas-sensitive, while irradiation-induced p21, which was mainly localized in the cytosol, rendered irradiated Tera cells resistant to Fas-induced apoptosis. ammonium ferrous sulfate 201-204 H3 histone pseudogene 16 Homo sapiens 109-112 15122333-7 2004 Sensitivity of irradiated Tera cells to Fas-induced apoptosis was restored by short interfering RNA-specific suppression of p21 expression. ammonium ferrous sulfate 40-43 H3 histone pseudogene 16 Homo sapiens 124-127 15122333-8 2004 These results strongly indicate that the low p21 protein levels are caused by reduced p21 gene transcription and sensitize cisplatin-treated TGCT cells to the Fas death pathway. Cisplatin 123-132 H3 histone pseudogene 16 Homo sapiens 45-48 14996704-4 2004 Treatment with depsipeptide, as well as other histone deacetylase inhibitors, caused induction of histone acetylation, induction of p21 expression, and substantial apoptosis without significant cell cycle arrest. Depsipeptides 15-27 H3 histone pseudogene 16 Homo sapiens 132-135 15147952-4 2004 Using the proteasome-specific inhibitors, MG132 and lactacystin, we show that the p53, the cdk inhibitors p21 and p27, and cyclin A are degraded by the ubiquitin-proteasome pathway in human osteosarcoma cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 42-47 H3 histone pseudogene 16 Homo sapiens 106-109 15147952-4 2004 Using the proteasome-specific inhibitors, MG132 and lactacystin, we show that the p53, the cdk inhibitors p21 and p27, and cyclin A are degraded by the ubiquitin-proteasome pathway in human osteosarcoma cells. lactacystin 52-63 H3 histone pseudogene 16 Homo sapiens 106-109 15174878-2 2004 The crystal structure prediction study, using a specifically developed anisotropic atom-atom potential for chlorothalonil, gave as the global minimum in the lattice energy a structure that was readily refined against powder diffraction data to the known form 1 (P2(1)/a). tetrachloroisophthalonitrile 107-121 H3 histone pseudogene 16 Homo sapiens 262-267 15059972-4 2004 Interestingly, the small GTP binding proteins of the p21Rho family and one of their effectors, p160 Rho-associated kinase, but not PKA, play a key role in redistribution of melanosomes at the extremities of the dendrites. Guanosine Triphosphate 25-28 H3 histone pseudogene 16 Homo sapiens 53-56 15135394-2 2004 During apoptosis, the N-terminal truncated version of Bax (p18 Bax) is often formed via cleavage of the p21 Bax by the calcium-dependent enzyme, calpain. Calcium 119-126 H3 histone pseudogene 16 Homo sapiens 104-107 15144874-4 2004 Pifithrin alpha reduced the number of apoptotic cells in the ischemic brain by inhibiting the binding of p53 to its DNA sites as it reduced the expression of the p53-related gene p21(WAF) without changing the amount of p53 protein itself. pifithrin 0-15 H3 histone pseudogene 16 Homo sapiens 179-182 15130767-0 2004 Anti-proliferation effect of 3-amino-2-imino-3,4-dihydro-2H-1,3-benzothiazin-4-one (BJ-601) on human vascular endothelial cells: G0/G1 p21-associated cell cycle arrest. 3-amino-2-imino-3,4-dihydro-2H-1,3-benzothiazin-4-one 29-82 H3 histone pseudogene 16 Homo sapiens 135-138 15130758-9 2004 Cantharidin alone induced the apoptosis by phosphorylation of p53, up-regulation of downstream target genes, MDM2 and p21 and also cleaved caspase-3, whereas SB202190 and SP600125 caused the down-regulation of p53, MDM-2, p21 and cleaved caspase-3 after a co-treatment with cantharidin. Cantharidin 0-11 H3 histone pseudogene 16 Homo sapiens 118-121 15130758-9 2004 Cantharidin alone induced the apoptosis by phosphorylation of p53, up-regulation of downstream target genes, MDM2 and p21 and also cleaved caspase-3, whereas SB202190 and SP600125 caused the down-regulation of p53, MDM-2, p21 and cleaved caspase-3 after a co-treatment with cantharidin. Cantharidin 0-11 H3 histone pseudogene 16 Homo sapiens 222-225 15323418-5 2004 Each cysteine mutant can increase endogenous p21 level, and also increased mortality rate of 293 cells when exposed to H2O2. Cysteine 5-13 H3 histone pseudogene 16 Homo sapiens 45-48 15064747-2 2004 In human U2OS cells, treatment with adriamycin causes p53 to be phosphorylated on all six serine residues tested, leading to the dissociation of p53 from MDM2 and transcription of the p21 and mdm2 genes. Doxorubicin 36-46 H3 histone pseudogene 16 Homo sapiens 184-187 15064747-5 2004 However, the increase of p21 and mdm2 mRNAs was indistinguishable following treatment with adriamycin or induction of p14ARF. Doxorubicin 91-101 H3 histone pseudogene 16 Homo sapiens 25-28 15130767-8 2004 Pretreatment of HDMVECs with a p21 antisense oligonucleotide, which blocked the expression of p21 protein, reversed the BJ-601-induced inhibition of [3H]thymidine incorporation into HDMVECs. Oligonucleotides 45-60 H3 histone pseudogene 16 Homo sapiens 31-34 15130767-8 2004 Pretreatment of HDMVECs with a p21 antisense oligonucleotide, which blocked the expression of p21 protein, reversed the BJ-601-induced inhibition of [3H]thymidine incorporation into HDMVECs. Oligonucleotides 45-60 H3 histone pseudogene 16 Homo sapiens 94-97 15130767-8 2004 Pretreatment of HDMVECs with a p21 antisense oligonucleotide, which blocked the expression of p21 protein, reversed the BJ-601-induced inhibition of [3H]thymidine incorporation into HDMVECs. Tritium 150-152 H3 histone pseudogene 16 Homo sapiens 31-34 15130767-8 2004 Pretreatment of HDMVECs with a p21 antisense oligonucleotide, which blocked the expression of p21 protein, reversed the BJ-601-induced inhibition of [3H]thymidine incorporation into HDMVECs. Tritium 150-152 H3 histone pseudogene 16 Homo sapiens 94-97 15130767-11 2004 In conclusion, these data suggest that BJ-601 inhibits HDMVECs proliferation by increasing the level of p21 protein, which in turn inhibits CDK2 kinase activity, and finally causes retardation of the cell cycle at the G0/G1 phase. 3-amino-2-imino-3,4-dihydro-2H-1,3-benzothiazin-4-one 39-45 H3 histone pseudogene 16 Homo sapiens 104-107 15132777-0 2004 The expressions of p21 and pRB may be good indicators for the sensitivity of esophageal squamous cell cancers to CPT-11: Cell proliferation activity correlates with the effect of CPT-11. Irinotecan 113-119 H3 histone pseudogene 16 Homo sapiens 19-22 15150125-0 2004 Flavopiridol induces p53 via initial inhibition of Mdm2 and p21 and, independently of p53, sensitizes apoptosis-reluctant cells to tumor necrosis factor. alvocidib 0-12 H3 histone pseudogene 16 Homo sapiens 60-63 15059930-0 2004 Phosphoinositide-dependent kinase 1 and p21-activated protein kinase mediate reactive oxygen species-dependent regulation of platelet-derived growth factor-induced smooth muscle cell migration. Reactive Oxygen Species 77-100 H3 histone pseudogene 16 Homo sapiens 40-43 15106975-2 2004 The single-crystal structure of the complex, [(PPh3)2Cu(mu-ppbCl2)Cu(PPh3)2](BF4)2 in the monoclinic space group P21/c, 18.2590(1), 21.1833(3), 23.2960(3) A with Z = 4 is reported. [(pph3)2cu 45-55 H3 histone pseudogene 16 Homo sapiens 113-116 15106975-2 2004 The single-crystal structure of the complex, [(PPh3)2Cu(mu-ppbCl2)Cu(PPh3)2](BF4)2 in the monoclinic space group P21/c, 18.2590(1), 21.1833(3), 23.2960(3) A with Z = 4 is reported. (mu-ppbcl2)cu(pph3)2](bf4)2 55-82 H3 histone pseudogene 16 Homo sapiens 113-116 15274354-8 2004 Within 24 hours of treatment, HMJ-38 influenced the CDK/cyclin B activity by increasing Chk1, Wee1 and p21 and decreasing Cdc25C protein levels. 2-(3'-methoxyphenyl)-6-pyrrolidinyl-4-quinazolinone 30-36 H3 histone pseudogene 16 Homo sapiens 103-106 15132777-0 2004 The expressions of p21 and pRB may be good indicators for the sensitivity of esophageal squamous cell cancers to CPT-11: Cell proliferation activity correlates with the effect of CPT-11. Irinotecan 179-185 H3 histone pseudogene 16 Homo sapiens 19-22 15132777-4 2004 Among these proteins, the expression levels of p21 and pRB showed significant differences that were associated with the IC50 values for CPT-11 (P = 0.0339 and P = 0.0109, respectively). Irinotecan 136-142 H3 histone pseudogene 16 Homo sapiens 47-50 15132777-5 2004 Namely, the expression of p21 or pRB independently could be a good indicator of CPT-11 efficacy in ESCC. Irinotecan 80-86 H3 histone pseudogene 16 Homo sapiens 26-29 15067336-9 2004 We also demonstrated that cerivastatin exerts growth inhibitory effect through induction of p21 cyclin-dependent kinase inhibitor and inhibition of cell cycle progression. cerivastatin 26-38 H3 histone pseudogene 16 Homo sapiens 92-95 15099969-3 2004 An association between endometrial cancer and the polymorphism at codon 31 (AGC/serine to AGA/arginine [Ser(31)Arg]) of the p21 gene, which is known to be a downstream mediator of p53, has also been reported. agc 76-79 H3 histone pseudogene 16 Homo sapiens 124-127 15099969-3 2004 An association between endometrial cancer and the polymorphism at codon 31 (AGC/serine to AGA/arginine [Ser(31)Arg]) of the p21 gene, which is known to be a downstream mediator of p53, has also been reported. Serine 80-86 H3 histone pseudogene 16 Homo sapiens 124-127 15099969-3 2004 An association between endometrial cancer and the polymorphism at codon 31 (AGC/serine to AGA/arginine [Ser(31)Arg]) of the p21 gene, which is known to be a downstream mediator of p53, has also been reported. polyethylene glycol-glutaminase-asparaginase 90-93 H3 histone pseudogene 16 Homo sapiens 124-127 15099969-3 2004 An association between endometrial cancer and the polymorphism at codon 31 (AGC/serine to AGA/arginine [Ser(31)Arg]) of the p21 gene, which is known to be a downstream mediator of p53, has also been reported. Arginine 94-102 H3 histone pseudogene 16 Homo sapiens 124-127 15099969-8 2004 Also, homozygous carriers of the p21 Ser allele showed a substantially increased risk of developing endometrial cancer (OR 2.68, 95% CI 1.59-4.51) as compared to homozygous and heterozygous carriers of the Arg allele. Serine 37-40 H3 histone pseudogene 16 Homo sapiens 33-36 15099969-8 2004 Also, homozygous carriers of the p21 Ser allele showed a substantially increased risk of developing endometrial cancer (OR 2.68, 95% CI 1.59-4.51) as compared to homozygous and heterozygous carriers of the Arg allele. Arginine 206-209 H3 histone pseudogene 16 Homo sapiens 33-36 15099969-9 2004 In addition, the combination of the pro allele containing genotypes of p53 and the Ser homozygous genotype of p21 posed a remarkably increased risk (OR 9.55, 95% CI 4.30-21.24) of endometrial cancer development. Serine 83-86 H3 histone pseudogene 16 Homo sapiens 110-113 15131062-9 2004 PS-341 not only inhibited nuclear localization of NF-kappaB but also activated the caspase cascade, increased p21 and Bax levels, and decreased Bcl-2 levels. Bortezomib 0-6 H3 histone pseudogene 16 Homo sapiens 110-113 15052205-11 2004 The proteins p21 and p53 were stabilized after treatment with bortezomib, correlating with a G(2)/M cell-cycle arrest. Bortezomib 62-72 H3 histone pseudogene 16 Homo sapiens 13-16 14976336-8 2004 In addition, the p21 mRNA level was elevated in 1,4-BQ-treated cells, suggesting that human CD34(+) cells utilize the p53 pathway in response to 1,4-BQ-induced DNA damage. quinone 48-54 H3 histone pseudogene 16 Homo sapiens 17-20 14976336-8 2004 In addition, the p21 mRNA level was elevated in 1,4-BQ-treated cells, suggesting that human CD34(+) cells utilize the p53 pathway in response to 1,4-BQ-induced DNA damage. quinone 145-151 H3 histone pseudogene 16 Homo sapiens 17-20 15252663-2 2004 The crystal structure has been determined for the triflate salt Ru(tpap)(CF3SO3)2.2H2O, which crystallizes in the monoclinic space group P2(1)/n. triflate salt ru(tpap)(cf3so3)2.2h2o 50-86 H3 histone pseudogene 16 Homo sapiens 137-142 14715082-3 2004 The present study describes the increased expression of both mRNA and protein for the cyclin-dependent kinase inhibitors p21 and p27 in response to deprivation of HepG2 cells for a single essential amino acid, histidine. Histidine 210-219 H3 histone pseudogene 16 Homo sapiens 121-124 14715082-5 2004 For p21, increase in mRNA by histidine depletion appeared to be independent of p53 transactivation, and the absolute level of p53 protein was unaffected by this treatment. Histidine 29-38 H3 histone pseudogene 16 Homo sapiens 4-7 14715082-6 2004 Histidine limitation caused an increase in the phosphorylation of ERK1/ERK2 (extracellular-signal-regulated kinase), and inhibition of the ERK signal transduction pathway resulted in a reduction in the starvation-dependent increase in p21 mRNA. Histidine 0-9 H3 histone pseudogene 16 Homo sapiens 235-238 15074972-3 2004 [Pt(bpp)Cl]Cl.2H(2)O: monoclinic, P2(1)/n, a = 11.3218(5) A, b = 6.7716(3) A, c = 20.6501(6) A, beta = 105.883(2) degrees, V = 1522.73(11) A(3), Z = 4. [pt(bpp)cl]cl.2h 0-16 H3 histone pseudogene 16 Homo sapiens 34-39 14715082-3 2004 The present study describes the increased expression of both mRNA and protein for the cyclin-dependent kinase inhibitors p21 and p27 in response to deprivation of HepG2 cells for a single essential amino acid, histidine. Amino Acids, Essential 188-208 H3 histone pseudogene 16 Homo sapiens 121-124 14977888-8 2004 Furthermore, this increase in intracellular ROS appeared to be responsible for the up-regulation of proapoptotic factor, p21, after treatment with 7-ketocholesterol but not in cells challenged with the oxysterol mixture. Reactive Oxygen Species 44-47 H3 histone pseudogene 16 Homo sapiens 121-124 14977888-8 2004 Furthermore, this increase in intracellular ROS appeared to be responsible for the up-regulation of proapoptotic factor, p21, after treatment with 7-ketocholesterol but not in cells challenged with the oxysterol mixture. 7-ketocholesterol 147-164 H3 histone pseudogene 16 Homo sapiens 121-124 14987952-7 2004 Taken together, emodin displays effective inhibitory effects on the growth of various human hepatoma cell lines and stimulates the expression of p53 and p21 that resulted in the cell cycle arrest of HepG2/C3A cells at G(2)/M phase. Emodin 16-22 H3 histone pseudogene 16 Homo sapiens 153-156 15200053-1 2004 ras-p21 protein binds to the son-of-sevenless (SOS) guanine nucleotide-exchange promoter that allows it to exchange GDP for GTP. Guanine Nucleotides 52-70 H3 histone pseudogene 16 Homo sapiens 4-7 15200053-1 2004 ras-p21 protein binds to the son-of-sevenless (SOS) guanine nucleotide-exchange promoter that allows it to exchange GDP for GTP. Guanosine Diphosphate 116-119 H3 histone pseudogene 16 Homo sapiens 4-7 15200053-1 2004 ras-p21 protein binds to the son-of-sevenless (SOS) guanine nucleotide-exchange promoter that allows it to exchange GDP for GTP. Guanosine Triphosphate 124-127 H3 histone pseudogene 16 Homo sapiens 4-7 15200053-8 2004 Overall, our current results suggest that SOS interactions with oncogenic ras-p21 may enhance ras-p21 mitogenic signaling through prolonging its activation by maintaining its binding to GTP and by allowing its effector domains to interact with intracellular targets. Guanosine Triphosphate 186-189 H3 histone pseudogene 16 Homo sapiens 78-81 15200053-8 2004 Overall, our current results suggest that SOS interactions with oncogenic ras-p21 may enhance ras-p21 mitogenic signaling through prolonging its activation by maintaining its binding to GTP and by allowing its effector domains to interact with intracellular targets. Guanosine Triphosphate 186-189 H3 histone pseudogene 16 Homo sapiens 98-101 15200054-1 2004 In the accompanying paper, we found, using molecular dynamics calculations, four domains of the ras-specific SOS guanine nucleotide exchange protein (residues 589-601, 654-675, 746-761, and 980-989) that differ markedly in conformation when SOS is complexed with either oncogenic (Val 12-) ras-p21 or wild-type ras-p21. sulfur monoxide 109-112 H3 histone pseudogene 16 Homo sapiens 294-297 15200054-1 2004 In the accompanying paper, we found, using molecular dynamics calculations, four domains of the ras-specific SOS guanine nucleotide exchange protein (residues 589-601, 654-675, 746-761, and 980-989) that differ markedly in conformation when SOS is complexed with either oncogenic (Val 12-) ras-p21 or wild-type ras-p21. sulfur monoxide 109-112 H3 histone pseudogene 16 Homo sapiens 315-318 15200054-1 2004 In the accompanying paper, we found, using molecular dynamics calculations, four domains of the ras-specific SOS guanine nucleotide exchange protein (residues 589-601, 654-675, 746-761, and 980-989) that differ markedly in conformation when SOS is complexed with either oncogenic (Val 12-) ras-p21 or wild-type ras-p21. Guanine Nucleotides 113-131 H3 histone pseudogene 16 Homo sapiens 294-297 15200054-1 2004 In the accompanying paper, we found, using molecular dynamics calculations, four domains of the ras-specific SOS guanine nucleotide exchange protein (residues 589-601, 654-675, 746-761, and 980-989) that differ markedly in conformation when SOS is complexed with either oncogenic (Val 12-) ras-p21 or wild-type ras-p21. Guanine Nucleotides 113-131 H3 histone pseudogene 16 Homo sapiens 315-318 15200054-3 2004 We have now synthesized peptides corresponding to these four domains and find that all of them block Val 12-ras-p21-induced oocyte maturation. Valine 101-104 H3 histone pseudogene 16 Homo sapiens 112-115 15200054-3 2004 We have now synthesized peptides corresponding to these four domains and find that all of them block Val 12-ras-p21-induced oocyte maturation. Radium 107-111 H3 histone pseudogene 16 Homo sapiens 112-115 15041706-9 2004 Treatment of lung carcinoma cells with the PPARgamma ligands PGJ2, ciglitazone, troglizaone, and GW1929 elevated p21 mRNA and protein levels and reduced cyclin D1 mRNA levels. ciglitazone 67-78 H3 histone pseudogene 16 Homo sapiens 113-116 14980826-2 2004 Two polymer chains and four iodide ions (I(-)) crystallized in a monoclinic unit cell with dimensions a = 9.46(2), b = 9.79(2)], c (fiber axis)=10.33(2)A, beta = 105.2(2) degrees and a space group P2(1). Polymers 4-11 H3 histone pseudogene 16 Homo sapiens 197-202 15001399-7 2004 In MCF-7 cells, the metal treatment increased the phosphorylation of p53 at serine 15, up-regulated p21 expression, and resulted in cell-cycle arrest in G1 phase with apoptosis. Metals 20-25 H3 histone pseudogene 16 Homo sapiens 100-103 15041706-9 2004 Treatment of lung carcinoma cells with the PPARgamma ligands PGJ2, ciglitazone, troglizaone, and GW1929 elevated p21 mRNA and protein levels and reduced cyclin D1 mRNA levels. troglizaone 80-91 H3 histone pseudogene 16 Homo sapiens 113-116 15041706-11 2004 In addition, p21 antisense oligonucleotides inhibited PPARgamma ligand-induced p21 protein expression and significantly blocked lung carcinoma cell growth inhibition induced by PPARgamma ligands. Oligonucleotides 27-43 H3 histone pseudogene 16 Homo sapiens 13-16 15041706-11 2004 In addition, p21 antisense oligonucleotides inhibited PPARgamma ligand-induced p21 protein expression and significantly blocked lung carcinoma cell growth inhibition induced by PPARgamma ligands. Oligonucleotides 27-43 H3 histone pseudogene 16 Homo sapiens 79-82 14592809-8 2004 Rapamycin also induced expression of the cyclin-dependent kinase inhibitors p21(cip) and p27(kip), consistent with cell cycle withdrawal. Sirolimus 0-9 H3 histone pseudogene 16 Homo sapiens 76-79 14975768-3 2004 The growth inhibitory effect induced by paclitaxel correlated with levels of intracellular p21 and resulted in cell cycle arrest at the G2/M phase. Paclitaxel 40-50 H3 histone pseudogene 16 Homo sapiens 91-94 14979728-0 2004 Mechanism of p21Ras S-nitrosylation and kinetics of nitric oxide-mediated guanine nucleotide exchange. Nitric Oxide 52-64 H3 histone pseudogene 16 Homo sapiens 13-16 15025498-3 2004 Our studies of the effects of noncytotoxic concentrations of Cd2+ on the levels of p53 and p21 in (+/-)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE)-treated human fibroblasts showed that Cd2+ decreased BPDE-induced p21 levels in a dose-dependent manner whereas p53 accumulation is attenuated only at higher noncytotoxic concentrations of cadmium. pyrene-7,8-diol-9,10-epoxide 117-145 H3 histone pseudogene 16 Homo sapiens 91-94 15025498-8 2004 Our findings indicate that cadmium not only inhibits NER pathway-dependent repair of BPDE-damaged DNA but also impairs p53 and p21 responses and overrides BPDE-induced G1-S cell cycle arrest. Cadmium 27-34 H3 histone pseudogene 16 Homo sapiens 127-130 14757188-5 2004 Furthermore, the nuclear export inhibitor leptomycin B showed a similar synergy with IR as did DRB regarding ser15 phosphorylation of p53 and p21 induction. leptomycin B 42-54 H3 histone pseudogene 16 Homo sapiens 142-145 14712481-5 2004 These effects, associated with an up-regulation of p53, p21 and bax, a shuttling of p53 protein into the nucleus and a down-regulation of bcl-2, survivin and p27 protein, were reversed by the simultaneous addition of guanine or guanosine and were more evident using nondialysed serum containing hypoxanthine. Guanine 217-224 H3 histone pseudogene 16 Homo sapiens 56-59 14757188-5 2004 Furthermore, the nuclear export inhibitor leptomycin B showed a similar synergy with IR as did DRB regarding ser15 phosphorylation of p53 and p21 induction. Dichlororibofuranosylbenzimidazole 95-98 H3 histone pseudogene 16 Homo sapiens 142-145 15075671-2 2004 MEN15658 induces p53 accumulation, and activation of gadd-45, p21, c-fos and bcl-2 family genes in human ovarian carcinoma A2780 cell line. 2-((1,10)phenanthrolin-2-ylhydrazono)-3,4-dihydro-2H-naphthalen-1-one 0-8 H3 histone pseudogene 16 Homo sapiens 62-65 14729643-3 2004 Here, we discovered a novel function of the chemopreventive agent resveratrol: resveratrol is a potent sensitizer of tumor cells for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through p53-independent induction of p21 and p21-mediated cell cycle arrest associated with survivin depletion. Resveratrol 66-77 H3 histone pseudogene 16 Homo sapiens 252-255 14871987-6 2004 Deguelin treatment did not affect Bcl-2 protein levels but increased expression levels of the proapoptotic protein p53 and the cyclin-dependent kinase inhibitors p21 and p27 in the squamous HBE cells. deguelin 0-8 H3 histone pseudogene 16 Homo sapiens 162-165 15051324-7 2004 With the aim to investigate the mechanisms underlying the quenching of 7K-dependent apoptosis by the oxysterol mixture, we found that the combined oxysterol mixture counteracted the ability of 7K given alone to strongly increase the steady-state level of reactive oxygen species (ROS) in macrophages as well as the up-regulation of the pro-apoptotic factor p21 and the triggering of the mitochondria-dependent pathway of apoptosis. Oxysterols 147-156 H3 histone pseudogene 16 Homo sapiens 357-360 14719078-0 2004 Protein levels of p21, p27, cyclin E and Bax predict sensitivity to cisplatin and paclitaxel in head and neck squamous cell carcinomas. Cisplatin 68-77 H3 histone pseudogene 16 Homo sapiens 18-21 14719078-0 2004 Protein levels of p21, p27, cyclin E and Bax predict sensitivity to cisplatin and paclitaxel in head and neck squamous cell carcinomas. Paclitaxel 82-92 H3 histone pseudogene 16 Homo sapiens 18-21 14719078-7 2004 Cells with strong expression of p21, p27, or Bax showed significantly higher sensitivity to cisplatin, and cells with strong expression of Bax or weak expression of cyclin E showed significantly higher sensitivity to paclitaxel. Cisplatin 92-101 H3 histone pseudogene 16 Homo sapiens 32-35 14719078-8 2004 Cisplatin most effectively killed cells expressing both p21 and p27 or either at G1 phase. Cisplatin 0-9 H3 histone pseudogene 16 Homo sapiens 56-59 14977084-0 2004 Molecular analysis of p21 promoter activity isolated from squamous carcinoma cell lines of the head and neck under the influence of 1,25(OH)2 vitamin D3 and its analogs. Calcitriol 132-152 H3 histone pseudogene 16 Homo sapiens 22-25 14977084-2 2004 For squamous carcinoma cell lines of the head and neck (SCCHN) we could show that this antiproliferative activity of 1,25(OH)2 vitamin D3 is due to induced expression of the cell-cycle inhibitory proteins p21 and p27, causing an arrest in the G0/G1 cell-cycle phase. Calcitriol 117-137 H3 histone pseudogene 16 Homo sapiens 205-208 14977084-8 2004 CONCLUSION: These results demonstrate that the cell-cycle inhibitor protein p21 is a direct target gene of biologically active 1,25(OH)2 vitamin D3, inducing G0/G1 cell-cycle arrest. Calcitriol 127-147 H3 histone pseudogene 16 Homo sapiens 76-79 14729643-3 2004 Here, we discovered a novel function of the chemopreventive agent resveratrol: resveratrol is a potent sensitizer of tumor cells for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through p53-independent induction of p21 and p21-mediated cell cycle arrest associated with survivin depletion. Resveratrol 79-90 H3 histone pseudogene 16 Homo sapiens 252-255 14729643-3 2004 Here, we discovered a novel function of the chemopreventive agent resveratrol: resveratrol is a potent sensitizer of tumor cells for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through p53-independent induction of p21 and p21-mediated cell cycle arrest associated with survivin depletion. Resveratrol 79-90 H3 histone pseudogene 16 Homo sapiens 260-263 14729643-6 2004 Likewise, resveratrol-mediated cell cycle arrest followed by survivin depletion and sensitization for TRAIL was impaired in p21- deficient cells. Resveratrol 10-21 H3 histone pseudogene 16 Homo sapiens 124-127 15093128-4 2004 This type of calcium signal promotes activation of the transcription factor CREB (cAMP response element binding protein) leading to cell cycle arrest in G1 phase via transactivation of p53/p21 signaling pathways. Calcium 13-20 H3 histone pseudogene 16 Homo sapiens 189-192 14734613-9 2004 We postulate that the immune stimulatory effect of allicin is mediated by redox-sensitive signaling such as activation of p21(ras). allicin 51-58 H3 histone pseudogene 16 Homo sapiens 122-125 14744786-1 2004 We have synthesized a histone deacetylase inhibitor, NVP-LAQ824, a cinnamic hydroxamic acid, that inhibited in vitro enzymatic activities and transcriptionally activated the p21 promoter in reporter gene assays. LAQ824 53-63 H3 histone pseudogene 16 Homo sapiens 174-177 14744786-1 2004 We have synthesized a histone deacetylase inhibitor, NVP-LAQ824, a cinnamic hydroxamic acid, that inhibited in vitro enzymatic activities and transcriptionally activated the p21 promoter in reporter gene assays. cinnamic hydroxamic acid 67-91 H3 histone pseudogene 16 Homo sapiens 174-177 14667929-5 2004 Western blot analysis revealed that the protein level of p21 increased after DPTH treated. diphenylthiohydantoin 77-81 H3 histone pseudogene 16 Homo sapiens 57-60 14667929-7 2004 Immunoprecipitation showed that the formations of the CDK2-p21 and CDK4-p21 complex, but not the CDK2-p27 and CDK4-p27 complex, were increased in the DPTH-treated HUVEC. diphenylthiohydantoin 150-154 H3 histone pseudogene 16 Homo sapiens 59-62 14667929-7 2004 Immunoprecipitation showed that the formations of the CDK2-p21 and CDK4-p21 complex, but not the CDK2-p27 and CDK4-p27 complex, were increased in the DPTH-treated HUVEC. diphenylthiohydantoin 150-154 H3 histone pseudogene 16 Homo sapiens 72-75 14667929-9 2004 Pretreatment of HUVEC with a p21 antisense oligonucleotide reversed the DPTH-induced inhibition of [3H]thymidine incorporation into HUVEC. Oligonucleotides 43-58 H3 histone pseudogene 16 Homo sapiens 29-32 14667929-9 2004 Pretreatment of HUVEC with a p21 antisense oligonucleotide reversed the DPTH-induced inhibition of [3H]thymidine incorporation into HUVEC. diphenylthiohydantoin 72-76 H3 histone pseudogene 16 Homo sapiens 29-32 14667929-9 2004 Pretreatment of HUVEC with a p21 antisense oligonucleotide reversed the DPTH-induced inhibition of [3H]thymidine incorporation into HUVEC. Tritium 100-102 H3 histone pseudogene 16 Homo sapiens 29-32 14667929-10 2004 In conclusion, these data suggest that DPTH inhibits HUVEC proliferation by increasing the level of p21 protein, which in turn inhibits CDK2 and CDK4 kinase activities, and finally interrupts the cell cycle. diphenylthiohydantoin 39-43 H3 histone pseudogene 16 Homo sapiens 100-103 14729643-3 2004 Here, we discovered a novel function of the chemopreventive agent resveratrol: resveratrol is a potent sensitizer of tumor cells for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through p53-independent induction of p21 and p21-mediated cell cycle arrest associated with survivin depletion. Resveratrol 66-77 H3 histone pseudogene 16 Homo sapiens 260-263 14751837-6 2003 The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Oligonucleotides 14-30 H3 histone pseudogene 16 Homo sapiens 82-85 15566959-8 2004 After 1 microM cisplatin treatment, Xrel3 had an anti-apoptotic effect, based on significantly lower levels of apoptotic proteins, including caspase-8, caspase-3 and p21. Cisplatin 15-24 H3 histone pseudogene 16 Homo sapiens 166-169 15566959-10 2004 After 5 microM cisplatin treatment, expression of HeLa Xrel3 had an apoptotic effect, based on significantly increased expression of the cell cycle inhibitor p21 and apoptotic proteins, including cleaved PARP, caspase-8, and caspase-3. Cisplatin 15-24 H3 histone pseudogene 16 Homo sapiens 158-161 15587392-10 2004 Both ATRA and/or sodium butyrate stimulated p21 expression at the mRNA levels. Tretinoin 5-9 H3 histone pseudogene 16 Homo sapiens 44-47 15587392-10 2004 Both ATRA and/or sodium butyrate stimulated p21 expression at the mRNA levels. Butyric Acid 17-32 H3 histone pseudogene 16 Homo sapiens 44-47 15587392-11 2004 Our results suggest that the effect of sodium butyrate on cell proliferation/differentiation might be linked to its ability to induce expression of p21 mRNA and inhibit the cyclin-cdk complexes. Butyric Acid 39-54 H3 histone pseudogene 16 Homo sapiens 148-151 14601052-7 2003 However, ActD, DOX and CDDP downregulated expression of cFLIP in OS cells as well as expression of p21 in normal hOBs. Doxorubicin 15-18 H3 histone pseudogene 16 Homo sapiens 99-102 14623034-6 2003 In addition, a short-time incubation of SH-SY5Y cells with phenformin induced enhanced and transient expression of the cell cycle inhibitor p21 suggesting that phenformin causes inhibition of cell cycle progression prior to induction of apoptosis. Phenformin 59-69 H3 histone pseudogene 16 Homo sapiens 140-143 14623034-6 2003 In addition, a short-time incubation of SH-SY5Y cells with phenformin induced enhanced and transient expression of the cell cycle inhibitor p21 suggesting that phenformin causes inhibition of cell cycle progression prior to induction of apoptosis. Phenformin 160-170 H3 histone pseudogene 16 Homo sapiens 140-143 14751837-6 2003 The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. 10-hydroxycamptothecin 123-145 H3 histone pseudogene 16 Homo sapiens 82-85 14751837-6 2003 The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Doxorubicin 147-157 H3 histone pseudogene 16 Homo sapiens 82-85 14751837-6 2003 The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Fluorouracil 159-173 H3 histone pseudogene 16 Homo sapiens 82-85 14751837-6 2003 The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Paclitaxel 179-189 H3 histone pseudogene 16 Homo sapiens 82-85 14676132-6 2003 EXPERIMENTAL DESIGN: The efficacy of combination of gamma-irradiation and flavopiridol was tested in vitro in MKN-74 and HCT-116 cells and correlated to changes in p21 expression. alvocidib 74-86 H3 histone pseudogene 16 Homo sapiens 164-167 14679005-5 2003 Coadministration of 17-AAG blocked SAHA-mediated induction of the cyclin-dependent kinase inhibitor p21(CIP1) and resulted in reduced expression of p27(KIP1) and p34(cdc2). tanespimycin 20-26 H3 histone pseudogene 16 Homo sapiens 100-103 14679005-5 2003 Coadministration of 17-AAG blocked SAHA-mediated induction of the cyclin-dependent kinase inhibitor p21(CIP1) and resulted in reduced expression of p27(KIP1) and p34(cdc2). Vorinostat 35-39 H3 histone pseudogene 16 Homo sapiens 100-103 14632777-4 2003 Western blotting of cell cycle proteins showed that STI571 increased the levels of p21 and p16. Imatinib Mesylate 52-58 H3 histone pseudogene 16 Homo sapiens 83-86 14676132-12 2003 Examination of the p21 status of HCT-116 and MKN-74 cells, after treatment with sequential gamma-irradiation and flavopiridol, indicated a loss of p21 protein expression. alvocidib 113-125 H3 histone pseudogene 16 Homo sapiens 19-22 14676132-14 2003 HCT-116 cells that lack p21 (p21(-/-)) also exhibited sensitization to gamma-irradiation and showed an even greater enhancement of gamma-irradiation-induced apoptosis by flavopiridol when compared with the parental HCT-116 cells. alvocidib 170-182 H3 histone pseudogene 16 Homo sapiens 29-32 14709802-5 2003 Treatment of cells with 1 mM NaB or 1 nM TGF 1 for 4 d decreased cell proliferation with a concomitant increase in the cell cycle protein p21. nab 29-32 H3 histone pseudogene 16 Homo sapiens 138-141 14607331-2 2003 One polymorphism in the p21 codon 31 produces variant proteins with an amino acid change (serine (ser) or arginine (arg)). Serine 90-96 H3 histone pseudogene 16 Homo sapiens 24-27 14679005-7 2003 Enforced expression of doxycycline-inducible p21(CIP1) or constitutively active MEK1 significantly diminished 17-AAG/SAHA-mediated lethality, indicating that interference with ERK activation and p21(CIP1) induction play important functional roles in the lethal effects of this regimen. Doxycycline 23-34 H3 histone pseudogene 16 Homo sapiens 45-48 14679005-7 2003 Enforced expression of doxycycline-inducible p21(CIP1) or constitutively active MEK1 significantly diminished 17-AAG/SAHA-mediated lethality, indicating that interference with ERK activation and p21(CIP1) induction play important functional roles in the lethal effects of this regimen. Doxycycline 23-34 H3 histone pseudogene 16 Homo sapiens 195-198 14679005-7 2003 Enforced expression of doxycycline-inducible p21(CIP1) or constitutively active MEK1 significantly diminished 17-AAG/SAHA-mediated lethality, indicating that interference with ERK activation and p21(CIP1) induction play important functional roles in the lethal effects of this regimen. tanespimycin 110-116 H3 histone pseudogene 16 Homo sapiens 45-48 14679005-7 2003 Enforced expression of doxycycline-inducible p21(CIP1) or constitutively active MEK1 significantly diminished 17-AAG/SAHA-mediated lethality, indicating that interference with ERK activation and p21(CIP1) induction play important functional roles in the lethal effects of this regimen. tanespimycin 110-116 H3 histone pseudogene 16 Homo sapiens 195-198 14679005-7 2003 Enforced expression of doxycycline-inducible p21(CIP1) or constitutively active MEK1 significantly diminished 17-AAG/SAHA-mediated lethality, indicating that interference with ERK activation and p21(CIP1) induction play important functional roles in the lethal effects of this regimen. Vorinostat 117-121 H3 histone pseudogene 16 Homo sapiens 45-48 14612423-8 2003 Chromatin immunoprecipitation was used to show that the proline repeat deletion mutant p53 is bound to the p21 promoter in vivo, but it is not acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event. Proline 56-63 H3 histone pseudogene 16 Homo sapiens 107-110 14612423-8 2003 Chromatin immunoprecipitation was used to show that the proline repeat deletion mutant p53 is bound to the p21 promoter in vivo, but it is not acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event. Proline 171-178 H3 histone pseudogene 16 Homo sapiens 107-110 14669326-13 2003 In response to oil A, P21 expression was increased, but P27 expression was not affected. Oil A 15-20 H3 histone pseudogene 16 Homo sapiens 22-25 14607331-2 2003 One polymorphism in the p21 codon 31 produces variant proteins with an amino acid change (serine (ser) or arginine (arg)). Serine 90-93 H3 histone pseudogene 16 Homo sapiens 24-27 14607331-2 2003 One polymorphism in the p21 codon 31 produces variant proteins with an amino acid change (serine (ser) or arginine (arg)). Arginine 106-114 H3 histone pseudogene 16 Homo sapiens 24-27 14607331-2 2003 One polymorphism in the p21 codon 31 produces variant proteins with an amino acid change (serine (ser) or arginine (arg)). Arginine 106-109 H3 histone pseudogene 16 Homo sapiens 24-27 14633737-9 2003 Treatment with Let, Tam, or E2W resulted in a dose- and time-dependent increase in active caspase-7 and up-regulation of p53 and p21 protein. Letrozole 15-18 H3 histone pseudogene 16 Homo sapiens 129-132 14606858-8 2003 Cr(N)(pyr-dtc)(2) (3) crystallizes as orange prisms in the monoclinic space group P21/c with cell parameters a = 14.8592(14) A, b = 8.5575(5) A, c = 11.8267(12) A, beta = 106.528(7) degrees, V = 1441.7(2) A(3), Z = 4. corrin 0-5 H3 histone pseudogene 16 Homo sapiens 82-85 14606858-8 2003 Cr(N)(pyr-dtc)(2) (3) crystallizes as orange prisms in the monoclinic space group P21/c with cell parameters a = 14.8592(14) A, b = 8.5575(5) A, c = 11.8267(12) A, beta = 106.528(7) degrees, V = 1441.7(2) A(3), Z = 4. pyrrolidine dithiocarbamic acid 6-13 H3 histone pseudogene 16 Homo sapiens 82-85 14633737-9 2003 Treatment with Let, Tam, or E2W resulted in a dose- and time-dependent increase in active caspase-7 and up-regulation of p53 and p21 protein. Tamoxifen 20-23 H3 histone pseudogene 16 Homo sapiens 129-132 14640056-2 2003 The mechanisms by which acetylsalicylic acid and other NSAIDs, including COX-2 inhibitors, exert this effect include: inhibition of COX-2, induction of apoptosis and induction of the P21 protein that controls the development of crypt cells. Aspirin 24-44 H3 histone pseudogene 16 Homo sapiens 183-186 14614447-2 2003 Here, we report that CP-31398 induces p53 reporter gene activity and p21 expression in all of 11 glioma cell lines harboring wild-type or mutant p53, but not in p53-null LN-308 cells. CP 31398 21-29 H3 histone pseudogene 16 Homo sapiens 69-72 12933701-6 2003 High glucose induced p21 and p27 in control cells but not in cells overexpressing HO-1. Glucose 5-12 H3 histone pseudogene 16 Homo sapiens 21-24 14688479-6 2003 We demonstrated that bortezomib induced p53, and activated its downstream genes p21, PUMA and Bax in a p53-dependent fashion. Bortezomib 21-31 H3 histone pseudogene 16 Homo sapiens 80-83 14688479-8 2003 Surprisingly, we found that bortezomib-induced apoptosis was markedly enhanced in the p21-knockout cells, while significantly decreased in the BAX-knockout cells. Bortezomib 28-38 H3 histone pseudogene 16 Homo sapiens 86-89 14532004-3 2003 Ubiquitinylated forms of p21 and p21(K0), a p21 mutant missing all lysines, are detected in vivo and in vitro, showing that the presence of lysines is dispensable for p21 ubiquitinylation. Lysine 67-74 H3 histone pseudogene 16 Homo sapiens 25-28 14532004-3 2003 Ubiquitinylated forms of p21 and p21(K0), a p21 mutant missing all lysines, are detected in vivo and in vitro, showing that the presence of lysines is dispensable for p21 ubiquitinylation. Lysine 67-74 H3 histone pseudogene 16 Homo sapiens 33-36 14532004-3 2003 Ubiquitinylated forms of p21 and p21(K0), a p21 mutant missing all lysines, are detected in vivo and in vitro, showing that the presence of lysines is dispensable for p21 ubiquitinylation. Lysine 67-74 H3 histone pseudogene 16 Homo sapiens 33-36 14532004-3 2003 Ubiquitinylated forms of p21 and p21(K0), a p21 mutant missing all lysines, are detected in vivo and in vitro, showing that the presence of lysines is dispensable for p21 ubiquitinylation. Lysine 67-74 H3 histone pseudogene 16 Homo sapiens 33-36 14532004-3 2003 Ubiquitinylated forms of p21 and p21(K0), a p21 mutant missing all lysines, are detected in vivo and in vitro, showing that the presence of lysines is dispensable for p21 ubiquitinylation. Lysine 140-147 H3 histone pseudogene 16 Homo sapiens 25-28 14532004-3 2003 Ubiquitinylated forms of p21 and p21(K0), a p21 mutant missing all lysines, are detected in vivo and in vitro, showing that the presence of lysines is dispensable for p21 ubiquitinylation. Lysine 140-147 H3 histone pseudogene 16 Homo sapiens 33-36 14532004-3 2003 Ubiquitinylated forms of p21 and p21(K0), a p21 mutant missing all lysines, are detected in vivo and in vitro, showing that the presence of lysines is dispensable for p21 ubiquitinylation. Lysine 140-147 H3 histone pseudogene 16 Homo sapiens 33-36 14532004-3 2003 Ubiquitinylated forms of p21 and p21(K0), a p21 mutant missing all lysines, are detected in vivo and in vitro, showing that the presence of lysines is dispensable for p21 ubiquitinylation. Lysine 140-147 H3 histone pseudogene 16 Homo sapiens 33-36 14532004-4 2003 Instead, the free amino group of the N-terminal methionine of p21 is a site for ubiquitinylation in vivo. Methionine 48-58 H3 histone pseudogene 16 Homo sapiens 62-65 14532004-5 2003 Although wild-type p21 is more abundantly ubiquitinylated than p21(K0) mutant due to the presence of internal lysine residues, their rates of proteolysis are indistinguishable. Lysine 110-116 H3 histone pseudogene 16 Homo sapiens 19-22 14532004-5 2003 Although wild-type p21 is more abundantly ubiquitinylated than p21(K0) mutant due to the presence of internal lysine residues, their rates of proteolysis are indistinguishable. Lysine 110-116 H3 histone pseudogene 16 Homo sapiens 63-66 14507860-0 2003 Vitamin D analogues increase p53, p21, and apoptosis in a xenograft model of human retinoblastoma. Vitamin D 0-9 H3 histone pseudogene 16 Homo sapiens 34-37 14507860-12 2003 There was an increase in staining for p53 and p21 in areas associated with cell death in specimens treated with vitamin D analogues. Vitamin D 112-121 H3 histone pseudogene 16 Homo sapiens 46-49 14981925-7 2003 Apoptosis induced by CAPE or CAO is associated with increased expression of p53, p21 and c-Jun. caffeic acid phenethyl ester 21-25 H3 histone pseudogene 16 Homo sapiens 81-84 14981925-7 2003 Apoptosis induced by CAPE or CAO is associated with increased expression of p53, p21 and c-Jun. cao 29-32 H3 histone pseudogene 16 Homo sapiens 81-84 14511359-10 2003 In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA. Serine 44-50 H3 histone pseudogene 16 Homo sapiens 136-139 14511359-10 2003 In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA. Aspirin 159-162 H3 histone pseudogene 16 Homo sapiens 136-139 14578467-6 2003 Treatment of these animals with a single dose of doxorubicin led to activation of the p53 pathway and a nearly 4-fold elevation of the plasma MIC-1 level, which was paralleled by p21 induction in the tumor xenografts. Doxorubicin 49-60 H3 histone pseudogene 16 Homo sapiens 179-182 14761400-0 2003 [Co-detection of P21, P53 and HSP70 and their possible role in diagnosis of polycyclic aromatic hydrocarbons (PAHs)-related lung cancer]. Polycyclic Aromatic Hydrocarbons 76-108 H3 histone pseudogene 16 Homo sapiens 17-20 14761400-0 2003 [Co-detection of P21, P53 and HSP70 and their possible role in diagnosis of polycyclic aromatic hydrocarbons (PAHs)-related lung cancer]. Polycyclic Aromatic Hydrocarbons 110-114 H3 histone pseudogene 16 Homo sapiens 17-20 12933701-7 2003 The addition of tin-mesoporphyrin (SnMP), an inhibitor of HO activity, reversed the HO-1-mediated decrease of p21 and p27 in cells overexpressing HO-1. tin mesoporphyrin 16-33 H3 histone pseudogene 16 Homo sapiens 110-113 12933701-7 2003 The addition of tin-mesoporphyrin (SnMP), an inhibitor of HO activity, reversed the HO-1-mediated decrease of p21 and p27 in cells overexpressing HO-1. tin mesoporphyrin 35-39 H3 histone pseudogene 16 Homo sapiens 110-113 12934082-13 2003 Interestingly, HCT cells lacking p21 (80S14(p21-/-)) are only slightly protected by SS from CD95L-induced apoptosis, but sensitized to Apo2L/TRAIL-induced apoptosis, indicating a link between the actions of SS and p21. Sulfasalazine 84-86 H3 histone pseudogene 16 Homo sapiens 44-47 12934082-13 2003 Interestingly, HCT cells lacking p21 (80S14(p21-/-)) are only slightly protected by SS from CD95L-induced apoptosis, but sensitized to Apo2L/TRAIL-induced apoptosis, indicating a link between the actions of SS and p21. Sulfasalazine 84-86 H3 histone pseudogene 16 Homo sapiens 44-47 12941844-2 2003 Exposure to LAQ824 induced the expression of the cell cycle-dependent kinase inhibitors p21 and p27 and caused cell cycle G(1)-phase accumulation and apoptosis of CML-BC cells. LAQ824 12-18 H3 histone pseudogene 16 Homo sapiens 88-91 12925221-5 2003 Lomefloxacin also triggered various stress responses: heme-oxygenase-1 expression in fibroblasts, changes in p53 status as shown by the accumulation of p53 and p21 proteins or the induction of MDM2 and GADD45 genes, and stimulation of melanogenesis by increasing the tyrosinase activity in melanocytes. lomefloxacin 0-12 H3 histone pseudogene 16 Homo sapiens 160-163 14555704-3 2003 We have shown previously that triptolide (PG490), an oxygenated diterpene derived from a Chinese medicinal plant, induces apoptosis in cultured tumor cells and sensitizes tumor cells to topoisomerase inhibitors by blocking p53-mediated induction of p21. triptolide 30-40 H3 histone pseudogene 16 Homo sapiens 249-252 14555704-3 2003 We have shown previously that triptolide (PG490), an oxygenated diterpene derived from a Chinese medicinal plant, induces apoptosis in cultured tumor cells and sensitizes tumor cells to topoisomerase inhibitors by blocking p53-mediated induction of p21. triptolide 42-47 H3 histone pseudogene 16 Homo sapiens 249-252 12883038-4 2003 Low adozelesin concentrations (e.g., 0.5 nM) induced a transient S-phase block and cell cycle arrest in G(2)-M, as well as increased induction of p53 and p21, whereas a high drug concentration (e.g., 2.5 nM) caused apoptosis but no p21 induction. adozelesin 4-14 H3 histone pseudogene 16 Homo sapiens 154-157 12951018-6 2003 Actinomycin D was found to induce redistribution of p14/p21 from the nucleolus to the nucleoplasm. Dactinomycin 0-13 H3 histone pseudogene 16 Homo sapiens 56-59 12883267-8 2003 Arsenic increased expression of the P21 protein and decreased levels of cyclin A, cyclin B1 and cyclin D1, but expression of CDK2, CDK4, CDK6, and cyclin E were not affected. Arsenic 0-7 H3 histone pseudogene 16 Homo sapiens 36-39 12885487-15 2003 Some studies have suggested an important role for the cell-cycle regulating protein p21 in mediating the chemopreventive effect of sulindac. Sulindac 131-139 H3 histone pseudogene 16 Homo sapiens 84-87 12823590-4 2003 To explain the p53-independent regulation of p21 by Core, we identified a Core-responsive element between positions -74 and -83 of the p21 promoter, exactly overlapped with a tumour growth factor beta (TGF-beta)/butyrate responsive element. Butyrates 212-220 H3 histone pseudogene 16 Homo sapiens 45-48 12823590-4 2003 To explain the p53-independent regulation of p21 by Core, we identified a Core-responsive element between positions -74 and -83 of the p21 promoter, exactly overlapped with a tumour growth factor beta (TGF-beta)/butyrate responsive element. Butyrates 212-220 H3 histone pseudogene 16 Homo sapiens 135-138 12823590-5 2003 Furthermore, we demonstrated that Core could activate the p21 through the element by stimulating a butyrate pathway, whereas this was inhibited through a TGF-beta pathway. Butyrates 99-107 H3 histone pseudogene 16 Homo sapiens 58-61 12883038-4 2003 Low adozelesin concentrations (e.g., 0.5 nM) induced a transient S-phase block and cell cycle arrest in G(2)-M, as well as increased induction of p53 and p21, whereas a high drug concentration (e.g., 2.5 nM) caused apoptosis but no p21 induction. adozelesin 4-14 H3 histone pseudogene 16 Homo sapiens 232-235 12883038-5 2003 In contrast, both low and high bizelesin concentrations enhanced p53 and p21 induction and triggered G(2)-M cell cycle arrest and eventual senescence without significant apoptotic cell death. bizelesin 31-40 H3 histone pseudogene 16 Homo sapiens 73-76 12883038-6 2003 However, in cells lacking p21, bizelesin, as well as adozelesin, triggered apoptosis, indicating that p21 was crucial to sustained bizelesin-induced G(2)-M arrest. bizelesin 131-140 H3 histone pseudogene 16 Homo sapiens 102-105 12794125-3 2003 The anergic cells showed a displacement of the CD4-p56(lck) signaling module from the GM1-rich plasma membrane microdomains (lipid rafts), and subsequently an increase in p59(fyn) kinase activity, a dominant expression of p21 inhibitory TCR zeta-chain, and a poor phosphorylation and recruitment of zeta-associated protein of 70 kDa kinase to the TCR"s immunoreceptor tyrosine-based activation motifs. Tyrosine 368-376 H3 histone pseudogene 16 Homo sapiens 222-225 12799645-3 2003 Pancreatic cancer frequently has a dysregulated p21(ras) pathway and therefore appears to be a suitable target for BPs that interfere with the prenylation of small GTP-binding proteins such as p21(ras). Diphosphonates 115-118 H3 histone pseudogene 16 Homo sapiens 48-51 12799645-3 2003 Pancreatic cancer frequently has a dysregulated p21(ras) pathway and therefore appears to be a suitable target for BPs that interfere with the prenylation of small GTP-binding proteins such as p21(ras). Diphosphonates 115-118 H3 histone pseudogene 16 Homo sapiens 193-196 12799645-3 2003 Pancreatic cancer frequently has a dysregulated p21(ras) pathway and therefore appears to be a suitable target for BPs that interfere with the prenylation of small GTP-binding proteins such as p21(ras). Guanosine Triphosphate 164-167 H3 histone pseudogene 16 Homo sapiens 193-196 12799645-8 2003 In conclusion, we demonstrated that ZOL induces growth inhibition and apoptosis on PC cells and interferes with growth and survival pathways downstream to p21(ras). Zoledronic Acid 36-39 H3 histone pseudogene 16 Homo sapiens 155-158 12877804-5 2003 In addition, LY294002 could induce time-course expressions of p16(INK4) and p21(Cip1) in 2BS cell lines. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 13-21 H3 histone pseudogene 16 Homo sapiens 76-79 12767524-0 2003 Effects of FK228, a novel histone deacetylase inhibitor, on tumor growth and expression of p21 and c-myc genes in vivo. romidepsin 11-16 H3 histone pseudogene 16 Homo sapiens 91-94 12767524-2 2003 FK228 induced the expression of p21 mRNA and decreased c-myc mRNA in tumor xenograft sensitive to FK228. romidepsin 0-5 H3 histone pseudogene 16 Homo sapiens 32-35 12767524-2 2003 FK228 induced the expression of p21 mRNA and decreased c-myc mRNA in tumor xenograft sensitive to FK228. romidepsin 98-103 H3 histone pseudogene 16 Homo sapiens 32-35 12767524-4 2003 The modulation of p21 and/or c-myc genes may be critical for the marked antitumor activity of FK228 in vivo. romidepsin 94-99 H3 histone pseudogene 16 Homo sapiens 18-21 12732930-7 2003 Under optimal conditions (a mixture of 0.25 microg ASO, 5 microl Effectene, 0.8 microl enhancer) SkMC transfected with p21 ASO reveal an average increase in cell proliferation of 32.5+/-11% after 24 h. p57 ASO shows the same effect, but concomitant transfection of p21 and p57 does not enhance it. Oligonucleotides, Antisense 123-126 H3 histone pseudogene 16 Homo sapiens 119-122 12732930-3 2003 In this context we are interested to improve the proliferation of primary human skeletal muscle cells (SkMC) by a reduction in the cell cycle proteins p21 and p57 using the appropriate antisense oligonucleotides (ASO). Oligonucleotides 195-211 H3 histone pseudogene 16 Homo sapiens 151-154 12732930-3 2003 In this context we are interested to improve the proliferation of primary human skeletal muscle cells (SkMC) by a reduction in the cell cycle proteins p21 and p57 using the appropriate antisense oligonucleotides (ASO). Oligonucleotides, Antisense 213-216 H3 histone pseudogene 16 Homo sapiens 151-154 12732930-7 2003 Under optimal conditions (a mixture of 0.25 microg ASO, 5 microl Effectene, 0.8 microl enhancer) SkMC transfected with p21 ASO reveal an average increase in cell proliferation of 32.5+/-11% after 24 h. p57 ASO shows the same effect, but concomitant transfection of p21 and p57 does not enhance it. Oligonucleotides, Antisense 51-54 H3 histone pseudogene 16 Homo sapiens 119-122 12732930-7 2003 Under optimal conditions (a mixture of 0.25 microg ASO, 5 microl Effectene, 0.8 microl enhancer) SkMC transfected with p21 ASO reveal an average increase in cell proliferation of 32.5+/-11% after 24 h. p57 ASO shows the same effect, but concomitant transfection of p21 and p57 does not enhance it. Oligonucleotides, Antisense 123-126 H3 histone pseudogene 16 Homo sapiens 119-122 12732930-7 2003 Under optimal conditions (a mixture of 0.25 microg ASO, 5 microl Effectene, 0.8 microl enhancer) SkMC transfected with p21 ASO reveal an average increase in cell proliferation of 32.5+/-11% after 24 h. p57 ASO shows the same effect, but concomitant transfection of p21 and p57 does not enhance it. Oligonucleotides, Antisense 123-126 H3 histone pseudogene 16 Homo sapiens 265-268 12732930-7 2003 Under optimal conditions (a mixture of 0.25 microg ASO, 5 microl Effectene, 0.8 microl enhancer) SkMC transfected with p21 ASO reveal an average increase in cell proliferation of 32.5+/-11% after 24 h. p57 ASO shows the same effect, but concomitant transfection of p21 and p57 does not enhance it. Oligonucleotides, Antisense 123-126 H3 histone pseudogene 16 Homo sapiens 265-268 12732930-10 2003 In contrast to both these formulations, SuperFect was found to be highly toxic for SkMC, with more than 70% dead cells after 24 h. The increase in proliferation, the functional biological effect of p21 ASO, is well correlated with a decrease in p21 detected by western blot analysis of 31.6% for Effectene. Oligonucleotides, Antisense 202-205 H3 histone pseudogene 16 Homo sapiens 198-201 12732930-12 2003 Taken together transient transfection of p21 or p57 ASO into primary human SkMC using Effectene significantly improves their proliferation compared to transfection with scrambled ASO without a major loss of cell vitality. Oligonucleotides, Antisense 179-182 H3 histone pseudogene 16 Homo sapiens 41-44 12802789-5 2003 However, TS induction abrogated p53, p21, Fas, and Bak induction in response to TDX, but not 5-FU. raltitrexed 80-83 H3 histone pseudogene 16 Homo sapiens 37-40 12773551-9 2003 Depsipeptide induced p21(Cip1) expression was reconstituted when cells were pretreated with 5-aza-2"-deoxycytidine. Depsipeptides 0-12 H3 histone pseudogene 16 Homo sapiens 21-24 12773551-9 2003 Depsipeptide induced p21(Cip1) expression was reconstituted when cells were pretreated with 5-aza-2"-deoxycytidine. Decitabine 92-114 H3 histone pseudogene 16 Homo sapiens 21-24 12642583-5 2003 1,5-Dihydroxyisoquinoline treatment prior to ionizing radiation delayed and attenuated the induction of two p53-responsive genes, p21 and mdm-2, and led to suppression of the p53-mediated G1-arrest response in MCF-7 and BJ/TERT cells. 1,5-dihydroxyisoquinoline 0-25 H3 histone pseudogene 16 Homo sapiens 130-133 12740440-0 2003 Structural and biochemical studies of p21Ras S-nitrosylation and nitric oxide-mediated guanine nucleotide exchange. Nitric Oxide 65-77 H3 histone pseudogene 16 Homo sapiens 38-41 12740440-0 2003 Structural and biochemical studies of p21Ras S-nitrosylation and nitric oxide-mediated guanine nucleotide exchange. Guanine Nucleotides 87-105 H3 histone pseudogene 16 Homo sapiens 38-41 12844404-2 2003 The results showed that the expression ratios of NF-kappaB, P21, MMP-2 and MMP-9 in untreated AL group were significantly higher than those in remission and normal control groups (P < 0.05), and no obvious difference was seen between remission and normal control groups. Aluminum 94-96 H3 histone pseudogene 16 Homo sapiens 60-63 12626521-6 2003 Phosphorylation of c-Raf1 serine 338 by p21-activated kinase has been recently reported to contribute to phosphoinositide 3-kinase-dependent activation of c-Raf1. Serine 26-32 H3 histone pseudogene 16 Homo sapiens 40-43 12761496-0 2003 Paclitaxel increases p21 synthesis and accumulation of its AKT-phosphorylated form in the cytoplasm of cancer cells. Paclitaxel 0-10 H3 histone pseudogene 16 Homo sapiens 21-24 12761496-1 2003 CKI p21 is a regulator of cellular responses to microtubule damage induced by drugs such as paclitaxel (PTX). Paclitaxel 92-102 H3 histone pseudogene 16 Homo sapiens 4-7 12761496-1 2003 CKI p21 is a regulator of cellular responses to microtubule damage induced by drugs such as paclitaxel (PTX). Paclitaxel 104-107 H3 histone pseudogene 16 Homo sapiens 4-7 12761496-3 2003 We demonstrated here that low doses of PTX that are unable to activate the spindle assembly checkpoint, upregulate p21 by a p53-dependent pathway and induce its translocation to the cytoplasm. Paclitaxel 39-42 H3 histone pseudogene 16 Homo sapiens 115-118 12761496-5 2003 Furthermore, the cytoplasmic p21 accumulation observed in PTX-treated cells was inhibited by LY 294002, a specific PI-3 kinase inhibitor or by the expression of a dominant-negative AKT mutant. Paclitaxel 58-61 H3 histone pseudogene 16 Homo sapiens 29-32 12761496-5 2003 Furthermore, the cytoplasmic p21 accumulation observed in PTX-treated cells was inhibited by LY 294002, a specific PI-3 kinase inhibitor or by the expression of a dominant-negative AKT mutant. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 93-102 H3 histone pseudogene 16 Homo sapiens 29-32 12761496-6 2003 However, the kinase activity of AKT was unchanged in PTX-treated cells, suggesting that low doses of PTX could regulate p21 phosphorylation via inhibition of its dephosphorylation. Paclitaxel 101-104 H3 histone pseudogene 16 Homo sapiens 120-123 12726921-3 2003 Exposure of cells to vanadate led to cell growth arrest at the G(2)/M phase and caused upregulation of p21 and phospho-cdc2 and degradation of cdc25C in a time- and dose-dependent manner. Vanadates 21-29 H3 histone pseudogene 16 Homo sapiens 103-106 12531799-4 2003 SAHA induced apoptosis in all tumor cells tested, with increased p21 and p53 protein levels and dephosphorylation of Rb. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 65-68 12726921-5 2003 PD98059, an inhibitor of ERK, and SB202190, an inhibitor of p38, inhibited vanadate-induced cell growth arrest, upregulation of p21 and cdc2, and degradation of cdc25C. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 0-7 H3 histone pseudogene 16 Homo sapiens 128-131 12726921-5 2003 PD98059, an inhibitor of ERK, and SB202190, an inhibitor of p38, inhibited vanadate-induced cell growth arrest, upregulation of p21 and cdc2, and degradation of cdc25C. 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole 34-42 H3 histone pseudogene 16 Homo sapiens 128-131 12726921-5 2003 PD98059, an inhibitor of ERK, and SB202190, an inhibitor of p38, inhibited vanadate-induced cell growth arrest, upregulation of p21 and cdc2, and degradation of cdc25C. Vanadates 75-83 H3 histone pseudogene 16 Homo sapiens 128-131 12726921-8 2003 ROS activate ERK and p38, which in turn upregulate p21 and cdc2 and cause degradation of cdc25C, leading to cell growth arrest at the G(2)/M phase. Reactive Oxygen Species 0-3 H3 histone pseudogene 16 Homo sapiens 51-54 12609999-0 2003 The activation domains, the proline-rich domain, and the C-terminal basic domain in p53 are necessary for acetylation of histones on the proximal p21 promoter and interaction with p300/CREB-binding protein. Proline 28-35 H3 histone pseudogene 16 Homo sapiens 146-149 12569550-7 2003 Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation. farnesylthiosalicylic acid 297-300 H3 histone pseudogene 16 Homo sapiens 236-239 12697268-5 2003 Furthermore, annonacin activated p21 in a p53-independent manner and arrested T24 cells at the G1 phase. annonacin 13-22 H3 histone pseudogene 16 Homo sapiens 33-36 12941159-8 2003 Further, we identified an increase in the level of superoxide and peroxynitrite in endothelial cells exposed to NO that was reduced by p21ras C118S transient transfection. Superoxides 51-61 H3 histone pseudogene 16 Homo sapiens 135-138 12941159-8 2003 Further, we identified an increase in the level of superoxide and peroxynitrite in endothelial cells exposed to NO that was reduced by p21ras C118S transient transfection. Peroxynitrous Acid 66-79 H3 histone pseudogene 16 Homo sapiens 135-138 12446442-1 2003 Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl-expressing K562 and LAMA-84 cells. Vorinostat 40-44 H3 histone pseudogene 16 Homo sapiens 145-148 12446442-1 2003 Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl-expressing K562 and LAMA-84 cells. Vorinostat 46-77 H3 histone pseudogene 16 Homo sapiens 145-148 12738242-4 2003 Bortezomib also appeared to increase the stabilization of p21 and p27, as well as transcription factor p53. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 58-61 12720299-6 2003 To clarify the roles of p21/Cip1 and p27/Kip1 protein expression, which was involved in G(0)/G(1) arrest and apoptosis induced by TF in human cancer cells, antisense oligodeoxynucleotides (ODNs) specific to p21/Cip1 and p27/Kip1 were used, and the expression of the p21/Cip1 and p27/Kip1 were monitored by immunoblotting analysis. Oligodeoxyribonucleotides 166-187 H3 histone pseudogene 16 Homo sapiens 24-27 12717016-1 2003 The hinge residues (Val29 and Ile36) of the switch I region (also known as the effector loop) of the Ha-ras-p21 protein have been mutated to glycines to accelerate the conformational changes typical for the effector loop. Glycine 141-149 H3 histone pseudogene 16 Homo sapiens 108-111 12717016-3 2003 Here, we use the fluorescence properties of the single tryptophan residue in the Y32W mutant of Ha-ras-p21. Tryptophan 55-65 H3 histone pseudogene 16 Homo sapiens 103-106 12594211-4 2003 Following cisplatin treatment, induction of p73 and its downstream effector p21(Cip1) was essentially blocked in SHP-2 mutant cells. Cisplatin 10-19 H3 histone pseudogene 16 Homo sapiens 76-79 12569550-7 2003 Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation. Hydrogen Peroxide 42-59 H3 histone pseudogene 16 Homo sapiens 236-239 12569550-7 2003 Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation. farnesylthiosalicylic acid 255-295 H3 histone pseudogene 16 Homo sapiens 236-239 12569550-7 2003 Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation. N-(5-(3-dimethylaminobenzamido)-2-methylphenyl)-4-hydroxybenzamide 323-332 H3 histone pseudogene 16 Homo sapiens 236-239 12569550-7 2003 Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 337-344 H3 histone pseudogene 16 Homo sapiens 236-239 12663718-1 2003 PURPOSE: R115777 is a selective nonpeptidomimetic inhibitor of farnesyltransferase (FTase), one of several enzymes responsible for posttranslational modification that is required for the function of p21(ras) and other proteins. tipifarnib 9-16 H3 histone pseudogene 16 Homo sapiens 199-202 12721754-0 2003 Staurosporine-induced apoptosis is independent of p16 and p21 and achieved via arrest at G2/M and at G1 in U251MG human glioma cell line. Staurosporine 0-13 H3 histone pseudogene 16 Homo sapiens 58-61 12721754-3 2003 METHODS: In the present study an adenovirus vector expressing p16 or p21 genes in human glioma cell lines was used to examine cell cycle regulation and cell death induced by staurosporine. Staurosporine 174-187 H3 histone pseudogene 16 Homo sapiens 69-72 12631353-12 2003 p21 was significantly and equally reduced in MCD (2.3%), DMH (0%), and FSGS (0.7%) compared to normal (66.6%). 1,2-Dimethylhydrazine 57-60 H3 histone pseudogene 16 Homo sapiens 0-3 12715170-23 2003 The increase in number of Bcl-2 positive cells after combined treatment and the consistently negative p21 status after any treatment in GLC4-CDDP may protect these tumor cells from apoptosis as a part of their resistance mechanism to cisplatin. glc4-cddp 136-145 H3 histone pseudogene 16 Homo sapiens 102-105 12690294-8 2003 Furthermore, examination of the levels of apoptosis regulatory proteins showed that, while levels of p53, Bax and p21 are higher, that of anti-apoptotic Bcl-2 is undetectable in cells treated with 2-ME compared with untreated controls. 2-Methoxyestradiol 197-201 H3 histone pseudogene 16 Homo sapiens 114-117 12715170-23 2003 The increase in number of Bcl-2 positive cells after combined treatment and the consistently negative p21 status after any treatment in GLC4-CDDP may protect these tumor cells from apoptosis as a part of their resistance mechanism to cisplatin. Cisplatin 234-243 H3 histone pseudogene 16 Homo sapiens 102-105 13678314-0 2003 Quantification of p21 gene expression in Caco-2 cells treated with sodium butyrate using real-time reverse transcription-PCR (RT-PCR) assay. Butyric Acid 67-82 H3 histone pseudogene 16 Homo sapiens 18-21 12618886-6 2003 Amifostine induced the expression of p53 protein in p53-proficient cells and the expression of p21 protein in both p53-proficient and -deficient cells. Amifostine 0-10 H3 histone pseudogene 16 Homo sapiens 95-98 12618886-7 2003 These findings indicate that amifostine-induced G1 arrest and cytoprotection are mediated via a pathway that is dependent on p53 protein and that amifostine-induced expression of p21 protein is not sufficient to sustain a G1 arrest or to mediate cytoprotection. Amifostine 146-156 H3 histone pseudogene 16 Homo sapiens 179-182 12711791-1 2003 The title compound is an ethanol-solvated salt, C(16)H(38)N(4)(2+) x -2C(11)H(7)O(2)(-) x -2C(2)H(6)O, in which the cation lies across a centre of inversion in P2(1)/c. Ethanol 25-32 H3 histone pseudogene 16 Homo sapiens 160-165 12711791-1 2003 The title compound is an ethanol-solvated salt, C(16)H(38)N(4)(2+) x -2C(11)H(7)O(2)(-) x -2C(2)H(6)O, in which the cation lies across a centre of inversion in P2(1)/c. Salts 42-46 H3 histone pseudogene 16 Homo sapiens 160-165 13678314-2 2003 Butyrate induced inhibition of cellular proliferation is considered to result from the induction of P21 gene expression through the activation of this gene transcription. Butyrates 0-8 H3 histone pseudogene 16 Homo sapiens 100-103 13678314-4 2003 In the present study the kinetics of the changes of the P21 transcription in Caco-2 colon adenocarcinoma cells treated with various concentrations of sodium butyrate was determined using a novel real-time quantitative RT-PCR (TaqMan) technique. Butyric Acid 150-165 H3 histone pseudogene 16 Homo sapiens 56-59 13678314-6 2003 Colonocytes were incubated with sodium butyrate at concentrations of 5 mM, 10 mM and 20 mM for 3, 6, 12, 24 and 48 h. The results of this study indicated that butyrate strongly induced P21 gene expression as early as 3 h after treatment. Butyric Acid 32-47 H3 histone pseudogene 16 Homo sapiens 185-188 13678314-6 2003 Colonocytes were incubated with sodium butyrate at concentrations of 5 mM, 10 mM and 20 mM for 3, 6, 12, 24 and 48 h. The results of this study indicated that butyrate strongly induced P21 gene expression as early as 3 h after treatment. Butyrates 39-47 H3 histone pseudogene 16 Homo sapiens 185-188 13678314-8 2003 The increases in P21 mRNA level were generally more pronounced at higher butyrate concentrations. Butyrates 73-81 H3 histone pseudogene 16 Homo sapiens 17-20 13678314-9 2003 Because Caco-2 cells are lacking the wild allele of the P53 gene, the present results support the hypothesis that butyrate induces P21 gene expression by P53-independent mechanism. Butyrates 114-122 H3 histone pseudogene 16 Homo sapiens 131-134 12610816-10 2003 The expression of the p53 response proteins, MDM2 and p21, was elevated in MG132 treated chondrocytes. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 75-80 H3 histone pseudogene 16 Homo sapiens 54-57 12663518-7 2003 IP6 strongly increased the expression of CDKIs (cyclin-dependent kinase inhibitors), Cip1/p21 and Kip1/p27, without any noticeable changes in G1 CDKs and cyclins, except a slight increase in cyclin D2. Phytic Acid 0-3 H3 histone pseudogene 16 Homo sapiens 90-93 12650433-5 2003 In MGMT-depleted cells, TMZ exposure led to DNA single-strand breaks and phosphorylation of cdc2, followed by G2-M arrest, induction of p53/p21, and DNA double-strand breaks. Temozolomide 24-27 H3 histone pseudogene 16 Homo sapiens 140-143 12795334-10 2003 An inhibitor of PKC, GF 109203X inhibited EGF-mediated suppression of TNF-alpha-induced accumulation of p53, p21 and induction of apoptosis. bisindolylmaleimide I 21-31 H3 histone pseudogene 16 Homo sapiens 109-112 12589822-7 2003 Treatment of quercetin, which induced a cell-cycle block in G1-phase, induced down-regulation of cyclins and CDKs and up-regulation of the CDK inhibitor p21 expression, whereas up-regulation of p27 or p53 by quercetin was not observed. Quercetin 13-22 H3 histone pseudogene 16 Homo sapiens 153-156 12839645-3 2003 The recombinant plasmid pcDNA-p53/p21 was constructed by inserting the p53/p21 fusion gene into eukaryotic expression vector pcDNA3.1 and subsequently transfected into human oral squamous cell carcinoma cell line (Tca8113) with lipofectamine. tca8113 214-221 H3 histone pseudogene 16 Homo sapiens 34-37 12839645-3 2003 The recombinant plasmid pcDNA-p53/p21 was constructed by inserting the p53/p21 fusion gene into eukaryotic expression vector pcDNA3.1 and subsequently transfected into human oral squamous cell carcinoma cell line (Tca8113) with lipofectamine. Lipofectamine 228-241 H3 histone pseudogene 16 Homo sapiens 34-37 12920809-4 2003 Targeting of Stat3 using antisense oligonucleotide which directed against the translation site resulted in growth inhibition, downregulation of Stat3, p-Stat3, Cyclins and CDKs, and up-regulation of p21 and p27. Oligonucleotides 35-50 H3 histone pseudogene 16 Homo sapiens 199-202 12475985-2 2003 Mevastatin, an inhibitor of cholesterol synthesis, inhibits cell growth through inhibition of cdk2 and this has been suggested to be due to enhancement of p21 levels. mevastatin 0-10 H3 histone pseudogene 16 Homo sapiens 155-158 12518324-7 2003 The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Oligonucleotides 14-29 H3 histone pseudogene 16 Homo sapiens 81-84 12518324-7 2003 The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. 10-hydroxycamptothecin 122-144 H3 histone pseudogene 16 Homo sapiens 81-84 12518324-7 2003 The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Doxorubicin 146-156 H3 histone pseudogene 16 Homo sapiens 81-84 12518324-7 2003 The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Fluorouracil 158-172 H3 histone pseudogene 16 Homo sapiens 81-84 12518324-7 2003 The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Paclitaxel 178-188 H3 histone pseudogene 16 Homo sapiens 81-84 12468545-6 2003 Basal levels as well as Vp16- or mitomycin C-stimulated levels of p53 and p21 protein were decreased in the catalase-overexpressing cells as compared with control cells; however, p53 mRNA levels were not decreased by catalase. Mitomycin 33-44 H3 histone pseudogene 16 Homo sapiens 74-77 12475985-3 2003 In a prostate cancer cell line, PC3, mevastatin treatment led to elevated levels of p21 and caused a small increase in the p21 associated with cdk2. mevastatin 37-47 H3 histone pseudogene 16 Homo sapiens 84-87 12475985-3 2003 In a prostate cancer cell line, PC3, mevastatin treatment led to elevated levels of p21 and caused a small increase in the p21 associated with cdk2. mevastatin 37-47 H3 histone pseudogene 16 Homo sapiens 123-126 12536077-0 2003 Anti-proliferative effects of 20-epi-vitamin-D3 analogue, KH1060 in human neuroblastoma: induction of RAR-beta and p21(Cip1). 20-epi-vitamin-d3 30-47 H3 histone pseudogene 16 Homo sapiens 115-118 12536077-9 2003 For the first time we demonstrate that KH1060 induces the expression of retinoic acid receptor-beta and p21(Cip1) suggesting that these proteins in part mediate the growth inhibitory effects. KH 1060 39-45 H3 histone pseudogene 16 Homo sapiens 104-107 12574638-2 2003 The monoclinic (P2(1)/c) structure consists of perovskite-like slabs of vertex-sharing TiO(6) octahedra, which are separated by additional oxygen layers. Oxygen 139-145 H3 histone pseudogene 16 Homo sapiens 16-23 12574211-2 2003 We found that manumycin induces endogenous expression of p21 Waf-1 in anaplastic thyroid cancer cells. manumycin 14-23 H3 histone pseudogene 16 Homo sapiens 57-60 12574638-2 2003 The monoclinic (P2(1)/c) structure consists of perovskite-like slabs of vertex-sharing TiO(6) octahedra, which are separated by additional oxygen layers. perovskite 47-57 H3 histone pseudogene 16 Homo sapiens 16-23 12574211-3 2003 Manumycin increased the activity of the p21promoter, the level of p21mRNA, and the amount of p21 protein. manumycin 0-9 H3 histone pseudogene 16 Homo sapiens 40-43 12574211-3 2003 Manumycin increased the activity of the p21promoter, the level of p21mRNA, and the amount of p21 protein. manumycin 0-9 H3 histone pseudogene 16 Homo sapiens 66-69 12574211-4 2003 We hypothesized that p21 had a proapoptotic effect in cells treated with manumycin, or paclitaxel, or both agents. manumycin 73-82 H3 histone pseudogene 16 Homo sapiens 21-24 12574211-4 2003 We hypothesized that p21 had a proapoptotic effect in cells treated with manumycin, or paclitaxel, or both agents. Paclitaxel 87-97 H3 histone pseudogene 16 Homo sapiens 21-24 12574211-5 2003 By measuring viability and caspase-3 activity, we found that stably transfected KAT-4 cells with p21 cDNA under the control of a metallothionein promoter were more sensitive to manumycin alone, paclitaxel alone, and manumycin plus paclitaxel when p21was induced. manumycin 177-186 H3 histone pseudogene 16 Homo sapiens 97-100 12574211-5 2003 By measuring viability and caspase-3 activity, we found that stably transfected KAT-4 cells with p21 cDNA under the control of a metallothionein promoter were more sensitive to manumycin alone, paclitaxel alone, and manumycin plus paclitaxel when p21was induced. Paclitaxel 194-204 H3 histone pseudogene 16 Homo sapiens 97-100 12574211-5 2003 By measuring viability and caspase-3 activity, we found that stably transfected KAT-4 cells with p21 cDNA under the control of a metallothionein promoter were more sensitive to manumycin alone, paclitaxel alone, and manumycin plus paclitaxel when p21was induced. manumycin 216-225 H3 histone pseudogene 16 Homo sapiens 97-100 12574211-5 2003 By measuring viability and caspase-3 activity, we found that stably transfected KAT-4 cells with p21 cDNA under the control of a metallothionein promoter were more sensitive to manumycin alone, paclitaxel alone, and manumycin plus paclitaxel when p21was induced. Paclitaxel 231-241 H3 histone pseudogene 16 Homo sapiens 97-100 12574211-7 2003 We also found that cells with both p21 alleles deleted were less sensitive to manumycin plus paclitaxel than its wild-type parent cells. manumycin 78-87 H3 histone pseudogene 16 Homo sapiens 35-38 12574211-7 2003 We also found that cells with both p21 alleles deleted were less sensitive to manumycin plus paclitaxel than its wild-type parent cells. Paclitaxel 93-103 H3 histone pseudogene 16 Homo sapiens 35-38 12574211-8 2003 Expression of p21 per se did not induce apoptosis but enhanced the cytotoxic effects of manumycin and paclitaxel. manumycin 88-97 H3 histone pseudogene 16 Homo sapiens 14-17 12574211-8 2003 Expression of p21 per se did not induce apoptosis but enhanced the cytotoxic effects of manumycin and paclitaxel. Paclitaxel 102-112 H3 histone pseudogene 16 Homo sapiens 14-17 12574211-9 2003 These findings suggested that p21 might be required to maintain cell sensitivity to the cytotoxic effects of manumycin and paclitaxel. manumycin 109-118 H3 histone pseudogene 16 Homo sapiens 30-33 12574211-9 2003 These findings suggested that p21 might be required to maintain cell sensitivity to the cytotoxic effects of manumycin and paclitaxel. Paclitaxel 123-133 H3 histone pseudogene 16 Homo sapiens 30-33 12499394-0 2003 Major loci influencing serum triglyceride levels on 2q14 and 9p21 localized by homozygosity-by-descent mapping in a large Hutterite pedigree. Triglycerides 29-41 H3 histone pseudogene 16 Homo sapiens 62-65 14977434-4 2003 The antiproliferative effect of resveratrol was associated with the inhibition of D-type cyclins and cyclin-dependent kinase (Cdk) 4 expression, and the induction of tumor suppressor p53 and Cdk inhibitor p21. Resveratrol 32-43 H3 histone pseudogene 16 Homo sapiens 205-208 12504097-3 2003 Maturation of p21(ras) was also inhibited in a mevalonate-dependent fashion. Mevalonic Acid 47-57 H3 histone pseudogene 16 Homo sapiens 14-17 12506223-1 2003 Crystallization of 2-amino-4-chloro-6-morpholinopyrimidine, C(8)H(11)ClN(4)O, (I), yields two polymorphs, both with space group P2(1)/c, having Z" = 1 (from diethyl ether solution) and Z" = 2 (from dichloromethane solution), denoted (Ia) and (Ib), respectively. 2-amino-4-chloro-6-morpholinopyrimidine 19-58 H3 histone pseudogene 16 Homo sapiens 128-135 12506223-4 2003 2-Amino-4-chloro-6-piperidinopyrimidine, C(9)H(13)ClN(4), (II), which is isomorphous with polymorph (Ib), also has Z" = 2 in P2(1)/c, and the molecules are linked by three N-H...N hydrogen bonds into a centrosymmetric four-molecule aggregate containing three R(2)(2)(8) rings. 2-amino-4-chloro-6-piperidinopyrimidine 0-39 H3 histone pseudogene 16 Homo sapiens 125-132 14526425-9 2003 Both sodium butyrate and trichostatin A could stimulate p21 expression of K562 cells at mRNA and protein levels. Butyric Acid 5-20 H3 histone pseudogene 16 Homo sapiens 56-59 14526425-9 2003 Both sodium butyrate and trichostatin A could stimulate p21 expression of K562 cells at mRNA and protein levels. trichostatin A 25-39 H3 histone pseudogene 16 Homo sapiens 56-59 14526425-10 2003 It may be concluded that sodium butyrate and trichostatin A could promote the proliferation/differentiation of the K562 cells, which might be contributed to the induced expression of cyclin D3 and p21 proteins. Butyric Acid 25-40 H3 histone pseudogene 16 Homo sapiens 197-200 14526425-10 2003 It may be concluded that sodium butyrate and trichostatin A could promote the proliferation/differentiation of the K562 cells, which might be contributed to the induced expression of cyclin D3 and p21 proteins. trichostatin A 45-59 H3 histone pseudogene 16 Homo sapiens 197-200 12670519-1 2003 AIMS: To determine the presence of Asp13-p21-ki-ras oncoprotein and p53 oncoprotein in the plasma of vinyl chloride monomer (VCM)-workers in Taiwan. Vinyl Chloride 101-115 H3 histone pseudogene 16 Homo sapiens 41-44 15015635-7 2003 These results indicate that the expression of HDAC1 is regulated by hypoxia and the effect of TSA is closely related to the expression of P21 under hypoxia condition. trichostatin A 94-97 H3 histone pseudogene 16 Homo sapiens 138-141 12759576-8 2003 However, the expression of vitamin D-dependent P21 gene on the mRNA level was not decreased in these cancers. Vitamin D 27-36 H3 histone pseudogene 16 Homo sapiens 47-50 12406558-5 2002 Cyclohexamide and TSA super-induced the expression of GADD45alpha and beta, but not p21(cip/waf). trichostatin A 18-21 H3 histone pseudogene 16 Homo sapiens 84-87 12429973-6 2002 Tetrandrine-induced growth inhibition was associated with induction of Cdk inhibitor p21, inhibition of cyclin D1 and activation of caspase-3. tetrandrine 0-11 H3 histone pseudogene 16 Homo sapiens 85-88 12213282-5 2002 The ability of glycolic acid to inhibit the UVB-induced cytotoxicity, apoptosis and expression of apoptosis-regulatory genes (p53 and p21) was examined. glycolic acid 15-28 H3 histone pseudogene 16 Homo sapiens 134-137 12213282-8 2002 Glycolic acid also inhibited the UVB-induced expression of c-fos and the activation of transcription factor AP-1, and inhibited mRNA levels of apoptosis-regulatory gene (p53 and p21). glycolic acid 0-13 H3 histone pseudogene 16 Homo sapiens 178-181 12466962-4 2002 Results showed that curcumin treatment causes p53- and p21-independent G(2)/M phase arrest and apoptosis in HCT-116(p53(+/+)), HCT-116(p53(-/-)) and HCT-116(p21(-/-)) cell lines. Curcumin 20-28 H3 histone pseudogene 16 Homo sapiens 55-58 12466962-4 2002 Results showed that curcumin treatment causes p53- and p21-independent G(2)/M phase arrest and apoptosis in HCT-116(p53(+/+)), HCT-116(p53(-/-)) and HCT-116(p21(-/-)) cell lines. Curcumin 20-28 H3 histone pseudogene 16 Homo sapiens 157-160 12510823-7 2002 This key post-translational modification is catalyzed by the enzyme Ras famesyltransferase (FTase), which transfers a famesyl group from farnesylpyrophosphate to the C-terminal cysteine of the Ras protein. farnesyl pyrophosphate 137-158 H3 histone pseudogene 16 Homo sapiens 68-71 12510823-7 2002 This key post-translational modification is catalyzed by the enzyme Ras famesyltransferase (FTase), which transfers a famesyl group from farnesylpyrophosphate to the C-terminal cysteine of the Ras protein. farnesyl pyrophosphate 137-158 H3 histone pseudogene 16 Homo sapiens 193-196 12510823-7 2002 This key post-translational modification is catalyzed by the enzyme Ras famesyltransferase (FTase), which transfers a famesyl group from farnesylpyrophosphate to the C-terminal cysteine of the Ras protein. Cysteine 177-185 H3 histone pseudogene 16 Homo sapiens 68-71 12510823-7 2002 This key post-translational modification is catalyzed by the enzyme Ras famesyltransferase (FTase), which transfers a famesyl group from farnesylpyrophosphate to the C-terminal cysteine of the Ras protein. Cysteine 177-185 H3 histone pseudogene 16 Homo sapiens 193-196 12473608-9 2002 Up-regulation of p53, bax, and p21 expression was induced in wild-type p53-expressing LNCaP cells only after cryptophycin 52 exposure. cryptophycin 109-121 H3 histone pseudogene 16 Homo sapiens 31-34 12428135-6 2002 These results suggest that the basal levels of activated NF-kappaB in cortical neurons are maintained partially by synaptic activity involving N-methyl- D-aspartate (NMDA) and AMPA/kainate glutamate receptors, coupled to activation of an Src-family tyrosine kinase and a p21(Ras)-like guanosine triphosphatase (GTPase) in a cGMP-dependent manner. N-Methylaspartate 143-164 H3 histone pseudogene 16 Homo sapiens 271-274 12428135-7 2002 The results are intriguing in the light of the recent identification of a synaptic p21(Ras) activator stimulated by cGMP. Cyclic GMP 116-120 H3 histone pseudogene 16 Homo sapiens 83-86 12417722-8 2002 Inhibition of Cdk2 activity was associated with increased binding of p21 and p27 to Cdk2 and decreased phosphorylation of Cdk2 on Thr(160). Threonine 130-133 H3 histone pseudogene 16 Homo sapiens 69-72 12409142-5 2002 Here we demonstrated that the resveratrol-treated cells were arrested in G1 phase and were associated with the increase of p21 expression. Resveratrol 30-41 H3 histone pseudogene 16 Homo sapiens 123-126 12642691-3 2002 The p53 induced by FR901228 was functional as evidenced by mdm-2 and p21 transactivation, and its further accumulation following DNA damage by doxorubicin. romidepsin 19-27 H3 histone pseudogene 16 Homo sapiens 69-72 12142081-5 2002 The median levels of ras p21 staining were higher in cases (7.04 IPU, P=0.03) compared to BBD controls (0.00 IPU) or healthy controls (0.00 IPU). ipu 65-68 H3 histone pseudogene 16 Homo sapiens 25-28 12142081-5 2002 The median levels of ras p21 staining were higher in cases (7.04 IPU, P=0.03) compared to BBD controls (0.00 IPU) or healthy controls (0.00 IPU). ipu 109-112 H3 histone pseudogene 16 Homo sapiens 25-28 12142081-5 2002 The median levels of ras p21 staining were higher in cases (7.04 IPU, P=0.03) compared to BBD controls (0.00 IPU) or healthy controls (0.00 IPU). ipu 109-112 H3 histone pseudogene 16 Homo sapiens 25-28 12392819-4 2002 In MDA-MB-231, resveratrol (up to 200 microM) lowered the expression and kinase activities of positive G1/S and G2/M cell cycle regulators and inhibited ribonucleotide reductase activity in a concentration dependent manner, without a significant effect on the low expression of tumor suppressors p21, p27, and p53. Resveratrol 15-26 H3 histone pseudogene 16 Homo sapiens 296-299 12397020-4 2002 This CO-induced cell growth arrest of HASMC was associated with upregulation of p21 and downregulation of cyclin D1 expression. hasmc 38-43 H3 histone pseudogene 16 Homo sapiens 80-83 12401724-4 2002 We found that glycated LDL (gly-LDL) triggered STAT5 activation, the formation of a prolactin inducible element (PIE)-binding complex containing STAT5, and increased p21(waf) expression through the activation of the receptor for AGE (RAGE). Glycine 14-17 H3 histone pseudogene 16 Homo sapiens 166-169 12441266-7 2002 Finally, treatment of two rhabdomyosarcoma cell lines, RH-30 and RD, with butyrate, resulted in complete growth inhibition and in the upregulation of the p21(Cip1) and p27(Kip1) levels. Butyrates 74-82 H3 histone pseudogene 16 Homo sapiens 154-157 12384528-5 2002 Herceptin plus Taxol treatment led to higher levels of p34(Cdc2) kinase activity and apoptosis in ErbB2-overexpressing breast cancer cells, which is likely attributable to inhibition of Cdc2-Tyr-15 phosphorylation and p21(Cip1) expression. Paclitaxel 15-20 H3 histone pseudogene 16 Homo sapiens 218-221 12198119-9 2002 Microarray analyses revealed changes in the expression of a small number of cell cycle-related genes (p21, GADD45A, cyclin G2, MCM5, and histones) that suggested their putative involvement in ET-743-induced cell cycle arrest. Trabectedin 192-198 H3 histone pseudogene 16 Homo sapiens 102-105 12370812-6 2002 Further, transactivation of p21 in response to replication blockade by hydroxyurea and aphidicolin is similar to that in response to ionizing radiation except that the latter is more immediate compared to the response to replication blockade. Hydroxyurea 71-82 H3 histone pseudogene 16 Homo sapiens 28-31 12370812-6 2002 Further, transactivation of p21 in response to replication blockade by hydroxyurea and aphidicolin is similar to that in response to ionizing radiation except that the latter is more immediate compared to the response to replication blockade. Aphidicolin 87-98 H3 histone pseudogene 16 Homo sapiens 28-31 12414635-7 2002 A common feature of MS-275 treatment of pediatric tumor cell lines was induction of p21mRNA. entinostat 20-26 H3 histone pseudogene 16 Homo sapiens 84-87 12441075-6 2002 U0126, a specific inhibitor of MEK, suppressed TGF-beta 1-mediated ERK 1/2 phosphorylation and p21 induction in HSC-39 cells and constitutive ERK 1/2 phosphorylation in GT38 cells. U 0126 0-5 H3 histone pseudogene 16 Homo sapiens 95-98 12384528-8 2002 Thus, Herceptin treatment of ErbB2-overexpressing cells can inhibit ErbB2-mediated Cdc2-Tyr-15 phosphorylation and p21(Cip1) up-regulation, which allows effective p34(Cdc2) activation and induction of apoptosis upon Taxol treatment. Paclitaxel 216-221 H3 histone pseudogene 16 Homo sapiens 115-118 12087103-4 2002 p21(SNFT) has been shown to replace Fos in dimerization with Jun on a consensus AP-1 binding site (12-O-tetradecanolyphorbol-13-acetate response element (TRE)) and to interact with Jun and NF-AT at the distal NF-AT/AP-1 enhancer element. 12-o-tetradecanolyphorbol-13-acetate 99-135 H3 histone pseudogene 16 Homo sapiens 0-3 12434292-8 2002 In our previous report, we proved that lovastatin, a pharmacological inhibitor of p21(ras) function, also reversed the increase of cortisol level in mutant K-ras stably transfected human adrenocortical cells. Lovastatin 39-49 H3 histone pseudogene 16 Homo sapiens 82-85 12434292-8 2002 In our previous report, we proved that lovastatin, a pharmacological inhibitor of p21(ras) function, also reversed the increase of cortisol level in mutant K-ras stably transfected human adrenocortical cells. Hydrocortisone 131-139 H3 histone pseudogene 16 Homo sapiens 82-85 12508641-11 2002 CONCLUSION: The results suggest that Ro 40-8757 inhibits the growth of human cancer cell lines in vitro by means of cell cycle arrest (mediated by up-regulating cell cycle protein P21 and P27) instead of cytotoxic effects, differentiation, or apoptosis. mofarotene 37-47 H3 histone pseudogene 16 Homo sapiens 180-183 12508652-13 2002 TSA acts as an anti-tumor agent could be through co-operation between p21 and p27 in growth inhibition, irrespective of endogenous p53 status. trichostatin A 0-3 H3 histone pseudogene 16 Homo sapiens 70-73 12270138-5 2002 However, it inhibited the transcriptional activity of the p21(WAF) promoter through Cdx1 binding to the p21(WAF) TATA-box and increased the transcriptional activity of the Bcl-2 promoter P2 through a consensus Cdx-binding site. Cefadroxil 84-87 H3 histone pseudogene 16 Homo sapiens 58-61 12270138-5 2002 However, it inhibited the transcriptional activity of the p21(WAF) promoter through Cdx1 binding to the p21(WAF) TATA-box and increased the transcriptional activity of the Bcl-2 promoter P2 through a consensus Cdx-binding site. Cefadroxil 84-87 H3 histone pseudogene 16 Homo sapiens 62-65 12270138-5 2002 However, it inhibited the transcriptional activity of the p21(WAF) promoter through Cdx1 binding to the p21(WAF) TATA-box and increased the transcriptional activity of the Bcl-2 promoter P2 through a consensus Cdx-binding site. Cefadroxil 84-87 H3 histone pseudogene 16 Homo sapiens 58-66 26680888-7 2002 The women who had p53 (Arg/Arg), p21 (Ser/Ser) and more than 3 children showed a 6.4 fold increased risk of cervical cancer than those women who had p53 (~Pro), p21 (~Arg) and had borne no child. Serine 38-41 H3 histone pseudogene 16 Homo sapiens 33-36 26680888-7 2002 The women who had p53 (Arg/Arg), p21 (Ser/Ser) and more than 3 children showed a 6.4 fold increased risk of cervical cancer than those women who had p53 (~Pro), p21 (~Arg) and had borne no child. Serine 42-45 H3 histone pseudogene 16 Homo sapiens 33-36 12354753-3 2002 In all three cell types, total K-ras p21 increased 2- to 4-fold at confluence, and active K-ras p21-GTP increased 10- to 200-fold. Guanosine Triphosphate 100-103 H3 histone pseudogene 16 Homo sapiens 96-99 12218155-9 2002 These data demonstrate that timing and magnitude of PtdIns(3,4,5)P3 accumulation in neutrophils correlate closely with O2- generation, that PI3-kinase-gamma is responsible for the enhanced PtdIns(3,4,5)P3 production seen in primed cells, and that factors other than activation of p21(ras) underlie this response. phosphatidylinositol 3,4,5-triphosphate 189-204 H3 histone pseudogene 16 Homo sapiens 280-283 12529993-9 2002 CD437 decreased levels of cdk inhibitor p21 in G2/M-arrested SC-M1 cells. CD 437 0-5 H3 histone pseudogene 16 Homo sapiens 40-43 12529993-15 2002 The differential regulation of p21 that leads to alteration in the activity of cdks may play a critical role in cell-line-dependent regulation of cell cycle arrest following treatment with CD437. CD 437 189-194 H3 histone pseudogene 16 Homo sapiens 31-34 12181740-5 2002 PD98059 and U0126 induced cell cycle arrest in G(0)/G(i) in cells with the highest levels of ERK1/2 activity, which correlated with induction of p27 but not p21. U 0126 12-17 H3 histone pseudogene 16 Homo sapiens 157-160 12354753-4 2002 It was estimated that 0.03% of total K-ras p21 was in the active GTP-bound state at 50% confluence, compared with 1.4% at postconfluence. Guanosine Triphosphate 65-68 H3 histone pseudogene 16 Homo sapiens 43-46 12198703-0 2002 JunD stabilization results in inhibition of normal intestinal epithelial cell growth through P21 after polyamine depletion. Polyamines 103-112 H3 histone pseudogene 16 Homo sapiens 93-96 12207334-6 2002 These results indicate that enforced p21(ras) functionality enhances primary T cells responses to calcium-generated signals, but is insufficient to prevent TCR-driven T cell unresponsiveness and suggest that additional biochemical mechanisms, independent of p21(ras), negatively regulate IL-2 production in unresponsive T cells. Calcium 98-105 H3 histone pseudogene 16 Homo sapiens 37-40 12198703-9 2002 Growth arrest following polyamine depletion also was accompanied by increases in both p21 expression and its promoter activity. Polyamines 24-33 H3 histone pseudogene 16 Homo sapiens 86-89 12198703-10 2002 Treatment with JunD antisense oligomers inhibited the p21 promoter and prevented the increase in p21 expression in the presence of DFMO. Eflornithine 131-135 H3 histone pseudogene 16 Homo sapiens 97-100 12198703-12 2002 CONCLUSIONS: Polyamines negatively regulate junD gene expression posttranscriptionally, and increased JunD/AP-1 inhibits intestinal epithelial cell proliferation at least partially through the activation of p21 promoter. Polyamines 13-23 H3 histone pseudogene 16 Homo sapiens 207-210 12218216-7 2002 We found that prolonged formalin fixation (>48 h) had a detrimental effect on quantitative RT polymerase chain reaction results that was most marked for MMP-1 and VEGF but less evident for p21 and EGFR. Formaldehyde 24-32 H3 histone pseudogene 16 Homo sapiens 192-195 12118068-6 2002 Fibroblasts from Alzheimer"s disease patients also have a profound impairment in the H(2)O(2)-activated, p53-dependent pathway, which results in a lack of activation of p53 or p53-target genes, including p21, GADD45 and bax. h(2)o 85-90 H3 histone pseudogene 16 Homo sapiens 204-207 12481415-2 2002 Here we show that the HDIs sodium butyrate (Bu), trichostatin A (TSA) and depsipeptide (FR901228) all induced p21, but only TSA and FR901228 caused mitotic arrest (in addition to arrest in G1 and G2). Butyric Acid 27-42 H3 histone pseudogene 16 Homo sapiens 110-113 12481415-2 2002 Here we show that the HDIs sodium butyrate (Bu), trichostatin A (TSA) and depsipeptide (FR901228) all induced p21, but only TSA and FR901228 caused mitotic arrest (in addition to arrest in G1 and G2). Butyrates 44-46 H3 histone pseudogene 16 Homo sapiens 110-113 12481415-2 2002 Here we show that the HDIs sodium butyrate (Bu), trichostatin A (TSA) and depsipeptide (FR901228) all induced p21, but only TSA and FR901228 caused mitotic arrest (in addition to arrest in G1 and G2). trichostatin A 49-63 H3 histone pseudogene 16 Homo sapiens 110-113 12481415-2 2002 Here we show that the HDIs sodium butyrate (Bu), trichostatin A (TSA) and depsipeptide (FR901228) all induced p21, but only TSA and FR901228 caused mitotic arrest (in addition to arrest in G1 and G2). trichostatin A 65-68 H3 histone pseudogene 16 Homo sapiens 110-113 12481415-2 2002 Here we show that the HDIs sodium butyrate (Bu), trichostatin A (TSA) and depsipeptide (FR901228) all induced p21, but only TSA and FR901228 caused mitotic arrest (in addition to arrest in G1 and G2). Depsipeptides 74-86 H3 histone pseudogene 16 Homo sapiens 110-113 12107073-6 2002 In addition, p21 mRNA abundance, a downstream target of p53 protein, was increased in the ZS cells compared with both the ZN control and ZD cells. Zinc 122-124 H3 histone pseudogene 16 Homo sapiens 13-16 12171906-5 2002 The p21-related cell cycle arrest was intimately linked to TMZ toxicity because tumors with wt p53 but lacking a robust increase in p21 protein level (D-54) were resistant to TMZ. Temozolomide 59-62 H3 histone pseudogene 16 Homo sapiens 4-7 12171906-5 2002 The p21-related cell cycle arrest was intimately linked to TMZ toxicity because tumors with wt p53 but lacking a robust increase in p21 protein level (D-54) were resistant to TMZ. Temozolomide 175-178 H3 histone pseudogene 16 Homo sapiens 4-7 12154299-1 2002 The title compound, alternatively called N-acridin-9(10H)-ylidene-2,2,2-trichloroacetamide monohydrate, C(15)H(9)Cl(3)N(2)O.H(2)O, crystallizes in space group P2(1)/c with Z = 4. n-acridin-9(10h)-ylidene-2,2,2-trichloroacetamide monohydrate 41-102 H3 histone pseudogene 16 Homo sapiens 159-164 12171907-9 2002 The overaccumulation of p21 and cyclin B1 protein was obvious at 24 h. Furthermore, CA4P treatment showed an increase in the expression of a marker of mitosis (mitotic protein monoclonal-2 antibody) and an overaccumulation of the cyclin B in the nucleus. CA4P 84-88 H3 histone pseudogene 16 Homo sapiens 24-27 12131363-14 2002 Resveratrol caused a p53 stimulated increase in p21 messenger RNA. Resveratrol 0-11 H3 histone pseudogene 16 Homo sapiens 48-51 12124333-0 2002 Growth inhibition of human hepatoma cells by acyclic retinoid is associated with induction of p21(CIP1) and inhibition of expression of cyclin D1. Retinoids 53-61 H3 histone pseudogene 16 Homo sapiens 94-97 12099876-3 2002 The copper(II) complex crystallized in the monoclinic space group P2(1)/c, with a =10.125(4), b = 14.103(6), and c = 14.537(6) A, beta = 91.049(8) degrees, V = 2075.4(16) A(3), and Z = 2. cupric ion 4-14 H3 histone pseudogene 16 Homo sapiens 66-71 12206509-3 2002 In order to infer which domains of GAP may be involved, we have performed molecular dynamics calculations of GAP complexed to wild-type and oncogenic (Val 12-containing) ras-p21, both bound to GTP. Guanosine Triphosphate 193-196 H3 histone pseudogene 16 Homo sapiens 174-177 12150453-3 2002 Taxol treatment resulted in elevated expression of p53 and of p21, which was more pronounced and persistent in cyclin D1 overexpressing cells. Paclitaxel 0-5 H3 histone pseudogene 16 Homo sapiens 62-65 12150453-4 2002 Overexpression of cyclin D1 altered sensitivity to taxol by modulating exit from mitosis, which is controlled by p21. Paclitaxel 51-56 H3 histone pseudogene 16 Homo sapiens 113-116 11980647-8 2002 In the analysis of cell cycle regulatory molecules, selenium-treated cells demonstrated a significant induction of cyclin-dependent kinase inhibitors Cip1/p21 and Kip1/p27. Selenium 52-60 H3 histone pseudogene 16 Homo sapiens 155-158 12067978-4 2002 Induction of the Sp1-regulated p21 gene by Trichostatin A (TSA) was blocked by ET-743 at concentrations that had minimal effect on uninduced (constitutive) expression. trichostatin A 43-57 H3 histone pseudogene 16 Homo sapiens 31-34 12067978-4 2002 Induction of the Sp1-regulated p21 gene by Trichostatin A (TSA) was blocked by ET-743 at concentrations that had minimal effect on uninduced (constitutive) expression. trichostatin A 59-62 H3 histone pseudogene 16 Homo sapiens 31-34 12067978-4 2002 Induction of the Sp1-regulated p21 gene by Trichostatin A (TSA) was blocked by ET-743 at concentrations that had minimal effect on uninduced (constitutive) expression. Trabectedin 79-85 H3 histone pseudogene 16 Homo sapiens 31-34 12051701-2 2002 Fibroblasts treated with pyruvate undergo a rapid growth arrest accompanied by elevated levels of the cell-cycle regulatory molecules p53, p21, and p16. Pyruvic Acid 25-33 H3 histone pseudogene 16 Homo sapiens 139-142 12107546-1 2002 PURPOSE: We have previously found that the staurosporine derivative, CGP 41 251, that has a high specificity for inhibiting protein kinase C (PKC), selectively blocks oncogenic ras-p21-induced oocyte maturation and that PKC and jun-N-terminal kinase (JNK), with which oncogenic ras-p21 directly interacts, reciprocally require each other"s activation. Staurosporine 43-56 H3 histone pseudogene 16 Homo sapiens 181-184 12107546-1 2002 PURPOSE: We have previously found that the staurosporine derivative, CGP 41 251, that has a high specificity for inhibiting protein kinase C (PKC), selectively blocks oncogenic ras-p21-induced oocyte maturation and that PKC and jun-N-terminal kinase (JNK), with which oncogenic ras-p21 directly interacts, reciprocally require each other"s activation. Staurosporine 43-56 H3 histone pseudogene 16 Homo sapiens 282-285 11877436-0 2002 Role of p21 in apoptosis and senescence of human colon cancer cells treated with camptothecin. Camptothecin 81-93 H3 histone pseudogene 16 Homo sapiens 8-11 11877436-5 2002 Interestingly, blocking of the apoptotic pathway, by Z-VAD-FMK, in p21(-/-) HCT116 cells following treatment with 20 nm CPT did not permit the cells to develop properties of senescence. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 53-62 H3 histone pseudogene 16 Homo sapiens 67-70 11877436-6 2002 These observations demonstrated that p21 was required for senescence development of HCT116 cells following treatment with low concentrations of CPT. Camptothecin 144-147 H3 histone pseudogene 16 Homo sapiens 37-40 12012007-3 2002 In this study, we investigated particularly the effect of 100 microM NS-398 on p53 and p21 expression, caspase activities and nuclear factor-kappaB (NF-kappaB). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 69-75 H3 histone pseudogene 16 Homo sapiens 87-90 12032863-0 2002 Enhanced tumor killing by Apo2L/TRAIL and CPT-11 co-treatment is associated with p21 cleavage and differential regulation of Apo2L/TRAIL ligand and its receptors. Irinotecan 42-48 H3 histone pseudogene 16 Homo sapiens 81-84 12032863-5 2002 CPT-11 treatment resulted in accumulation of cells at G(2)M-phase and correlated with a substantial increase in the protein levels of the cyclin-dependent kinase inhibitor p21. Irinotecan 0-6 H3 histone pseudogene 16 Homo sapiens 172-175 12032863-6 2002 However, cells co-treated with CPT-11 and Apo2L/TRAIL, or pretreated with CPT-11 for up to 24 h followed by 2 h Apo2L/TRAIL, resulted in a caspase-dependent degradation of p21, reversal of G(2)-M phase arrest with a concomitant increase in apoptosis. Irinotecan 31-37 H3 histone pseudogene 16 Homo sapiens 172-175 12032863-6 2002 However, cells co-treated with CPT-11 and Apo2L/TRAIL, or pretreated with CPT-11 for up to 24 h followed by 2 h Apo2L/TRAIL, resulted in a caspase-dependent degradation of p21, reversal of G(2)-M phase arrest with a concomitant increase in apoptosis. Irinotecan 74-80 H3 histone pseudogene 16 Homo sapiens 172-175 12032863-8 2002 These data indicate that the up-regulation of Apo2L/TRAIL ligand and its death receptors as well as cleavage of p21 protein in the Apo2L/TRAIL plus CPT-11 treatment contributes to the positive cooperation between these agents in enhancing tumor cell apoptosis. Irinotecan 148-154 H3 histone pseudogene 16 Homo sapiens 112-115 11980662-9 2002 Both inducible TS expression and the addition of exogenous thymidine (10 microM) blocked p53 and p21 induction by the antifolates but not by 5-FU in the M7TS90 cell line. Thymidine 59-68 H3 histone pseudogene 16 Homo sapiens 97-100 21320405-7 2002 CONCLUSIONS: Tanshinone IIA can inhibit cell growth and clone formation in human lung cancer cell line (SPC-A-1) and its possible molecular mechanism may be inhibiting DNA synthesis by up-regulating p53, p21 and down-regulating CDKN2. tanshinone 13-27 H3 histone pseudogene 16 Homo sapiens 204-207 12027902-0 2002 Interaction between p21-activated protein kinase and Rac during differentiation of HL-60 human promyelocytic leukemia cell induced by all-trans-retinoic acid. Tretinoin 134-157 H3 histone pseudogene 16 Homo sapiens 20-23 12479270-15 2002 Silibinin-treated cells showed up to 2.4- and 3.6-fold increases in Cip1/p21 and Kip1/p27 levels, respectively, and a decrease in CDK2 (80%), CDK4 (98%), and cyclin D1 (60%). Silybin 0-9 H3 histone pseudogene 16 Homo sapiens 73-76 11952383-8 2002 The novel compound crystallizes with one solvent molecule CH(2)Cl(2) in the monoclinic space group P2(1)/n with a = 1151.8(1) pm, b = 1498.1(2) pm, c = 2018.2(2) pm, beta = 102.58(1) degrees, and Z = 4. (2)cl(2) 60-68 H3 histone pseudogene 16 Homo sapiens 99-104 11925210-6 2002 The perchlorate anion in 3 (orthorhombic, space group P2(1)2(1)2(1)) and 5 (orthorhombic, space group P2(1)) is far from O(+) and close to S(+). perchlorate anion 4-21 H3 histone pseudogene 16 Homo sapiens 54-59 11821415-7 2002 Inhibition of ERK activation by PD98059 or U0126 attenuated p21(CIP1) induction, resulting in partial release of the G(2)/M cell cycle arrest induced by ETOP. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 32-39 H3 histone pseudogene 16 Homo sapiens 60-63 11821415-7 2002 Inhibition of ERK activation by PD98059 or U0126 attenuated p21(CIP1) induction, resulting in partial release of the G(2)/M cell cycle arrest induced by ETOP. U 0126 43-48 H3 histone pseudogene 16 Homo sapiens 60-63 11821415-7 2002 Inhibition of ERK activation by PD98059 or U0126 attenuated p21(CIP1) induction, resulting in partial release of the G(2)/M cell cycle arrest induced by ETOP. Etoposide 153-157 H3 histone pseudogene 16 Homo sapiens 60-63 11782491-3 2002 We report that the phosphorylation of merlin at serine 518 is induced by the p21-activated kinase PAK2. Serine 48-54 H3 histone pseudogene 16 Homo sapiens 77-80 12452013-3 2002 RESULT: The c-myc, c-jun, and HNF-1 alpha mRNA of K562 cells treated by 0.2 mg/ml matrine were dramatically decreased at the early stage (3 h), while the H-ras and p21 mRNA were increased obviously at the same time. matrine 82-89 H3 histone pseudogene 16 Homo sapiens 164-167 11894120-5 2002 In LS174T cells, the antisense oligonucleotide, but not the mismatch oligonucleotide, specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p53 activation and p21 induction. Oligonucleotides 31-46 H3 histone pseudogene 16 Homo sapiens 206-209 11894120-6 2002 In DLD-1 cells, the antisense oligonucleotide specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p21 induction although mutant p53 levels remained unchanged. Oligonucleotides 30-45 H3 histone pseudogene 16 Homo sapiens 147-150 11894120-6 2002 In DLD-1 cells, the antisense oligonucleotide specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p21 induction although mutant p53 levels remained unchanged. Irinotecan 125-135 H3 histone pseudogene 16 Homo sapiens 147-150 11960380-5 2002 Surprisingly, we found that hydroxyurea-treated BLM-deficient cells exhibit an intact S phase arrest, proper recovery from the S phase arrest, and intact p53 and p21 responses. Hydroxyurea 28-39 H3 histone pseudogene 16 Homo sapiens 162-165 11856825-5 2002 However, in the P2(1) crystal form dimers of S100A12 are arranged in a spherical hexameric assembly with an external diameter of about 55 A stabilized by calcium ions bound between adjacent dimers. Calcium 154-161 H3 histone pseudogene 16 Homo sapiens 16-21 11874354-3 2002 Ethyltellurium(IV) triazide, C(2)H(5)Te(N(3))(3) (12), crystallizes in the monoclinic space group P2(1)/n, a = 8.4530(2) A, b = 7.9094(2) A, c = 12.6288(3) A, beta = 91.876(1). ethyltellurium(iv) triazide 0-27 H3 histone pseudogene 16 Homo sapiens 98-103 11874354-4 2002 n-Propyltellurium(IV) triazide, n-C(3)H(7)Te(N(3))(3) (13), crystallizes in the monoclinic space group P2(1)/n as well, a = 8.7999(2) A, b = 7.9674(2) A, c = 13.2334(3) A, beta = 94.626(1). n-propyltellurium 0-17 H3 histone pseudogene 16 Homo sapiens 103-108 11874354-4 2002 n-Propyltellurium(IV) triazide, n-C(3)H(7)Te(N(3))(3) (13), crystallizes in the monoclinic space group P2(1)/n as well, a = 8.7999(2) A, b = 7.9674(2) A, c = 13.2334(3) A, beta = 94.626(1). Trichlormethiazide 22-30 H3 histone pseudogene 16 Homo sapiens 103-108 11874354-6 2002 Mesityltellurium(IV) triazide, 2,4,6-(CH(3))(3)C(6)H(2)Te(N(3))(3) (16), crystallizes monoclinic as well; the space group is P2(1)/c, a = 7.5503(6) A, b = 23.581(1) A, c = 7.5094(6) A, beta = 91.295(9). mesityltellurium(iv) triazide 0-29 H3 histone pseudogene 16 Homo sapiens 125-132 11874354-6 2002 Mesityltellurium(IV) triazide, 2,4,6-(CH(3))(3)C(6)H(2)Te(N(3))(3) (16), crystallizes monoclinic as well; the space group is P2(1)/c, a = 7.5503(6) A, b = 23.581(1) A, c = 7.5094(6) A, beta = 91.295(9). 2,4,6-(ch(3)) 31-44 H3 histone pseudogene 16 Homo sapiens 125-132 11751903-6 2002 The ability of p21(Cip1) to inhibit cyclin D1 nuclear export correlates with its ability to bind to Thr-286-phosphorylated cyclin D1 and thereby prevents cyclin D1.CRM1 association. Threonine 100-103 H3 histone pseudogene 16 Homo sapiens 15-18 11882313-4 2002 The treatment of VSMCs with lipophilic statins was associated with decreased prenylation of p-21 Rho A and mevalonate, farnesyl pyrophosphate (F-PP) and geranylgeranyl pyrophosphate (G-PP) reversed prenylation to basal levels. vsmcs 17-22 H3 histone pseudogene 16 Homo sapiens 92-96 11882313-4 2002 The treatment of VSMCs with lipophilic statins was associated with decreased prenylation of p-21 Rho A and mevalonate, farnesyl pyrophosphate (F-PP) and geranylgeranyl pyrophosphate (G-PP) reversed prenylation to basal levels. geranylgeranyl pyrophosphate 183-187 H3 histone pseudogene 16 Homo sapiens 92-96 12168940-0 2002 Correlation of clinical outcome with p53 and p21 status in patients with advanced transitional-cell carcinoma treated with paclitaxel and carboplatin. Paclitaxel 123-133 H3 histone pseudogene 16 Homo sapiens 45-48 12168940-0 2002 Correlation of clinical outcome with p53 and p21 status in patients with advanced transitional-cell carcinoma treated with paclitaxel and carboplatin. Carboplatin 138-149 H3 histone pseudogene 16 Homo sapiens 45-48 12168940-1 2002 BACKGROUND: The purpose of the present study was to correlate the nuclear expression of p53 and p21 with response to paclitaxel and carboplatin, progression-free survival (PFS) as well as overall survival (OS), in patients with urothelial metastatic transitional-cell carcinoma (TCC). Paclitaxel 117-127 H3 histone pseudogene 16 Homo sapiens 96-99 12168940-1 2002 BACKGROUND: The purpose of the present study was to correlate the nuclear expression of p53 and p21 with response to paclitaxel and carboplatin, progression-free survival (PFS) as well as overall survival (OS), in patients with urothelial metastatic transitional-cell carcinoma (TCC). Carboplatin 132-143 H3 histone pseudogene 16 Homo sapiens 96-99 12071473-9 2002 These data support the hypothesis that melatonin reduces MCF-7 cell proliferation by modulating cell-cycle length through the control of the p53-p21 pathway, but without clearly inducing apoptosis. Melatonin 39-48 H3 histone pseudogene 16 Homo sapiens 145-148 12429923-5 2002 In the studies analyzing whether this effect of silibinin is via modulation of cell cycle regulators, silibinin-treated cells showed a strong increase (up to 13- and 6-fold) in Cip1/p21 and Kip1/p27 levels, respectively. Silybin 48-57 H3 histone pseudogene 16 Homo sapiens 182-185 12429923-5 2002 In the studies analyzing whether this effect of silibinin is via modulation of cell cycle regulators, silibinin-treated cells showed a strong increase (up to 13- and 6-fold) in Cip1/p21 and Kip1/p27 levels, respectively. Silybin 102-111 H3 histone pseudogene 16 Homo sapiens 182-185 11889192-4 2002 Addition of pifithrin-alpha, a specific inhibitor of p53, or transfection of p53 antisense oligonucleotides caused decreased RV-induced p53 and p21 expression in PTC and FTC cells. pifithrin 12-27 H3 histone pseudogene 16 Homo sapiens 144-147 11889192-4 2002 Addition of pifithrin-alpha, a specific inhibitor of p53, or transfection of p53 antisense oligonucleotides caused decreased RV-induced p53 and p21 expression in PTC and FTC cells. Oligonucleotides 91-107 H3 histone pseudogene 16 Homo sapiens 144-147 11864927-12 2002 Modulation of cell reactivity to oxidative stress by p21 Ras points to the specific and predictive effects of Ras inhibitors in vivo as potential therapeutic drugs in disorders produced by increase of reactive oxygen species inside the cells. Reactive Oxygen Species 201-224 H3 histone pseudogene 16 Homo sapiens 53-56 12474524-11 2002 An individual possessing one allele of arginine form in p21 codon 31 has a higher risk of developing bladder cancer than the serine form. Arginine 39-47 H3 histone pseudogene 16 Homo sapiens 56-59 12474524-11 2002 An individual possessing one allele of arginine form in p21 codon 31 has a higher risk of developing bladder cancer than the serine form. Serine 125-131 H3 histone pseudogene 16 Homo sapiens 56-59 11818660-2 2002 The onset of ordering of the lactone ring at 300 K proceeds continuously, changes the space group from P2(1)/m to P2(1)/c and doubles the unit cell; the abrupt inversion of the lactone rings at 225 K changes the crystal translational symmetry in the (010) plane. Lactones 29-36 H3 histone pseudogene 16 Homo sapiens 114-121 11807783-6 2002 In accord with these findings, in undifferentiated cells, beta-carotene was more effective in decreasing cyclin A and Bcl-2 expression and in increasing p21 and p27 expression. beta Carotene 58-71 H3 histone pseudogene 16 Homo sapiens 153-156 11707453-6 2002 Analysis of p53-dependent transcription following UV revealed that the phosphorylation of threonine 18 is required for transactivation of the p21, Hdm2 (the human ortholog of Mdm2), and GADD45 genes. Threonine 90-99 H3 histone pseudogene 16 Homo sapiens 142-145 11866879-11 2002 CONCLUSION: Heparin and ADM appear to interact in a synergistic manner, which may be related to the over-expression of p53 and p21 mRNA and the elevated ratio of Bax/Bcl-2 mRNA. Heparin 12-19 H3 histone pseudogene 16 Homo sapiens 127-130 11866879-11 2002 CONCLUSION: Heparin and ADM appear to interact in a synergistic manner, which may be related to the over-expression of p53 and p21 mRNA and the elevated ratio of Bax/Bcl-2 mRNA. Doxorubicin 24-27 H3 histone pseudogene 16 Homo sapiens 127-130 11955311-6 2002 (2) p21WAF1 gene transduction mediated by lipofectaminetrade mark reagent could increase the p21 protein expression in the keratocyte, and inhibit the keratocyte proliferation during 2 - 10 days after transduction. lipofectaminetrade 42-60 H3 histone pseudogene 16 Homo sapiens 4-7 11885700-3 2002 We showed that VCA induced apoptosis in both SK-Hep-1 (p53-positive) and Hep 3B (p53-negative) cells through p53- and p21-independent pathways. cis-vaccenic acid 15-18 H3 histone pseudogene 16 Homo sapiens 118-121 11887880-2 2002 The compound was recrystallized from a mixture of ethylacetate and n-hexane in monoclinic, space group P21/c, with a = 16.622(1), b = 6.215(1), c = 15.802(1) A, P= 104.97(1), and Z = 4. n-hexane 67-75 H3 histone pseudogene 16 Homo sapiens 103-108 11830533-6 2002 Equitoxic doses of AN-238, AN-201, or DOX affected p53, p21, and PCNA differently. Doxorubicin 38-41 H3 histone pseudogene 16 Homo sapiens 56-59 11830533-8 2002 In HCT-15 cells, PCNA:p21 ratios, which are indicators of proliferation and repair processes, remained unchanged after exposure to AN-238 but were increased by DOX. Doxorubicin 160-163 H3 histone pseudogene 16 Homo sapiens 22-25 11739523-8 2001 On the basis of information obtained in these and other studies, we localize down-regulation of IgE-mediated LTC(4) secretion to a region of the signaling cascade antecedent to p21(ras) activation, downstream of phosphatidylinositol 3 kinase activity and probably involving regulation of phosphatidylinositol-3,4,5-trisphosphate levels. phosphatidylinositol 3,4,5-triphosphate 288-328 H3 histone pseudogene 16 Homo sapiens 177-180 11987241-16 2002 Thus, ALA could exhibit chemoselectivity in 9p21/MTAP-deleted cells, even if DHFR amplification occurs. ala 6-9 H3 histone pseudogene 16 Homo sapiens 45-48 11782367-6 2002 Conversely, treatment with the B[a]P metabolite 7r,8t-dihydroxy-9t,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) repressed BRCA-1 promoter activity and protein, while increasing p53 and p21 protein levels. 7r,8t-dihydroxy-9t,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene 48-109 H3 histone pseudogene 16 Homo sapiens 190-193 11813258-5 2002 Moreover, the magnolol-induced cell cycle arrest occurred when the cyclin-CDK system was inhibited, just as p21 protein expression was augmented. magnolol 14-22 H3 histone pseudogene 16 Homo sapiens 108-111 11741176-8 2002 CONCLUSION: Troglitazone had growth inhibitory and differentiation induction effects on the pancreatic cancer cell lines through the upregulation of p21 expression, suggesting that ligand activation of PPAR gamma is a new molecular target for effective therapy against pancreatic cancer. Troglitazone 12-24 H3 histone pseudogene 16 Homo sapiens 149-152 12017271-4 2002 Synergistic effects on p53 and p21 levels between the oligonucleotide and chemotherapeutic agents were also observed in vitro. Oligonucleotides 54-69 H3 histone pseudogene 16 Homo sapiens 31-34 11855756-11 2002 p21 was upregulated following p53 activation at low doses of DOX in HepG2 cells, but at higher doses, p21 was downregulated in Huh-7 and HepG2 cells. Doxorubicin 61-64 H3 histone pseudogene 16 Homo sapiens 0-3 11813266-5 2002 P53, p21, and MDM2 were induced in E6-transfected TK6 cells, as well as in parental TK6 cells after arsenite treatment. arsenite 100-108 H3 histone pseudogene 16 Homo sapiens 5-8 11721009-0 2001 Molecular dynamics simulations of Gly-12-->Val mutant of p21(ras): dynamic inhibition mechanism. Glycine 34-37 H3 histone pseudogene 16 Homo sapiens 60-63 11747348-5 2001 Western blot analysis indicated that Tyrphostin AG 1024-induced apoptosis was associated with a downregulation of expression of phospho-Akt1, increased expression of Bax, p53 and p21, and a decreased expression of bcl-2 expression, especially when combined with irradiation. Tyrphostins 37-47 H3 histone pseudogene 16 Homo sapiens 179-182 11721009-0 2001 Molecular dynamics simulations of Gly-12-->Val mutant of p21(ras): dynamic inhibition mechanism. Valine 46-49 H3 histone pseudogene 16 Homo sapiens 60-63 11721009-3 2001 In our previous study, we have clarified the mechanism of the GTP-->GDP hydrolysis reaction in the wild-type p21(ras) at the atomic level and concluded that GTPase-activating protein plays a significant role in the supply of H2O molecules for the hydrolysis. Guanosine Triphosphate 62-65 H3 histone pseudogene 16 Homo sapiens 112-115 11721009-3 2001 In our previous study, we have clarified the mechanism of the GTP-->GDP hydrolysis reaction in the wild-type p21(ras) at the atomic level and concluded that GTPase-activating protein plays a significant role in the supply of H2O molecules for the hydrolysis. Water 228-231 H3 histone pseudogene 16 Homo sapiens 112-115 11721009-5 2001 However, by performing molecular dynamic calculations, we found that the structure of the active site of the enzyme substrate complex in the oncogenic mutant p21(ras) continuously changes, and these continuous changes in the active site would make it difficult for the GTP-->GDP hydrolysis reaction to occur in the mutant. Guanosine Triphosphate 269-272 H3 histone pseudogene 16 Homo sapiens 158-161 11721009-5 2001 However, by performing molecular dynamic calculations, we found that the structure of the active site of the enzyme substrate complex in the oncogenic mutant p21(ras) continuously changes, and these continuous changes in the active site would make it difficult for the GTP-->GDP hydrolysis reaction to occur in the mutant. Guanosine Diphosphate 278-281 H3 histone pseudogene 16 Homo sapiens 158-161 11740818-6 2001 PS-341 inhibits p44/42 mitogen-activated protein kinase (MAPK) growth signaling triggered by IL-6 and induces apoptosis, despite induction of p21 and p27, in p53 wild-type and p53 mutant MM cells. Bortezomib 0-6 H3 histone pseudogene 16 Homo sapiens 142-145 11751522-4 2001 Exposure of parental Hct116 cells to clinically achievable concentrations of SN-38 (the active metabolite of CPT-11) induces p21 and a G(2) arrest. Irinotecan 77-82 H3 histone pseudogene 16 Homo sapiens 125-128 11751522-4 2001 Exposure of parental Hct116 cells to clinically achievable concentrations of SN-38 (the active metabolite of CPT-11) induces p21 and a G(2) arrest. Irinotecan 109-115 H3 histone pseudogene 16 Homo sapiens 125-128 11751522-6 2001 In contrast, Hct116 cells that are p21 deficient (p21-/- Hct116) readily undergo apoptosis after treatment with SN-38. Irinotecan 112-117 H3 histone pseudogene 16 Homo sapiens 35-38 11751522-6 2001 In contrast, Hct116 cells that are p21 deficient (p21-/- Hct116) readily undergo apoptosis after treatment with SN-38. Irinotecan 112-117 H3 histone pseudogene 16 Homo sapiens 50-53 11751522-10 2001 Sequential treatment with SN-38 followed by flavopiridol was associated with higher activation of caspase-3 and greater cleavage of both p21 and XIAP, an inhibitor of apoptosis, compared with other treatment schedules. Irinotecan 26-31 H3 histone pseudogene 16 Homo sapiens 137-140 11751522-10 2001 Sequential treatment with SN-38 followed by flavopiridol was associated with higher activation of caspase-3 and greater cleavage of both p21 and XIAP, an inhibitor of apoptosis, compared with other treatment schedules. alvocidib 44-56 H3 histone pseudogene 16 Homo sapiens 137-140 11751523-6 2001 In cells treated with EGCG, there was a decrease in the cyclin D1 protein, an increase in the p21(Cip1) and p27(Kip1) proteins, and a reduction in the hyperphosphorylated form of pRB, changes that may account for the arrest in G(1). epigallocatechin gallate 22-26 H3 histone pseudogene 16 Homo sapiens 94-97 11746677-0 2001 Revisiting the structural flexibility of the complex p21(ras)-GTP: the catalytic conformation of the molecular switch II. Guanosine Triphosphate 62-65 H3 histone pseudogene 16 Homo sapiens 53-56 11746677-1 2001 The hydrolysis of GTP in p21(ras) triggers conformational changes that regulate the ras/ERK signaling pathway. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 25-28 11753676-4 2001 However, RA sensitive CA-OV3 cells expressed higher levels of p53, p27, p21, and p16 compared to RA resistant SK-OV3 cells. Tretinoin 9-11 H3 histone pseudogene 16 Homo sapiens 72-75 11709727-7 2001 Furthermore, treatment with LY294002 resulted in the selective increase of cyclin-dependent kinase inhibitors p21(Cip1) or p27(Kip1) and suppression of cyclin E-associated Cdk2 kinase activity in ErbB2-overexpressing lines, which may account for their hypersensitivity toward inhibitors of the PI3K pathway in anchorage-independent growth. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 28-36 H3 histone pseudogene 16 Homo sapiens 110-113 16200730-2 2001 METHODS: A human colorectal carcinoma cell line DLD1 whose p21 expression can be controlled by isopropyl-beta-D-thiogalactoside (IPTG) was established. Isopropyl Thiogalactoside 95-127 H3 histone pseudogene 16 Homo sapiens 59-62 16200730-2 2001 METHODS: A human colorectal carcinoma cell line DLD1 whose p21 expression can be controlled by isopropyl-beta-D-thiogalactoside (IPTG) was established. Isopropyl Thiogalactoside 129-133 H3 histone pseudogene 16 Homo sapiens 59-62 11727266-13 2001 Expression of p21(cip1) and p27(kip1) was observed in 40% of ACs and 37.5% and 12.5% of DCs. Cycloserine 88-91 H3 histone pseudogene 16 Homo sapiens 14-17 11698350-5 2001 We observed that both SAM-486A and DFMO, either alone or in combination, inhibited cell proliferation, induced p21 and arrested cells in the G(0)-G(1) phase of the cell cycle but failed to activate caspase-3 as assessed by enzymatic assay of caspase-3, western blot analysis of the proteolytic cleavage of caspase-3 protein as well as TUNEL assay. 4-amidinoindan-1-one 2'-amidinohydrazone 22-30 H3 histone pseudogene 16 Homo sapiens 111-114 11698350-5 2001 We observed that both SAM-486A and DFMO, either alone or in combination, inhibited cell proliferation, induced p21 and arrested cells in the G(0)-G(1) phase of the cell cycle but failed to activate caspase-3 as assessed by enzymatic assay of caspase-3, western blot analysis of the proteolytic cleavage of caspase-3 protein as well as TUNEL assay. Eflornithine 35-39 H3 histone pseudogene 16 Homo sapiens 111-114 11694645-0 2001 Short-chain fatty acids inhibit invasive human colon cancer by modulating uPA, TIMP-1, TIMP-2, mutant p53, Bcl-2, Bax, p21 and PCNA protein expression in an in vitro cell culture model. Fatty Acids, Volatile 0-23 H3 histone pseudogene 16 Homo sapiens 119-122 11668507-3 2001 NaB-mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unphosphorylation. nab 0-3 H3 histone pseudogene 16 Homo sapiens 13-16 11694593-7 2001 TNF-alpha, sphingomyelinase, and C(2)-ceramide translocated Cdc42, Rac, and RhoA to membranes, and stimulated p21-activated protein kinase downstream of Ras-GTP, PI 3-K, and SK. N-acetylsphingosine 33-46 H3 histone pseudogene 16 Homo sapiens 110-113 11694593-7 2001 TNF-alpha, sphingomyelinase, and C(2)-ceramide translocated Cdc42, Rac, and RhoA to membranes, and stimulated p21-activated protein kinase downstream of Ras-GTP, PI 3-K, and SK. Radium 153-156 H3 histone pseudogene 16 Homo sapiens 110-113 11694593-7 2001 TNF-alpha, sphingomyelinase, and C(2)-ceramide translocated Cdc42, Rac, and RhoA to membranes, and stimulated p21-activated protein kinase downstream of Ras-GTP, PI 3-K, and SK. Guanosine Triphosphate 157-160 H3 histone pseudogene 16 Homo sapiens 110-113 11687965-10 2001 These observations suggest that the interaction of COX-2 with p53 may cause p21-independent suppression of tumor cell growth upon flurbiprofen treatment. Flurbiprofen 130-142 H3 histone pseudogene 16 Homo sapiens 76-79 11704859-8 2001 The results suggested that down regulation of p21(Cip1) expression is linked to the tumorigenic conversion of BEP2D cells by asbestos. Asbestos 125-133 H3 histone pseudogene 16 Homo sapiens 46-49 11690683-3 2001 PATIENTS AND METHODS: Bcl-2, Bax and p21 positivity were detected immunohistochemically on paraffin-embedded pre-treatment biopsies from 83 patients with invasive transitional cell cancer (TCC) of the bladder, treated with radiotherapy. Paraffin 91-99 H3 histone pseudogene 16 Homo sapiens 37-40 11668507-8 2001 This suggested that NaB had the potential to elicit SLPs through p21-mediated withdrawal from cell cycle progression. nab 20-23 H3 histone pseudogene 16 Homo sapiens 65-68 11477076-5 2001 However, glutathione S-transferase-fused and thus dimerized p63 and p53 core domains had similar affinity and specificity for the p53 consensus sites p21, gadd45, cyclin G, and bax. Glutathione 9-20 H3 histone pseudogene 16 Homo sapiens 150-153 11511210-5 2001 For 5, C20H20S3O3Ag, crystal data are as follows: monoclinic, space group P2(1)/n, a = 11.8117(5) A, b = 7.8813(5) A, c = 22.3316(10) A, beta = 102.245(5) degrees, V = 2031.6(2) A(3), Z = 4. c20h20s3o3ag 7-19 H3 histone pseudogene 16 Homo sapiens 74-79 11525649-1 2001 Oncogenic ras (Val 12-containing)-p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 (that block Val 12-p21-activated raf) and 96-110 and 115-126, which do not affect the ability of insulin-activated cellular p21 to induce maturation. val 12 15-21 H3 histone pseudogene 16 Homo sapiens 34-37 11525649-1 2001 Oncogenic ras (Val 12-containing)-p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 (that block Val 12-p21-activated raf) and 96-110 and 115-126, which do not affect the ability of insulin-activated cellular p21 to induce maturation. val 12 15-21 H3 histone pseudogene 16 Homo sapiens 142-145 11525649-1 2001 Oncogenic ras (Val 12-containing)-p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 (that block Val 12-p21-activated raf) and 96-110 and 115-126, which do not affect the ability of insulin-activated cellular p21 to induce maturation. val 12 15-21 H3 histone pseudogene 16 Homo sapiens 142-145 11525649-1 2001 Oncogenic ras (Val 12-containing)-p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 (that block Val 12-p21-activated raf) and 96-110 and 115-126, which do not affect the ability of insulin-activated cellular p21 to induce maturation. val 12 15-21 H3 histone pseudogene 16 Homo sapiens 142-145 11525649-1 2001 Oncogenic ras (Val 12-containing)-p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 (that block Val 12-p21-activated raf) and 96-110 and 115-126, which do not affect the ability of insulin-activated cellular p21 to induce maturation. val 12 180-186 H3 histone pseudogene 16 Homo sapiens 34-37 11525649-1 2001 Oncogenic ras (Val 12-containing)-p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 (that block Val 12-p21-activated raf) and 96-110 and 115-126, which do not affect the ability of insulin-activated cellular p21 to induce maturation. val 12 180-186 H3 histone pseudogene 16 Homo sapiens 142-145 11525649-1 2001 Oncogenic ras (Val 12-containing)-p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 (that block Val 12-p21-activated raf) and 96-110 and 115-126, which do not affect the ability of insulin-activated cellular p21 to induce maturation. val 12 180-186 H3 histone pseudogene 16 Homo sapiens 142-145 11525649-1 2001 Oncogenic ras (Val 12-containing)-p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 (that block Val 12-p21-activated raf) and 96-110 and 115-126, which do not affect the ability of insulin-activated cellular p21 to induce maturation. val 12 180-186 H3 histone pseudogene 16 Homo sapiens 142-145 11585744-0 2001 Growth inhibitory effects of 1alpha, 25-dihydroxyvitamin D(3) are mediated by increased levels of p21 in the prostatic carcinoma cell line ALVA-31. Calcitriol 29-61 H3 histone pseudogene 16 Homo sapiens 98-101 11725347-5 2001 We measured ras p21 proteins in lung cancer patients, patients with chronic obstructive pulmonary disease (COPD) and workers exposed to emissions from petrochemical plants and 1,3-butadiene and 1,3-butadiene/styrene. 1,3-butadiene 176-189 H3 histone pseudogene 16 Homo sapiens 16-19 11725347-5 2001 We measured ras p21 proteins in lung cancer patients, patients with chronic obstructive pulmonary disease (COPD) and workers exposed to emissions from petrochemical plants and 1,3-butadiene and 1,3-butadiene/styrene. 1,3-butadiene 194-207 H3 histone pseudogene 16 Homo sapiens 16-19 11725347-5 2001 We measured ras p21 proteins in lung cancer patients, patients with chronic obstructive pulmonary disease (COPD) and workers exposed to emissions from petrochemical plants and 1,3-butadiene and 1,3-butadiene/styrene. Styrene 208-215 H3 histone pseudogene 16 Homo sapiens 16-19 11447225-2 2001 In addition, H(2)O(2)-induced phosphorylation of p53 was followed by induction of p21, suggesting functional activation of p53. Hydrogen Peroxide 13-21 H3 histone pseudogene 16 Homo sapiens 82-85 11593437-1 2001 The small GTP-binding protein Rac is a downstream effector of the oncogene product p21-ras. Guanosine Triphosphate 10-13 H3 histone pseudogene 16 Homo sapiens 83-86 11511226-1 2001 Thermal decomposition of monochlorogallane, [H2GaCl]n, at ambient temperatures releases H2 and results in the formation of gallium(I) species, including the new compound Ga[GaHCl3], which has been characterized crystallographically at 100 K (monoclinic P2(1)/n, a = 5.730(1), b = 6.787(1), c = 14.508(1) A, beta = 97.902(5) degrees ) and by its Raman spectrum. monochlorogallane 25-42 H3 histone pseudogene 16 Homo sapiens 253-258 11511226-1 2001 Thermal decomposition of monochlorogallane, [H2GaCl]n, at ambient temperatures releases H2 and results in the formation of gallium(I) species, including the new compound Ga[GaHCl3], which has been characterized crystallographically at 100 K (monoclinic P2(1)/n, a = 5.730(1), b = 6.787(1), c = 14.508(1) A, beta = 97.902(5) degrees ) and by its Raman spectrum. Hydrogen 45-47 H3 histone pseudogene 16 Homo sapiens 253-258 11498783-7 2001 Although the basal mRNA levels of these genes did not depend on the presence of p53, we observed a p53-dependent induction of all these targets in response to gamma-irradiation and a p53-independent regulation for p21 and KILLER/DR5 in response to dexamethasone. Dexamethasone 248-261 H3 histone pseudogene 16 Homo sapiens 214-217 11507071-3 2001 We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines. Melphalan 93-102 H3 histone pseudogene 16 Homo sapiens 53-56 11507071-3 2001 We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines. Melphalan 104-109 H3 histone pseudogene 16 Homo sapiens 53-56 11488607-8 2001 Vanadate also increased p21 and Chk1 levels and reduced Cdc25C expression, leading to phosphorylation of Cdc2 and a slight increase in cyclin B1 expression as analyzed by Western blot. Vanadates 0-8 H3 histone pseudogene 16 Homo sapiens 24-27 11488607-9 2001 Catalase, a specific antioxidant for H2O2, decreased vanadate-induced expression of p21 and Chk1, reduced phosphorylation of Cdc2Tyr15, and decreased cyclin B1 levels. Vanadates 53-61 H3 histone pseudogene 16 Homo sapiens 84-87 11523059-10 2001 It is concluded that sennosides acutely induce apoptosis of colonic epithelial cells, presumably by a p53, p21/WAF-mediated pathway, resulting in shorter crypts. senokot 21-31 H3 histone pseudogene 16 Homo sapiens 107-110 11440896-3 2001 Induction of fetal hyperinsulinemia by direct infusion of insulin into the fetus and by either fetal or maternal infusions of glucose resulted in significant increases in the activity of FTase and the amounts of farnesylated p21 Ras in fetal liver, skeletal muscle, fat, and white blood cells. Glucose 126-133 H3 histone pseudogene 16 Homo sapiens 225-228 11408350-6 2001 Cell cycle inhibitors p21 and p27 were significantly upregulated by mevastatin. mevastatin 68-78 H3 histone pseudogene 16 Homo sapiens 22-25 11439344-0 2001 Low concentrations of paclitaxel induce cell type-dependent p53, p21 and G1/G2 arrest instead of mitotic arrest: molecular determinants of paclitaxel-induced cytotoxicity. Paclitaxel 22-32 H3 histone pseudogene 16 Homo sapiens 65-68 11488531-1 2001 PURPOSE: We have previously found that a synthetic peptide corresponding to ras-p21 residues 96 110 (PNC2) selectively blocks oncogenic (Val 12-containing) ras-p21 protein-induced oocyte maturation. val 12 137-143 H3 histone pseudogene 16 Homo sapiens 80-83 11488531-1 2001 PURPOSE: We have previously found that a synthetic peptide corresponding to ras-p21 residues 96 110 (PNC2) selectively blocks oncogenic (Val 12-containing) ras-p21 protein-induced oocyte maturation. val 12 137-143 H3 histone pseudogene 16 Homo sapiens 160-163 11488531-5 2001 RESULTS: Microinjection of this plasmid into oocytes together with Val 12-p21 resulted in complete inhibition of maturation in the presence of inducer. val 12 67-73 H3 histone pseudogene 16 Homo sapiens 74-77 11390204-10 2001 However, in the presence of melatonin, this apoptotic population decreased up to 4.5% at 10(-5) M. The p53 and p21 protein levels of skin fibroblasts increased 4 h after 8 Gy irradiation, but melatonin pretreatment did not change those levels. Melatonin 28-37 H3 histone pseudogene 16 Homo sapiens 111-114 11390204-10 2001 However, in the presence of melatonin, this apoptotic population decreased up to 4.5% at 10(-5) M. The p53 and p21 protein levels of skin fibroblasts increased 4 h after 8 Gy irradiation, but melatonin pretreatment did not change those levels. Melatonin 192-201 H3 histone pseudogene 16 Homo sapiens 111-114 11406180-6 2001 Both long-term, low dose and short-term, high dose exposure to arsenite greatly suppressed the radiation-induced increase in p21 abundance. arsenite 63-71 H3 histone pseudogene 16 Homo sapiens 125-128 11406180-8 2001 These results show that in cells treated with arsenite, p53-dependent increase in p21 expression, normally a block to cell cycle progression after DNA damage, is deficient. arsenite 46-54 H3 histone pseudogene 16 Homo sapiens 82-85 11453316-5 2001 Thirty-three per cent of the DMPMs were positive for p53, 35% for p21 and 52% for metallothionein. dmpms 29-34 H3 histone pseudogene 16 Homo sapiens 66-69 11453316-7 2001 For p21 and metallothionein there was a statistically significant difference between the exposure characteristics: patients with environmental asbestos exposure had shown more immunopositivity. Asbestos 143-151 H3 histone pseudogene 16 Homo sapiens 4-7 11453316-8 2001 There were statistically significant differences between age groups and between asbestos exposure times for metallothionein, and between asbestos exposure times and p21. Asbestos 137-145 H3 histone pseudogene 16 Homo sapiens 165-168 11439344-5 2001 Furthermore, we observed that the levels of p53 and p21 induced by adriamycin and by low concentrations of PTX in A549 cells were comparable. Doxorubicin 67-77 H3 histone pseudogene 16 Homo sapiens 52-55 11439344-5 2001 Furthermore, we observed that the levels of p53 and p21 induced by adriamycin and by low concentrations of PTX in A549 cells were comparable. Paclitaxel 107-110 H3 histone pseudogene 16 Homo sapiens 52-55 11439344-6 2001 This observation led us to conclude that low concentrations of PTX can induce p53 and p21 sufficiently to cause G1 and G2. Paclitaxel 63-66 H3 histone pseudogene 16 Homo sapiens 86-89 11439344-3 2001 At these low concentrations that are insufficient to inhibit mitotic progression, PTX induced both p53 and p21 causing G1 and G2 arrest in A549. Paclitaxel 82-85 H3 histone pseudogene 16 Homo sapiens 107-110 11389075-8 2001 We found that vinblastine treatment caused down-regulation of p53 and its target p21 and up-regulation of tumor necrosis factor alpha, Bak, and several other genes in control but not in KB3-TAM67 cells, identifying these genes as putative targets of vinblastine-inducible AP-1. Vinblastine 14-25 H3 histone pseudogene 16 Homo sapiens 81-84 11380423-4 2001 This erythroid differentiation was linked to a dose- and time-dependent inhibition of cell proliferation associated with an equivalent increased expression of p21 mRNA, but with a higher increased level of p21 protein (sixfold) for cells treated with resveratrol than for those treated with hydroxyurea (1.5-fold). Resveratrol 251-262 H3 histone pseudogene 16 Homo sapiens 159-162 11376010-3 2001 Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G(1), regardless of whether they carry a diploid or polyploid genome after mitotic exit. Nocodazole 29-39 H3 histone pseudogene 16 Homo sapiens 83-86 11376010-3 2001 Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G(1), regardless of whether they carry a diploid or polyploid genome after mitotic exit. Nocodazole 144-154 H3 histone pseudogene 16 Homo sapiens 83-86 11376126-7 2001 Oestradiol and IGF-1 regulate the expression of two cyclin dependent kinase inhibitors, p21 and p27, differently. Estradiol 0-10 H3 histone pseudogene 16 Homo sapiens 88-91 11380423-4 2001 This erythroid differentiation was linked to a dose- and time-dependent inhibition of cell proliferation associated with an equivalent increased expression of p21 mRNA, but with a higher increased level of p21 protein (sixfold) for cells treated with resveratrol than for those treated with hydroxyurea (1.5-fold). Resveratrol 251-262 H3 histone pseudogene 16 Homo sapiens 206-209 11306695-7 2001 The accumulation of the cell cycle inhibitor p21(cip1) was only apparent after sst(2) and sst(4) receptor activation in the presence of bFGF, which was sensitive to PD 169316 or pertussis toxin. 2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole 165-174 H3 histone pseudogene 16 Homo sapiens 45-48 11391852-1 2001 INTRODUCTION: Phenylbutyrate (PB) and its metabolite phenylacetate (PA) demonstrate anticancer activity in vitro through promotion of cell differentiation, induction of apoptosis through the p21 pathway, inhibition of histone deacetylase, and in the case of PB, direct cytotoxicity. Phenylbutyrates 14-28 H3 histone pseudogene 16 Homo sapiens 191-194 11391852-1 2001 INTRODUCTION: Phenylbutyrate (PB) and its metabolite phenylacetate (PA) demonstrate anticancer activity in vitro through promotion of cell differentiation, induction of apoptosis through the p21 pathway, inhibition of histone deacetylase, and in the case of PB, direct cytotoxicity. Phenylbutyrates 30-32 H3 histone pseudogene 16 Homo sapiens 191-194 11391852-1 2001 INTRODUCTION: Phenylbutyrate (PB) and its metabolite phenylacetate (PA) demonstrate anticancer activity in vitro through promotion of cell differentiation, induction of apoptosis through the p21 pathway, inhibition of histone deacetylase, and in the case of PB, direct cytotoxicity. phenylacetic acid 53-66 H3 histone pseudogene 16 Homo sapiens 191-194 11391852-1 2001 INTRODUCTION: Phenylbutyrate (PB) and its metabolite phenylacetate (PA) demonstrate anticancer activity in vitro through promotion of cell differentiation, induction of apoptosis through the p21 pathway, inhibition of histone deacetylase, and in the case of PB, direct cytotoxicity. phenylacetic acid 68-70 H3 histone pseudogene 16 Homo sapiens 191-194 11313183-7 2001 In astrocytoma cells, cisplatin treatment resulted in the upregulation of p53, p21 and bax, while only p21 induction was observed after BBR3464 treatment. Cisplatin 22-31 H3 histone pseudogene 16 Homo sapiens 79-82 11313183-7 2001 In astrocytoma cells, cisplatin treatment resulted in the upregulation of p53, p21 and bax, while only p21 induction was observed after BBR3464 treatment. BBR 3464 136-143 H3 histone pseudogene 16 Homo sapiens 103-106 11313183-8 2001 In cisplatin-resistant cells, the reduced sensitivity to cisplatin paralleled a resistance to the induction of p53/p21 pathway by cisplatin, while the same doses of BBR3464 induced p21 to a similar extent in the resistant cells as in the parental cells. Cisplatin 3-12 H3 histone pseudogene 16 Homo sapiens 115-118 11313183-8 2001 In cisplatin-resistant cells, the reduced sensitivity to cisplatin paralleled a resistance to the induction of p53/p21 pathway by cisplatin, while the same doses of BBR3464 induced p21 to a similar extent in the resistant cells as in the parental cells. Cisplatin 57-66 H3 histone pseudogene 16 Homo sapiens 115-118 11313183-8 2001 In cisplatin-resistant cells, the reduced sensitivity to cisplatin paralleled a resistance to the induction of p53/p21 pathway by cisplatin, while the same doses of BBR3464 induced p21 to a similar extent in the resistant cells as in the parental cells. Cisplatin 57-66 H3 histone pseudogene 16 Homo sapiens 115-118 11313183-8 2001 In cisplatin-resistant cells, the reduced sensitivity to cisplatin paralleled a resistance to the induction of p53/p21 pathway by cisplatin, while the same doses of BBR3464 induced p21 to a similar extent in the resistant cells as in the parental cells. BBR 3464 165-172 H3 histone pseudogene 16 Homo sapiens 181-184 11248419-7 2001 We found that the codon 31 Ser/Ser homozygote of the p21 gene could be a risk factor for the development of cervical adenocarcinoma associated with high-risk HPV. Serine 27-30 H3 histone pseudogene 16 Homo sapiens 53-56 11286989-5 2001 In addition, genistein enhanced the expression of the cell cycle inhibitor p21(waf/cip1) by 10- to 15-fold, increased p21(waf/cip1) association with Cdc2 by 2-fold, and increased the expression of the tumor suppressor p53 by 2.8-fold. Genistein 13-22 H3 histone pseudogene 16 Homo sapiens 75-78 11286989-5 2001 In addition, genistein enhanced the expression of the cell cycle inhibitor p21(waf/cip1) by 10- to 15-fold, increased p21(waf/cip1) association with Cdc2 by 2-fold, and increased the expression of the tumor suppressor p53 by 2.8-fold. Genistein 13-22 H3 histone pseudogene 16 Homo sapiens 118-121 11286989-8 2001 From these results, we conclude that genistein inhibits the growth of nonneoplastic MCF-10F human breast cells by preventing the G2/M phase transition, induces the expression of the cell cycle inhibitor p21(waf/cip1) as well as its interaction with Cdc2, and inhibits the activity of Cdc2 in a phosphorylation-related manner. Genistein 37-46 H3 histone pseudogene 16 Homo sapiens 203-206 11304152-6 2001 [Ni(o-MeO-dppe)I2] crystallizes in the monoclinic space group P2(1)/c with Z = 4, a = 12.1309(1) A, b = 16.5759(3) A, c = 17.6474(2) A, beta = 119.3250(10) degrees. ni(o-meo-dppe)i2 1-17 H3 histone pseudogene 16 Homo sapiens 62-67 11248419-7 2001 We found that the codon 31 Ser/Ser homozygote of the p21 gene could be a risk factor for the development of cervical adenocarcinoma associated with high-risk HPV. Serine 31-34 H3 histone pseudogene 16 Homo sapiens 53-56 11313592-1 2001 The title compound, N-hydroxypropanamide, C(3)H(7)NO(2), crystallizes with Z" = 3 in P2(1)/c. n-hydroxypropanamide 20-40 H3 histone pseudogene 16 Homo sapiens 85-90 11400165-8 2001 Levels of p21 increased in both of the genistein-treated cell lines, suggesting that p21 gene expression was activated but in a p53-independent manner, whereas no significant changes in levels of the pro-apoptotic protein, Bax, were found. Genistein 39-48 H3 histone pseudogene 16 Homo sapiens 10-13 11400165-8 2001 Levels of p21 increased in both of the genistein-treated cell lines, suggesting that p21 gene expression was activated but in a p53-independent manner, whereas no significant changes in levels of the pro-apoptotic protein, Bax, were found. Genistein 39-48 H3 histone pseudogene 16 Homo sapiens 85-88 11313592-1 2001 The title compound, N-hydroxypropanamide, C(3)H(7)NO(2), crystallizes with Z" = 3 in P2(1)/c. c(3)h(7)no 42-52 H3 histone pseudogene 16 Homo sapiens 85-90 11329487-0 2001 Ethanol decreases expression of p21 and increases hyperphosphorylated pRb in cell lines of squamous cell carcinomas of the head and neck. Ethanol 0-7 H3 histone pseudogene 16 Homo sapiens 32-35 11329487-9 2001 CONCLUSIONS: In the acute alcohol in vitro experiments, the marked downregulation of the important cell cycle inhibitor p21 and the corresponding increase of hyperphosphorylated pRb accelerate the progression of cells from the G1 to the S phase in the cell cycle. Alcohols 26-33 H3 histone pseudogene 16 Homo sapiens 120-123 11306489-3 2001 In this study, we demonstrate that the proteasome inhibitor PS-341 directly inhibits proliferation and induces apoptosis of human MM cell lines and freshly isolated patient MM cells; inhibits mitogen-activated protein kinase growth signaling in MM cells; induces apoptosis despite induction of p21 and p27 in both p53 wild-type and p53 mutant MM cells; overcomes drug resistance; adds to the anti-MM activity of dexamethasone; and overcomes the resistance to apoptosis in MM cells conferred by interleukin-6. Bortezomib 60-66 H3 histone pseudogene 16 Homo sapiens 294-297 11106643-3 2001 Treatment of K562(pTet-on/p53) cells with doxycycline resulted in a dose-dependent expression of p53 protein and transcripts, increased p21 protein, decreased dihydrofolate reductase, and G(1) arrest with decreased numbers of cells in S-phase. Doxycycline 42-53 H3 histone pseudogene 16 Homo sapiens 136-139 12577360-1 2001 OBJECTIVE: To investigate the common regulative effects of the Chinese drug Bailong and hexamethylen bisacetamide (HMBA) on expressions of oncogenes (c-H-ras and c-myc), and tumor suppressor genes (Rb, p53 and p21) of MGC80-3 in human cancer cell cycle. hexamethylene bisacetamide 88-113 H3 histone pseudogene 16 Homo sapiens 210-213 12577360-1 2001 OBJECTIVE: To investigate the common regulative effects of the Chinese drug Bailong and hexamethylen bisacetamide (HMBA) on expressions of oncogenes (c-H-ras and c-myc), and tumor suppressor genes (Rb, p53 and p21) of MGC80-3 in human cancer cell cycle. hexamethylene bisacetamide 115-119 H3 histone pseudogene 16 Homo sapiens 210-213 11261970-6 2001 [PdCl2(Ph2PCH2CH(Ph)NHPh-kappaP,kappaN)] crystallizes at 298 K in the space group P2(1)/n with cell parameters a = 10.689(2) A, b = 21.345(3) A, c = 12.282(2) A, beta = 90.294(12) degrees, Z = 4, D(calcd) = 1.526. palladium chloride 1-6 H3 histone pseudogene 16 Homo sapiens 82-87 11307620-3 2001 Lovastatin and phenylacetate promote p21 accumulation but fail to induce cell cycle arrest. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 37-40 11313862-3 2001 Recent evidence indicates that p21 Ras is required for TSH-induced mitogenesis, but the molecular mechanism(s) is not known. Thyrotropin 55-58 H3 histone pseudogene 16 Homo sapiens 31-34 11307620-3 2001 Lovastatin and phenylacetate promote p21 accumulation but fail to induce cell cycle arrest. phenylacetic acid 15-28 H3 histone pseudogene 16 Homo sapiens 37-40 11314044-6 2001 Analysis of p53-dependent transcription revealed that phosphorylation of serine 15 is required to maintain basal levels of p21 mRNA. Serine 73-79 H3 histone pseudogene 16 Homo sapiens 123-126 11171632-4 2001 Flow cytometric analysis revealed a time-dependent growth suppression along with early induction of p21 mRNA in the butyrate, T, and TR groups. Butyrates 116-124 H3 histone pseudogene 16 Homo sapiens 100-103 11462153-11 2001 Western blot analysis of p53 and p21 revealed a gradual increase in the level of these proteins when RPE cells were exposed to increasing concentrations of MMC. Mitomycin 156-159 H3 histone pseudogene 16 Homo sapiens 33-36 11177741-4 2001 Preliminary data suggest that gene expression levels of topoisomerase I, p21, bcl-2, and ICE may be predictive of response to therapy with CPT-11. Irinotecan 139-145 H3 histone pseudogene 16 Homo sapiens 73-76 11314044-7 2001 These results provide new evidence for an important function of serine 37 phosphorylation, clearly distinguish the pathways of p53 activation in response to ultraviolet radiation or DNA damage inflicted by adriamycin, and reveal that serine 15 is crucial to support the p53-mediated basal expression of p21. Serine 234-240 H3 histone pseudogene 16 Homo sapiens 303-306 11181044-5 2001 In addition, mevastatin caused a significant increase in the cell cycle inhibitor p21. mevastatin 13-23 H3 histone pseudogene 16 Homo sapiens 82-85 11456571-4 2001 Single crystals of both salts are suitable for an X-ray diffraction study at 180 K. Both isostructural salts crystallize in the monoclinic space group P2(1)/c (No. Salts 24-29 H3 histone pseudogene 16 Homo sapiens 151-158 11170137-8 2001 In other studies, silymarin, genistein or EGCG caused a strong induction of Cip1/p21 (up to 2.4-fold) and Kip1/p27 (up to 150-fold), and a strong decrease in CDK4 (40-90%) but had moderate effect on CDK2, and cyclins D1 and E. Silymarin 18-27 H3 histone pseudogene 16 Homo sapiens 81-84 11170137-8 2001 In other studies, silymarin, genistein or EGCG caused a strong induction of Cip1/p21 (up to 2.4-fold) and Kip1/p27 (up to 150-fold), and a strong decrease in CDK4 (40-90%) but had moderate effect on CDK2, and cyclins D1 and E. Genistein 29-38 H3 histone pseudogene 16 Homo sapiens 81-84 11170137-8 2001 In other studies, silymarin, genistein or EGCG caused a strong induction of Cip1/p21 (up to 2.4-fold) and Kip1/p27 (up to 150-fold), and a strong decrease in CDK4 (40-90%) but had moderate effect on CDK2, and cyclins D1 and E. epigallocatechin gallate 42-46 H3 histone pseudogene 16 Homo sapiens 81-84 11209606-5 2001 The crystal of H3tachta.3HCl.2H2O is monoclinic, of the space group P2(1)/c, with a = 15.1688(4) A, b = 8.4708(2) A, c = 15.9408(2) A, beta = 108.058(1) degrees, and Z = 4; that of [Ga(tachta)] is cubic, of space group Pa3, with a = 14.0762(1) A and Z = 8. h3tachta.3hcl.2h2o 15-33 H3 histone pseudogene 16 Homo sapiens 68-73 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 0-4 H3 histone pseudogene 16 Homo sapiens 142-145 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 0-4 H3 histone pseudogene 16 Homo sapiens 296-299 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 0-4 H3 histone pseudogene 16 Homo sapiens 296-299 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 205-209 H3 histone pseudogene 16 Homo sapiens 142-145 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 205-209 H3 histone pseudogene 16 Homo sapiens 296-299 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 205-209 H3 histone pseudogene 16 Homo sapiens 296-299 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 205-209 H3 histone pseudogene 16 Homo sapiens 142-145 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 205-209 H3 histone pseudogene 16 Homo sapiens 296-299 11029459-10 2001 Antisense oligonucleotides directed to Ki-Ras decreased both TbetaRIII post-translational modification in Ki-ras(G12V) cells and TGF-beta1 down-regulation of p21, demonstrating the direct effect of mutant Ras. Oligonucleotides 10-26 H3 histone pseudogene 16 Homo sapiens 158-161 11162600-5 2001 DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively. Eflornithine 205-209 H3 histone pseudogene 16 Homo sapiens 296-299 11173413-1 2001 The title compound, C17H23NO2, a tetrahydronaphthalenic analogue of melatonin, crystallizes in the monoclinic space group P2(1) with one molecule in the asymmetric unit. c17h23no2 20-29 H3 histone pseudogene 16 Homo sapiens 122-127 11173413-1 2001 The title compound, C17H23NO2, a tetrahydronaphthalenic analogue of melatonin, crystallizes in the monoclinic space group P2(1) with one molecule in the asymmetric unit. Melatonin 68-77 H3 histone pseudogene 16 Homo sapiens 122-127 11299739-6 2001 We therefore concluded that immunohistochemical studies for p53 and p21 were useful for predicting the chemosensitivities of colon and gastric cancer to MMC and 5-FU. Mitomycin 153-156 H3 histone pseudogene 16 Homo sapiens 68-71 11270487-0 2001 1,25(OH)2 vitamin D3 induces elevated expression of the cell cycle-regulating genes P21 and P27 in squamous carcinoma cell lines of the head and neck. Calcitriol 0-20 H3 histone pseudogene 16 Homo sapiens 84-87 11270487-3 2001 To further explore the molecular mechanisms of the antiproliferative activity in SCCHN we studied the influence of 1,25(OH)2D3 on the expression of the G1 phase-regulating proteins cyclin D1, p21 and p27. Calcitriol 115-126 H3 histone pseudogene 16 Homo sapiens 192-195 11270487-7 2001 In all cell lines tested 1,25(OH)2D3 caused an arrest of cells in the G0/G1 phase of the cell cycle and markedly induced the expression of the inhibitors p21 and p27. oh)2d3 30-36 H3 histone pseudogene 16 Homo sapiens 154-157 11270487-11 2001 Our results demonstrate that the biologically active form of vitamin D3 directly regulates the expression of p21 and p27, inducing a G0/G1 phase arrest: one mechanism by which 1,25(OH)2D3 controls cell proliferation inSCCHN. Cholecalciferol 61-71 H3 histone pseudogene 16 Homo sapiens 109-112 11299762-3 2001 Here, we show that ellagic acid, a natural, dietary phenolic antioxidant when given at 10(-5) M for 48 hours to colon cancer cells (SW 480), induced down regulation of insulin like growth factor IGF-II, activated p21(waf1/Cip1), mediated a cumulative effect on G1/S transition phase and caused apoptotic cell death. Ellagic Acid 19-31 H3 histone pseudogene 16 Homo sapiens 213-216 11299762-5 2001 Collectively, these observations suggest that growth inhibition by ellagic acid is mediated by signaling pathways that mediate DNA damage, triggers p53, which in turn activates p21 and at the same time alters the growth factor expression, resulting in the down regulation of IGF-II. Ellagic Acid 67-79 H3 histone pseudogene 16 Homo sapiens 177-180 11299739-6 2001 We therefore concluded that immunohistochemical studies for p53 and p21 were useful for predicting the chemosensitivities of colon and gastric cancer to MMC and 5-FU. Fluorouracil 161-165 H3 histone pseudogene 16 Homo sapiens 68-71 11299740-5 2001 RESULTS: We found that adriamycin induced a p53 and p21 response as well as a G1 arrest in 184B5 cells, but not in its E6 transformed cells. Doxorubicin 23-33 H3 histone pseudogene 16 Homo sapiens 52-55 11054406-6 2000 TGF-beta induction of PAI-1 and p21 is blocked by the Sp1 inhibitor mithramycin, implicating Sp1 in the in vivo regulation of these genes by TGF-beta. Plicamycin 68-79 H3 histone pseudogene 16 Homo sapiens 32-35 11436200-4 2001 The gene polymorphism for p21 codon 31 involved a base change from AGC to AGA and amino acid changes from serine (Ser) to arginine (Arg). Arginine 132-135 H3 histone pseudogene 16 Homo sapiens 26-29 11436200-0 2001 p21 gene codon 31 arginine/serine polymorphism: non-association with endometriosis. Arginine 18-26 H3 histone pseudogene 16 Homo sapiens 0-3 11436200-0 2001 p21 gene codon 31 arginine/serine polymorphism: non-association with endometriosis. Serine 27-33 H3 histone pseudogene 16 Homo sapiens 0-3 11436200-4 2001 The gene polymorphism for p21 codon 31 involved a base change from AGC to AGA and amino acid changes from serine (Ser) to arginine (Arg). Serine 106-112 H3 histone pseudogene 16 Homo sapiens 26-29 11436200-4 2001 The gene polymorphism for p21 codon 31 involved a base change from AGC to AGA and amino acid changes from serine (Ser) to arginine (Arg). Serine 114-117 H3 histone pseudogene 16 Homo sapiens 26-29 11436200-4 2001 The gene polymorphism for p21 codon 31 involved a base change from AGC to AGA and amino acid changes from serine (Ser) to arginine (Arg). Arginine 122-130 H3 histone pseudogene 16 Homo sapiens 26-29 11104898-3 2000 Very recent studies clarified that P53 independent expression of p21 and gadd 45, activation of PPARgamma are involved in antitumor mechanism of these PGs. Phosphatidylglycerols 151-154 H3 histone pseudogene 16 Homo sapiens 65-68 11188692-1 2000 BACKGROUND: The means by which the protein GAP accelerates GTP hydrolysis, and thereby downregulates growth signaling by p21Ras, is of considerable interest, particularly inasmuch as p21 mutants are implicated in a number of human cancers. Guanosine Triphosphate 59-62 H3 histone pseudogene 16 Homo sapiens 121-124 11188692-3 2000 Mutagenesis studies, however, have shown that the arginine can only partially account for the 10(5)-fold increase in the GAP-accelerated GTPase rate of p21. Arginine 50-58 H3 histone pseudogene 16 Homo sapiens 152-155 11188692-4 2000 RESULTS: We report electron spin-echo envelope modulation (ESEEM) studies of GAP-334 complexed with GMPPNP bound p21 in frozen solution, together with molecular-dynamics simulations. Guanylyl Imidodiphosphate 100-106 H3 histone pseudogene 16 Homo sapiens 113-116 11188692-5 2000 Our results indicate that, in solution, the association of GAP-334 with GTP bound p21 induces a conformational change near the metal ion active site of p21. Guanosine Triphosphate 72-75 H3 histone pseudogene 16 Homo sapiens 82-85 11188692-5 2000 Our results indicate that, in solution, the association of GAP-334 with GTP bound p21 induces a conformational change near the metal ion active site of p21. Guanosine Triphosphate 72-75 H3 histone pseudogene 16 Homo sapiens 152-155 11188692-5 2000 Our results indicate that, in solution, the association of GAP-334 with GTP bound p21 induces a conformational change near the metal ion active site of p21. Metals 127-132 H3 histone pseudogene 16 Homo sapiens 82-85 11188692-5 2000 Our results indicate that, in solution, the association of GAP-334 with GTP bound p21 induces a conformational change near the metal ion active site of p21. Metals 127-132 H3 histone pseudogene 16 Homo sapiens 152-155 11188692-6 2000 This change significantly reduces the distances from the amide groups of p21 glycine residues 60 and 13 to the divalent metal ion. Amides 57-62 H3 histone pseudogene 16 Homo sapiens 73-76 11188692-6 2000 This change significantly reduces the distances from the amide groups of p21 glycine residues 60 and 13 to the divalent metal ion. Glycine 77-84 H3 histone pseudogene 16 Homo sapiens 73-76 11188692-6 2000 This change significantly reduces the distances from the amide groups of p21 glycine residues 60 and 13 to the divalent metal ion. Metals 120-125 H3 histone pseudogene 16 Homo sapiens 73-76 11188692-7 2000 CONCLUSIONS: The movement of glycine residues 60 and 13 upon the binding of GAP-334 in solution provides a physical basis to interpret prior mutagenesis studies, which indicated that Gly-60 and Gly-13 of p21 play important roles in the GAP-dependent GTPase reaction. Glycine 29-36 H3 histone pseudogene 16 Homo sapiens 204-207 11188692-7 2000 CONCLUSIONS: The movement of glycine residues 60 and 13 upon the binding of GAP-334 in solution provides a physical basis to interpret prior mutagenesis studies, which indicated that Gly-60 and Gly-13 of p21 play important roles in the GAP-dependent GTPase reaction. Glycine 183-186 H3 histone pseudogene 16 Homo sapiens 204-207 11188692-7 2000 CONCLUSIONS: The movement of glycine residues 60 and 13 upon the binding of GAP-334 in solution provides a physical basis to interpret prior mutagenesis studies, which indicated that Gly-60 and Gly-13 of p21 play important roles in the GAP-dependent GTPase reaction. Glycine 194-197 H3 histone pseudogene 16 Homo sapiens 204-207 11188692-8 2000 Gly-60 and Gly-13 may play direct catalytic roles and stabilize the attacking water molecule and beta,gamma-bridging oxygen, respectively, in p21. Glycine 0-3 H3 histone pseudogene 16 Homo sapiens 142-145 11188692-8 2000 Gly-60 and Gly-13 may play direct catalytic roles and stabilize the attacking water molecule and beta,gamma-bridging oxygen, respectively, in p21. Glycine 11-14 H3 histone pseudogene 16 Homo sapiens 142-145 11188692-8 2000 Gly-60 and Gly-13 may play direct catalytic roles and stabilize the attacking water molecule and beta,gamma-bridging oxygen, respectively, in p21. Water 78-83 H3 histone pseudogene 16 Homo sapiens 142-145 11188692-8 2000 Gly-60 and Gly-13 may play direct catalytic roles and stabilize the attacking water molecule and beta,gamma-bridging oxygen, respectively, in p21. Oxygen 117-123 H3 histone pseudogene 16 Homo sapiens 142-145 11151508-3 2000 The solid-state structure of the ZnII derivative, NN-SQZnTpCum,Me (C56H69BN8O4Zn), was determined: monoclinic, P2(1)/c, a = 12.5781(12) A, b = 17.7408(17) A, c = 24.440(2) A, alpha = 90.00 degrees, beta = 98.240(2) degrees, gamma = 90.00 degrees, Z = 4. Zinc 33-37 H3 histone pseudogene 16 Homo sapiens 111-118 11151508-3 2000 The solid-state structure of the ZnII derivative, NN-SQZnTpCum,Me (C56H69BN8O4Zn), was determined: monoclinic, P2(1)/c, a = 12.5781(12) A, b = 17.7408(17) A, c = 24.440(2) A, alpha = 90.00 degrees, beta = 98.240(2) degrees, gamma = 90.00 degrees, Z = 4. nn 50-52 H3 histone pseudogene 16 Homo sapiens 111-118 11716435-8 2000 At an ASO concentration of 300 nM, p53 protein was induced 12.5-fold and p21 was induced 8-fold over background levels, 24 h after start of ASO treatment. Oligonucleotides, Antisense 6-9 H3 histone pseudogene 16 Homo sapiens 73-76 11073759-5 2000 The likelihood of relapse was 39% versus 27% (P=.21) on azithromycin compared with clarithromycin, respectively. Azithromycin 56-68 H3 histone pseudogene 16 Homo sapiens 46-51 11139434-4 2000 Levamisole increased in ECs integrin-dependent matrix adhesion, inhibited proliferation (-70%), reduced expression of survival factors such as clusterin (-30%), endothelin-1 (-43%), bcl-2 (-34%), endothelial NO-synthase (-32%) and pRb (Retinoblastoma protein: -89%), and increased that of growth arrest/death signals such as p21 (+73%) and bak (+50%). Levamisole 0-10 H3 histone pseudogene 16 Homo sapiens 325-328 11154558-4 2000 An X-ray single-crystal analysis was carried out on the phenylalanine derivative 3a (monoclinic space group P2(1), a = 10.301(1) A, b = 9.647(1) A, c = 18.479(2) A, beta = 102.98(2) degrees, Z = 4). Phenylalanine 56-69 H3 histone pseudogene 16 Homo sapiens 108-113 11103796-6 2000 p53 downstream proteins, such as p21 and the human homologue of murine double minute-2, were also significantly induced by arsenite treatment. arsenite 123-131 H3 histone pseudogene 16 Homo sapiens 33-36 11129289-9 2000 After SCH58500 treatment, 3-11-fold elevations of p21 expression were observed in tumor xenografts containing nonfunctional p53 (MDA-MB-468, MDA-MB-231, MIAPaCa2, DU-145, and SK-OV-3), but no change in p21 mRNA in wild-type p53 PA-1 tumors. sch58500 6-14 H3 histone pseudogene 16 Homo sapiens 50-53 11129289-9 2000 After SCH58500 treatment, 3-11-fold elevations of p21 expression were observed in tumor xenografts containing nonfunctional p53 (MDA-MB-468, MDA-MB-231, MIAPaCa2, DU-145, and SK-OV-3), but no change in p21 mRNA in wild-type p53 PA-1 tumors. sch58500 6-14 H3 histone pseudogene 16 Homo sapiens 202-205 11129289-12 2000 However, paclitaxel suppressed p21 expression induced by SCH58500 4-fold in DU-145 and SK-OV-3 tumors. Paclitaxel 9-19 H3 histone pseudogene 16 Homo sapiens 31-34 11129289-12 2000 However, paclitaxel suppressed p21 expression induced by SCH58500 4-fold in DU-145 and SK-OV-3 tumors. sch58500 57-65 H3 histone pseudogene 16 Homo sapiens 31-34 11196914-2 2000 beta-Hg2MoO4: P2(1)/c, Z = 4, a = 511.31(6) pm, b = 901.83(7) pm, c = 1086.0(1) pm, beta = 101.01(3) degrees. beta-hg2moo4 0-12 H3 histone pseudogene 16 Homo sapiens 14-21 11092986-1 2000 UCN-01 (7-hydroxystaurosporine) is a newly developed cell cycle inhibitor known to have several modes of action, including inhibition of cyclin-dependent kinase, induction of p21 and suppression of pRb phosphorylation. 7-hydroxystaurosporine 0-6 H3 histone pseudogene 16 Homo sapiens 175-178 11092986-1 2000 UCN-01 (7-hydroxystaurosporine) is a newly developed cell cycle inhibitor known to have several modes of action, including inhibition of cyclin-dependent kinase, induction of p21 and suppression of pRb phosphorylation. 7-hydroxystaurosporine 8-30 H3 histone pseudogene 16 Homo sapiens 175-178 11111922-0 2000 The p21 GTP-binding proteins and bacterial toxins. Guanosine Triphosphate 8-11 H3 histone pseudogene 16 Homo sapiens 4-7 11025661-2 2000 Treatment with vincristine or paclitaxel before DNA-damage or before leptomycin B treatment reduces nuclear accumulation of p53 and expression of mdm2 and p21. Vincristine 15-26 H3 histone pseudogene 16 Homo sapiens 155-158 11025661-2 2000 Treatment with vincristine or paclitaxel before DNA-damage or before leptomycin B treatment reduces nuclear accumulation of p53 and expression of mdm2 and p21. Paclitaxel 30-40 H3 histone pseudogene 16 Homo sapiens 155-158 10925268-0 2000 In vitro and in vivo transfection of p21 gene enhances cyclosporin A-mediated inhibition of lymphocyte proliferation. Cyclosporine 55-68 H3 histone pseudogene 16 Homo sapiens 37-40 10925268-1 2000 Cyclosporine has potent antiproliferative properties, some of which may be via the induction of the cyclin inhibitor p21. Cyclosporine 0-12 H3 histone pseudogene 16 Homo sapiens 117-120 10925268-4 2000 This in vitro transfection of p21 resulted in the inhibition of spontaneous and mitogen-induced cellular proliferation ([3H]thymidine uptake) and also augmented the antiproliferative effects of cyclosporine. Tritium 121-123 H3 histone pseudogene 16 Homo sapiens 30-33 10925268-4 2000 This in vitro transfection of p21 resulted in the inhibition of spontaneous and mitogen-induced cellular proliferation ([3H]thymidine uptake) and also augmented the antiproliferative effects of cyclosporine. Thymidine 124-133 H3 histone pseudogene 16 Homo sapiens 30-33 10925268-4 2000 This in vitro transfection of p21 resulted in the inhibition of spontaneous and mitogen-induced cellular proliferation ([3H]thymidine uptake) and also augmented the antiproliferative effects of cyclosporine. Cyclosporine 194-206 H3 histone pseudogene 16 Homo sapiens 30-33 10918446-7 2000 Here, we report that the mitochondrial role, especially for ATP synthesis, and PKA are necessary for the procaspase 3/p21 complex formation to resist Fas-mediated cell death. Adenosine Triphosphate 60-63 H3 histone pseudogene 16 Homo sapiens 118-121 10972198-6 2000 Taken our results together, we suggested that ginsenoside Rg3 activated the expression of cyclin-kinase inhibitors, p21 and p27, arrested LNCaP cells at G1 phase, and subsequently inhibited cell growth through a caspase3-mediated apoptosis mechanism. Ginsenosides 46-57 H3 histone pseudogene 16 Homo sapiens 116-119 10918446-0 2000 Procaspase 3/p21 complex formation to resist fas-mediated cell death is initiated as a result of the phosphorylation of p21 by protein kinase A. ammonium ferrous sulfate 45-48 H3 histone pseudogene 16 Homo sapiens 13-16 10918446-0 2000 Procaspase 3/p21 complex formation to resist fas-mediated cell death is initiated as a result of the phosphorylation of p21 by protein kinase A. ammonium ferrous sulfate 45-48 H3 histone pseudogene 16 Homo sapiens 120-123 10918446-7 2000 Here, we report that the mitochondrial role, especially for ATP synthesis, and PKA are necessary for the procaspase 3/p21 complex formation to resist Fas-mediated cell death. ammonium ferrous sulfate 150-153 H3 histone pseudogene 16 Homo sapiens 118-121 10918446-5 2000 This mitochondrial damage occurs before an estrangement of the procaspase 3/p21 complex, and we demonstrate that intracellular ATP-deprivation also initiates an estrangement of procaspase 3/p21 complex formation and accelerates Fas-mediated cell death. Adenosine Triphosphate 127-130 H3 histone pseudogene 16 Homo sapiens 76-79 10921903-7 2000 Hus1(-/-)p21(-/-) cells display a unique profile of significantly heightened sensitivity to hydroxyurea, a DNA replication inhibitor, and ultraviolet light, but only slightly increased sensitivity to ionizing radiation. Hydroxyurea 92-103 H3 histone pseudogene 16 Homo sapiens 9-12 10918446-5 2000 This mitochondrial damage occurs before an estrangement of the procaspase 3/p21 complex, and we demonstrate that intracellular ATP-deprivation also initiates an estrangement of procaspase 3/p21 complex formation and accelerates Fas-mediated cell death. Adenosine Triphosphate 127-130 H3 histone pseudogene 16 Homo sapiens 190-193 11196863-3 2000 However, the second oxidation process breaks the dimolybdenum bond, giving a bioctahedral complex, [Mo2(DPhIP)4](BF4)2.5CH3CN.Et2O (2.5CH3CN.Et2O), with Mo...Mo separation of 2.9954(7) A. Crystallographic data for 1.2CH2Cl2 are space group C2/c, a = 17.1891(9) A, b = 17.807(1) A, c = 24.210(2) A, beta = 106.403(4) degrees, Z = 4; for 2.5CH3CN.Et2O, space group P2(1)/n, a = 16.523(5) A, b = 27.418(5) A, c = 18.163(3) A, beta = 93.48(2) degrees, Z = 4. [mo2(dphip)4](bf4)2.5ch3cn 99-125 H3 histone pseudogene 16 Homo sapiens 363-368 10897038-7 2000 In A2780 cells, glutathione exposure was followed by p21 and Bax induction and p53 up-regulation, as expected for genotoxic stress. Glutathione 16-27 H3 histone pseudogene 16 Homo sapiens 53-56 11196863-3 2000 However, the second oxidation process breaks the dimolybdenum bond, giving a bioctahedral complex, [Mo2(DPhIP)4](BF4)2.5CH3CN.Et2O (2.5CH3CN.Et2O), with Mo...Mo separation of 2.9954(7) A. Crystallographic data for 1.2CH2Cl2 are space group C2/c, a = 17.1891(9) A, b = 17.807(1) A, c = 24.210(2) A, beta = 106.403(4) degrees, Z = 4; for 2.5CH3CN.Et2O, space group P2(1)/n, a = 16.523(5) A, b = 27.418(5) A, c = 18.163(3) A, beta = 93.48(2) degrees, Z = 4. Ether 126-130 H3 histone pseudogene 16 Homo sapiens 363-368 11196863-3 2000 However, the second oxidation process breaks the dimolybdenum bond, giving a bioctahedral complex, [Mo2(DPhIP)4](BF4)2.5CH3CN.Et2O (2.5CH3CN.Et2O), with Mo...Mo separation of 2.9954(7) A. Crystallographic data for 1.2CH2Cl2 are space group C2/c, a = 17.1891(9) A, b = 17.807(1) A, c = 24.210(2) A, beta = 106.403(4) degrees, Z = 4; for 2.5CH3CN.Et2O, space group P2(1)/n, a = 16.523(5) A, b = 27.418(5) A, c = 18.163(3) A, beta = 93.48(2) degrees, Z = 4. 5ch3cn 119-125 H3 histone pseudogene 16 Homo sapiens 363-368 11196866-8 2000 [ReCl(PhN2)(PPh(OEt)2)4][BPh4] (7) crystallizes in space group P2(1)/n with a = 19.613(5) A, b = 20.101(5) A, c = 19.918(5) A, beta = 115.12(2) degrees, and Z = 4. phn2 6-10 H3 histone pseudogene 16 Homo sapiens 63-68 11196866-8 2000 [ReCl(PhN2)(PPh(OEt)2)4][BPh4] (7) crystallizes in space group P2(1)/n with a = 19.613(5) A, b = 20.101(5) A, c = 19.918(5) A, beta = 115.12(2) degrees, and Z = 4. sapropterin 25-29 H3 histone pseudogene 16 Homo sapiens 63-68 11196898-3 2000 These Cs-symmetric molecules crystallize with two molecules in the monoclinic space group P2(1)/m. Cesium 6-8 H3 histone pseudogene 16 Homo sapiens 90-95 10817929-5 2000 Then, we studied the expression of two p53 downstream genes that could participate in the glutamate-induced pro-apoptotic pathway: p21, which codes for an inhibitor of different cyclin dependent kinases, and MSH2, which codes for a protein involved in the recognition and repair of DNA mismatches. Glutamic Acid 90-99 H3 histone pseudogene 16 Homo sapiens 131-134 10817929-7 2000 However, very soon after a brief exposure of the cells to glutamate, the expression of both proteins was dramatically enhanced.On these bases, we propose NF-kappaB, p53, p21 and MSH2 as relevant contributors of the glutamate-induced pro-apoptotic pathway. Glutamic Acid 58-67 H3 histone pseudogene 16 Homo sapiens 170-173 10817929-7 2000 However, very soon after a brief exposure of the cells to glutamate, the expression of both proteins was dramatically enhanced.On these bases, we propose NF-kappaB, p53, p21 and MSH2 as relevant contributors of the glutamate-induced pro-apoptotic pathway. Glutamic Acid 215-224 H3 histone pseudogene 16 Homo sapiens 170-173 10911952-9 2000 By inducing premature senescence with a pulse treatment of H2O2, we can study the role of the cell cycle checkpoint proteins p53, p21, p16 and Rb in gaining each feature of senescence. Hydrogen Peroxide 59-63 H3 histone pseudogene 16 Homo sapiens 130-133 11197019-6 2000 In contrast, clear, orange Ca4GeN4 with fully oxidized germanium contains isolated GeN4(8-) tetrahedra and is monoclinic P2(1)/c (no. ca4gen4 27-34 H3 histone pseudogene 16 Homo sapiens 121-128 11197020-10 2000 The crystal of 4 (C36H49B2N12TeSm.C7H8) was monoclinic, P2(1)/c, a = 18.7440(10) A, b = 10.3892(6) A, c = 23.8351(13) A, beta = 94.854(2) degrees, Z = 4. c7h8 34-38 H3 histone pseudogene 16 Homo sapiens 56-63 10837373-0 2000 Polycyclic aromatic hydrocarbon carcinogens increase ubiquitination of p21 protein after the stabilization of p53 and the expression of p21. Polycyclic Aromatic Hydrocarbons 0-31 H3 histone pseudogene 16 Homo sapiens 71-74 10837373-0 2000 Polycyclic aromatic hydrocarbon carcinogens increase ubiquitination of p21 protein after the stabilization of p53 and the expression of p21. Polycyclic Aromatic Hydrocarbons 0-31 H3 histone pseudogene 16 Homo sapiens 136-139 10837373-8 2000 With the addition of MG-132, a proteasome inhibitor, to B[a]P or 1-NP treatments, both p21 and p53 protein levels were increased; however, the increase in p21 protein levels was significantly larger than the increase in p53 protein levels. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 21-27 H3 histone pseudogene 16 Homo sapiens 87-90 10837373-8 2000 With the addition of MG-132, a proteasome inhibitor, to B[a]P or 1-NP treatments, both p21 and p53 protein levels were increased; however, the increase in p21 protein levels was significantly larger than the increase in p53 protein levels. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 21-27 H3 histone pseudogene 16 Homo sapiens 155-158 10866325-8 2000 N-Hydroxy-L-arginine (NOHA), a stable intermediate product formed during conversion of L-arginine to NO, inhibited proliferation of the high arginase-expressing MDA-MB-468 cells and induced apoptosis after 48 h. NOHA arrested these cells in the S phase, increased the expression of p21, and reduced spermine content. n-hydroxy-l-arginine 0-20 H3 histone pseudogene 16 Homo sapiens 282-285 10866325-8 2000 N-Hydroxy-L-arginine (NOHA), a stable intermediate product formed during conversion of L-arginine to NO, inhibited proliferation of the high arginase-expressing MDA-MB-468 cells and induced apoptosis after 48 h. NOHA arrested these cells in the S phase, increased the expression of p21, and reduced spermine content. NG-Hydroxy-L-arginine, Monoacetate Salt 22-26 H3 histone pseudogene 16 Homo sapiens 282-285 10866325-8 2000 N-Hydroxy-L-arginine (NOHA), a stable intermediate product formed during conversion of L-arginine to NO, inhibited proliferation of the high arginase-expressing MDA-MB-468 cells and induced apoptosis after 48 h. NOHA arrested these cells in the S phase, increased the expression of p21, and reduced spermine content. Arginine 10-20 H3 histone pseudogene 16 Homo sapiens 282-285 12526531-4 2000 [W(CO)6(FSbF5)][Sb2F11] crystallizes in the monoclinic space group P21 (No. [w(co)6(fsbf5)][sb2f11 0-22 H3 histone pseudogene 16 Homo sapiens 67-70 10850458-0 2000 Arsenic trioxide-mediated growth inhibition in MC/CAR myeloma cells via cell cycle arrest in association with induction of cyclin-dependent kinase inhibitor, p21, and apoptosis. Arsenic Trioxide 0-16 H3 histone pseudogene 16 Homo sapiens 158-161 10850458-6 2000 The mRNA and protein levels of CDKI, p21 were increased by treatment with As2O3, but those of p27 were not. Arsenic Trioxide 74-79 H3 histone pseudogene 16 Homo sapiens 37-40 10850458-7 2000 In addition, As2O3 markedly enhanced the binding of p21 with CDK6, cdc2, cyclin E, and cyclin A compared with untreated control cells. Arsenic Trioxide 13-18 H3 histone pseudogene 16 Homo sapiens 52-55 10850458-12 2000 These results suggest that As2O3 inhibits the proliferation of myeloma cells, especially MC/CAR cells, via cell cycle arrest in association with induction of p21 and apoptosis. Arsenic Trioxide 27-32 H3 histone pseudogene 16 Homo sapiens 158-161 10842159-6 2000 A similar reduction in cellular proliferation and upregulation of p21 expression were achieved with iNOS gene transfer as well as treatment with the NO-donor S-nitroso-N-acetylpenicillamine (SNAP), demonstrating the p53-independent nature of these NO-mediated pathways. S-Nitroso-N-Acetylpenicillamine 158-189 H3 histone pseudogene 16 Homo sapiens 66-69 10842159-7 2000 The transfer of the iNOS gene activated the p42/44 MAPK, and inhibition of this MAPK pathway with PD98059 partially blocked the antiproliferative effects of NO and completely inhibited the p21 stimulatory effects of NO. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 98-105 H3 histone pseudogene 16 Homo sapiens 189-192 10842159-10 2000 CONCLUSION: Nitric oxide inhibits VSMC proliferation in association with the upregulation of p21; both occur independent of p53 and cGMP while being partially mediated through the p42/44 MAPK signaling cascade. Nitric Oxide 12-24 H3 histone pseudogene 16 Homo sapiens 93-96 10842159-10 2000 CONCLUSION: Nitric oxide inhibits VSMC proliferation in association with the upregulation of p21; both occur independent of p53 and cGMP while being partially mediated through the p42/44 MAPK signaling cascade. vsmc 34-38 H3 histone pseudogene 16 Homo sapiens 93-96 10837517-7 2000 The most abundant variants in coding sequence of p21 gene were a C to A transversion at codon 31 which resulted in Ser to Arg and had been identified being polymorphism. Serine 115-118 H3 histone pseudogene 16 Homo sapiens 49-52 10837517-7 2000 The most abundant variants in coding sequence of p21 gene were a C to A transversion at codon 31 which resulted in Ser to Arg and had been identified being polymorphism. Arginine 122-125 H3 histone pseudogene 16 Homo sapiens 49-52 10817508-5 2000 In addition, p21 mRNA was regulated by irradiation and dexamethasone in accordance with the observed changes in p53. Dexamethasone 55-68 H3 histone pseudogene 16 Homo sapiens 13-16 10929428-15 2000 Although RA at the concentration of 10(-6) mmol/l caused lower p21 expression, Ni(RA)2.3H2O did not affect p21 expression in EJ cells. Tretinoin 9-11 H3 histone pseudogene 16 Homo sapiens 63-66 10785598-4 2000 Exposure to 5-FU (50 and 100 microM) and ZD1694 (50 and 100 nM) for 24 and 48 h induced p53 and p21 expression in wt p53 cells, but not in mt p53 cells. Fluorouracil 12-16 H3 histone pseudogene 16 Homo sapiens 96-99 10771089-0 2000 Phosphatidylinositol 3-kinase inhibitors, Wortmannin or LY294002, inhibited accumulation of p21 protein after gamma-irradiation by stabilization of the protein. Wortmannin 42-52 H3 histone pseudogene 16 Homo sapiens 92-95 11042529-9 2000 In conclusion, As(2) O(3) might become a new therapeutic tool in the treatment of ATL as As(2) O(3) induces apoptosis by destruction of the bcl-2 protein and enhancement of the bak protein production proceeding to activate caspases, and also induces G(1) phase accumulation by enhancement of p53, Cip1/p21, Kip1/p27 and dephosphorylation of pRb to HTLV-I infected T-cell lines. (2) o(3) 17-25 H3 histone pseudogene 16 Homo sapiens 302-305 10771089-9 2000 Accumulation of p21 protein by gamma-irradiation was similar to that of DNA-PK intact cells and was reduced by Wortmannin or LY294002 pretreatment. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 125-133 H3 histone pseudogene 16 Homo sapiens 16-19 10771089-11 2000 ATM deficient cells induced p21 after gamma-irradiation, gamma-irradiation-induced p21 protein was diminished by pretreatment of cells with Wortmannin or LY294002. Wortmannin 140-150 H3 histone pseudogene 16 Homo sapiens 28-31 10771089-11 2000 ATM deficient cells induced p21 after gamma-irradiation, gamma-irradiation-induced p21 protein was diminished by pretreatment of cells with Wortmannin or LY294002. Wortmannin 140-150 H3 histone pseudogene 16 Homo sapiens 83-86 10771089-11 2000 ATM deficient cells induced p21 after gamma-irradiation, gamma-irradiation-induced p21 protein was diminished by pretreatment of cells with Wortmannin or LY294002. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 154-162 H3 histone pseudogene 16 Homo sapiens 83-86 10771089-12 2000 We conclude that the p21 stabilization mechanism functions after gamma-irradiation, was sensitive to Wortmannin or LY294002, and required neither DNA-PK nor ATM gene product for activity. Wortmannin 101-111 H3 histone pseudogene 16 Homo sapiens 21-24 10771089-12 2000 We conclude that the p21 stabilization mechanism functions after gamma-irradiation, was sensitive to Wortmannin or LY294002, and required neither DNA-PK nor ATM gene product for activity. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 115-123 H3 histone pseudogene 16 Homo sapiens 21-24 10771089-0 2000 Phosphatidylinositol 3-kinase inhibitors, Wortmannin or LY294002, inhibited accumulation of p21 protein after gamma-irradiation by stabilization of the protein. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 56-64 H3 histone pseudogene 16 Homo sapiens 92-95 10771089-5 2000 Enhanced p21 protein expression in ML-1 cells resulting from 15 Gy gamma-irradiation was diminished by Wortmannin or LY294002 pretreatment of cells. Wortmannin 103-113 H3 histone pseudogene 16 Homo sapiens 9-12 10771089-5 2000 Enhanced p21 protein expression in ML-1 cells resulting from 15 Gy gamma-irradiation was diminished by Wortmannin or LY294002 pretreatment of cells. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 117-125 H3 histone pseudogene 16 Homo sapiens 9-12 10771089-9 2000 Accumulation of p21 protein by gamma-irradiation was similar to that of DNA-PK intact cells and was reduced by Wortmannin or LY294002 pretreatment. Wortmannin 111-121 H3 histone pseudogene 16 Homo sapiens 16-19 10713676-0 2000 Survivin initiates procaspase 3/p21 complex formation as a result of interaction with Cdk4 to resist Fas-mediated cell death. ammonium ferrous sulfate 101-104 H3 histone pseudogene 16 Homo sapiens 32-35 12526456-3 2000 [Mn4O2(O2CPh)6(py)(dbm)2] (8): monoclinic, P2(1)/c, a = 14.743(6) A, b = 15.536(8) A, c = 30.006(13) A, beta = 102.79(1) degrees, V = 6702 A3, Z = 4, T = -155 degrees C, R (Rw) = 4.32 (4.44)%. [mn4o2(o2cph)6(py)(dbm)2 0-24 H3 histone pseudogene 16 Homo sapiens 43-50 10716680-0 2000 Butyrate and trichostatin A effects on the proliferation/differentiation of human intestinal epithelial cells: induction of cyclin D3 and p21 expression. Butyrates 0-8 H3 histone pseudogene 16 Homo sapiens 138-141 10716680-0 2000 Butyrate and trichostatin A effects on the proliferation/differentiation of human intestinal epithelial cells: induction of cyclin D3 and p21 expression. trichostatin A 13-27 H3 histone pseudogene 16 Homo sapiens 138-141 10716680-12 2000 Butyrate and trichostatin A stimulated p21 expression both at the mRNA and protein levels, whereas their effects on the expression of cyclin dependent kinases were slightly different. Butyrates 0-8 H3 histone pseudogene 16 Homo sapiens 39-42 10716680-12 2000 Butyrate and trichostatin A stimulated p21 expression both at the mRNA and protein levels, whereas their effects on the expression of cyclin dependent kinases were slightly different. trichostatin A 13-27 H3 histone pseudogene 16 Homo sapiens 39-42 10762058-7 2000 These results suggest that cisplatin induced p53 protein phosphorylation and may activate the downstream of p53 gene expression such as p21 and Bax. Cisplatin 27-36 H3 histone pseudogene 16 Homo sapiens 136-139 11272564-4 2000 The complex [Rh(NBD)(PePy2)]PF6.Cl2CH2 crystallizes in the monoclinic space group P21/n with a = 8.455(1) A, b = 18.068(3) A, c = 19.729(3) A, beta = 99.658(3)degrees, and Z = 4. [rh(nbd)(pepy2)]pf6.cl2ch2 12-38 H3 histone pseudogene 16 Homo sapiens 82-85 10831277-0 2000 Inhibition of Ras p21 synthesis by antisense undecamers with uniform and specifically arranged phosphorothioate linkages. Parathion 95-111 H3 histone pseudogene 16 Homo sapiens 18-21 10831277-5 2000 Both the antisense PPS and PS undecamers produced well-defined inhibition of Ras p21 synthesis in both cell-free and cell-based assays. Pentosan Sulfuric Polyester 19-22 H3 histone pseudogene 16 Homo sapiens 81-84 10831277-5 2000 Both the antisense PPS and PS undecamers produced well-defined inhibition of Ras p21 synthesis in both cell-free and cell-based assays. Parathion 20-22 H3 histone pseudogene 16 Homo sapiens 81-84 10831277-7 2000 In contrast, the antisense PPS undecamer, when delivered to RS485 cells with Lipofectin reagent, inhibits human Ras p21 synthesis by more than 90% at a concentration of 3.2 microM, while the effect of controls with inverted, mismatched or scrambled sequence was minimal (5% or less) on p21 synthesis and RS485 cell growth. Pentosan Sulfuric Polyester 27-30 H3 histone pseudogene 16 Homo sapiens 116-119 10831277-7 2000 In contrast, the antisense PPS undecamer, when delivered to RS485 cells with Lipofectin reagent, inhibits human Ras p21 synthesis by more than 90% at a concentration of 3.2 microM, while the effect of controls with inverted, mismatched or scrambled sequence was minimal (5% or less) on p21 synthesis and RS485 cell growth. Pentosan Sulfuric Polyester 27-30 H3 histone pseudogene 16 Homo sapiens 286-289 10831277-7 2000 In contrast, the antisense PPS undecamer, when delivered to RS485 cells with Lipofectin reagent, inhibits human Ras p21 synthesis by more than 90% at a concentration of 3.2 microM, while the effect of controls with inverted, mismatched or scrambled sequence was minimal (5% or less) on p21 synthesis and RS485 cell growth. 1,2-dielaidoylphosphatidylethanolamine 77-87 H3 histone pseudogene 16 Homo sapiens 116-119 10725091-6 2000 Here we show that anti-ras PPS-C(16) ODN retains the high sequence-specificity of PPS ODNs and provides maximal inhibition of Ras p21 synthesis with minimal toxicity even without the use of a cellular uptake enhancer. pps 27-30 H3 histone pseudogene 16 Homo sapiens 130-133 10725091-6 2000 Here we show that anti-ras PPS-C(16) ODN retains the high sequence-specificity of PPS ODNs and provides maximal inhibition of Ras p21 synthesis with minimal toxicity even without the use of a cellular uptake enhancer. pps 82-85 H3 histone pseudogene 16 Homo sapiens 130-133 10732765-2 2000 Immunoblot analysis of isolated cell membranes and total cellular lysates of COLO320-DM cells demonstrated that manumycin dose-dependently reduced p21 ras farnesylation with a 50% inhibitory concentration (IC50) of 2.51 +/- 0.11 microM and 2.68 +/- 0.20 microM, respectively, while the geranylgeranylation of p21 rhoA and p21rap1 was not affected. manumycin 112-121 H3 histone pseudogene 16 Homo sapiens 147-150 10671549-2 2000 Tumor suppressor protein p53 and cell cycle inhibitor p21 accumulate as an early sign of S-nitrosoglutathione-mediated toxicity. S-Nitrosoglutathione 89-109 H3 histone pseudogene 16 Homo sapiens 54-57 11229577-3 2000 The mercuric chloride complex crystallizes in the monoclinic space group P2(1/c) with unit cell dimensions a = 8.5768(8) A, b = 19.1718(17) A, c = 8.5956(8) A, beta = 90.405 degrees, and V = 1413.4(2) A3. Chlorides 13-21 H3 histone pseudogene 16 Homo sapiens 73-79 11229578-10 2000 Data for crystal I of H3Os6(CO)16B: monoclinic P2(1/n), a = 9.954(2) A, b = 15.780(4) A, c = 16.448(3) A, beta = 91.07(1) degrees, Z = 4. h3os6 22-27 H3 histone pseudogene 16 Homo sapiens 47-53 11229578-11 2000 Data for crystal II of H3Os6(CO)16B: monoclinic P2(1/n), a = 9.927(2) A, beta = 16.623(2) A, b = 16.0233(10) A, beta = 97.78(1) degrees, Z = 4. 16b 32-35 H3 histone pseudogene 16 Homo sapiens 48-54 10732765-2 2000 Immunoblot analysis of isolated cell membranes and total cellular lysates of COLO320-DM cells demonstrated that manumycin dose-dependently reduced p21 ras farnesylation with a 50% inhibitory concentration (IC50) of 2.51 +/- 0.11 microM and 2.68 +/- 0.20 microM, respectively, while the geranylgeranylation of p21 rhoA and p21rap1 was not affected. manumycin 112-121 H3 histone pseudogene 16 Homo sapiens 309-312 10618436-0 2000 Requirement for nitric oxide activation of p21(ras)/extracellular regulated kinase in neuronal ischemic preconditioning. Nitric Oxide 16-28 H3 histone pseudogene 16 Homo sapiens 43-51 10652438-0 2000 Quercetin inhibits p21-RAS expression in human colon cancer cell lines and in primary colorectal tumors. Quercetin 0-9 H3 histone pseudogene 16 Homo sapiens 19-22 10652438-1 2000 Immunocytochemical studies have revealed that 10 microM quercetin reduced the steady state levels of p21-ras proteins in both colon cancer cell lines and primary colorectal tumors. Quercetin 56-65 H3 histone pseudogene 16 Homo sapiens 101-104 10652438-2 2000 These findings were confirmed by Western blot and flow cytometric analysis showing that the inhibition of p21-ras expression by quercetin was time- and concentration-dependent. Quercetin 128-137 H3 histone pseudogene 16 Homo sapiens 106-109 10652438-3 2000 Twenty-four-hour treatment with 10 microM quercetin reduced p21-ras levels to about 50% of control values. Quercetin 42-51 H3 histone pseudogene 16 Homo sapiens 60-63 10683383-8 2000 Therefore, (a) p53-dependent p21 induction caused by doxorubicin protects from microtubule drug-induced cytotoxicity, and (b) pretreatment with cytostatic doses of DNA-damaging drugs before treatment with microtubule drugs results in selective cytotoxicity to cancer cells with defective p53/p21-dependent checkpoint. Doxorubicin 53-64 H3 histone pseudogene 16 Homo sapiens 29-32 10735543-1 2000 BACKGROUND: Previous in vitro experiments have indicated that if the ninth codon of the hepatitis C virus (HCV) core gene is mutated from arginine to lysine, a short 16-kDa (P16) instead of a 21-kDa (P21) core protein will be produced. Arginine 138-146 H3 histone pseudogene 16 Homo sapiens 200-203 10735543-1 2000 BACKGROUND: Previous in vitro experiments have indicated that if the ninth codon of the hepatitis C virus (HCV) core gene is mutated from arginine to lysine, a short 16-kDa (P16) instead of a 21-kDa (P21) core protein will be produced. Lysine 150-156 H3 histone pseudogene 16 Homo sapiens 200-203 10661494-9 2000 Pearce, R. Levi, A. Novogrodsky, Nitric oxide-stimulated guanine nucleotide exchange on p21 ras, J. Biol. Nitric Oxide 33-45 H3 histone pseudogene 16 Homo sapiens 88-91 10661494-9 2000 Pearce, R. Levi, A. Novogrodsky, Nitric oxide-stimulated guanine nucleotide exchange on p21 ras, J. Biol. Guanine Nucleotides 57-75 H3 histone pseudogene 16 Homo sapiens 88-91 10618436-3 2000 We report here that OGD preconditioning induces p21(ras) (Ras) activation in an N-methyl-D-aspartate receptor- and NO-dependent, but cGMP-independent, manner. Cyclic GMP 133-137 H3 histone pseudogene 16 Homo sapiens 48-56 10618436-3 2000 We report here that OGD preconditioning induces p21(ras) (Ras) activation in an N-methyl-D-aspartate receptor- and NO-dependent, but cGMP-independent, manner. Cyclic GMP 133-137 H3 histone pseudogene 16 Homo sapiens 58-61 10642304-0 2000 Cyclic AMP inhibited proliferation of human aortic vascular smooth muscle cells, accompanied by induction of p53 and p21. Cyclic AMP 0-10 H3 histone pseudogene 16 Homo sapiens 117-120 10874474-0 2000 Induction of p53-independent p21 during ceramide-induced G1 arrest in human hepatocarcinoma cells. Ceramides 40-48 H3 histone pseudogene 16 Homo sapiens 29-32 10874474-2 2000 In this paper, we investigated whether p21, a cdk (cyclin-dependent kinase) inhibitor, is involved in the induction of pRb dephosphorylation during ceramide-induced G1 arrest. Ceramides 148-156 H3 histone pseudogene 16 Homo sapiens 39-42 10874474-6 2000 p21 induction was also observed in the Hep3B cells lacking a functional p53 after exposure to ceramide. Ceramides 94-102 H3 histone pseudogene 16 Homo sapiens 0-3 10874474-7 2000 Although p21 is induced in ceramide-treated Hep3B cells, Hep3B cells do not induce G1 arrest, because Hep3B cells are deficient in a functional pRb protein. Ceramides 27-35 H3 histone pseudogene 16 Homo sapiens 9-12 10874474-10 2000 In pRb+/+ cells, ceramide-mediated G1 arrest was accompanied by the accumulation of hypophosphorylated pRb and p21 associated with cdk2. Ceramides 17-25 H3 histone pseudogene 16 Homo sapiens 111-114 10874474-11 2000 Together, these results suggest that p21, induced through p53-independent pathway, participates in the induction of pRb dephosphorylation by inhibiting cdk2 activity during ceramide-mediated G1 arrest in hepatocarcinoma cells. Ceramides 173-181 H3 histone pseudogene 16 Homo sapiens 37-40 10642304-6 2000 Upregulation of p53 protein by cAMP was further confirmed by the observation that the decrease in p21, a p53-inducible protein, by PDGF was significantly attenuated by cilostazol in a dose-dependent manner (P<0.01). Cyclic AMP 31-35 H3 histone pseudogene 16 Homo sapiens 98-101 10642304-6 2000 Upregulation of p53 protein by cAMP was further confirmed by the observation that the decrease in p21, a p53-inducible protein, by PDGF was significantly attenuated by cilostazol in a dose-dependent manner (P<0.01). Cilostazol 168-178 H3 histone pseudogene 16 Homo sapiens 98-101 10642304-7 2000 These results revealed that accumulation of cAMP inhibited VSMC proliferation, which was at least in part due to an increase in p53-p21 expression. Cyclic AMP 44-48 H3 histone pseudogene 16 Homo sapiens 132-135 10642304-7 2000 These results revealed that accumulation of cAMP inhibited VSMC proliferation, which was at least in part due to an increase in p53-p21 expression. vsmc 59-63 H3 histone pseudogene 16 Homo sapiens 132-135 10642304-11 2000 Overall, these results demonstrated that cAMP inhibited the proliferation of human aortic VSMCs, accompanied by p53-p21-mediated apoptosis. Cyclic AMP 41-45 H3 histone pseudogene 16 Homo sapiens 116-119 10905503-9 2000 However, there was an additive effect on the expression of p21 when cells were exposed to CH and CSS simultaneously for 24 hours. thiocysteine 97-100 H3 histone pseudogene 16 Homo sapiens 59-62 11196807-3 2000 Crystals of trenphen.H2O.CH3CN, 1, are monoclinic, space group P2(1)/n, a = 14.9923(8) A, b = 17.4451(10) A, c = 17.1880(10) A, beta = 114.8290(10) degrees, V = 4079.9(4) A3, Z = 4. trenphen 12-20 H3 histone pseudogene 16 Homo sapiens 63-68 11196807-3 2000 Crystals of trenphen.H2O.CH3CN, 1, are monoclinic, space group P2(1)/n, a = 14.9923(8) A, b = 17.4451(10) A, c = 17.1880(10) A, beta = 114.8290(10) degrees, V = 4079.9(4) A3, Z = 4. Water 21-24 H3 histone pseudogene 16 Homo sapiens 63-68 10905503-10 2000 When cells were exposed to CH and CSS simultaneously three times (24 hours each time), then passaged for 1 month, the expression of p21 increased synergistically. thiocysteine 34-37 H3 histone pseudogene 16 Homo sapiens 132-135 11341037-6 2000 Methionine restriction led to accumulation of the cyclin-dependent kinase inhibitors p21 and p27, as determined by Western blot analysis, and inhibited the enzymatic activities of the cyclin-dependent kinases CDK2 and cdc2, as determined by an in vitro kinase assay: However, methionine restriction had little or no effect on CDK2 or cdc2 protein levels. Methionine 0-10 H3 histone pseudogene 16 Homo sapiens 85-88 10672584-6 2000 At P21, the cells are severely damaged and further intracellular changes include a decrease in N-acetylaspartate (NAA) and loss of amino acids and many organic osmolytes. N-acetylaspartate 95-112 H3 histone pseudogene 16 Homo sapiens 3-6 10672584-6 2000 At P21, the cells are severely damaged and further intracellular changes include a decrease in N-acetylaspartate (NAA) and loss of amino acids and many organic osmolytes. N-acetylaspartate 114-117 H3 histone pseudogene 16 Homo sapiens 3-6 10585263-0 1999 p21 promotes ceramide-induced apoptosis and antagonizes the antideath effect of Bcl-2 in human hepatocarcinoma cells. Ceramides 13-21 H3 histone pseudogene 16 Homo sapiens 0-3 10585263-3 1999 Previously, we reported that p21 was induced in a p53-independent manner during ceramide-induced apoptosis in human hepatocarcinoma cell lines. Ceramides 80-88 H3 histone pseudogene 16 Homo sapiens 29-32 10585263-4 1999 In the present study, we investigated the precise role of p21 in ceramide-induced apoptosis in human hepatocarcinoma cells by using a tetracycline-inducible expression system. Ceramides 65-73 H3 histone pseudogene 16 Homo sapiens 58-61 10585263-6 1999 However, Hep3B/p21 cells were more sensitive to ceramide-induced apoptosis. Ceramides 48-56 H3 histone pseudogene 16 Homo sapiens 15-18 10585263-8 1999 The expression level of Bax was increased in Hep3B/p21 cells treated with ceramide and its expression was more accelerated under the p21-overexpressed condition compared to that of the p21-repressed condition. Ceramides 74-82 H3 histone pseudogene 16 Homo sapiens 51-54 10585263-8 1999 The expression level of Bax was increased in Hep3B/p21 cells treated with ceramide and its expression was more accelerated under the p21-overexpressed condition compared to that of the p21-repressed condition. Ceramides 74-82 H3 histone pseudogene 16 Homo sapiens 133-136 10641285-1 1999 The title aldehyde, C15H14O3, crystallized in the centrosymmetric space group P2(1)/c with one molecule in the asymmetric unit. Aldehydes 10-18 H3 histone pseudogene 16 Homo sapiens 78-83 10585263-8 1999 The expression level of Bax was increased in Hep3B/p21 cells treated with ceramide and its expression was more accelerated under the p21-overexpressed condition compared to that of the p21-repressed condition. Ceramides 74-82 H3 histone pseudogene 16 Homo sapiens 133-136 10585263-10 1999 On the other hand, the levels of p21 and Bax protein were increased by ceramide in another hepatocarcinoma cell line, SK-Hep-1, while the Bcl-2 protein level was not changed. Ceramides 71-79 H3 histone pseudogene 16 Homo sapiens 33-36 10641285-1 1999 The title aldehyde, C15H14O3, crystallized in the centrosymmetric space group P2(1)/c with one molecule in the asymmetric unit. c15h14o3 20-28 H3 histone pseudogene 16 Homo sapiens 78-83 10585263-11 1999 Overexpression of Bcl-2 not only suppressed apoptosis but also completely prevented induction of p21 and Bax caused by ceramide in SK-Hep-1 cells. Ceramides 119-127 H3 histone pseudogene 16 Homo sapiens 97-100 10585263-13 1999 These results suggest that p21 promotes ceramide-induced apoptosis by enhancing the expression of Bax, thereby modulating the molecular ratio of Bcl-2:Bax in human hepatocarcinoma cells. Ceramides 40-48 H3 histone pseudogene 16 Homo sapiens 27-30 10585203-3 1999 We have demonstrated that the natural product cerulenin ([2R,3S]-2,3-epoxy-4-oxo-7,10-trans,trans-dodecadienamide) inhibits the palmitoylation of H-ras- and N-ras-encoded p21s in parallel with inhibition of cell proliferation. Cerulenin 46-55 H3 histone pseudogene 16 Homo sapiens 171-174 10585464-9 1999 cis-Diamminedichloroplatinum (II) (CDDP) induced p53 activation and p21 transactivation. Cisplatin 0-33 H3 histone pseudogene 16 Homo sapiens 68-71 10585464-9 1999 cis-Diamminedichloroplatinum (II) (CDDP) induced p53 activation and p21 transactivation. Cisplatin 35-39 H3 histone pseudogene 16 Homo sapiens 68-71 10585464-10 1999 The p53-dependent p21 transactivation induced by CDDP was inhibited by mTRX overexpression, suggesting that TRX-dependent redox regulation is physiologically involved in p53 regulation. Cisplatin 49-53 H3 histone pseudogene 16 Homo sapiens 18-21 10585203-3 1999 We have demonstrated that the natural product cerulenin ([2R,3S]-2,3-epoxy-4-oxo-7,10-trans,trans-dodecadienamide) inhibits the palmitoylation of H-ras- and N-ras-encoded p21s in parallel with inhibition of cell proliferation. [2r,3s]-2,3-epoxy-4-oxo-7,10-trans,trans-dodecadienamide 57-113 H3 histone pseudogene 16 Homo sapiens 171-174 10585203-6 1999 Several compounds inhibited the incorporation of [(3)H]palmitate into p21 in intact T24 cells, with the unsubstituted carboxamides being more active than N,N-dimethyl compounds. [(3)h]palmitate 49-64 H3 histone pseudogene 16 Homo sapiens 70-73 10585203-6 1999 Several compounds inhibited the incorporation of [(3)H]palmitate into p21 in intact T24 cells, with the unsubstituted carboxamides being more active than N,N-dimethyl compounds. carboxamides 118-130 H3 histone pseudogene 16 Homo sapiens 70-73 10927436-2 1999 Single-crystal X-ray diffraction (performed at room temperature) revealed Cs(2)(HSO(4))(H(2)PO(4)) to crystallize in space group P2(1)/n with lattice parameters a = 7.856 (8), b = 7.732 (7), c = 7.827 (7) A, and beta = 99.92 (4) degrees. Cesium 74-76 H3 histone pseudogene 16 Homo sapiens 129-134 10585950-2 1999 Lys(16) was demonstrated to be crucial to the function of Ras p21, and the hydrolysis of GTP to GDP was found to be an one-step reaction. Lysine 0-3 H3 histone pseudogene 16 Homo sapiens 62-65 10585950-2 1999 Lys(16) was demonstrated to be crucial to the function of Ras p21, and the hydrolysis of GTP to GDP was found to be an one-step reaction. Guanosine Triphosphate 89-92 H3 histone pseudogene 16 Homo sapiens 62-65 10585950-0 1999 Ab initio study of the role of lysine 16 for the molecular switching mechanism of Ras protein p21. Lysine 31-37 H3 histone pseudogene 16 Homo sapiens 94-97 10585950-2 1999 Lys(16) was demonstrated to be crucial to the function of Ras p21, and the hydrolysis of GTP to GDP was found to be an one-step reaction. Guanosine Diphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 62-65 10604659-0 1999 Proliferation arrest and induction of CDK inhibitors p21 and p27 by depleting the calcium store in cultured C6 glioma cells. Calcium 82-89 H3 histone pseudogene 16 Homo sapiens 53-56 10661763-4 1999 In this model, TAM resistance resulted in an increase in the detectable basal levels of cyclin E, GADD 153, p16, BAX, Bcl-XL, and wild-type and mutant p53, an increase in TAM induction of p16, and a decrease in the detectable basal levels of cyclin D1, p21 and p27. Tamoxifen 15-18 H3 histone pseudogene 16 Homo sapiens 253-256 10661763-6 1999 In the TAM-resistant variant, p21 levels were essentially undetectable, while p27 was present and maintained its response to TAM Induction, albeit at a much lower level. Tamoxifen 7-10 H3 histone pseudogene 16 Homo sapiens 30-33 10574788-0 1999 The pre-hydrolysis state of p21(ras) in complex with GTP: new insights into the role of water molecules in the GTP hydrolysis reaction of ras-like proteins. Guanosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 28-31 10574788-0 1999 The pre-hydrolysis state of p21(ras) in complex with GTP: new insights into the role of water molecules in the GTP hydrolysis reaction of ras-like proteins. Water 88-93 H3 histone pseudogene 16 Homo sapiens 28-31 10574788-0 1999 The pre-hydrolysis state of p21(ras) in complex with GTP: new insights into the role of water molecules in the GTP hydrolysis reaction of ras-like proteins. Guanosine Triphosphate 111-114 H3 histone pseudogene 16 Homo sapiens 28-31 10574788-5 1999 RESULTS: The structure of the complex formed between p21(ras) and GTP has been determined by X-ray diffraction at 1.6 A using a combination of photolysis of an inactive GTP precursor (caged GTP) and rapid freezing (100K). Guanosine Triphosphate 66-69 H3 histone pseudogene 16 Homo sapiens 53-56 10574788-5 1999 RESULTS: The structure of the complex formed between p21(ras) and GTP has been determined by X-ray diffraction at 1.6 A using a combination of photolysis of an inactive GTP precursor (caged GTP) and rapid freezing (100K). Guanosine Triphosphate 169-172 H3 histone pseudogene 16 Homo sapiens 53-56 10574788-5 1999 RESULTS: The structure of the complex formed between p21(ras) and GTP has been determined by X-ray diffraction at 1.6 A using a combination of photolysis of an inactive GTP precursor (caged GTP) and rapid freezing (100K). Guanosine Triphosphate 169-172 H3 histone pseudogene 16 Homo sapiens 53-56 10574788-6 1999 The structure of this complex differs from that of p21(ras)-GppNHp (determined at 277K) with respect to the degree of order and conformation of the catalytic loop (loop 4 of the switch II region) and the positioning of water molecules around the gamma-phosphate group. Water 219-224 H3 histone pseudogene 16 Homo sapiens 51-54 10574788-6 1999 The structure of this complex differs from that of p21(ras)-GppNHp (determined at 277K) with respect to the degree of order and conformation of the catalytic loop (loop 4 of the switch II region) and the positioning of water molecules around the gamma-phosphate group. Phosphates 252-261 H3 histone pseudogene 16 Homo sapiens 51-54 10551809-1 1999 p21-activated kinases (Pak)/Ste20 kinases are regulated in vitro and in vivo by the small GTP-binding proteins Rac and Cdc42 and lipids, such as sphingosine, which stimulate autophosphorylation and phosphorylation of exogenous substrates. Guanosine Triphosphate 90-93 H3 histone pseudogene 16 Homo sapiens 0-3 10551809-1 1999 p21-activated kinases (Pak)/Ste20 kinases are regulated in vitro and in vivo by the small GTP-binding proteins Rac and Cdc42 and lipids, such as sphingosine, which stimulate autophosphorylation and phosphorylation of exogenous substrates. Sphingosine 145-156 H3 histone pseudogene 16 Homo sapiens 0-3 10544021-5 1999 Activation of p53 was accompanied by phosphorylation of p53 at Ser-15 and elevated p21 and MDM2, both of which were at least partly blocked by wortmannin, a kinase inhibitor against proteins with a PI3 kinase domain. Wortmannin 143-153 H3 histone pseudogene 16 Homo sapiens 83-86 10706449-7 1999 The ATRA-mediated increase in p21 preceded the change in RB phosphorylation and G1 arrest and was not reversed by the addition of exogenous IL-6. Tretinoin 4-8 H3 histone pseudogene 16 Homo sapiens 30-33 10839623-2 1999 The X-ray crystal structure of the ras oncogene-encoded p21 protein bound to SOS, the guanine nucleotide exchange-promoting protein, has been determined. Guanine Nucleotides 86-104 H3 histone pseudogene 16 Homo sapiens 56-59 10502413-0 1999 The biphasic induction of p21 and p27 in breast cancer cells by modulators of cAMP is posttranscriptionally regulated and independent of the PKA pathway. Cyclic AMP 78-82 H3 histone pseudogene 16 Homo sapiens 26-29 10502413-2 1999 Previous studies linked cAMP-mediated growth arrest in breast tumor cells to increased levels of cyclin kinase inhibitor (CKI), p21. Cyclic AMP 24-28 H3 histone pseudogene 16 Homo sapiens 128-131 10502413-3 1999 In the present study we examined the role of cAMP-dependent protein kinase (PKA) on p21 and p27 induction in the breast cancer cell line, MDA-MB-157. Cyclic AMP 45-49 H3 histone pseudogene 16 Homo sapiens 84-87 10502413-4 1999 The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity. Cyclic AMP 43-47 H3 histone pseudogene 16 Homo sapiens 345-348 10502413-4 1999 The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity. 1-Methyl-3-isobutylxanthine 106-110 H3 histone pseudogene 16 Homo sapiens 345-348 10502413-4 1999 The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity. Lovastatin 116-126 H3 histone pseudogene 16 Homo sapiens 345-348 10502413-7 1999 This analysis revealed that the cAMP activators were capable of inducing p21 even though PKA activity was completely eliminated. Cyclic AMP 32-36 H3 histone pseudogene 16 Homo sapiens 73-76 10502413-8 1999 In the second approach PKA dominant negative stable clones of MDA-MB-157 treated with CT + IBMX or forskolin also resulted in p21 induction, in the absence of any PKA activity. ct + ibmx 86-95 H3 histone pseudogene 16 Homo sapiens 126-129 10502413-8 1999 In the second approach PKA dominant negative stable clones of MDA-MB-157 treated with CT + IBMX or forskolin also resulted in p21 induction, in the absence of any PKA activity. Colforsin 99-108 H3 histone pseudogene 16 Homo sapiens 126-129 10502413-9 1999 Last, treatment of MDA-MB-157 cells with lovastatin, another known cAMP modulator which also causes growth arrest, resulted in the induction of p21 and p27 without any increase in PKA activity. Lovastatin 41-51 H3 histone pseudogene 16 Homo sapiens 144-147 10502413-9 1999 Last, treatment of MDA-MB-157 cells with lovastatin, another known cAMP modulator which also causes growth arrest, resulted in the induction of p21 and p27 without any increase in PKA activity. Cyclic AMP 67-71 H3 histone pseudogene 16 Homo sapiens 144-147 10502413-10 1999 Collectively, the above results suggest that the induction of p21 by cAMP is through a novel pathway, independent of PKA activity. Cyclic AMP 69-73 H3 histone pseudogene 16 Homo sapiens 62-65 10706449-8 1999 The levels of CDK2 activity were inhibited approximately 60% in ATRA-treated cells, suggesting that the increased p21 levels were sufficient to inhibit CDK activity and cause RB hypophosphorylation. Tretinoin 64-68 H3 histone pseudogene 16 Homo sapiens 114-117 10706449-9 1999 Increased levels of p21 have recently been observed in human myeloma cells exposed to dexamethasone, and we suggest that the common ability of these two agents to inhibit myeloma cell growth depends on their induction of p21. Dexamethasone 86-99 H3 histone pseudogene 16 Homo sapiens 20-23 10706449-9 1999 Increased levels of p21 have recently been observed in human myeloma cells exposed to dexamethasone, and we suggest that the common ability of these two agents to inhibit myeloma cell growth depends on their induction of p21. Dexamethasone 86-99 H3 histone pseudogene 16 Homo sapiens 221-224 10706449-7 1999 The ATRA-mediated increase in p21 preceded the change in RB phosphorylation and G1 arrest and was not reversed by the addition of exogenous IL-6. Rubidium 57-59 H3 histone pseudogene 16 Homo sapiens 30-33 10559936-2 1999 Here we show that p21-activated kinase (Pak1) phosphorylates LIM-kinase at threonine residue 508 within LIM-kinase"s activation loop, and increases LIM-kinase-mediated phosphorylation of the actin-regulatory protein cofilin tenfold in vitro. Threonine 75-84 H3 histone pseudogene 16 Homo sapiens 18-21 10480882-6 1999 In accordance with its inhibitory action on protein synthesis, activation of cyclin D1 and p21 proteins by growth factors is also blocked by preincubation with rapamycin. Sirolimus 160-169 H3 histone pseudogene 16 Homo sapiens 91-94 10619494-6 1999 Both Bcl-2 and Bcl-xL were down-regulated by glutamate at 24 h and further at 48 h. The apoptosis-promoting product p21 Bax-alpha was also down-regulated in GB-12 but slightly up-regulated in GB-4, accompanied by generation of variant form of p18 Bax-alpha in both cell lines. Glutamic Acid 45-54 H3 histone pseudogene 16 Homo sapiens 116-119 10619494-6 1999 Both Bcl-2 and Bcl-xL were down-regulated by glutamate at 24 h and further at 48 h. The apoptosis-promoting product p21 Bax-alpha was also down-regulated in GB-12 but slightly up-regulated in GB-4, accompanied by generation of variant form of p18 Bax-alpha in both cell lines. gb-12 157-162 H3 histone pseudogene 16 Homo sapiens 116-119 10619494-6 1999 Both Bcl-2 and Bcl-xL were down-regulated by glutamate at 24 h and further at 48 h. The apoptosis-promoting product p21 Bax-alpha was also down-regulated in GB-12 but slightly up-regulated in GB-4, accompanied by generation of variant form of p18 Bax-alpha in both cell lines. GB-4 192-196 H3 histone pseudogene 16 Homo sapiens 116-119 12541388-2 1999 METHOD: The SP immunohistochemical method was used to detect the expression of p16, p21 and p53 protein in 116 cases of NPC and 15 cases of non-tumour nasopharyngeal tissue. TFF2 protein, human 12-14 H3 histone pseudogene 16 Homo sapiens 84-87 10460485-5 1999 Retinoic acid (RA) treatment will drive these cells to differentiation toward the neuronal lineage and cause an increase in expression of the cyclin-dependent kinase inhibitor p21 protein, which leads to an inhibition in cellular proliferation. Tretinoin 0-13 H3 histone pseudogene 16 Homo sapiens 176-179 10460485-5 1999 Retinoic acid (RA) treatment will drive these cells to differentiation toward the neuronal lineage and cause an increase in expression of the cyclin-dependent kinase inhibitor p21 protein, which leads to an inhibition in cellular proliferation. Tretinoin 15-17 H3 histone pseudogene 16 Homo sapiens 176-179 11671061-16 1999 VO(alpha-D-HMe(3)MP)(L-psal).H(2)O: chemical formula, C(25)H(32)NO(11)V; crystal system, monoclinic; space group, P2(1); a = 13.645(4) A, b = 7.022(2) A, c = 15.500(4) A; beta = 113.98(2) degrees; Z = 2. Vanadium(II) oxide 0-2 H3 histone pseudogene 16 Homo sapiens 114-119 10428811-0 1999 A tyrosine-phosphorylated protein that binds to an important regulatory region on the cool family of p21-activated kinase-binding proteins. Tyrosine 2-10 H3 histone pseudogene 16 Homo sapiens 101-104 10543370-6 1999 Although phorbol 12-myristate 13-acetate strongly induced p21 and stabilised p53 in the resting transfected Jurkat cells, neither apoptosis nor cell arrest was observed. Tetradecanoylphorbol Acetate 9-40 H3 histone pseudogene 16 Homo sapiens 58-61 10493587-1 1999 Kinetics of binding of beryllium trifluoride to V29G and I36G mutants of Ha-ras-p21. beryllium trifluoride 23-44 H3 histone pseudogene 16 Homo sapiens 80-83 10417423-4 1999 Selenomethionine-containing crystals have been grown in both forms, and anomalous data from the P2(1) selenomethionine enzyme provided the location of 17 of the 19 Se atoms in the protein. Selenomethionine 102-118 H3 histone pseudogene 16 Homo sapiens 96-101 10424768-6 1999 FUra exposure resulted in transient induction of p53 and p21, which returned to basal levels 24 hr after drug removal. Fluorouracil 0-4 H3 histone pseudogene 16 Homo sapiens 57-60 10424768-7 1999 p53 and p21 protein content also increased markedly during paclitaxel exposure, accompanied by phosphorylation of Bcl-2. Paclitaxel 59-69 H3 histone pseudogene 16 Homo sapiens 8-11 10444820-1 1999 The title acid, C10H12O2S, crystallized in the centrosymmetric space group P2(1)/c with one molecule in the asymmetric unit. Ethyl (phenylthio)acetate 16-25 H3 histone pseudogene 16 Homo sapiens 75-80 10348819-10 1999 Nocodazole treatment of constitutive IGF-II-expressing cells stimulated p21 expression in the presence of hyperphosphorylated pRb. Nocodazole 0-10 H3 histone pseudogene 16 Homo sapiens 72-75 10408088-1 1999 The title substance, C12H6O3, crystallized in the centrosymmetric space group P2(1)/c with one molecule in the asymmetric unit. c12h6o3 21-28 H3 histone pseudogene 16 Homo sapiens 78-83 10399961-4 1999 We show that p21 ras processing is blocked by lovastatin, suggesting that inhibition of isoprenylation may be important in lovastatin-induced apoptosis. Lovastatin 46-56 H3 histone pseudogene 16 Homo sapiens 13-16 10399961-4 1999 We show that p21 ras processing is blocked by lovastatin, suggesting that inhibition of isoprenylation may be important in lovastatin-induced apoptosis. Lovastatin 123-133 H3 histone pseudogene 16 Homo sapiens 13-16 10494844-5 1999 Using caged GTP the intrinsic and GAP catalyzed GTPase activity of H-ras p21 is studied. Guanosine Triphosphate 12-15 H3 histone pseudogene 16 Homo sapiens 73-76 10321832-6 1999 E2 prevented down-regulation of p21 and Bcl-2 induced by taxol but did not prevent the down-regulation of p21 induced by etoposide, consistent with the failure of E2 to inhibit etoposide-induced cell death. Paclitaxel 57-62 H3 histone pseudogene 16 Homo sapiens 32-35 10321832-7 1999 However, ECM prevented p21 and Bcl-2 down-regulation induced by taxol or etoposide. Paclitaxel 64-69 H3 histone pseudogene 16 Homo sapiens 23-26 10336521-3 1999 BA-induced apoptosis requires new protein, but not RNA, synthesis, is independent of p53, and results in p21 protein accumulation in the absence of a cell cycle arrest. betulinic acid 0-2 H3 histone pseudogene 16 Homo sapiens 105-108 10321832-7 1999 However, ECM prevented p21 and Bcl-2 down-regulation induced by taxol or etoposide. Etoposide 73-82 H3 histone pseudogene 16 Homo sapiens 23-26 10469393-8 1999 The number of p21-positive H & RS cells was significantly related with that of the p53-positive cells. Adenosine Monophosphate 30-33 H3 histone pseudogene 16 Homo sapiens 14-17 10342319-0 1999 Cyclosporine induces the expression of the cyclin inhibitor p21. Cyclosporine 0-12 H3 histone pseudogene 16 Homo sapiens 60-63 10342319-3 1999 In this study, we examined whether cyclosporine A (CsA) suppresses the cell cycle progression through the induction of the cell cycle inhibitor p21. Cyclosporine 35-49 H3 histone pseudogene 16 Homo sapiens 144-147 10342319-3 1999 In this study, we examined whether cyclosporine A (CsA) suppresses the cell cycle progression through the induction of the cell cycle inhibitor p21. Cyclosporine 51-54 H3 histone pseudogene 16 Homo sapiens 144-147 10360653-7 1999 p21 expression is induced by boswellic acids via a p53-independent pathway. boswellic acid 29-44 H3 histone pseudogene 16 Homo sapiens 0-3 10342319-7 1999 The dependence of CsA"s induction of p21 was studied using anti-TGF-beta antibody and TGF-beta altered A-549 cells. Cyclosporine 18-21 H3 histone pseudogene 16 Homo sapiens 37-40 10342319-8 1999 RESULTS: CsA induced p21 mRNA protein expression and stimulated its promoter activity in lymphoid (T cells) and nonlymphoid (human lung adenocarcinoma, A-549 cells).CsA"s induction of p21 was inhibited both by a neutralizing anti-TGF-beta antibody and in TGF-beta-altered A-549 cells, consistent with its effects on p21 requiring TGF-beta. Cyclosporine 9-12 H3 histone pseudogene 16 Homo sapiens 21-24 10342319-8 1999 RESULTS: CsA induced p21 mRNA protein expression and stimulated its promoter activity in lymphoid (T cells) and nonlymphoid (human lung adenocarcinoma, A-549 cells).CsA"s induction of p21 was inhibited both by a neutralizing anti-TGF-beta antibody and in TGF-beta-altered A-549 cells, consistent with its effects on p21 requiring TGF-beta. Cyclosporine 9-12 H3 histone pseudogene 16 Homo sapiens 184-187 10342319-8 1999 RESULTS: CsA induced p21 mRNA protein expression and stimulated its promoter activity in lymphoid (T cells) and nonlymphoid (human lung adenocarcinoma, A-549 cells).CsA"s induction of p21 was inhibited both by a neutralizing anti-TGF-beta antibody and in TGF-beta-altered A-549 cells, consistent with its effects on p21 requiring TGF-beta. Cyclosporine 9-12 H3 histone pseudogene 16 Homo sapiens 184-187 10212255-0 1999 A novel pathway for tumor necrosis factor-alpha and ceramide signaling involving sequential activation of tyrosine kinase, p21(ras), and phosphatidylinositol 3-kinase. Ceramides 52-60 H3 histone pseudogene 16 Homo sapiens 123-126 10207107-0 1999 Mitochondrial regulation of cell death: mitochondria are essential for procaspase 3-p21 complex formation to resist Fas-mediated cell death. ammonium ferrous sulfate 116-119 H3 histone pseudogene 16 Homo sapiens 84-87 10207107-2 1999 Recently, we reported that the cell cycle regulator p21 interacts with procaspase 3 to resist Fas-mediated cell death. ammonium ferrous sulfate 94-97 H3 histone pseudogene 16 Homo sapiens 52-55 10227127-1 1999 A racemic mixture of the title compound, C12H15NO3, crystallizes in the chiral, monoclinic space group P2(1), with one enantiomerically related pair of molecules per asymmetric unit. Carbofuran 41-50 H3 histone pseudogene 16 Homo sapiens 103-108 10087060-6 1999 Estrogen produces a rapid, transient activation of src-family tyrosine kinases and tyrosine phosphorylation of p21(ras)-guanine nucleotide activating protein. Guanine Nucleotides 120-138 H3 histone pseudogene 16 Homo sapiens 111-114 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Histamine 254-263 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Potassium Chloride 281-284 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Carbachol 0-9 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Guanosine Triphosphate 37-40 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Phosphorus-32 105-108 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Guanosine Triphosphate 109-112 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Phosphorus-32 118-121 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Guanosine Triphosphate 109-112 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Phosphorus-32 118-121 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Guanosine Diphosphate 133-136 H3 histone pseudogene 16 Homo sapiens 47-50 10198354-4 1999 Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect. Carbachol 178-187 H3 histone pseudogene 16 Homo sapiens 47-50 10101031-6 1999 Stimulation of HMC-1 with the stable adenosine analog NECA (5"-N-ethylcarboxamidoadenosine) activated p21(ras) and both p42 and p44 isoforms of extracellular signal-regulated kinase (ERK). Adenosine 37-46 H3 histone pseudogene 16 Homo sapiens 102-105 10101031-6 1999 Stimulation of HMC-1 with the stable adenosine analog NECA (5"-N-ethylcarboxamidoadenosine) activated p21(ras) and both p42 and p44 isoforms of extracellular signal-regulated kinase (ERK). Adenosine-5'-(N-ethylcarboxamide) 54-58 H3 histone pseudogene 16 Homo sapiens 102-105 10101031-6 1999 Stimulation of HMC-1 with the stable adenosine analog NECA (5"-N-ethylcarboxamidoadenosine) activated p21(ras) and both p42 and p44 isoforms of extracellular signal-regulated kinase (ERK). Adenosine-5'-(N-ethylcarboxamide) 60-90 H3 histone pseudogene 16 Homo sapiens 102-105 10194059-2 1999 These interactions not only allow colonization of the human mucosa but also stimulate cellular signaling cascades involving phosphatidylcholine-dependent phospholipase C, acidic sphingomyelinase and protein kinase C in epithelial cells, and Src-related kinases, Rac1, p21-activated kinase, and Jun N-terminal kinase in phagocytic cells. Phosphatidylcholines 124-143 H3 histone pseudogene 16 Homo sapiens 268-271 10469432-2 1999 GTP to inactive Ras.GDP. Guanosine Triphosphate 0-3 H3 histone pseudogene 16 Homo sapiens 16-19 10469432-2 1999 GTP to inactive Ras.GDP. Guanosine Diphosphate 20-23 H3 histone pseudogene 16 Homo sapiens 16-19 10037143-2 1999 We found that phorbol 12-myristate 13-acetate (PMA) induced upregulation of p21, not only in MCF-7 cells arrested in the G1 phase as previously shown, but also in cells delayed in the G2 phase. Tetradecanoylphorbol Acetate 14-45 H3 histone pseudogene 16 Homo sapiens 76-79 11812373-2 1999 METHODS: The p16, p21 and p53 genes mediated by Stearylamine/DOPE (SA liposome) were introduced alone and jointly into the non-small cell lung cancer (NSCLC) cell line A549 and small cell lung cancer (SCLC) SH77. 2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine 67-69 H3 histone pseudogene 16 Homo sapiens 18-21 11812373-4 1999 RESULTS: The p16, p53 and p21 genes alone mediated by SA liposome can inhibit obviously the growth of NSCLC cell line A549 cells, while the genes were slightly effective on SCLC cell line SH77 cells at day 1, 3, 5 after transfecting the genes. 2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine 54-56 H3 histone pseudogene 16 Homo sapiens 26-29 10071846-1 1999 The title compound, C18H18O4, crystallizes in the centrosymmetric space group P2(1)/c, with two molecules in the asymmetric unit. c18h18o4 20-28 H3 histone pseudogene 16 Homo sapiens 78-83 10331244-3 1999 The crystal of [Pd(en)(pyridine)Cl]NO3 is monoclinic, space group P21/c (a = 7.990(2), b = 16.058(3), c = 9.846(2) A, beta = 103.81(3) degrees, Z = 4, R = 0.067, Rw = 0.066). [pd(en)(pyridine)cl]no3 15-38 H3 histone pseudogene 16 Homo sapiens 66-71 11812373-2 1999 METHODS: The p16, p21 and p53 genes mediated by Stearylamine/DOPE (SA liposome) were introduced alone and jointly into the non-small cell lung cancer (NSCLC) cell line A549 and small cell lung cancer (SCLC) SH77. stearylamine 48-60 H3 histone pseudogene 16 Homo sapiens 18-21 11812373-2 1999 METHODS: The p16, p21 and p53 genes mediated by Stearylamine/DOPE (SA liposome) were introduced alone and jointly into the non-small cell lung cancer (NSCLC) cell line A549 and small cell lung cancer (SCLC) SH77. dioleoyl phosphatidylethanolamine 61-65 H3 histone pseudogene 16 Homo sapiens 18-21 9935156-8 1999 Mutation-matched anti-sense oligonucleotides effectively inhibited the growth of these pancreatic cancer cell lines, except for BxPC-3, by suppressing K-ras mRNA expression and K-ras p21 protein synthesis. Oligonucleotides 28-44 H3 histone pseudogene 16 Homo sapiens 183-186 10037143-2 1999 We found that phorbol 12-myristate 13-acetate (PMA) induced upregulation of p21, not only in MCF-7 cells arrested in the G1 phase as previously shown, but also in cells delayed in the G2 phase. Tetradecanoylphorbol Acetate 47-50 H3 histone pseudogene 16 Homo sapiens 76-79 10037143-3 1999 This increase in p21 in cells accumulated in the G1 and G2/M phases of the cell cycle after PMA treatment was inhibited by the PKC inhibitor GF109203X. bisindolylmaleimide I 141-150 H3 histone pseudogene 16 Homo sapiens 17-20 10037143-7 1999 Furthermore, we found that after PMA treatment p21 was able to associate with the active Tyr-15 dephosphorylated form of cdc2, but this complex was devoid of kinase activity indicating that p21 may play a role in inhibition of cdc2 induced by PMA. Tyrosine 89-92 H3 histone pseudogene 16 Homo sapiens 47-50 10037143-7 1999 Furthermore, we found that after PMA treatment p21 was able to associate with the active Tyr-15 dephosphorylated form of cdc2, but this complex was devoid of kinase activity indicating that p21 may play a role in inhibition of cdc2 induced by PMA. Tyrosine 89-92 H3 histone pseudogene 16 Homo sapiens 190-193 11670740-10 1998 X-ray data for complex Re(2)Cl(4)(PEt(2)H)(4) 3 are as follows: P2(1)/n with a = 10.445(2) A, b = 10.113(3) A, c = 13.473(2) A, beta = 102.17(2) degrees, and Z = 2. (2)cl 25-30 H3 histone pseudogene 16 Homo sapiens 64-69 10927344-7 1999 L-Leucyl-L-valine-methanol (1/1) crystallizes in the space group P2(1) with Z = 2. H-LEU-VAL-OH 0-17 H3 histone pseudogene 16 Homo sapiens 65-70 10927344-7 1999 L-Leucyl-L-valine-methanol (1/1) crystallizes in the space group P2(1) with Z = 2. Methanol 18-26 H3 histone pseudogene 16 Homo sapiens 65-70 10927344-10 1999 The solution shows a structure which formally belongs to the space group P2(1), with four dipeptide molecules and four solvent molecules in the asymmetric unit (Z = 8). Dipeptides 90-99 H3 histone pseudogene 16 Homo sapiens 73-78 9916711-8 1999 While the tyrosine phosphorylated forms of zeta (p21 and p23) could be observed during Ag stimulation, downstream signaling events such as the generation of phospho-p36, higher m.w. Tyrosine 10-18 H3 histone pseudogene 16 Homo sapiens 49-52 9878368-2 1998 When the structure of GDP-RanQ69L from monoclinic crystals with P21 symmetry was compared with the structure of wild-type Ran obtained from monoclinic crystals, the Q69L mutant showed a large conformational change in residues 68-74, which are in the switch II region of the molecule which changes conformation in response to nucleotide state and which forms the major interaction interface with nuclear transport factor 2 (NTF2, sometimes called p10). Guanosine Diphosphate 22-25 H3 histone pseudogene 16 Homo sapiens 64-67 10048181-1 1999 The title compound, C20H26O4, crystallized in the centrosymmetric space group P21/c with a single molecule as the asymmetric unit. C20H26O4 20-28 H3 histone pseudogene 16 Homo sapiens 78-81 9921693-1 1998 The title acid, C10H7NO2, crystallized in the centrosymmetric space group P2(1)/c with one molecule in the asymmetric unit. c10h7no2 16-24 H3 histone pseudogene 16 Homo sapiens 74-79 9921696-1 1998 The title compound, C14H10O, crystallized in the centrosymmetric space group P2(1)/c with a single molecule in the asymmetric unit. c14h10o 20-27 H3 histone pseudogene 16 Homo sapiens 77-82 9811471-0 1998 Lovastatin mediated G1 arrest in normal and tumor breast cells is through inhibition of CDK2 activity and redistribution of p21 and p27, independent of p53. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 124-127 9823899-5 1998 Here we show that the p21-activated protein kinase Pak3 phosphorylates Raf-1 on serine 338 in vitro and in vivo. Serine 80-86 H3 histone pseudogene 16 Homo sapiens 22-25 9811471-2 1998 In the present study we have investigated the nature of the CKIs (p21 and p27) alterations resulting in G1 arrest in both normal and tumor breast cell lines by lovastatin. Lovastatin 160-170 H3 histone pseudogene 16 Homo sapiens 66-69 9811471-3 1998 We show that even though lovastatin treatment causes G1 arrest in a wide variety of normal and tumor breast cells irrespective of their p53 or pRb status, the p21 and p27 protein levels are not increased in all cell lines treated suggesting that the increase in p21 and p27 protein expression per se is not necessary for lovastatin mediated G1 arrest. Lovastatin 25-35 H3 histone pseudogene 16 Homo sapiens 262-265 9811471-4 1998 However, the binding of p21 and p27 to CDK2 increases significantly following treatment of cells with lovastatin leading to inhibition of CDK2 activity and a subsequent arrest of cells in G1. Lovastatin 102-112 H3 histone pseudogene 16 Homo sapiens 24-27 9878214-5 1998 Camptothecin, but not beta-lapachone, induced accumulation of p53 and the major growth arrest-associated p53 response protein, p21. Camptothecin 0-12 H3 histone pseudogene 16 Homo sapiens 127-130 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 H3 histone pseudogene 16 Homo sapiens 76-79 10047792-0 1998 Polyamine analogue-mediated cell cycle responses in human melanoma cells involves the p53, p21, Rb regulatory pathway. Polyamines 0-9 H3 histone pseudogene 16 Homo sapiens 91-94 9930367-0 1998 p53- and p21-independent apoptosis of squamous cell carcinoma cells induced by 5-fluorouracil and radiation. Fluorouracil 79-93 H3 histone pseudogene 16 Homo sapiens 9-12 9778364-3 1998 The urea-induced equilibrium unfolding transitions for the ternary (p21.GDP.Mg2+), binary (p21.GDP) and apo (p21) forms of p21(H-ras) at pH 7.5 and 25 degreesC were monitored by absorbance and circular dichroism spectroscopies. Urea 4-8 H3 histone pseudogene 16 Homo sapiens 68-71 9778364-3 1998 The urea-induced equilibrium unfolding transitions for the ternary (p21.GDP.Mg2+), binary (p21.GDP) and apo (p21) forms of p21(H-ras) at pH 7.5 and 25 degreesC were monitored by absorbance and circular dichroism spectroscopies. Urea 4-8 H3 histone pseudogene 16 Homo sapiens 91-94 9778364-3 1998 The urea-induced equilibrium unfolding transitions for the ternary (p21.GDP.Mg2+), binary (p21.GDP) and apo (p21) forms of p21(H-ras) at pH 7.5 and 25 degreesC were monitored by absorbance and circular dichroism spectroscopies. Urea 4-8 H3 histone pseudogene 16 Homo sapiens 91-94 9778364-3 1998 The urea-induced equilibrium unfolding transitions for the ternary (p21.GDP.Mg2+), binary (p21.GDP) and apo (p21) forms of p21(H-ras) at pH 7.5 and 25 degreesC were monitored by absorbance and circular dichroism spectroscopies. Urea 4-8 H3 histone pseudogene 16 Homo sapiens 91-94 9778364-6 1998 Near- and far-UV circular dichroism spectra of these three forms of p21(H-ras) show that removal of the Mg2+ from the ternary complex loosens the aromatic side chain packing but leaves the secondary structure largely unchanged. magnesium ion 104-108 H3 histone pseudogene 16 Homo sapiens 68-71 9778364-8 1998 These results demonstrate that ligands play a significant role in the stability and structure of the p21.GDP.Mg2+ complex. Guanosine Diphosphate 105-108 H3 histone pseudogene 16 Homo sapiens 101-104 9778364-8 1998 These results demonstrate that ligands play a significant role in the stability and structure of the p21.GDP.Mg2+ complex. magnesium ion 109-113 H3 histone pseudogene 16 Homo sapiens 101-104 9778365-1 1998 p21(H-ras) plays a critical role in signal transduction pathways by cycling between an active, GTP/Mg2+ ternary complex and an inactive, GDP/Mg2+ complex. Guanosine Triphosphate 95-98 H3 histone pseudogene 16 Homo sapiens 0-3 9778365-1 1998 p21(H-ras) plays a critical role in signal transduction pathways by cycling between an active, GTP/Mg2+ ternary complex and an inactive, GDP/Mg2+ complex. magnesium ion 99-103 H3 histone pseudogene 16 Homo sapiens 0-3 9778365-1 1998 p21(H-ras) plays a critical role in signal transduction pathways by cycling between an active, GTP/Mg2+ ternary complex and an inactive, GDP/Mg2+ complex. Guanosine Diphosphate 137-140 H3 histone pseudogene 16 Homo sapiens 0-3 9778365-1 1998 p21(H-ras) plays a critical role in signal transduction pathways by cycling between an active, GTP/Mg2+ ternary complex and an inactive, GDP/Mg2+ complex. magnesium ion 141-145 H3 histone pseudogene 16 Homo sapiens 0-3 9778365-11 1998 Only the faster unfolding reaction is observed in the absence of Mg2+, suggesting that this reaction corresponds to the unfolding of the binary complex, p21(H-ras)*GDP. magnesium ion 65-69 H3 histone pseudogene 16 Homo sapiens 153-156 9778365-11 1998 Only the faster unfolding reaction is observed in the absence of Mg2+, suggesting that this reaction corresponds to the unfolding of the binary complex, p21(H-ras)*GDP. Guanosine Diphosphate 164-167 H3 histone pseudogene 16 Homo sapiens 153-156 9778365-12 1998 The slower unfolding reaction presumably corresponds to the unfolding of the ternary complex, p21(H-ras)*GDP. Guanosine Diphosphate 105-108 H3 histone pseudogene 16 Homo sapiens 94-97 9778365-14 1998 The kinetic data show that the refolding/unfolding of p21(H-ras) occurs through parallel channels that are strongly influenced by the binding/release of GDP and Mg2+ to/from a pair of native conformers. Guanosine Diphosphate 153-156 H3 histone pseudogene 16 Homo sapiens 54-57 9778365-14 1998 The kinetic data show that the refolding/unfolding of p21(H-ras) occurs through parallel channels that are strongly influenced by the binding/release of GDP and Mg2+ to/from a pair of native conformers. magnesium ion 161-165 H3 histone pseudogene 16 Homo sapiens 54-57 9930367-12 1998 These findings indicate that 5-FU and gamma-rays induce apoptosis of squamous cell carcinoma cells in p53- and p21-independent manners, in the S and G2/M phases, respectively. Fluorouracil 29-33 H3 histone pseudogene 16 Homo sapiens 111-114 11939039-5 1998 It indicates that CTP and COV can cause the p21 protein level increase in the occupational population. Cytidine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 44-47 9778042-7 1998 In addition, sulindac sulfide can impair the nucleotide exchange on p21ras by CDC25 as well as the acceleration of the p21ras GTPase reaction by p120GAP. sulindac sulfide 13-29 H3 histone pseudogene 16 Homo sapiens 68-71 9774361-6 1998 Both Ang II and A23187 caused a rapid increase in the binding of GTP to p21(Ras), which was nearly abolished by genistein and calmidazolium. Calcimycin 16-22 H3 histone pseudogene 16 Homo sapiens 72-75 9774361-6 1998 Both Ang II and A23187 caused a rapid increase in the binding of GTP to p21(Ras), which was nearly abolished by genistein and calmidazolium. Guanosine Triphosphate 65-68 H3 histone pseudogene 16 Homo sapiens 72-75 9774361-6 1998 Both Ang II and A23187 caused a rapid increase in the binding of GTP to p21(Ras), which was nearly abolished by genistein and calmidazolium. Genistein 112-121 H3 histone pseudogene 16 Homo sapiens 72-75 9774361-6 1998 Both Ang II and A23187 caused a rapid increase in the binding of GTP to p21(Ras), which was nearly abolished by genistein and calmidazolium. calmidazolium 126-139 H3 histone pseudogene 16 Homo sapiens 72-75 9774361-9 1998 Overexpression of the dominant negative mutant of Pyk2 significantly attenuated Ang II or A23187-induced ERK activities (36% and 38% inhibition compared with that in mock-transfected cells, respectively) and ERK tyrosine phosphorylation levels, as well as an increase in the binding of GTP to p21(Ras). Calcimycin 90-96 H3 histone pseudogene 16 Homo sapiens 293-296 11939039-5 1998 It indicates that CTP and COV can cause the p21 protein level increase in the occupational population. (1S,3R,5Z,7E,14beta,17alpha)-17-[(2S,4S)-4-(2-hydroxy-2-methylpropyl)-2-methyltetrahydrofuran-2-yl]-9,10-secoandrosta-5,7,10-triene-1,3-diol 26-29 H3 histone pseudogene 16 Homo sapiens 44-47 9712657-5 1998 The activation of alpha-Bgt-AChRs by nicotine results in the induction of the tumor suppressor protein p53 and the cdk inhibitor p21. Nicotine 37-45 H3 histone pseudogene 16 Homo sapiens 129-132 9740740-5 1998 The effect of glycerol and MG on the ESEEM amplitudes of various protein nucleiwas studied in ras p21.Mn(II). methylglucoside 27-29 H3 histone pseudogene 16 Homo sapiens 98-101 9740740-7 1998 In particular, in p21 incorporating [2H-3]Thr, the Mn(II)-[2H-3]Thr35 distance was found to be unaffected by the concentration of cryoprotectant or the rate of freezing. Deuterium 36-39 H3 histone pseudogene 16 Homo sapiens 18-21 9740740-7 1998 In particular, in p21 incorporating [2H-3]Thr, the Mn(II)-[2H-3]Thr35 distance was found to be unaffected by the concentration of cryoprotectant or the rate of freezing. Manganese(2+) 51-57 H3 histone pseudogene 16 Homo sapiens 18-21 9706145-2 1998 Previous studies have shown that p21 and histone hyperacetylation are important in basal growth inhibition by butyrate. Butyrates 110-118 H3 histone pseudogene 16 Homo sapiens 33-36 9740740-9 1998 In p21.Mn(II)GMPPNP, the large deuterium modulations from the d5-glycerol exhibit saturation behavior with increasing d5-glycerol concentration, implying that glycerol, a widely used cryoprotectant, replaces the aquo ligands of the Mn(II) ion. mn(ii)gmppnp 7-19 H3 histone pseudogene 16 Homo sapiens 3-6 9740740-9 1998 In p21.Mn(II)GMPPNP, the large deuterium modulations from the d5-glycerol exhibit saturation behavior with increasing d5-glycerol concentration, implying that glycerol, a widely used cryoprotectant, replaces the aquo ligands of the Mn(II) ion. Deuterium 31-40 H3 histone pseudogene 16 Homo sapiens 3-6 9740740-9 1998 In p21.Mn(II)GMPPNP, the large deuterium modulations from the d5-glycerol exhibit saturation behavior with increasing d5-glycerol concentration, implying that glycerol, a widely used cryoprotectant, replaces the aquo ligands of the Mn(II) ion. d5-glycerol 62-73 H3 histone pseudogene 16 Homo sapiens 3-6 9740740-9 1998 In p21.Mn(II)GMPPNP, the large deuterium modulations from the d5-glycerol exhibit saturation behavior with increasing d5-glycerol concentration, implying that glycerol, a widely used cryoprotectant, replaces the aquo ligands of the Mn(II) ion. Glycerol 65-73 H3 histone pseudogene 16 Homo sapiens 3-6 9740740-9 1998 In p21.Mn(II)GMPPNP, the large deuterium modulations from the d5-glycerol exhibit saturation behavior with increasing d5-glycerol concentration, implying that glycerol, a widely used cryoprotectant, replaces the aquo ligands of the Mn(II) ion. Manganese(2+) 7-13 H3 histone pseudogene 16 Homo sapiens 3-6 9740740-10 1998 The interaction between the Mn(II) ion of p21 and MG, however, is less intimate: the deuterium ESEEM amplitudes are much smaller for samples prepared with d7-MG than with d5-glycerol. Manganese(2+) 28-34 H3 histone pseudogene 16 Homo sapiens 42-45 9740740-10 1998 The interaction between the Mn(II) ion of p21 and MG, however, is less intimate: the deuterium ESEEM amplitudes are much smaller for samples prepared with d7-MG than with d5-glycerol. Deuterium 85-94 H3 histone pseudogene 16 Homo sapiens 42-45 9740740-10 1998 The interaction between the Mn(II) ion of p21 and MG, however, is less intimate: the deuterium ESEEM amplitudes are much smaller for samples prepared with d7-MG than with d5-glycerol. d7-mg 155-160 H3 histone pseudogene 16 Homo sapiens 42-45 9740740-10 1998 The interaction between the Mn(II) ion of p21 and MG, however, is less intimate: the deuterium ESEEM amplitudes are much smaller for samples prepared with d7-MG than with d5-glycerol. d5-glycerol 171-182 H3 histone pseudogene 16 Homo sapiens 42-45 11670523-14 1998 Complex Zn(py)(2)Br(2) crystallizes in the monoclinic P2(1)/c space group with a = 8.534(2) A, b = 18.316(4) A, c = 8.461(2) A, beta = 101.07(3) degrees, V = 1297.9(5) A(3), and Z = 4. zn(py 8-13 H3 histone pseudogene 16 Homo sapiens 54-59 9732400-4 1998 Prolonged exposure for 72 hr to high nanomolar to low micromolar concentrations of topotecan augmented p21 protein levels and induced G2/M arrest but failed to consistently alter BCL-2 and BAX protein levels, did not induce significant DNA/topoisomerase I complex formation and did not inhibit RNA synthesis. Topotecan 83-92 H3 histone pseudogene 16 Homo sapiens 103-106 9693007-1 1998 The vibrational spectra of phosphate modes for GDP and GTP bound to the c-Harvey p21(ras) protein have been determined using 18O isotope edited Raman difference spectroscopy. Phosphates 27-36 H3 histone pseudogene 16 Homo sapiens 81-84 9693007-1 1998 The vibrational spectra of phosphate modes for GDP and GTP bound to the c-Harvey p21(ras) protein have been determined using 18O isotope edited Raman difference spectroscopy. Guanosine Diphosphate 47-50 H3 histone pseudogene 16 Homo sapiens 81-84 9693007-1 1998 The vibrational spectra of phosphate modes for GDP and GTP bound to the c-Harvey p21(ras) protein have been determined using 18O isotope edited Raman difference spectroscopy. Guanosine Triphosphate 55-58 H3 histone pseudogene 16 Homo sapiens 81-84 9664115-3 1998 Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2. Cisplatin 15-24 H3 histone pseudogene 16 Homo sapiens 91-94 9664115-3 1998 Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2. Carboplatin 29-40 H3 histone pseudogene 16 Homo sapiens 91-94 9726816-5 1998 In contrast, PDTC, DDTC, and ammonium dithiocarbamate (ADTC) did not induce apoptosis; rather they led to the induction of p53 and p21 followed by G1/S arrest. prolinedithiocarbamate 13-17 H3 histone pseudogene 16 Homo sapiens 131-134 9726816-5 1998 In contrast, PDTC, DDTC, and ammonium dithiocarbamate (ADTC) did not induce apoptosis; rather they led to the induction of p53 and p21 followed by G1/S arrest. Ditiocarb 19-23 H3 histone pseudogene 16 Homo sapiens 131-134 9726816-5 1998 In contrast, PDTC, DDTC, and ammonium dithiocarbamate (ADTC) did not induce apoptosis; rather they led to the induction of p53 and p21 followed by G1/S arrest. AMMONIUM DITHIOCARBAMATE 29-53 H3 histone pseudogene 16 Homo sapiens 131-134 9726816-5 1998 In contrast, PDTC, DDTC, and ammonium dithiocarbamate (ADTC) did not induce apoptosis; rather they led to the induction of p53 and p21 followed by G1/S arrest. adtc 55-59 H3 histone pseudogene 16 Homo sapiens 131-134 9706145-11 1998 CONCLUSIONS: Butyrate appears to inhibit colon cancer cell growth by two mechanisms, one involving histone hyperacetylation and p21 induction and the other related to impaired EGF-responsiveness. Butyrates 13-21 H3 histone pseudogene 16 Homo sapiens 128-131 9739543-1 1998 Phenanthrene-4-carboxylic acid, C15H10O2, crystallized in the centrosymmetric space group P2(1)/n, while 1,2-dihydrophenanthrene-4-carboxylic acid, C15H12O2, crystallized in the centrosymmetric space group Pbca. phenanthrene-4-carboxylic acid 0-30 H3 histone pseudogene 16 Homo sapiens 90-95 9783903-0 1998 Action of 1,25(OH)2D3 on the cell cycle genes, cyclin D1, p21 and p27 in MCF-7 cells. Calcitriol 10-21 H3 histone pseudogene 16 Homo sapiens 58-61 9719464-0 1998 Induction of p21 during ceramide-mediated apoptosis in human hepatocarcinoma cells. Ceramides 24-32 H3 histone pseudogene 16 Homo sapiens 13-16 9719464-2 1998 In this study, we investigated the expression of the p21 gene and its relationship to apoptosis induced by ceramide. Ceramides 107-115 H3 histone pseudogene 16 Homo sapiens 53-56 9719464-5 1998 This apoptotic cell death with p21 induction was also observed in the Hep 3B cells lacking functional p53 after exposure to C6-ceramide. N-caproylsphingosine 124-135 H3 histone pseudogene 16 Homo sapiens 31-34 9719464-6 1998 These findings suggest that ceramide-induced apoptosis is associated with the upregulation of p21 mRNA and protein in a p53-independent pathway. Ceramides 28-36 H3 histone pseudogene 16 Homo sapiens 94-97 9665734-0 1998 Time-resolved FTIR studies of the GTPase reaction of H-ras p21 reveal a key role for the beta-phosphate. beta-phosphate 89-103 H3 histone pseudogene 16 Homo sapiens 59-62 9739543-1 1998 Phenanthrene-4-carboxylic acid, C15H10O2, crystallized in the centrosymmetric space group P2(1)/n, while 1,2-dihydrophenanthrene-4-carboxylic acid, C15H12O2, crystallized in the centrosymmetric space group Pbca. c15h10o2 32-40 H3 histone pseudogene 16 Homo sapiens 90-95 9739544-1 1998 The title acid, 8-aminooctanoic acid, C8H17NO2, crystallized in the centrosymmetric space group P2(1)/n in the zwitterionic form. acid, 8-aminooctanoic acid 10-36 H3 histone pseudogene 16 Homo sapiens 96-101 9739544-1 1998 The title acid, 8-aminooctanoic acid, C8H17NO2, crystallized in the centrosymmetric space group P2(1)/n in the zwitterionic form. c8h17no2 38-46 H3 histone pseudogene 16 Homo sapiens 96-101 9601032-7 1998 It is suggested that, by analogy to the GTPase activity of p21(ras) and by examining the crystallographic structure of Spo0F, that the carboxyamide of the mutant Asn 56 may favorably position a catalytic water near the protein acyl phosphate to promote Spo0F approximately P K56N hydrolysis. Carbamates 135-147 H3 histone pseudogene 16 Homo sapiens 59-62 9624165-9 1998 p21(Cdc42Hs/Rac)-activated kinase (PAK) phosphorylates p67(phox) amino acid residues adjacent to the Rac1/2-binding site, and this phosphorylation is stimulated by deletion of the C-terminal SH3 domain or the polyproline-rich motif. polyproline 209-220 H3 histone pseudogene 16 Homo sapiens 0-3 9642224-5 1998 Increasing p21(ras) activity by expressing v-ras or by treatment with an antisense oligonucleotide to the GTPase-activating protein was found to accelerate the Fas-mediated apoptotic process in Jurkat and mouse LF cells. Oligonucleotides 83-98 H3 histone pseudogene 16 Homo sapiens 11-14 9642224-5 1998 Increasing p21(ras) activity by expressing v-ras or by treatment with an antisense oligonucleotide to the GTPase-activating protein was found to accelerate the Fas-mediated apoptotic process in Jurkat and mouse LF cells. ammonium ferrous sulfate 160-163 H3 histone pseudogene 16 Homo sapiens 11-14 9642224-7 1998 In contrast, Fas engagement, although inducing a vigorous and PKC-independent activation of endogenous p21(ras), did not alter cell cycle progression, nor did it require such progression for apoptosis. ammonium ferrous sulfate 13-16 H3 histone pseudogene 16 Homo sapiens 103-106 9624180-6 1998 alpha2-Adrenergic stimulation also led to an increase in GDP/GTP exchange on p21(rhoA), as well as to an increase in the amount of p21(rhoA) in the particulate fraction of alpha2AF2 preadipocytes. Guanosine Diphosphate 57-60 H3 histone pseudogene 16 Homo sapiens 77-80 9624180-6 1998 alpha2-Adrenergic stimulation also led to an increase in GDP/GTP exchange on p21(rhoA), as well as to an increase in the amount of p21(rhoA) in the particulate fraction of alpha2AF2 preadipocytes. Guanosine Triphosphate 61-64 H3 histone pseudogene 16 Homo sapiens 77-80 9675842-1 1998 The title molecule, C12H18O3, crystallized in the centrosymmetric space group P2(1)/c with two molecules in the asymmetric unit. c12h18o3 20-28 H3 histone pseudogene 16 Homo sapiens 78-83 9675843-1 1998 The title acid, C13H10O2, crystallized in the centrosymmetric space group P2(1)/c with four molecules in the asymmetric unit. c13h10o2 16-24 H3 histone pseudogene 16 Homo sapiens 74-79 9626359-8 1998 These results suggest that SB induces cellular differentiation and suppresses growth and tumorigenicity of HCC cells in vitro and in viva by a mechanism independent of p53 but possibly dependent on p21. Butyric Acid 27-29 H3 histone pseudogene 16 Homo sapiens 198-201 9601032-7 1998 It is suggested that, by analogy to the GTPase activity of p21(ras) and by examining the crystallographic structure of Spo0F, that the carboxyamide of the mutant Asn 56 may favorably position a catalytic water near the protein acyl phosphate to promote Spo0F approximately P K56N hydrolysis. Asparagine 162-165 H3 histone pseudogene 16 Homo sapiens 59-62 9601032-7 1998 It is suggested that, by analogy to the GTPase activity of p21(ras) and by examining the crystallographic structure of Spo0F, that the carboxyamide of the mutant Asn 56 may favorably position a catalytic water near the protein acyl phosphate to promote Spo0F approximately P K56N hydrolysis. Phosphates 232-241 H3 histone pseudogene 16 Homo sapiens 59-62 9871712-1 1998 Assuming that substrate-assisted catalysis is the mechanism of GTP hydrolysis for ras p21 and other GTP-binding proteins, we used the PM3 semiempirical molecular orbital method to predict from the calculated reaction profiles of GTP hydrolysis reactions the changes in GTPase activities caused by mutations. Guanosine Triphosphate 63-66 H3 histone pseudogene 16 Homo sapiens 86-89 9576849-3 1998 To understand the molecular basis for the H2O2-induced growth arrest, we determined the cell cycle distribution, levels of p53 tumour suppressor and p21 cyclin-dependent kinase inhibitor proteins, and the status of Rb phosphorylation in H2O2-treated cells. Hydrogen Peroxide 42-46 H3 histone pseudogene 16 Homo sapiens 149-152 9576849-8 1998 The level of p21 protein increased about 18 h after H2O2 exposure and remained elevated for at least 21 days. Hydrogen Peroxide 52-56 H3 histone pseudogene 16 Homo sapiens 13-16 9576849-14 1998 Thus H2O2-treated cells show a transient elevation of p53, high level of p21, lack of Rb phosphorylation, G1 arrest and inability to replicate when G1 arrest is inactivated. Hydrogen Peroxide 5-9 H3 histone pseudogene 16 Homo sapiens 73-76 9871712-1 1998 Assuming that substrate-assisted catalysis is the mechanism of GTP hydrolysis for ras p21 and other GTP-binding proteins, we used the PM3 semiempirical molecular orbital method to predict from the calculated reaction profiles of GTP hydrolysis reactions the changes in GTPase activities caused by mutations. Guanosine Triphosphate 100-103 H3 histone pseudogene 16 Homo sapiens 86-89 9871712-1 1998 Assuming that substrate-assisted catalysis is the mechanism of GTP hydrolysis for ras p21 and other GTP-binding proteins, we used the PM3 semiempirical molecular orbital method to predict from the calculated reaction profiles of GTP hydrolysis reactions the changes in GTPase activities caused by mutations. Guanosine Triphosphate 100-103 H3 histone pseudogene 16 Homo sapiens 86-89 9574518-4 1998 The combined stimulation of either CD3 and CD28 or CD3 concurrently with C2-ceramide largely enhanced the activity of p21-activated kinase and MEK kinase 1. N-acetylsphingosine 73-84 H3 histone pseudogene 16 Homo sapiens 118-121 9531502-7 1998 In contrast, altering the p21(ras)-dependent pathway with either manumycin, an inhibitor of Ras farnesylation, or PD98059, an inhibitor of the mitogen-activated protein kinase/extracellular signal-regulated protein kinase (ERK) kinase, suppressed the induction of ERCC-1 mRNA by insulin (P<0.001). manumycin 65-74 H3 histone pseudogene 16 Homo sapiens 26-29 9438391-2 1998 Using the proteasome-specific inhibitors, MG132 (N-acetyl-L-leucinyl-L-leucinal-L-leucinal) and lactacystin, here we show that the p53-response proteins, bax and mdm2 as well as p21, are degraded by the ubiquitin-proteasome pathway in HeLa cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 42-47 H3 histone pseudogene 16 Homo sapiens 178-181 9528787-11 1998 Coexpression of this PAK inhibitor with Cdc42G12V prevented the formation of peripheral actin microspikes and associated loss of stress fibers normally induced by the p21. cdc42g12v 40-49 H3 histone pseudogene 16 Homo sapiens 167-170 9761883-1 1998 Balhimycin is a naturally occurring glycopeptide antibiotic, related to vancomycin which acts by binding nascent bacterial cell-wall peptide ending in the sequence D-Ala-D-Ala. Crystals of balhimycin are monoclinic, space group P21, a = 20.48 (10), b = 43.93 (21), c = 27.76 (14) A, beta = 100.5 (5) degrees with four independent antibiotic molecules, three molecules of 2-methyl-2,4-pentanediol, two citrate ions, three acetate ions and 127.5 water molecules in the asymmetric unit. balhimycin 0-10 H3 histone pseudogene 16 Homo sapiens 228-231 9761883-1 1998 Balhimycin is a naturally occurring glycopeptide antibiotic, related to vancomycin which acts by binding nascent bacterial cell-wall peptide ending in the sequence D-Ala-D-Ala. Crystals of balhimycin are monoclinic, space group P21, a = 20.48 (10), b = 43.93 (21), c = 27.76 (14) A, beta = 100.5 (5) degrees with four independent antibiotic molecules, three molecules of 2-methyl-2,4-pentanediol, two citrate ions, three acetate ions and 127.5 water molecules in the asymmetric unit. Vancomycin 72-82 H3 histone pseudogene 16 Homo sapiens 228-231 9761883-1 1998 Balhimycin is a naturally occurring glycopeptide antibiotic, related to vancomycin which acts by binding nascent bacterial cell-wall peptide ending in the sequence D-Ala-D-Ala. Crystals of balhimycin are monoclinic, space group P21, a = 20.48 (10), b = 43.93 (21), c = 27.76 (14) A, beta = 100.5 (5) degrees with four independent antibiotic molecules, three molecules of 2-methyl-2,4-pentanediol, two citrate ions, three acetate ions and 127.5 water molecules in the asymmetric unit. balhimycin 189-199 H3 histone pseudogene 16 Homo sapiens 228-231 9452502-4 1998 We present in vitro evidence for a plasma membrane binding protein for p21(ras) that can recognize the isoprenoid substituent and, therefore, may facilitate the localization of p21ras. Terpenes 103-113 H3 histone pseudogene 16 Homo sapiens 71-74 9476915-5 1998 Renaturation of apical membrane proteins within polyacrylamide gels showed that p19s and p21s autophosphorylated with either gamma[32P]GTP or gamma[32P]ATP as substrates, suggesting that the two proteins were kinases. polyacrylamide 48-62 H3 histone pseudogene 16 Homo sapiens 89-92 9476915-5 1998 Renaturation of apical membrane proteins within polyacrylamide gels showed that p19s and p21s autophosphorylated with either gamma[32P]GTP or gamma[32P]ATP as substrates, suggesting that the two proteins were kinases. gamma[32p]gtp 125-138 H3 histone pseudogene 16 Homo sapiens 89-92 9476915-5 1998 Renaturation of apical membrane proteins within polyacrylamide gels showed that p19s and p21s autophosphorylated with either gamma[32P]GTP or gamma[32P]ATP as substrates, suggesting that the two proteins were kinases. Phosphorus-32 130-135 H3 histone pseudogene 16 Homo sapiens 89-92 9533953-7 1998 The vimar protein contains 15 tandem copies of the Armadillo repeat, a protein interaction domain, and is similar to mammalian Smg guanine dissociation stimulator protein, which stimulates the activity of a number of different p21 small G-proteins. Guanine 131-138 H3 histone pseudogene 16 Homo sapiens 227-230 9476915-5 1998 Renaturation of apical membrane proteins within polyacrylamide gels showed that p19s and p21s autophosphorylated with either gamma[32P]GTP or gamma[32P]ATP as substrates, suggesting that the two proteins were kinases. Adenosine Triphosphate 152-155 H3 histone pseudogene 16 Homo sapiens 89-92 9438391-2 1998 Using the proteasome-specific inhibitors, MG132 (N-acetyl-L-leucinyl-L-leucinal-L-leucinal) and lactacystin, here we show that the p53-response proteins, bax and mdm2 as well as p21, are degraded by the ubiquitin-proteasome pathway in HeLa cells. lactacystin 96-107 H3 histone pseudogene 16 Homo sapiens 178-181 9659915-2 1998 We have purified and cloned a new class of Rho-p21 guanine nucleotide exchange factor binding tightly through its N-terminal SH3 domain to a conserved proline-rich PAK sequence with a Kd of 24 nM. Proline 151-158 H3 histone pseudogene 16 Homo sapiens 47-50 9717256-2 1998 CNF1 covalently and specifically modifies the p21 Rho GTP-binding protein in mammalian cells by deamidation of the p21 Rho glutamine 63. Glutamine 123-132 H3 histone pseudogene 16 Homo sapiens 46-49 9717256-2 1998 CNF1 covalently and specifically modifies the p21 Rho GTP-binding protein in mammalian cells by deamidation of the p21 Rho glutamine 63. Glutamine 123-132 H3 histone pseudogene 16 Homo sapiens 115-118 10682555-1 1998 To study the relationship between the expressions of tumor supressor protein p21 and p53 and malignant growth of gastric carcinoma, 88 paraffin embedded specimens of gastric carcinoma and gastric ulcer were examined with immunohistochemical method. Paraffin 135-143 H3 histone pseudogene 16 Homo sapiens 77-80 9661152-9 1998 As an example of such investigations, the time-resolved FTIR studies on the GTPase reaction of H-ras p21 using caged GTP is presented. Guanosine Triphosphate 76-79 H3 histone pseudogene 16 Homo sapiens 101-104 9398294-3 1997 The same phenomenon may also account for the diminished GTPase activity of the homologous transforming Gly42 --> Val mutation in p21(ras). Valine 116-119 H3 histone pseudogene 16 Homo sapiens 132-135 9876011-0 1998 Modulation of ras p21 oncoprotein levels and DNA strand breakage in human cells with chemotherapeutic agents and/or deferoxamine. Deferoxamine 116-128 H3 histone pseudogene 16 Homo sapiens 18-21 9876011-3 1998 In the present study, therefore, ras p21 protein expression was examined in in vitro cultures of human lymphocytes treated with mitomycin C and in the human colon adenocarcinoma Caco-2 cell line treated with doxorubicin with and without deferoxamine. Mitomycin 128-139 H3 histone pseudogene 16 Homo sapiens 37-40 9876011-3 1998 In the present study, therefore, ras p21 protein expression was examined in in vitro cultures of human lymphocytes treated with mitomycin C and in the human colon adenocarcinoma Caco-2 cell line treated with doxorubicin with and without deferoxamine. Doxorubicin 208-219 H3 histone pseudogene 16 Homo sapiens 37-40 9876011-5 1998 Increases in p21 protein levels were seen with mitomycin C but no clear response was seen with doxorubicin. Mitomycin 47-58 H3 histone pseudogene 16 Homo sapiens 13-16 9876011-6 1998 However, deferoxamine, with and without doxorubicin, altered p21 expression. Deferoxamine 9-21 H3 histone pseudogene 16 Homo sapiens 61-64 9876011-6 1998 However, deferoxamine, with and without doxorubicin, altered p21 expression. Doxorubicin 40-51 H3 histone pseudogene 16 Homo sapiens 61-64 9876011-7 1998 Deferoxamine is an iron chelator so these results support the hypothesis that oxygen radicals were responsible for the altered p21 protein levels. Deferoxamine 0-12 H3 histone pseudogene 16 Homo sapiens 127-130 9876011-7 1998 Deferoxamine is an iron chelator so these results support the hypothesis that oxygen radicals were responsible for the altered p21 protein levels. Reactive Oxygen Species 78-93 H3 histone pseudogene 16 Homo sapiens 127-130 9396728-2 1997 The covalent complex has been prepared by introducing a disulphide bond between Cys-1 of P21 and Lys-13 of Mp, previously modified with a thiol-containing reagent. disulphide 56-66 H3 histone pseudogene 16 Homo sapiens 89-92 9396728-2 1997 The covalent complex has been prepared by introducing a disulphide bond between Cys-1 of P21 and Lys-13 of Mp, previously modified with a thiol-containing reagent. Lysine 97-100 H3 histone pseudogene 16 Homo sapiens 89-92 9396728-2 1997 The covalent complex has been prepared by introducing a disulphide bond between Cys-1 of P21 and Lys-13 of Mp, previously modified with a thiol-containing reagent. Sulfhydryl Compounds 138-143 H3 histone pseudogene 16 Homo sapiens 89-92 9396728-4 1997 The results obtained indicate that His-13 of P21 co-ordinates to the sixth co-ordination position of the haem iron, thus leading to the formation of a complex characterized by an equilibrium between an "open" and a "closed" structure, as confirmed by molecular dynamics simulations. Histidine 35-38 H3 histone pseudogene 16 Homo sapiens 45-48 9396728-4 1997 The results obtained indicate that His-13 of P21 co-ordinates to the sixth co-ordination position of the haem iron, thus leading to the formation of a complex characterized by an equilibrium between an "open" and a "closed" structure, as confirmed by molecular dynamics simulations. Iron 110-114 H3 histone pseudogene 16 Homo sapiens 45-48 9419978-1 1997 It has been shown recently that expression of p21 is enhanced by paclitaxel. Paclitaxel 65-75 H3 histone pseudogene 16 Homo sapiens 46-49 9396728-5 1997 Under acidic pH conditions, where His-13 of P21 is loosely bound to the haem iron ("open" conformation), MKP displays appreciable, quasi-reversible electrochemical activity; in contrast, at neutral pH ("closed" conformation) electrochemical behaviour is negligible, indicating that P21 interferes with the electron-transfer properties typical of Mp. Histidine 34-37 H3 histone pseudogene 16 Homo sapiens 44-47 9396728-5 1997 Under acidic pH conditions, where His-13 of P21 is loosely bound to the haem iron ("open" conformation), MKP displays appreciable, quasi-reversible electrochemical activity; in contrast, at neutral pH ("closed" conformation) electrochemical behaviour is negligible, indicating that P21 interferes with the electron-transfer properties typical of Mp. Heme 72-76 H3 histone pseudogene 16 Homo sapiens 44-47 9396728-5 1997 Under acidic pH conditions, where His-13 of P21 is loosely bound to the haem iron ("open" conformation), MKP displays appreciable, quasi-reversible electrochemical activity; in contrast, at neutral pH ("closed" conformation) electrochemical behaviour is negligible, indicating that P21 interferes with the electron-transfer properties typical of Mp. Iron 77-81 H3 histone pseudogene 16 Homo sapiens 44-47 9419978-0 1997 Involvement of p21 in mitotic exit after paclitaxel treatment in MCF-7 breast adenocarcinoma cell line. Paclitaxel 41-51 H3 histone pseudogene 16 Homo sapiens 15-18 9419978-3 1997 In the present study, we showed that, in MCF-7 cells, paclitaxel induced accumulation of p21 in cells with a G2/M DNA content, corresponding to cells either in abnormal mitosis or in an interphase-like state (decondensed chromatin) with multiple nuclei. Paclitaxel 54-64 H3 histone pseudogene 16 Homo sapiens 89-92 9419978-6 1997 High levels of p21 protein were also found to be associated with inactive p34cdc2/cyclin B protein complex after treatment with paclitaxel. Paclitaxel 128-138 H3 histone pseudogene 16 Homo sapiens 15-18 9419978-7 1997 Treatment with p21 antisense oligonucleotide partially blocked induction of p21 expression by paclitaxel and significantly reduced survival of MCF-7 cells exposed to this agent. Oligonucleotides 29-44 H3 histone pseudogene 16 Homo sapiens 15-18 9419978-7 1997 Treatment with p21 antisense oligonucleotide partially blocked induction of p21 expression by paclitaxel and significantly reduced survival of MCF-7 cells exposed to this agent. Oligonucleotides 29-44 H3 histone pseudogene 16 Homo sapiens 76-79 9419978-7 1997 Treatment with p21 antisense oligonucleotide partially blocked induction of p21 expression by paclitaxel and significantly reduced survival of MCF-7 cells exposed to this agent. Paclitaxel 94-104 H3 histone pseudogene 16 Homo sapiens 15-18 9419978-7 1997 Treatment with p21 antisense oligonucleotide partially blocked induction of p21 expression by paclitaxel and significantly reduced survival of MCF-7 cells exposed to this agent. Paclitaxel 94-104 H3 histone pseudogene 16 Homo sapiens 76-79 9419978-8 1997 In NIH-OVCAR-3 cells, which are deficient in basal and paclitaxel-induced p21 expression, paclitaxel led to a prolonged activation of p34cdc2 and a delayed mitotic exit associated with apoptotic cell death. Paclitaxel 55-65 H3 histone pseudogene 16 Homo sapiens 74-77 9419978-8 1997 In NIH-OVCAR-3 cells, which are deficient in basal and paclitaxel-induced p21 expression, paclitaxel led to a prolonged activation of p34cdc2 and a delayed mitotic exit associated with apoptotic cell death. Paclitaxel 90-100 H3 histone pseudogene 16 Homo sapiens 74-77 9434871-0 1997 Examination of ras (P21) proteins in plasma from workers exposed to benzene emissions from petrochemical plants and healthy controls. Benzene 68-75 H3 histone pseudogene 16 Homo sapiens 15-23 9374488-3 1997 SL-GTP was hydrolyzed by p21 with rates similar to those for GTP hydrolysis and appears to be an excellent substrate analog. sl-gtp 0-6 H3 histone pseudogene 16 Homo sapiens 25-28 9374488-3 1997 SL-GTP was hydrolyzed by p21 with rates similar to those for GTP hydrolysis and appears to be an excellent substrate analog. Guanosine Triphosphate 3-6 H3 histone pseudogene 16 Homo sapiens 25-28 9374488-4 1997 The ESR spectra of SL-GTP and SL-GDP in complex with p21 differ significantly when acquired at 0 degrees C or 5 degrees C indicating different environments (conformations) of the protein-bound radicals depending on the phosphorylation state of the bound nucleotide. sl-gtp 19-25 H3 histone pseudogene 16 Homo sapiens 53-56 9374488-4 1997 The ESR spectra of SL-GTP and SL-GDP in complex with p21 differ significantly when acquired at 0 degrees C or 5 degrees C indicating different environments (conformations) of the protein-bound radicals depending on the phosphorylation state of the bound nucleotide. Guanosine Diphosphate 33-36 H3 histone pseudogene 16 Homo sapiens 53-56 9374488-5 1997 We calculated the rate constant for the conformational change as deduced from the changes in the corresponding ESR spectra upon incubation of the p21.SL-GTP complex at 25 degrees C and compared it to the rate constant of hydrolysis of SL-GTP at the same temperature. sl-gtp 150-156 H3 histone pseudogene 16 Homo sapiens 146-149 9374488-5 1997 We calculated the rate constant for the conformational change as deduced from the changes in the corresponding ESR spectra upon incubation of the p21.SL-GTP complex at 25 degrees C and compared it to the rate constant of hydrolysis of SL-GTP at the same temperature. sl-gtp 235-241 H3 histone pseudogene 16 Homo sapiens 146-149 9374488-7 1997 The data are in agreement with the idea that a conformational change during GTP hydrolysis by p21 occurs simultaneously with the actual hydrolysis step. Guanosine Triphosphate 76-79 H3 histone pseudogene 16 Homo sapiens 94-97 9431662-1 1997 The title compound, (+/-)-cis-2-phenylcyclopropanecarboxylic acid, C10H10O2, crystallized in the centrosymmetric space group P2(1)/n. (1S,2R)-2-Phenylcyclopropanecarboxylic acid 20-65 H3 histone pseudogene 16 Homo sapiens 125-130 9431662-1 1997 The title compound, (+/-)-cis-2-phenylcyclopropanecarboxylic acid, C10H10O2, crystallized in the centrosymmetric space group P2(1)/n. 1-phenylbut-2-yne-1,4-diol 67-75 H3 histone pseudogene 16 Homo sapiens 125-130 9431663-5 1997 1,4,5,8-Naphthalenetetracarboxylic 1,8:4,5-dianhydride, C14H4O6, crystallized in the centrosymmetric space group P2(1)/c with half the molecule as the asymmetric unit. naphthalenetetracarboxylic dianhydride 0-54 H3 histone pseudogene 16 Homo sapiens 113-118 9431663-5 1997 1,4,5,8-Naphthalenetetracarboxylic 1,8:4,5-dianhydride, C14H4O6, crystallized in the centrosymmetric space group P2(1)/c with half the molecule as the asymmetric unit. c14h4o6 56-63 H3 histone pseudogene 16 Homo sapiens 113-118 9415415-8 1997 A dramatic increase in the level of p21 mRNA was seen in epirubicin-treated MCF-7 cells, while no such increase was seen in SK-BR-3 cells. Epirubicin 57-67 H3 histone pseudogene 16 Homo sapiens 36-39 9434871-2 1997 Altogether 97 plasma samples from workers and 40 from unexposed matched referents from two samplings in different seasons were analyzed for the presence of ras (P21) proteins; of the workers 50 were exposed to benzene in the benzene production plant and 47 to polyaromatic hydrocarbons and benzene in a cokery. Benzene 210-217 H3 histone pseudogene 16 Homo sapiens 161-164 9494538-3 1997 Only two of three MCF10-2A clones which expressed mutant p21 protein acquired the ability to form colonies in soft agar. Agar 115-119 H3 histone pseudogene 16 Homo sapiens 57-60 9398050-6 1997 LN-229 cells which have partial p53-wild-type activity show enhanced expression of p53, p21 and bax protein, whereas bcl-2 levels decrease, after exposure to camptothecin. Camptothecin 158-170 H3 histone pseudogene 16 Homo sapiens 88-91 9398520-1 1997 A normal mode and energy minimization of ras p21 is used to determine the flexibility of the protein and the origin of the conformational differences between GTP and GDP-bound forms. Guanosine Triphosphate 158-161 H3 histone pseudogene 16 Homo sapiens 45-48 9398520-1 1997 A normal mode and energy minimization of ras p21 is used to determine the flexibility of the protein and the origin of the conformational differences between GTP and GDP-bound forms. Guanosine Diphosphate 166-169 H3 histone pseudogene 16 Homo sapiens 45-48 9358730-2 1997 Two depsipeptides and one ethanol molecule per asymmetric unit crystallize in space group P2(1) (Z = 4); a = 14.579, b = 39.795, c = 13.928 A, beta = 116.90, Rl = 0.0757. Ethanol 26-33 H3 histone pseudogene 16 Homo sapiens 90-95 9348195-4 1997 Both 1,25-(OH)2D3 and TPA independently up-regulated the vitamin D receptor, p21, and the hypophosphorylated form of retinoblastoma (Rb) protein. Calcitriol 5-17 H3 histone pseudogene 16 Homo sapiens 77-80 9348195-4 1997 Both 1,25-(OH)2D3 and TPA independently up-regulated the vitamin D receptor, p21, and the hypophosphorylated form of retinoblastoma (Rb) protein. Tetradecanoylphorbol Acetate 22-25 H3 histone pseudogene 16 Homo sapiens 77-80 9348195-8 1997 In MCF-7D3Res cells, 1,25-(OH)2D3 treatment had minimal effects on p21 or Rb protein expression, whereas TPA down-regulated Rb protein and transiently up-regulated p21. Tetradecanoylphorbol Acetate 105-108 H3 histone pseudogene 16 Homo sapiens 164-167 9312159-6 1997 Because the MAP kinases have been implicated in cell growth, the p21(ras)-MAP kinase pathway may represent one of the mechanisms that mediates homocysteine"s effect on VEC growth. Homocysteine 143-155 H3 histone pseudogene 16 Homo sapiens 65-68 9342335-1 1997 Conformational changes in ras p21 triggered by the hydrolysis of GTP play an essential role in the signal transduction pathway. Guanosine Triphosphate 65-68 H3 histone pseudogene 16 Homo sapiens 30-33 9362552-1 1997 The title compound, C13H12O4, crystallized in the centrosymmetric space group P2(1)/c and exhibits cyclic dimer hydrogen bonding about a center of symmetry. c13h12o4 20-28 H3 histone pseudogene 16 Homo sapiens 78-83 9362554-4 1997 Tyr-D-Tic-NH2 crystals are monoclinic (P2(1)), the asymmetric unit containing one peptide molecule and one molecule of water. Tyr-D-Tic-NH2 0-13 H3 histone pseudogene 16 Homo sapiens 39-44 9378960-7 1997 Although both p21 and p23 tyrosine-phosphorylated forms of zeta as well as phospho-CD3 epsilon molecules were constitutively present in human thymocytes and could be immunoprecipitated with ZAP-70- or CD3 epsilon-specific Abs, the p21 species of zeta was predominant in CD5 immune complexes. Tyrosine 26-34 H3 histone pseudogene 16 Homo sapiens 231-234 9312159-4 1997 Homocysteine decreased carboxyl methylation of p21(ras) (a G1 regulator whose activity is regulated by prenylation and methylation in addition to GTP-GDP exchange) by 50% in VEC but not VSMC, a difference that may be explained by the ability of homocysteine to dramatically increase levels of S-adenosylhomocysteine, a potent inhibitor of methyltransferase, in VEC but not VSMC. Homocysteine 0-12 H3 histone pseudogene 16 Homo sapiens 47-50 9312159-5 1997 Moreover, homocysteine-induced hypomethylation in VEC was associated with a 66% reduction in membrane-associated p21(ras) and a 67% reduction in extracellular signal-regulated kinase 1/2, which is a member of the mitogen-activated protein (MAP) kinase family. Homocysteine 10-22 H3 histone pseudogene 16 Homo sapiens 113-116 9312058-7 1997 In vivo generation of a C-terminal cleavage product of endogenous p53 similar in size to p50(DeltaC) correlated with up-regulation of p21 expression in ML-1 cells exposed to either adriamycin or cisplatin. Doxorubicin 181-191 H3 histone pseudogene 16 Homo sapiens 134-137 9312058-7 1997 In vivo generation of a C-terminal cleavage product of endogenous p53 similar in size to p50(DeltaC) correlated with up-regulation of p21 expression in ML-1 cells exposed to either adriamycin or cisplatin. Cisplatin 195-204 H3 histone pseudogene 16 Homo sapiens 134-137 9328342-10 1997 Instead, a second progesterone dose delays the fall of p21 and enhances the rise of p27(Kip1), thereby intensifying the progesterone resistance in an autoinhibitory loop. Progesterone 18-30 H3 histone pseudogene 16 Homo sapiens 55-58 9287316-6 1997 In this work, we have used a fluorescent active mutant (Y32W) of p21(Ha-)ras to demonstrate that BeF3- binds to the GDP. Guanosine Diphosphate 116-119 H3 histone pseudogene 16 Homo sapiens 65-68 11670106-5 1997 An X-ray structure of the thf solvate of the latter compound was determined: space group P2(1)/c, a = 11.612(1) A, b = 10.759(2) A, c = 14.291(2) A, beta = 105.50(1) degrees, V = 1720.5(4) A(3), Z = 4, R = 0.062. tetrahydrofuran 26-29 H3 histone pseudogene 16 Homo sapiens 89-96 9313336-1 1997 The title compound, C17H10O9,2H2O, crystallizes in the centrosymmetric space group P2(1)/a but does not exhibit strong eight-membered cyclic dimer hydrogen bonds about centers of symmetry or otherwise. c17h10o9 20-28 H3 histone pseudogene 16 Homo sapiens 83-88 9313337-1 1997 The title compound, C18H16O2, crystallized in the centrosymmetric space group P2(1)/a. c18h16o2 20-28 H3 histone pseudogene 16 Homo sapiens 78-83 9313339-0 1997 Hydrogen bonding and ring asymmetry in a substituted cyclopropane: (+)-trans-(1S,2S)-2-phenylcyclopropanecarboxylic acid at 208 K. The title compound, C10H10O2, crystallized in space group P2(1) with two molecules in the asymmetric unit. cyclopropane 53-65 H3 histone pseudogene 16 Homo sapiens 189-194 9278434-3 1997 However, inducible overexpression and activation of the protein kinase Calpha isozyme or the addition of 12-O-tetradecanoylphorbol-13-acetate in the prostate epithelial cell line, LNCaP, resulted in apoptosis preceded by induction of p21 and dephosphorylation of the retinoblastoma protein. Tetradecanoylphorbol Acetate 105-141 H3 histone pseudogene 16 Homo sapiens 234-237 9276920-1 1997 The title compound, C15H10O2, was found to crystallize in the centrosymmetric space group P2(1)/n. c15h10o2 20-28 H3 histone pseudogene 16 Homo sapiens 90-95 9311595-8 1997 These data demonstrate that peptide vaccination with a single mutant p21-ras-derived peptide induces CD4+ and CD8+ CTL specific for nested epitopes, including the Gly --> Val substitution at codon 12, and that both these T-cell sub-sets specifically recognize tumour cells harbouring the corresponding K-ras mutation. Glycine 163-166 H3 histone pseudogene 16 Homo sapiens 69-72 9311595-8 1997 These data demonstrate that peptide vaccination with a single mutant p21-ras-derived peptide induces CD4+ and CD8+ CTL specific for nested epitopes, including the Gly --> Val substitution at codon 12, and that both these T-cell sub-sets specifically recognize tumour cells harbouring the corresponding K-ras mutation. Valine 174-177 H3 histone pseudogene 16 Homo sapiens 69-72 9199341-2 1997 Addition of estradiol relieves the cell cycle block created by tamoxifen treatment, leading to marked activation of cyclin E-cdk2 complexes and phosphorylation of the retinoblastoma protein within 6 h. Cyclin D1 levels increase significantly while the levels of cyclin E, cdk2, and the p21 and p27 cdk inhibitors are relatively constant. Estradiol 12-21 H3 histone pseudogene 16 Homo sapiens 286-289 9309221-8 1997 CONCLUSIONS: The 13C beta of Thr35 is more distant from the active site Mn2+ in the frozen solution structure than in the crystal structure of p21.Mg2+ GMPPNP, indicating that Thr35 only weakly coordinates the metal ion in frozen solution. mg2+ gmppnp 147-158 H3 histone pseudogene 16 Homo sapiens 143-146 9260897-3 1997 RA did not induce p16 and p27 expression, but obviously reduced p21 level in MCF-7 cells. Tretinoin 0-2 H3 histone pseudogene 16 Homo sapiens 64-67 9241813-1 1997 The title compound, C12H12O6, crystallized in the centrosymmetric space group P21/n. c12h12o6 20-28 H3 histone pseudogene 16 Homo sapiens 78-81 9309221-0 1997 The frozen solution structure of p21 ras determined by ESEEM spectroscopy reveals weak coordination of Thr35 to the active site metal ion. Metals 128-133 H3 histone pseudogene 16 Homo sapiens 33-36 9309221-2 1997 Hydrolysis of tightly bound GTP alters the conformation of p21, terminating the signal. Guanosine Triphosphate 28-31 H3 histone pseudogene 16 Homo sapiens 59-62 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. magnesium ion 45-49 H3 histone pseudogene 16 Homo sapiens 24-27 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. magnesium ion 45-49 H3 histone pseudogene 16 Homo sapiens 122-125 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. Guanosine Triphosphate 144-147 H3 histone pseudogene 16 Homo sapiens 24-27 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. Guanosine Triphosphate 144-147 H3 histone pseudogene 16 Homo sapiens 122-125 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. Guanylyl Imidodiphosphate 155-161 H3 histone pseudogene 16 Homo sapiens 24-27 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. Guanylyl Imidodiphosphate 155-161 H3 histone pseudogene 16 Homo sapiens 122-125 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. Guanosine Diphosphate 175-178 H3 histone pseudogene 16 Homo sapiens 24-27 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. Guanosine Triphosphate 297-300 H3 histone pseudogene 16 Homo sapiens 24-27 9309221-3 1997 The coordination of the p21 residue Thr35 to Mg2+ in its active site, which has been observed in the crystal structure of p21 in complex with a GTP-analog GMPPNP but not with GDP, has been proposed to drive the conformational change accompanying nucleotide substitution and may have a role in the GTP hydrolysis reaction itself. Guanosine Triphosphate 297-300 H3 histone pseudogene 16 Homo sapiens 122-125 9309221-4 1997 However, previous electron spin-echo envelope modulation (ESEEM) studies of selectively 2H beta-threonine and 15N-threonine labeled p21.Mn2+ GMPPNP suggest that Thr35 only weakly coordinates the metal ion in the growth-active GTP-bound state of p21. 15n-threonine 110-123 H3 histone pseudogene 16 Homo sapiens 132-135 9199341-2 1997 Addition of estradiol relieves the cell cycle block created by tamoxifen treatment, leading to marked activation of cyclin E-cdk2 complexes and phosphorylation of the retinoblastoma protein within 6 h. Cyclin D1 levels increase significantly while the levels of cyclin E, cdk2, and the p21 and p27 cdk inhibitors are relatively constant. Tamoxifen 63-72 H3 histone pseudogene 16 Homo sapiens 286-289 9223188-0 1997 Calculation of pathways for the conformational transition between the GTP- and GDP-bound states of the Ha-ras-p21 protein: calculations with explicit solvent simulations and comparison with calculations in vacuum. Guanosine Triphosphate 70-73 H3 histone pseudogene 16 Homo sapiens 110-113 9223188-0 1997 Calculation of pathways for the conformational transition between the GTP- and GDP-bound states of the Ha-ras-p21 protein: calculations with explicit solvent simulations and comparison with calculations in vacuum. Guanosine Diphosphate 79-82 H3 histone pseudogene 16 Homo sapiens 110-113 9223188-1 1997 The transitions between the water-equilibrated structures of the GTP and GDP forms of Ha-ras-p21 have been calculated by using the targeted molecular dynamics (TMD) method (Schlitter et al., Mol. Water 28-33 H3 histone pseudogene 16 Homo sapiens 93-96 9223188-1 1997 The transitions between the water-equilibrated structures of the GTP and GDP forms of Ha-ras-p21 have been calculated by using the targeted molecular dynamics (TMD) method (Schlitter et al., Mol. Guanosine Triphosphate 65-68 H3 histone pseudogene 16 Homo sapiens 93-96 9223188-1 1997 The transitions between the water-equilibrated structures of the GTP and GDP forms of Ha-ras-p21 have been calculated by using the targeted molecular dynamics (TMD) method (Schlitter et al., Mol. Guanosine Diphosphate 73-76 H3 histone pseudogene 16 Homo sapiens 93-96 9188453-9 1997 For example, the p21(ras).GTP loading, p44 MAPK activity, and induction of transcription factor c-fos all were inhibited by NAC and DPI as well as an antioxidant pyrrolidine dithiocarbamate or reduced glutathione (GSH). Guanosine Triphosphate 26-29 H3 histone pseudogene 16 Homo sapiens 17-20 11038767-2 1997 METHODS: p21 H-ras expression and H-ras codon 12 mutation was detected in the same paraffin embedded tissues of 171 cases of cervical carcinoma, 68 cases of SIL, and 29 cases of chronic cervicitis, by using immunohistochemical and PCR-RFLP techniques. Paraffin 83-91 H3 histone pseudogene 16 Homo sapiens 9-12 9812584-3 1997 Lanthanum chloride, cerium chloride and mixed rare-earth chloride at levels of 0.5 to 1.5 mmol/L could inhibit obviously growth of cancer cells and change cell morphology and microtubule structure of PAMC82, similar to that of normal cells, their colony-forming ability lowered in soft agar, and expression of tumor suppressor gene p53, p16 and p21 increased and that of gene nm23 lowered. lanthanum chloride 0-18 H3 histone pseudogene 16 Homo sapiens 345-348 9812584-3 1997 Lanthanum chloride, cerium chloride and mixed rare-earth chloride at levels of 0.5 to 1.5 mmol/L could inhibit obviously growth of cancer cells and change cell morphology and microtubule structure of PAMC82, similar to that of normal cells, their colony-forming ability lowered in soft agar, and expression of tumor suppressor gene p53, p16 and p21 increased and that of gene nm23 lowered. Chlorides 10-18 H3 histone pseudogene 16 Homo sapiens 345-348 9188453-1 1997 Previously, our laboratory reported that lactosylceramide (LacCer) stimulated human aortic smooth muscle cell proliferation via specific activation of p44 mitogen-activated protein kinase (MAPK) in the p21(ras)/Raf-1/MEK2 pathway and induced expression of the transcription factor c-fos downstream to the p44 MAPK signaling cascade (Bhunia A. K., Han, H., Snowden, A., and Chatterjee S. (1996) J. Biol. CDw17 antigen 41-57 H3 histone pseudogene 16 Homo sapiens 202-205 9188453-9 1997 For example, the p21(ras).GTP loading, p44 MAPK activity, and induction of transcription factor c-fos all were inhibited by NAC and DPI as well as an antioxidant pyrrolidine dithiocarbamate or reduced glutathione (GSH). diphenyleneiodonium 132-135 H3 histone pseudogene 16 Homo sapiens 17-20 9188453-1 1997 Previously, our laboratory reported that lactosylceramide (LacCer) stimulated human aortic smooth muscle cell proliferation via specific activation of p44 mitogen-activated protein kinase (MAPK) in the p21(ras)/Raf-1/MEK2 pathway and induced expression of the transcription factor c-fos downstream to the p44 MAPK signaling cascade (Bhunia A. K., Han, H., Snowden, A., and Chatterjee S. (1996) J. Biol. CDw17 antigen 59-65 H3 histone pseudogene 16 Homo sapiens 202-205 9188453-9 1997 For example, the p21(ras).GTP loading, p44 MAPK activity, and induction of transcription factor c-fos all were inhibited by NAC and DPI as well as an antioxidant pyrrolidine dithiocarbamate or reduced glutathione (GSH). pyrrolidine dithiocarbamic acid 162-189 H3 histone pseudogene 16 Homo sapiens 17-20 9188453-9 1997 For example, the p21(ras).GTP loading, p44 MAPK activity, and induction of transcription factor c-fos all were inhibited by NAC and DPI as well as an antioxidant pyrrolidine dithiocarbamate or reduced glutathione (GSH). Glutathione 201-212 H3 histone pseudogene 16 Homo sapiens 17-20 9188453-9 1997 For example, the p21(ras).GTP loading, p44 MAPK activity, and induction of transcription factor c-fos all were inhibited by NAC and DPI as well as an antioxidant pyrrolidine dithiocarbamate or reduced glutathione (GSH). Glutathione 214-217 H3 histone pseudogene 16 Homo sapiens 17-20 9102473-5 1997 To determine the role of the metal ion, the crystal structure of p21(G12P). Metals 29-34 H3 histone pseudogene 16 Homo sapiens 65-68 9208460-1 1997 Anthracene-1,8-dimethanol, C16H14O2, crystallized in the centrosymmetric space group P21/n. anthracene-1,8-dimethanol 0-25 H3 histone pseudogene 16 Homo sapiens 85-88 9208460-1 1997 Anthracene-1,8-dimethanol, C16H14O2, crystallized in the centrosymmetric space group P21/n. c16h14o2 27-35 H3 histone pseudogene 16 Homo sapiens 85-88 9112760-0 1997 Inhibition of the GDP/GTP exchange reaction of ras p21 by aluminum ion. Guanosine Diphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 51-54 9112760-0 1997 Inhibition of the GDP/GTP exchange reaction of ras p21 by aluminum ion. Guanosine Triphosphate 22-25 H3 histone pseudogene 16 Homo sapiens 51-54 9112760-0 1997 Inhibition of the GDP/GTP exchange reaction of ras p21 by aluminum ion. Aluminum 58-66 H3 histone pseudogene 16 Homo sapiens 51-54 9112760-1 1997 In an effort to understand the biochemical mechanisms of aluminum-induced neurotoxicity, we investigated the effects of aluminum ion, Al3+, on the Mg(2+)- and nucleotide-dependent protein, ras p21. Aluminum 120-128 H3 histone pseudogene 16 Homo sapiens 193-196 9112760-2 1997 Picomolar Al3+ concentrations inhibited the GTPase activity of ras p21 in an Mg(2+)-dependent manner, consistent with an Al3+/Mg2+ competition mechanism. ALUMINUM ION 10-14 H3 histone pseudogene 16 Homo sapiens 67-70 9112760-2 1997 Picomolar Al3+ concentrations inhibited the GTPase activity of ras p21 in an Mg(2+)-dependent manner, consistent with an Al3+/Mg2+ competition mechanism. magnesium ion 77-83 H3 histone pseudogene 16 Homo sapiens 67-70 9112760-2 1997 Picomolar Al3+ concentrations inhibited the GTPase activity of ras p21 in an Mg(2+)-dependent manner, consistent with an Al3+/Mg2+ competition mechanism. ALUMINUM ION 121-125 H3 histone pseudogene 16 Homo sapiens 67-70 9112760-2 1997 Picomolar Al3+ concentrations inhibited the GTPase activity of ras p21 in an Mg(2+)-dependent manner, consistent with an Al3+/Mg2+ competition mechanism. magnesium ion 126-130 H3 histone pseudogene 16 Homo sapiens 67-70 9112760-4 1997 Kinetic studies demonstrated that the mode of Al(3+)-induced inhibition of ras p21 GTPase activity changed from competitive to mixed non-competitive as the number of ras p21 turnovers increased. ALUMINUM ION 46-52 H3 histone pseudogene 16 Homo sapiens 79-82 9112760-4 1997 Kinetic studies demonstrated that the mode of Al(3+)-induced inhibition of ras p21 GTPase activity changed from competitive to mixed non-competitive as the number of ras p21 turnovers increased. ALUMINUM ION 46-52 H3 histone pseudogene 16 Homo sapiens 170-173 9112760-5 1997 Further dissection of the ras p21 cycle revealed that Mg(2+)-dependent GDP/GTP exchange was the Al(3+)-sensitive step. magnesium ion 54-60 H3 histone pseudogene 16 Homo sapiens 30-33 9112760-5 1997 Further dissection of the ras p21 cycle revealed that Mg(2+)-dependent GDP/GTP exchange was the Al(3+)-sensitive step. Guanosine Diphosphate 71-74 H3 histone pseudogene 16 Homo sapiens 30-33 9112760-5 1997 Further dissection of the ras p21 cycle revealed that Mg(2+)-dependent GDP/GTP exchange was the Al(3+)-sensitive step. Guanosine Triphosphate 75-78 H3 histone pseudogene 16 Homo sapiens 30-33 9112760-5 1997 Further dissection of the ras p21 cycle revealed that Mg(2+)-dependent GDP/GTP exchange was the Al(3+)-sensitive step. ALUMINUM ION 96-102 H3 histone pseudogene 16 Homo sapiens 30-33 9331847-5 1997 In 34 patients who had tumors designated p53-/p21+ or p53+/p21+, CHPP reduced the percentage of patients who died from recurrence of cancer from 10/20 (50%) to 3/14 (21.4%, P = 0.184). chpp 65-69 H3 histone pseudogene 16 Homo sapiens 46-49 9331847-5 1997 In 34 patients who had tumors designated p53-/p21+ or p53+/p21+, CHPP reduced the percentage of patients who died from recurrence of cancer from 10/20 (50%) to 3/14 (21.4%, P = 0.184). chpp 65-69 H3 histone pseudogene 16 Homo sapiens 59-62 9331847-7 1997 In the case of patients who had p21-positive tumors, the 5-year survival rate of 11 patients who were treated with CHPP (72.7%) was higher than that of 17 patients who were not treated with CHPP (41.2%, p = 0.027). chpp 115-119 H3 histone pseudogene 16 Homo sapiens 32-35 9331847-8 1997 However, in the case of patients with p21-negative tumors, the 5-year survival rate of 10 patients who were treated with CHPP (50%) was not very different from that of 28 patients who were not treated with CHPP (42.9%, p = 0.308). chpp 121-125 H3 histone pseudogene 16 Homo sapiens 38-41 9331847-9 1997 CONCLUSIONS: These results indicate that the CHPP might be effective in preventing the recurrence of cancer in patients with p21-positive regardless of the expression of p53. chpp 45-49 H3 histone pseudogene 16 Homo sapiens 125-128 9194162-0 1997 Comparison of ras-p21 bound to GDP and GTP: differences in protein and ligand dynamics. Guanosine Diphosphate 31-34 H3 histone pseudogene 16 Homo sapiens 18-21 9194162-0 1997 Comparison of ras-p21 bound to GDP and GTP: differences in protein and ligand dynamics. Guanosine Triphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 18-21 9194162-2 1997 Essential dynamics analysis of 300 ps of full solvent molecular dynamics simulations revealed differences in structure and dynamics between GDP- and GTP-bound forms of H-ras-p21. Guanosine Diphosphate 140-143 H3 histone pseudogene 16 Homo sapiens 174-177 9054359-1 1997 NIH 3T3 fibroblasts stably transformed with a constitutively active isoform of p21(Ras), H-RasV12 (v-H-Ras or EJ-Ras), produced large amounts of the reactive oxygen species superoxide (.O2-). Reactive Oxygen Species 149-172 H3 histone pseudogene 16 Homo sapiens 79-82 9054359-1 1997 NIH 3T3 fibroblasts stably transformed with a constitutively active isoform of p21(Ras), H-RasV12 (v-H-Ras or EJ-Ras), produced large amounts of the reactive oxygen species superoxide (.O2-). Superoxides 173-183 H3 histone pseudogene 16 Homo sapiens 79-82 9054359-1 1997 NIH 3T3 fibroblasts stably transformed with a constitutively active isoform of p21(Ras), H-RasV12 (v-H-Ras or EJ-Ras), produced large amounts of the reactive oxygen species superoxide (.O2-). Superoxides 186-188 H3 histone pseudogene 16 Homo sapiens 79-82 9236898-2 1997 The ras family of genes consists of three functional genes which encode highly similar, guanine nucleotide-binding, proteins (p21) of 21kDa, with GTPase activity. Guanine Nucleotides 88-106 H3 histone pseudogene 16 Homo sapiens 126-129 9125526-0 1997 Conformational and dynamic differences between N-ras P21 bound to GTPgammaS and to GMPPNP as studied by NMR. Guanylyl Imidodiphosphate 83-89 H3 histone pseudogene 16 Homo sapiens 53-56 9125526-1 1997 Heteronuclear-edited proton-detected NMR methods are used to study the nucleotide-dependent conformational changes between the GMPPNP form of human N-ras P21 as compared to GDP and GTPgammaS forms. Guanylyl Imidodiphosphate 127-133 H3 histone pseudogene 16 Homo sapiens 154-157 9209430-4 1997 This chloroquine-induced change suggests that the increase in intracellular pH and the upregulation of p21 with subsequent downregulation of cdc2 kinase are triggers for basophilic differentiation of this cell line. Chloroquine 5-16 H3 histone pseudogene 16 Homo sapiens 103-106 9194162-2 1997 Essential dynamics analysis of 300 ps of full solvent molecular dynamics simulations revealed differences in structure and dynamics between GDP- and GTP-bound forms of H-ras-p21. Guanosine Triphosphate 149-152 H3 histone pseudogene 16 Homo sapiens 174-177 9194162-4 1997 Differences in dynamics between H-ras-p21 GDP and H-ras-p21 GTP may be related to interactions of ras with GAP and its receptor and effector. Guanosine Diphosphate 42-45 H3 histone pseudogene 16 Homo sapiens 38-41 9194162-4 1997 Differences in dynamics between H-ras-p21 GDP and H-ras-p21 GTP may be related to interactions of ras with GAP and its receptor and effector. Guanosine Triphosphate 60-63 H3 histone pseudogene 16 Homo sapiens 56-59 9016871-4 1997 In addition, T cells exposed to wild-type ligand in the presence of anti-CD4 antibodies show a pattern of TCR signaling resembling that seen using partial agonists, with predominant accumulation of the p21 tyrosine-phosphorylated form of TCR-zeta, reduced tyrosine phosphorylation of CD3epsilon, and no detectable phosphorylation of ZAP-70. Tyrosine 206-214 H3 histone pseudogene 16 Homo sapiens 202-205 9038193-7 1997 Activation of the A2A-adenosine receptor is associated with increased levels of GTP-bound p21(ras). Guanosine Triphosphate 80-83 H3 histone pseudogene 16 Homo sapiens 90-93 9020151-1 1997 Structural basis for the nitric oxide-p21(ras) interaction. Nitric Oxide 25-37 H3 histone pseudogene 16 Homo sapiens 38-41 9020151-2 1997 We have identified the site of molecular interaction between nitric oxide (NO) and p21(ras) responsible for initiation of signal transduction. Nitric Oxide 61-73 H3 histone pseudogene 16 Homo sapiens 83-86 9020151-5 1997 NO-related species stimulated guanine nucleotide exchange on wild-type p21(ras), resulting in an active form, but not on p21(ras)C118S. Guanine Nucleotides 30-48 H3 histone pseudogene 16 Homo sapiens 71-74 9020151-7 1997 These data indicate that Cys118 is a critical site of redox regulation of p21(ras), and S-nitrosylation of this residue triggers guanine nucleotide exchange and downstream signaling. Guanine Nucleotides 129-147 H3 histone pseudogene 16 Homo sapiens 74-77 10325614-0 1997 [Effects of sterigmatocystin on ras p21 expression and ultrastructure of human lung fibroblasts in vitro]. Sterigmatocystin 12-28 H3 histone pseudogene 16 Homo sapiens 36-39 10325614-1 1997 Effects of Sterigmatocystin (ST) on ras p21 expression and ultrastructure of human lung fibroblasts in vitro were studied with immunological flow cytometry and electron microscopy. Sterigmatocystin 29-31 H3 histone pseudogene 16 Homo sapiens 40-43 9016871-4 1997 In addition, T cells exposed to wild-type ligand in the presence of anti-CD4 antibodies show a pattern of TCR signaling resembling that seen using partial agonists, with predominant accumulation of the p21 tyrosine-phosphorylated form of TCR-zeta, reduced tyrosine phosphorylation of CD3epsilon, and no detectable phosphorylation of ZAP-70. Tyrosine 256-264 H3 histone pseudogene 16 Homo sapiens 202-205 8988173-5 1997 In a search for cellular factors that could activate p21 during phorbol ester (TPA)-induced differentiation, we identified AP2 as a regulator of p21 expression. Phorbol Esters 64-77 H3 histone pseudogene 16 Homo sapiens 53-56 9000576-2 1997 We show that despite p21 induction in 7 of 12 human cancer cell lines treated with PMA, growth inhibition was observed only in two cell lines (SKBr3 breast and LNCaP prostate cancer cells). Tetradecanoylphorbol Acetate 83-86 H3 histone pseudogene 16 Homo sapiens 21-24 9000576-7 1997 Our findings suggest that induction of p21 and down-regulation of c-myc may be necessary steps in a PMA-induced growth-inhibitory pathway in cancer cells. Tetradecanoylphorbol Acetate 100-103 H3 histone pseudogene 16 Homo sapiens 39-42 9021406-5 1997 C27 also exhibited a much stronger response to a mutated p21 Ras whole-protein molecule-carrying Val at position 12, as compared with the wild-type protein. Valine 97-100 H3 histone pseudogene 16 Homo sapiens 57-60 9037749-1 1997 Anthracene-9-carboxylic acid, C15H10O2, was found to crystallize in the centrosymmetric space group P2(1)/n. 9-anthroic acid 0-28 H3 histone pseudogene 16 Homo sapiens 100-105 9037749-1 1997 Anthracene-9-carboxylic acid, C15H10O2, was found to crystallize in the centrosymmetric space group P2(1)/n. c15h10o2 30-38 H3 histone pseudogene 16 Homo sapiens 100-105 8996528-1 1997 PURPOSE: DNA damage-inducible genes, such as gadd153, gadd45, p21 and c-jun, have previously been shown to be induced by the chemotherapeutic agent cisplatin. Cisplatin 148-157 H3 histone pseudogene 16 Homo sapiens 62-65 8988173-5 1997 In a search for cellular factors that could activate p21 during phorbol ester (TPA)-induced differentiation, we identified AP2 as a regulator of p21 expression. Phorbol Esters 64-77 H3 histone pseudogene 16 Homo sapiens 145-148 8988173-5 1997 In a search for cellular factors that could activate p21 during phorbol ester (TPA)-induced differentiation, we identified AP2 as a regulator of p21 expression. Tetradecanoylphorbol Acetate 79-82 H3 histone pseudogene 16 Homo sapiens 53-56 8988173-5 1997 In a search for cellular factors that could activate p21 during phorbol ester (TPA)-induced differentiation, we identified AP2 as a regulator of p21 expression. Tetradecanoylphorbol Acetate 79-82 H3 histone pseudogene 16 Homo sapiens 145-148 8988173-6 1997 Mutagenesis of an AP2 DNA-binding site within a p21 promoter-luciferase reporter inhibited its activation by either AP2 transfection or TPA stimulation. Tetradecanoylphorbol Acetate 136-139 H3 histone pseudogene 16 Homo sapiens 48-51 9067995-3 1997 The amount of rho p21 in cells or tissues is determined by the in vitro ADP-ribosylation reaction with C3 exoenzyme and 32P NAD. Adenosine Diphosphate 72-75 H3 histone pseudogene 16 Homo sapiens 18-21 9067995-3 1997 The amount of rho p21 in cells or tissues is determined by the in vitro ADP-ribosylation reaction with C3 exoenzyme and 32P NAD. 32p nad 120-127 H3 histone pseudogene 16 Homo sapiens 18-21 9067995-0 1997 [Analysis of the cellular functions of the small GTP-binding protein rho p21 with Clostridium botulinum C3 exoenzyme]. Guanosine Triphosphate 49-52 H3 histone pseudogene 16 Homo sapiens 73-76 8939963-4 1996 Within 2 min of stimulation, we also observed increased tyrosine phosphorylation of SHC, activation of the guanidine nucleotide exchange activity on p21(ras), and an electrophoretic mobility shift of MAP kinase. guanidine nucleotide 107-127 H3 histone pseudogene 16 Homo sapiens 149-152 9015898-1 1996 4-(2-Naphthyl)butanoic acid, C14H14O2, crystallizes in the centrosymmetric space group P2(1)/a. 4-(2-naphthyl)butanoic acid 0-27 H3 histone pseudogene 16 Homo sapiens 87-92 9015898-1 1996 4-(2-Naphthyl)butanoic acid, C14H14O2, crystallizes in the centrosymmetric space group P2(1)/a. 2,6-dimethoxybiphenyl 29-37 H3 histone pseudogene 16 Homo sapiens 87-92 11666874-8 1996 [Pb(NO(3))(2)(EO6)] is monoclinic P2(1)/c, with a = 16.289(4) A, b = 10.773(4) A, c = 12.329(4) A, beta = 106.77(2) degrees, and Z = 4. Lead 1-3 H3 histone pseudogene 16 Homo sapiens 34-39 11666884-8 1996 Crystallographic data (-173 degrees C) for [P(t)()Bu(2)MeH][Ru(2)Cl(5)(CO)(2)(P(t)()Bu(2)Me)(2)]: a = 16.418(2)A, b = 12.578(2)A, c = 20.044(3)A, beta = 103.38(1) degrees with Z = 4 in space group P2(1)/a. (2)meh 52-58 H3 histone pseudogene 16 Homo sapiens 197-202 8972729-1 1996 Peptide specific polyclonal antibodies directed against C-termini of ras p21 related GTP-binding proteins, ralA and ralB, were generated. Guanosine Triphosphate 85-88 H3 histone pseudogene 16 Homo sapiens 73-76 8916907-7 1996 Further, the reduced GTPase reaction rate that characterizes the oncogenic effect of many of the p21 mutants found in human tumors seems to be a consequence of a slightly reduced pKa of the gamma-phosphate group of bound GTP. Phosphates 196-205 H3 histone pseudogene 16 Homo sapiens 97-100 8916907-7 1996 Further, the reduced GTPase reaction rate that characterizes the oncogenic effect of many of the p21 mutants found in human tumors seems to be a consequence of a slightly reduced pKa of the gamma-phosphate group of bound GTP. Guanosine Triphosphate 21-24 H3 histone pseudogene 16 Homo sapiens 97-100 8910345-1 1996 Activation of p21(ras) by GTP loading is a critical step in a cascade of intracellular insulin signaling. Guanosine Triphosphate 26-29 H3 histone pseudogene 16 Homo sapiens 14-17 11666844-0 1996 X-ray Crystallographic Study of the Ruthenium Blue Complexes [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O, [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, and [Ru(2)I(3)(tacn)(2)](PF(6))(2): Steric Interactions and the Ru-Ru "Bond Length" X-ray crystal structures are reported for the following complexes: [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O (tacn = 1,4,7-triazacyclononane), monoclinic P2(1)/n, Z = 4, a = 14.418(8) A, b = 11.577(3) A, c = 18.471(1) A, beta = 91.08(5) degrees, V = 3082 A(3), R(R(w)) = 0.039 (0.043) using 4067 unique data with I > 2.5sigma(I) at 293 K; [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, monoclinic P2(1)/a, Z = 4, a = 13.638(4) A, b = 12.283(4) A, c = 18.679(6) A, beta = 109.19(2) degrees, V = 3069.5 A(3), R(R(w)) = 0.052 (0.054) using 3668 unique data with I > 2.5sigma(I) at 293 K; [Ru(2)I(3)(tacn)(2)](PF(6))(2), cubic P2(1)/3, Z = 3, a = 14.03(4) A, beta = 90.0 degrees, V = 2763.1(1) A(3), R (R(w)) = 0.022 (0.025) using 896 unique data with I > 2.5sigma(I) at 293 K. All of the cations have cofacial bioctahedral geometries, although [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O, [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, and [Ru(2)I(3)(tacn)(2)](PF(6))(2) are not isomorphous. ruthenium blue 36-50 H3 histone pseudogene 16 Homo sapiens 377-382 11666844-0 1996 X-ray Crystallographic Study of the Ruthenium Blue Complexes [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O, [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, and [Ru(2)I(3)(tacn)(2)](PF(6))(2): Steric Interactions and the Ru-Ru "Bond Length" X-ray crystal structures are reported for the following complexes: [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O (tacn = 1,4,7-triazacyclononane), monoclinic P2(1)/n, Z = 4, a = 14.418(8) A, b = 11.577(3) A, c = 18.471(1) A, beta = 91.08(5) degrees, V = 3082 A(3), R(R(w)) = 0.039 (0.043) using 4067 unique data with I > 2.5sigma(I) at 293 K; [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, monoclinic P2(1)/a, Z = 4, a = 13.638(4) A, b = 12.283(4) A, c = 18.679(6) A, beta = 109.19(2) degrees, V = 3069.5 A(3), R(R(w)) = 0.052 (0.054) using 3668 unique data with I > 2.5sigma(I) at 293 K; [Ru(2)I(3)(tacn)(2)](PF(6))(2), cubic P2(1)/3, Z = 3, a = 14.03(4) A, beta = 90.0 degrees, V = 2763.1(1) A(3), R (R(w)) = 0.022 (0.025) using 896 unique data with I > 2.5sigma(I) at 293 K. All of the cations have cofacial bioctahedral geometries, although [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O, [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, and [Ru(2)I(3)(tacn)(2)](PF(6))(2) are not isomorphous. ruthenium blue 36-50 H3 histone pseudogene 16 Homo sapiens 616-621 11666844-0 1996 X-ray Crystallographic Study of the Ruthenium Blue Complexes [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O, [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, and [Ru(2)I(3)(tacn)(2)](PF(6))(2): Steric Interactions and the Ru-Ru "Bond Length" X-ray crystal structures are reported for the following complexes: [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O (tacn = 1,4,7-triazacyclononane), monoclinic P2(1)/n, Z = 4, a = 14.418(8) A, b = 11.577(3) A, c = 18.471(1) A, beta = 91.08(5) degrees, V = 3082 A(3), R(R(w)) = 0.039 (0.043) using 4067 unique data with I > 2.5sigma(I) at 293 K; [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, monoclinic P2(1)/a, Z = 4, a = 13.638(4) A, b = 12.283(4) A, c = 18.679(6) A, beta = 109.19(2) degrees, V = 3069.5 A(3), R(R(w)) = 0.052 (0.054) using 3668 unique data with I > 2.5sigma(I) at 293 K; [Ru(2)I(3)(tacn)(2)](PF(6))(2), cubic P2(1)/3, Z = 3, a = 14.03(4) A, beta = 90.0 degrees, V = 2763.1(1) A(3), R (R(w)) = 0.022 (0.025) using 896 unique data with I > 2.5sigma(I) at 293 K. All of the cations have cofacial bioctahedral geometries, although [Ru(2)Cl(3)(tacn)(2)](PF(6))(2).4H(2)O, [Ru(2)Br(3)(tacn)(2)](PF(6))(2).2H(2)O, and [Ru(2)I(3)(tacn)(2)](PF(6))(2) are not isomorphous. ruthenium blue 36-50 H3 histone pseudogene 16 Homo sapiens 845-859 11666847-2 1996 [Cu(H(2)O)(tpa)](ClO(4))(2) (1) crystallized in the monoclinic system, space group P2(1)/a, with a = 15.029(7) A, b = 9.268(2) A, c = 17.948(5) A, beta = 113.80(3) degrees, and Z = 4 (R = 0.061, R(w) = 0.059). tris(2-pyridylmethyl)amine 11-14 H3 histone pseudogene 16 Homo sapiens 83-88 11666847-2 1996 [Cu(H(2)O)(tpa)](ClO(4))(2) (1) crystallized in the monoclinic system, space group P2(1)/a, with a = 15.029(7) A, b = 9.268(2) A, c = 17.948(5) A, beta = 113.80(3) degrees, and Z = 4 (R = 0.061, R(w) = 0.059). clo 17-20 H3 histone pseudogene 16 Homo sapiens 83-88 11666847-4 1996 [CuCl(Me(2)tpa)]ClO(4) (3) crystallized in the monoclinic system, space group P2(1)/n, with a = 19.650(4) A, b = 13.528(4) A, c = 8.55(1) A, beta = 101.51(5) degrees, and Z = 4 (R = 0.071, R(w) = 0.050). cuprous chloride 1-5 H3 histone pseudogene 16 Homo sapiens 78-83 11666847-5 1996 [CuCl(Me(3)tpa)][CuCl(2)(Me(3)tpa)]ClO(4) (4) crystallized in the monoclinic system, space group P2(1)/a, with a = 15.698(6) A, b = 14.687(7) A, c = 19.475(4) A, beta = 97.13(2) degrees, and Z = 4 (R = 0.054, R(w) = 0.038). cuprous chloride 1-5 H3 histone pseudogene 16 Homo sapiens 97-102 11666847-5 1996 [CuCl(Me(3)tpa)][CuCl(2)(Me(3)tpa)]ClO(4) (4) crystallized in the monoclinic system, space group P2(1)/a, with a = 15.698(6) A, b = 14.687(7) A, c = 19.475(4) A, beta = 97.13(2) degrees, and Z = 4 (R = 0.054, R(w) = 0.038). me(3)tpa 6-14 H3 histone pseudogene 16 Homo sapiens 97-102 11666847-5 1996 [CuCl(Me(3)tpa)][CuCl(2)(Me(3)tpa)]ClO(4) (4) crystallized in the monoclinic system, space group P2(1)/a, with a = 15.698(6) A, b = 14.687(7) A, c = 19.475(4) A, beta = 97.13(2) degrees, and Z = 4 (R = 0.054, R(w) = 0.038). cupric chloride 17-24 H3 histone pseudogene 16 Homo sapiens 97-102 11666847-5 1996 [CuCl(Me(3)tpa)][CuCl(2)(Me(3)tpa)]ClO(4) (4) crystallized in the monoclinic system, space group P2(1)/a, with a = 15.698(6) A, b = 14.687(7) A, c = 19.475(4) A, beta = 97.13(2) degrees, and Z = 4 (R = 0.054, R(w) = 0.038). me(3)tpa) 6-15 H3 histone pseudogene 16 Homo sapiens 97-102 11666847-5 1996 [CuCl(Me(3)tpa)][CuCl(2)(Me(3)tpa)]ClO(4) (4) crystallized in the monoclinic system, space group P2(1)/a, with a = 15.698(6) A, b = 14.687(7) A, c = 19.475(4) A, beta = 97.13(2) degrees, and Z = 4 (R = 0.054, R(w) = 0.038). clo 35-38 H3 histone pseudogene 16 Homo sapiens 97-102 8910345-7 1996 Insulin challenge of 3T3-L1 adipocytes increased incorporation of tritiated mevalonic acid in p21(ras) in a dose-dependent manner and stimulated a 2-fold increase in phosphorylation of the alpha-subunit of FTase at 5 min and a 4-fold increase at 60 min. tritiated mevalonic acid 66-90 H3 histone pseudogene 16 Homo sapiens 94-97 8960661-3 1996 He developed AML (M4) in February 1993 after long-term treatment with oral etoposide (total dose 14,650 mg) t(9; 11) (p21; q23) with rearrangement of MLL genes was recognized. Etoposide 75-84 H3 histone pseudogene 16 Homo sapiens 118-121 8887687-3 1996 p21(ras), a guanine nucleotide binding factor, mediates T-cell signal transduction through PKC-dependent and PKC-independent pathways. Guanine Nucleotides 12-30 H3 histone pseudogene 16 Homo sapiens 0-3 8887687-4 1996 The involvement of p21(ras) in the regulation of calcium-dependent signals has been suggested through analysis of its role in the activation of NF-AT. Calcium 49-56 H3 histone pseudogene 16 Homo sapiens 19-22 8887687-5 1996 We have investigated the inductions of the IE genes in response to calcium signals in Jurkat cells (in the presence of activated p21(ras)) and their correlated consequences. Calcium 67-74 H3 histone pseudogene 16 Homo sapiens 129-132 8887687-6 1996 The expression of activated p21(ras) negatively regulated the induction of IE genes by calcium ionophore. Calcium 87-94 H3 histone pseudogene 16 Homo sapiens 28-31 8947526-5 1996 The proportion of cellular p21-ras bound to GTP (ras-GTP level) was determined using immunoprecipitation of 32P-labeled cell lysates followed by thin layer chromatography and phosphoimaging analysis. Guanosine Triphosphate 44-47 H3 histone pseudogene 16 Homo sapiens 27-30 8947526-5 1996 The proportion of cellular p21-ras bound to GTP (ras-GTP level) was determined using immunoprecipitation of 32P-labeled cell lysates followed by thin layer chromatography and phosphoimaging analysis. Radium 31-34 H3 histone pseudogene 16 Homo sapiens 27-30 8947526-5 1996 The proportion of cellular p21-ras bound to GTP (ras-GTP level) was determined using immunoprecipitation of 32P-labeled cell lysates followed by thin layer chromatography and phosphoimaging analysis. Guanosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 27-30 8947526-5 1996 The proportion of cellular p21-ras bound to GTP (ras-GTP level) was determined using immunoprecipitation of 32P-labeled cell lysates followed by thin layer chromatography and phosphoimaging analysis. Phosphorus-32 108-111 H3 histone pseudogene 16 Homo sapiens 27-30 8810926-5 1996 By analysis of high-frequency EPR spectra, we determine the number of water molecules in the first coordination sphere of the manganous ion to be four in p21.Mn(II).GDP, consistent with prior low-frequency EPR and X-ray crystallographic studies. Water 70-75 H3 histone pseudogene 16 Homo sapiens 154-157 8810926-0 1996 High frequency (139.5 GHz) electron paramagnetic resonance characterization of Mn(II)-H2(17)O interactions in GDP and GTP forms of p21 ras. Manganese(2+) 79-85 H3 histone pseudogene 16 Homo sapiens 131-134 8810926-5 1996 By analysis of high-frequency EPR spectra, we determine the number of water molecules in the first coordination sphere of the manganous ion to be four in p21.Mn(II).GDP, consistent with prior low-frequency EPR and X-ray crystallographic studies. Guanosine Diphosphate 165-168 H3 histone pseudogene 16 Homo sapiens 154-157 8810926-0 1996 High frequency (139.5 GHz) electron paramagnetic resonance characterization of Mn(II)-H2(17)O interactions in GDP and GTP forms of p21 ras. Hydrogen 86-88 H3 histone pseudogene 16 Homo sapiens 131-134 8810926-0 1996 High frequency (139.5 GHz) electron paramagnetic resonance characterization of Mn(II)-H2(17)O interactions in GDP and GTP forms of p21 ras. Guanosine Diphosphate 110-113 H3 histone pseudogene 16 Homo sapiens 131-134 8810926-0 1996 High frequency (139.5 GHz) electron paramagnetic resonance characterization of Mn(II)-H2(17)O interactions in GDP and GTP forms of p21 ras. Guanosine Triphosphate 118-121 H3 histone pseudogene 16 Homo sapiens 131-134 8810926-1 1996 As a molecular switch, the ras protein p21 undergoes structural changes that couple recognition sites on the protein surface to the guanine nucleotide-divalent metal ion binding site. Guanine Nucleotides 132-150 H3 histone pseudogene 16 Homo sapiens 39-42 8810926-1 1996 As a molecular switch, the ras protein p21 undergoes structural changes that couple recognition sites on the protein surface to the guanine nucleotide-divalent metal ion binding site. Metals 160-165 H3 histone pseudogene 16 Homo sapiens 39-42 8810926-2 1996 X-ray crystallographic studies of p21 suggest that coordination between threonine-35 and the divalent metal ion plays an important role in these conformational changes. Threonine 72-81 H3 histone pseudogene 16 Homo sapiens 34-37 8810926-6 1996 In the complex of p21 with a GTP analog, p21.Mn(II).GMPPNP, we determine the hydration number to be 2, also consistent with crystal structures. Guanosine Triphosphate 29-32 H3 histone pseudogene 16 Homo sapiens 18-21 8810926-2 1996 X-ray crystallographic studies of p21 suggest that coordination between threonine-35 and the divalent metal ion plays an important role in these conformational changes. Metals 102-107 H3 histone pseudogene 16 Homo sapiens 34-37 8810926-3 1996 Recent ESEEM studies of p21 in solution, however, place threonine-35 more distant from the metal and were interpreted as weak or indirect coordination of this residue. Threonine 56-65 H3 histone pseudogene 16 Homo sapiens 24-27 8810926-6 1996 In the complex of p21 with a GTP analog, p21.Mn(II).GMPPNP, we determine the hydration number to be 2, also consistent with crystal structures. Guanosine Triphosphate 29-32 H3 histone pseudogene 16 Homo sapiens 41-44 8810926-4 1996 We report high frequency (139.5 GHz) EPR spectroscopy of p21.Mn(II) complexes of two guanine nucleotides that probes the link between threonine-35 and the divalent metal ion. Manganese(2+) 61-67 H3 histone pseudogene 16 Homo sapiens 57-60 8810926-6 1996 In the complex of p21 with a GTP analog, p21.Mn(II).GMPPNP, we determine the hydration number to be 2, also consistent with crystal structures. Manganese(2+) 45-51 H3 histone pseudogene 16 Homo sapiens 18-21 8810926-4 1996 We report high frequency (139.5 GHz) EPR spectroscopy of p21.Mn(II) complexes of two guanine nucleotides that probes the link between threonine-35 and the divalent metal ion. Guanine Nucleotides 85-104 H3 histone pseudogene 16 Homo sapiens 57-60 8810926-4 1996 We report high frequency (139.5 GHz) EPR spectroscopy of p21.Mn(II) complexes of two guanine nucleotides that probes the link between threonine-35 and the divalent metal ion. Threonine 134-143 H3 histone pseudogene 16 Homo sapiens 57-60 8810926-6 1996 In the complex of p21 with a GTP analog, p21.Mn(II).GMPPNP, we determine the hydration number to be 2, also consistent with crystal structures. Manganese(2+) 45-51 H3 histone pseudogene 16 Homo sapiens 41-44 8810926-4 1996 We report high frequency (139.5 GHz) EPR spectroscopy of p21.Mn(II) complexes of two guanine nucleotides that probes the link between threonine-35 and the divalent metal ion. Metals 164-169 H3 histone pseudogene 16 Homo sapiens 57-60 8810926-6 1996 In the complex of p21 with a GTP analog, p21.Mn(II).GMPPNP, we determine the hydration number to be 2, also consistent with crystal structures. Guanylyl Imidodiphosphate 52-58 H3 histone pseudogene 16 Homo sapiens 18-21 8810926-6 1996 In the complex of p21 with a GTP analog, p21.Mn(II).GMPPNP, we determine the hydration number to be 2, also consistent with crystal structures. Guanylyl Imidodiphosphate 52-58 H3 histone pseudogene 16 Homo sapiens 41-44 8810926-7 1996 This result rules out indirect coordination of threonine-35 in the solution structure of p21.Mn(II).GMPPNP, and implicates direct, weak coordination of this residue as suggested by Halkides et al. Threonine 47-56 H3 histone pseudogene 16 Homo sapiens 89-92 8810926-7 1996 This result rules out indirect coordination of threonine-35 in the solution structure of p21.Mn(II).GMPPNP, and implicates direct, weak coordination of this residue as suggested by Halkides et al. Manganese(2+) 93-99 H3 histone pseudogene 16 Homo sapiens 89-92 8810926-7 1996 This result rules out indirect coordination of threonine-35 in the solution structure of p21.Mn(II).GMPPNP, and implicates direct, weak coordination of this residue as suggested by Halkides et al. Guanylyl Imidodiphosphate 100-106 H3 histone pseudogene 16 Homo sapiens 89-92 8810927-0 1996 High frequency (139.5 GHz) electron paramagnetic resonance spectroscopy of the GTP form of p21 ras with selective 17O labeling of threonine. Guanosine Triphosphate 79-82 H3 histone pseudogene 16 Homo sapiens 91-94 8810927-0 1996 High frequency (139.5 GHz) electron paramagnetic resonance spectroscopy of the GTP form of p21 ras with selective 17O labeling of threonine. 17o 114-117 H3 histone pseudogene 16 Homo sapiens 91-94 8810927-0 1996 High frequency (139.5 GHz) electron paramagnetic resonance spectroscopy of the GTP form of p21 ras with selective 17O labeling of threonine. Threonine 130-139 H3 histone pseudogene 16 Homo sapiens 91-94 8810927-1 1996 Electron paramagnetic resonance spectroscopy at 139.5 GHz has been used to study p21 ras complexed with Mn(II) and guanosine 5"-(beta, gamma-imidotriphosphate), an analog of GTP. Manganese(2+) 104-110 H3 histone pseudogene 16 Homo sapiens 81-84 8810927-1 1996 Electron paramagnetic resonance spectroscopy at 139.5 GHz has been used to study p21 ras complexed with Mn(II) and guanosine 5"-(beta, gamma-imidotriphosphate), an analog of GTP. Guanylyl Imidodiphosphate 115-158 H3 histone pseudogene 16 Homo sapiens 81-84 8810927-1 1996 Electron paramagnetic resonance spectroscopy at 139.5 GHz has been used to study p21 ras complexed with Mn(II) and guanosine 5"-(beta, gamma-imidotriphosphate), an analog of GTP. Guanosine Triphosphate 174-177 H3 histone pseudogene 16 Homo sapiens 81-84 8810927-2 1996 The p21 sample studied was selectively labeled with [17O gamma]threonine to a final enrichment of 30%. [17o gamma]threonine 52-72 H3 histone pseudogene 16 Homo sapiens 4-7 8810927-6 1996 This contrast underscores the peculiar weakness of this Mn(II)-O interaction in p21 and persuasively argues that the nucleotide-induced conformational change, which is known to encompass the region of p21 involving Thr35, is not driven by Mn(II) coordination of the Thr35 hydroxyl group. Manganese(2+) 56-62 H3 histone pseudogene 16 Homo sapiens 80-83 8810927-6 1996 This contrast underscores the peculiar weakness of this Mn(II)-O interaction in p21 and persuasively argues that the nucleotide-induced conformational change, which is known to encompass the region of p21 involving Thr35, is not driven by Mn(II) coordination of the Thr35 hydroxyl group. Manganese(2+) 56-62 H3 histone pseudogene 16 Homo sapiens 201-204 8810927-6 1996 This contrast underscores the peculiar weakness of this Mn(II)-O interaction in p21 and persuasively argues that the nucleotide-induced conformational change, which is known to encompass the region of p21 involving Thr35, is not driven by Mn(II) coordination of the Thr35 hydroxyl group. Manganese(2+) 239-245 H3 histone pseudogene 16 Homo sapiens 201-204 8661432-2 1996 Nucleotide substitutions introduced into the -3 and +4 positions of the p21 AUG codon (where the A of the AUG is +1) verified that purines in these positions are favored and demonstrated the similar contribution of the -3 and +4 positions to the efficiency of initiation codon selection in plants. Purines 131-138 H3 histone pseudogene 16 Homo sapiens 72-75 8764406-1 1996 The fold of the von Willebrand Factor type A domain (vWF-A) was predicted to be similar to an alpha/beta doubly wound fold in the GTP-binding domain of ras-p21, despite the lack of sequence or functional similarity. Guanosine Triphosphate 130-133 H3 histone pseudogene 16 Homo sapiens 156-159 11666630-6 1996 Light yellow polyhedrons of the title compound crystallize from the aqueous solvent of acetonitrile and aqueous solution as the formula of alpha-H(4)SiW(12)O(40).4HMPA.2H(2)O in the monoclinic, space group P2(1). acetonitrile 87-99 H3 histone pseudogene 16 Homo sapiens 206-211 11666630-6 1996 Light yellow polyhedrons of the title compound crystallize from the aqueous solvent of acetonitrile and aqueous solution as the formula of alpha-H(4)SiW(12)O(40).4HMPA.2H(2)O in the monoclinic, space group P2(1). alpha-h 139-146 H3 histone pseudogene 16 Homo sapiens 206-211 11666630-6 1996 Light yellow polyhedrons of the title compound crystallize from the aqueous solvent of acetonitrile and aqueous solution as the formula of alpha-H(4)SiW(12)O(40).4HMPA.2H(2)O in the monoclinic, space group P2(1). 4hmpa 162-167 H3 histone pseudogene 16 Homo sapiens 206-211 11666630-6 1996 Light yellow polyhedrons of the title compound crystallize from the aqueous solvent of acetonitrile and aqueous solution as the formula of alpha-H(4)SiW(12)O(40).4HMPA.2H(2)O in the monoclinic, space group P2(1). 2h(2)o 168-174 H3 histone pseudogene 16 Homo sapiens 206-211 8702787-4 1996 As with the small GTP-binding protein Ha-Ras p21 and with EF-Tu, nucleotide binding occurs in at least two steps and is describable in terms of a relatively weak initial interaction followed by a highly irreversible isomerization of the protein-nucleotide complex, which results in a change in the fluorescence properties. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 45-48 8702787-9 1996 The results demonstrate a high degree of mechanistic similarity between the Rab proteins and other GTP-binding proteins, which have been examined in detail, including Ha-Ras p21, Ran, and EF-Tu. Guanosine Triphosphate 99-102 H3 histone pseudogene 16 Homo sapiens 174-177 8702674-3 1996 We have demonstrated that NOx-induced activation of the guanine nucleotide-binding protein p21(ras) leads to nuclear translocation of the transcription factor NFkappaB. nicotine 1-N-oxide 26-29 H3 histone pseudogene 16 Homo sapiens 91-94 8663295-1 1996 Desensitization of p21(ras) after stimulation of cells by growth factors and phorbol 12-myristate 13-acetate (PMA) correlates with hyperphosphorylation of the guanine nucleotide exchange factor Son-of-sevenless (Sos) and its dissociation from the adaptor protein Grb2 (Cherniack, A., Klarlund, J. K., Conway, B. R., and Czech, M. P. (1995) J. Biol. Tetradecanoylphorbol Acetate 77-108 H3 histone pseudogene 16 Homo sapiens 19-22 8663295-1 1996 Desensitization of p21(ras) after stimulation of cells by growth factors and phorbol 12-myristate 13-acetate (PMA) correlates with hyperphosphorylation of the guanine nucleotide exchange factor Son-of-sevenless (Sos) and its dissociation from the adaptor protein Grb2 (Cherniack, A., Klarlund, J. K., Conway, B. R., and Czech, M. P. (1995) J. Biol. Tetradecanoylphorbol Acetate 110-113 H3 histone pseudogene 16 Homo sapiens 19-22 8663295-1 1996 Desensitization of p21(ras) after stimulation of cells by growth factors and phorbol 12-myristate 13-acetate (PMA) correlates with hyperphosphorylation of the guanine nucleotide exchange factor Son-of-sevenless (Sos) and its dissociation from the adaptor protein Grb2 (Cherniack, A., Klarlund, J. K., Conway, B. R., and Czech, M. P. (1995) J. Biol. Guanine Nucleotides 159-177 H3 histone pseudogene 16 Homo sapiens 19-22 8668337-5 1996 Furthermore, when levels of activated p21 ras were decreased in astrocytoma cells expressing the ras inhibitory Asn-17 dominant-negative mutant, levels of neurofibromin expression decreased. asn-17 112-118 H3 histone pseudogene 16 Homo sapiens 38-41 8687373-9 1996 Newly identified vitamin D-dependent target genes include those for Ca2+/Mg(2+)-ATPase in the intestine and p21 in the myelomonocytic U937 cell line. Vitamin D 17-26 H3 histone pseudogene 16 Homo sapiens 108-111 8832375-1 1996 rap-1A is a membrane-bound G-protein in the ras superfamily that, like the ras-p21 protein, is activated by binding GTP in place of GDP. Guanosine Diphosphate 132-135 H3 histone pseudogene 16 Homo sapiens 79-82 8832375-9 1996 In addition, we have found that ras-p21 and rap-M proteins are superimposable in the region 96-110 except at Asp 105. Aspartic Acid 109-112 H3 histone pseudogene 16 Homo sapiens 36-39 8832375-1 1996 rap-1A is a membrane-bound G-protein in the ras superfamily that, like the ras-p21 protein, is activated by binding GTP in place of GDP. Guanosine Triphosphate 116-119 H3 histone pseudogene 16 Homo sapiens 79-82 8608802-1 1996 The role of rho proteins, which are ras p21-related small GTP-binding proteins, in megakaryocyte endomitosis was examined using a botulinum C3 exoenzyme (C3), a rho inactivating enzyme. Guanosine Triphosphate 58-61 H3 histone pseudogene 16 Homo sapiens 40-43 8740369-1 1996 BACKGROUND: p21ras is one of the GTP-binding proteins that act as intercellular molecular switches. Guanosine Triphosphate 33-36 H3 histone pseudogene 16 Homo sapiens 12-15 11666422-10 1996 In Cu(2)(HL-H)(NCS)(3)OH.2H(2)O.3CH(3)OH.Et(2)O, 5 (a = 18.322(5) A, b = 15.543(6) A, c = 19.428(7) A, beta = 102.78(3) degrees, Z = 4, monoclinic, P2(1)/c), the hydroxide ion does not coordinate. Deuterium 25-27 H3 histone pseudogene 16 Homo sapiens 148-155 9206209-2 1996 Elevated PDGF-beta chain and P21 protein levels were found in hepatocytes in the early stages after DENA administration. Diethylnitrosamine 100-104 H3 histone pseudogene 16 Homo sapiens 29-32 8735493-5 1996 Radiation-induced phosphorylation of RPA p34 is nearly absent in non-cycling cells, while the expression of p21cipl/wafl/sdil remains inducible. sdil 121-125 H3 histone pseudogene 16 Homo sapiens 108-111 8649838-7 1996 Microinjection of rho GDP dissociation inhibitor or Clostridium botulinum ADP-ribosyltransferase C3 which is known to impair the function of a small GTP-binding protein, rho p21, inhibited the stress fiber formation by CCK-8 as well as by PDGF. Guanosine Triphosphate 149-152 H3 histone pseudogene 16 Homo sapiens 174-177 8838585-1 1996 rap-1A, an anti-oncogene-encoded protein, is a ras-p21-like protein whose sequence is over 80% homologous to p21 and which interacts with the same intracellular target proteins and is activated by the same mechanisms as p21, e.g., by binding GTP in place of GDP. Guanosine Triphosphate 242-245 H3 histone pseudogene 16 Homo sapiens 51-54 8566748-0 1996 Transcriptional activation of the Cdk inhibitor p21 by vitamin D3 leads to the induced differentiation of the myelomonocytic cell line U937. Cholecalciferol 55-65 H3 histone pseudogene 16 Homo sapiens 48-51 8566748-5 1996 Furthermore, we show that p21 is transcriptionally induced by 1,25-dihydroxyvitamin D3 in a VDR-dependent, but not p53-dependent, manner, and we identify a functional vitamin D response element in the p21 promoter. Calcitriol 62-86 H3 histone pseudogene 16 Homo sapiens 26-29 8615653-0 1996 Regulation of TNF-alpha and IL-1 gene expression during TPA-induced differentiation of "Malignant histiocytosis" DEL cell line t(5;6) (q35:p21). Tetradecanoylphorbol Acetate 56-59 H3 histone pseudogene 16 Homo sapiens 139-142 8642043-6 1996 7-Hydroxycoumarin decreased the relative amount of intracellular p21ras, and concomitantly a PMA-induced decrease of p21ras GTPase activity could be partially antagonized by 7-hydroxycoumarin. 7-hydroxycoumarin 0-17 H3 histone pseudogene 16 Homo sapiens 65-68 8642043-6 1996 7-Hydroxycoumarin decreased the relative amount of intracellular p21ras, and concomitantly a PMA-induced decrease of p21ras GTPase activity could be partially antagonized by 7-hydroxycoumarin. Tetradecanoylphorbol Acetate 93-96 H3 histone pseudogene 16 Homo sapiens 65-68 8642043-6 1996 7-Hydroxycoumarin decreased the relative amount of intracellular p21ras, and concomitantly a PMA-induced decrease of p21ras GTPase activity could be partially antagonized by 7-hydroxycoumarin. 7-hydroxycoumarin 174-191 H3 histone pseudogene 16 Homo sapiens 65-68 8631299-0 1996 The heterotrimeric G q protein-coupled angiotensin II receptor activates p21 ras via the tyrosine kinase-Shc-Grb2-Sos pathway in cardiac myocytes. sulfur monoxide 114-117 H3 histone pseudogene 16 Homo sapiens 73-76 8631299-5 1996 The p21 ras activation by Ang II is mediated by an increase in the guanine nucleotide exchange activity, but not by an inhibition of the GTPase-activating protein. Guanine Nucleotides 67-85 H3 histone pseudogene 16 Homo sapiens 4-7 8631299-6 1996 Ang II causes rapid tyrosine phosphorylation of Shc and its association with Grb2 and mSos-1, a guanine nucleotide exchange factor of p21 ras. Tyrosine 20-28 H3 histone pseudogene 16 Homo sapiens 134-137 8566748-5 1996 Furthermore, we show that p21 is transcriptionally induced by 1,25-dihydroxyvitamin D3 in a VDR-dependent, but not p53-dependent, manner, and we identify a functional vitamin D response element in the p21 promoter. Vitamin D 76-85 H3 histone pseudogene 16 Homo sapiens 26-29 8566748-5 1996 Furthermore, we show that p21 is transcriptionally induced by 1,25-dihydroxyvitamin D3 in a VDR-dependent, but not p53-dependent, manner, and we identify a functional vitamin D response element in the p21 promoter. Vitamin D 76-85 H3 histone pseudogene 16 Homo sapiens 201-204 8713572-4 1996 HMBA induces an increase in the level of p21 which inhibits cyclin-dependent kinase activity and, in turn, may cause cells to arrest in G1. hexamethylene bisacetamide 0-4 H3 histone pseudogene 16 Homo sapiens 41-44 8838585-1 1996 rap-1A, an anti-oncogene-encoded protein, is a ras-p21-like protein whose sequence is over 80% homologous to p21 and which interacts with the same intracellular target proteins and is activated by the same mechanisms as p21, e.g., by binding GTP in place of GDP. Guanosine Triphosphate 242-245 H3 histone pseudogene 16 Homo sapiens 109-112 8838585-1 1996 rap-1A, an anti-oncogene-encoded protein, is a ras-p21-like protein whose sequence is over 80% homologous to p21 and which interacts with the same intracellular target proteins and is activated by the same mechanisms as p21, e.g., by binding GTP in place of GDP. Guanosine Triphosphate 242-245 H3 histone pseudogene 16 Homo sapiens 109-112 8838585-1 1996 rap-1A, an anti-oncogene-encoded protein, is a ras-p21-like protein whose sequence is over 80% homologous to p21 and which interacts with the same intracellular target proteins and is activated by the same mechanisms as p21, e.g., by binding GTP in place of GDP. Guanosine Diphosphate 258-261 H3 histone pseudogene 16 Homo sapiens 51-54 8838585-1 1996 rap-1A, an anti-oncogene-encoded protein, is a ras-p21-like protein whose sequence is over 80% homologous to p21 and which interacts with the same intracellular target proteins and is activated by the same mechanisms as p21, e.g., by binding GTP in place of GDP. Guanosine Diphosphate 258-261 H3 histone pseudogene 16 Homo sapiens 109-112 8838585-1 1996 rap-1A, an anti-oncogene-encoded protein, is a ras-p21-like protein whose sequence is over 80% homologous to p21 and which interacts with the same intracellular target proteins and is activated by the same mechanisms as p21, e.g., by binding GTP in place of GDP. Guanosine Diphosphate 258-261 H3 histone pseudogene 16 Homo sapiens 109-112 8838585-5 1996 We have constructed the three-dimensional structure of rap-1A bound to GTP by using the energy-minimized three-dimensional structure of ras-p21 as the basis for the modeling using a stepwise procedure in which identical and homologous amino acid residues in rap-1A are assumed to adopt the same conformation as the corresponding residues in p21. Guanosine Triphosphate 71-74 H3 histone pseudogene 16 Homo sapiens 140-143 8838585-5 1996 We have constructed the three-dimensional structure of rap-1A bound to GTP by using the energy-minimized three-dimensional structure of ras-p21 as the basis for the modeling using a stepwise procedure in which identical and homologous amino acid residues in rap-1A are assumed to adopt the same conformation as the corresponding residues in p21. Guanosine Triphosphate 71-74 H3 histone pseudogene 16 Homo sapiens 341-344 8590632-5 1995 Although increases in wild type p53 protein in ML-1 cells resulted in increases in a p53 target gene, p21cipl/wafl/sdil, this effect was not observed in Raji cells which express a mutant p53 protein. sdil 115-119 H3 histone pseudogene 16 Homo sapiens 102-105 8983024-6 1996 Analysis of the binding and dissociation of GTP and GDP to normal and mutated p21 expressed in Escherichia coli showed that [V12D28]p21 and [D28]p21 do not bind GTP. Guanosine Triphosphate 44-47 H3 histone pseudogene 16 Homo sapiens 78-81 8983024-6 1996 Analysis of the binding and dissociation of GTP and GDP to normal and mutated p21 expressed in Escherichia coli showed that [V12D28]p21 and [D28]p21 do not bind GTP. Guanosine Diphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 78-81 8747433-0 1995 Structural effects of the binding of GTP to the wild-type and oncogenic forms of the ras-gene-encoded p21 proteins. Guanosine Triphosphate 37-40 H3 histone pseudogene 16 Homo sapiens 102-105 8747433-1 1995 Molecular dynamics calculations have been performed to determine the average structures of ras-gene-encoded p21 proteins bound to GTP, i.e., the normal (wild-type) protein and two oncogenic forms of this protein, the Val 12- and Leu 61-p21 proteins. Guanosine Triphosphate 130-133 H3 histone pseudogene 16 Homo sapiens 108-111 8747433-1 1995 Molecular dynamics calculations have been performed to determine the average structures of ras-gene-encoded p21 proteins bound to GTP, i.e., the normal (wild-type) protein and two oncogenic forms of this protein, the Val 12- and Leu 61-p21 proteins. Valine 217-220 H3 histone pseudogene 16 Homo sapiens 108-111 8747433-1 1995 Molecular dynamics calculations have been performed to determine the average structures of ras-gene-encoded p21 proteins bound to GTP, i.e., the normal (wild-type) protein and two oncogenic forms of this protein, the Val 12- and Leu 61-p21 proteins. Leucine 229-232 H3 histone pseudogene 16 Homo sapiens 108-111 8747433-9 1995 However, they still differ in structure at specific amino acid residues rather than in whole regions, in contradistinction to the results found for the p21-GDP complexes. Guanosine Diphosphate 156-159 H3 histone pseudogene 16 Homo sapiens 152-155 8607982-5 1995 Other aspects of Ras p21 regulation will be discussed, including the existence of RasGDl proteins that inhibit GDP dissociation from Ras, and may thus regulate the level of active Ras in the cell. Guanosine Diphosphate 111-114 H3 histone pseudogene 16 Homo sapiens 21-24 7479845-2 1995 This effect is mediated by increased phosphorylation of JNK in the presence of wild-type and oncogenic (Val-12) p21 protein in a dose-dependent manner. val-12 104-110 H3 histone pseudogene 16 Homo sapiens 112-115 8583229-4 1995 Treatment with NGF increased the amount of GTP bound p21ras 3-fold, within 20 min exposure. Guanosine Triphosphate 43-46 H3 histone pseudogene 16 Homo sapiens 53-56 7547978-2 1995 Formation of a complex with nucleotide-free H-ras p21 could be analyzed on native gel electrophoresis by combining C-CDC25Mm and p21.GDP, as the result of the fast separation of GDP from p21. c-cdc25mm 115-124 H3 histone pseudogene 16 Homo sapiens 50-53 7547978-2 1995 Formation of a complex with nucleotide-free H-ras p21 could be analyzed on native gel electrophoresis by combining C-CDC25Mm and p21.GDP, as the result of the fast separation of GDP from p21. Guanosine Diphosphate 133-136 H3 histone pseudogene 16 Homo sapiens 50-53 7547978-2 1995 Formation of a complex with nucleotide-free H-ras p21 could be analyzed on native gel electrophoresis by combining C-CDC25Mm and p21.GDP, as the result of the fast separation of GDP from p21. Guanosine Diphosphate 178-181 H3 histone pseudogene 16 Homo sapiens 50-53 7547978-3 1995 Therefore, in order to obtain highly purified heterodimer in preparative amounts, p21.GDP and C-CDC25Mm were exposed to an electric field and the complex purified by anionic chromatography. Guanosine Diphosphate 86-89 H3 histone pseudogene 16 Homo sapiens 82-85 7547978-4 1995 The rate of the C-CDC25Mm-mediated nucleotide exchange on p21 depended on the nature of the bound nucleotide (6 times faster for p21.GDP than p21.GTP) but was uninfluenced by the nature of the free nucleotide acting as second substrate. Guanosine Triphosphate 146-149 H3 histone pseudogene 16 Homo sapiens 58-61 7547978-8 1995 The "on-rate" of the nucleotide on the p21.C-CDC25Mm complex was similar for GDP and GTP and was little increased vs that on p21 alone. Guanosine Diphosphate 77-80 H3 histone pseudogene 16 Homo sapiens 39-42 7547978-8 1995 The "on-rate" of the nucleotide on the p21.C-CDC25Mm complex was similar for GDP and GTP and was little increased vs that on p21 alone. Guanosine Triphosphate 85-88 H3 histone pseudogene 16 Homo sapiens 39-42 7547942-0 1995 Molecular dynamics simulation of the solution structures of Ha-ras-p21 GDP and GTP complexes: flexibility, possible hinges, and levers of the conformational transition. Guanosine Diphosphate 71-74 H3 histone pseudogene 16 Homo sapiens 67-70 7547942-0 1995 Molecular dynamics simulation of the solution structures of Ha-ras-p21 GDP and GTP complexes: flexibility, possible hinges, and levers of the conformational transition. Guanosine Triphosphate 79-82 H3 histone pseudogene 16 Homo sapiens 67-70 7547942-1 1995 Unconstrained molecular dynamics simulations of the GDP and GTP complexes of Ha-ras p21 protein are performed in aqueous environment for 500 ps, using the GROMOS force field. Guanosine Diphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 84-87 7547942-1 1995 Unconstrained molecular dynamics simulations of the GDP and GTP complexes of Ha-ras p21 protein are performed in aqueous environment for 500 ps, using the GROMOS force field. Guanosine Triphosphate 60-63 H3 histone pseudogene 16 Homo sapiens 84-87 7677742-2 1995 Both H7 (serine/threonine kinase inhibitor) and staurosporine (protein kinase C inhibitor) were able to induce p21 protein in a time- and dose-dependent manner. Staurosporine 48-61 H3 histone pseudogene 16 Homo sapiens 111-114 7673152-7 1995 Finally, using recombinant p21ras in vitro, we found that redox modulators directly promoted guanine nucleotide exchange on p21ras. Guanine Nucleotides 93-111 H3 histone pseudogene 16 Homo sapiens 27-30 7656216-9 1995 Since the activity of p21(ras) is thought to be involved in pathways of T cell activation, we set out to determine whether down-regulation of ras expression in T cells could be the mechanism by which T cell proliferation was inhibited in GSH-depleted T lymphocytes. Glutathione 238-241 H3 histone pseudogene 16 Homo sapiens 22-25 7595467-3 1995 The complex [Cu(Cx)2].2H2O crystallizes in the monoclinic system, space group P2(1)/c. bis(cinoxacinate)copper(II) 13-20 H3 histone pseudogene 16 Homo sapiens 78-83 7595467-3 1995 The complex [Cu(Cx)2].2H2O crystallizes in the monoclinic system, space group P2(1)/c. 2h2o 22-26 H3 histone pseudogene 16 Homo sapiens 78-83 7663644-0 1995 Measurement of ras p21 in urine of people occupationally exposed to chromium compounds. Chromium Compounds 68-86 H3 histone pseudogene 16 Homo sapiens 19-22 8593186-0 1995 Comparison of the computed three-dimensional structures of oncogenic forms (bound to GDP) of the ras-gene-encoded p21 protein with the structure of the normal (non-transforming) wild-type protein. Guanosine Diphosphate 85-88 H3 histone pseudogene 16 Homo sapiens 114-117 8593186-3 1995 To determine the effects of these substitutions on the three-dimensional structure of the whole p21 protein, we have performed molecular dynamics calculations on each of these three proteins bound to GDP and magnesium ion to compute the average structures of each of the three forms. Guanosine Diphosphate 200-203 H3 histone pseudogene 16 Homo sapiens 96-99 8593186-3 1995 To determine the effects of these substitutions on the three-dimensional structure of the whole p21 protein, we have performed molecular dynamics calculations on each of these three proteins bound to GDP and magnesium ion to compute the average structures of each of the three forms. Magnesium 208-217 H3 histone pseudogene 16 Homo sapiens 96-99 7880841-0 1995 Mutagenesis of the H-ras p21 at glycine-60 residue disrupts GTP-induced conformational change. Glycine 32-39 H3 histone pseudogene 16 Homo sapiens 25-28 7565497-5 1995 Reminiscent of previous findings obtained in C40 offspring at P11 (35), P21 C40 offspring exhibited a slightly reduced sensitivity to haloperidol relative to LC controls both in terms of DA ratios in the NAc as well as plasma prolactin levels. Haloperidol 134-145 H3 histone pseudogene 16 Homo sapiens 72-75 7565497-5 1995 Reminiscent of previous findings obtained in C40 offspring at P11 (35), P21 C40 offspring exhibited a slightly reduced sensitivity to haloperidol relative to LC controls both in terms of DA ratios in the NAc as well as plasma prolactin levels. Dopamine 187-189 H3 histone pseudogene 16 Homo sapiens 72-75 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. farnesyl pyrophosphate 54-75 H3 histone pseudogene 16 Homo sapiens 152-155 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. farnesyl pyrophosphate 54-75 H3 histone pseudogene 16 Homo sapiens 207-210 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. farnesyl pyrophosphate 54-75 H3 histone pseudogene 16 Homo sapiens 207-210 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. farnesyl pyrophosphate 77-80 H3 histone pseudogene 16 Homo sapiens 152-155 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. farnesyl pyrophosphate 77-80 H3 histone pseudogene 16 Homo sapiens 207-210 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. farnesyl pyrophosphate 77-80 H3 histone pseudogene 16 Homo sapiens 207-210 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. Cysteine 85-93 H3 histone pseudogene 16 Homo sapiens 152-155 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. Cysteine 85-93 H3 histone pseudogene 16 Homo sapiens 207-210 7494090-2 1995 FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. Cysteine 85-93 H3 histone pseudogene 16 Homo sapiens 207-210 7494090-5 1995 The radioactivity associated with ras p21 bound to the phosphocellulose paper was determined by scintillation counting after soaking the paper in trichloroacetic acid and washing with distilled water. phosphocellulose 55-71 H3 histone pseudogene 16 Homo sapiens 38-41 7494090-5 1995 The radioactivity associated with ras p21 bound to the phosphocellulose paper was determined by scintillation counting after soaking the paper in trichloroacetic acid and washing with distilled water. Trichloroacetic Acid 146-166 H3 histone pseudogene 16 Homo sapiens 38-41 7494090-5 1995 The radioactivity associated with ras p21 bound to the phosphocellulose paper was determined by scintillation counting after soaking the paper in trichloroacetic acid and washing with distilled water. Water 194-199 H3 histone pseudogene 16 Homo sapiens 38-41 7494090-6 1995 Utilizing [3H]FPP and recombinant Ha-ras p21 as substrates in the reaction, the FTase followed Michaelis-Menten kinetics with Km values of 1.0 and 7.69 microM for respectively [3H]FPP and recombinant Ha-ras p21. Tritium 11-13 H3 histone pseudogene 16 Homo sapiens 41-44 7494090-6 1995 Utilizing [3H]FPP and recombinant Ha-ras p21 as substrates in the reaction, the FTase followed Michaelis-Menten kinetics with Km values of 1.0 and 7.69 microM for respectively [3H]FPP and recombinant Ha-ras p21. Tritium 11-13 H3 histone pseudogene 16 Homo sapiens 207-210 7494090-6 1995 Utilizing [3H]FPP and recombinant Ha-ras p21 as substrates in the reaction, the FTase followed Michaelis-Menten kinetics with Km values of 1.0 and 7.69 microM for respectively [3H]FPP and recombinant Ha-ras p21. Tritium 177-179 H3 histone pseudogene 16 Homo sapiens 41-44 7494090-6 1995 Utilizing [3H]FPP and recombinant Ha-ras p21 as substrates in the reaction, the FTase followed Michaelis-Menten kinetics with Km values of 1.0 and 7.69 microM for respectively [3H]FPP and recombinant Ha-ras p21. Tritium 177-179 H3 histone pseudogene 16 Homo sapiens 207-210 7738010-1 1995 Cdc42Hs and Rac1 are members of the Ras superfamily of small molecular weight (p21) GTP binding proteins. Guanosine Triphosphate 84-87 H3 histone pseudogene 16 Homo sapiens 79-82 7730301-0 1995 Switching nucleotide specificity of Ha-Ras p21 by a single amino acid substitution at aspartate 119. Aspartic Acid 86-95 H3 histone pseudogene 16 Homo sapiens 43-46 7647555-1 1995 The relaxation rates of the multiple-quantum coherence for the amide hydrogen of Gly13 in ras p21.GDP were determined in the presence and absence of 17O labeling in the beta-phosphate of GDP. Amides 63-68 H3 histone pseudogene 16 Homo sapiens 94-97 7647555-1 1995 The relaxation rates of the multiple-quantum coherence for the amide hydrogen of Gly13 in ras p21.GDP were determined in the presence and absence of 17O labeling in the beta-phosphate of GDP. Hydrogen 69-77 H3 histone pseudogene 16 Homo sapiens 94-97 7647555-1 1995 The relaxation rates of the multiple-quantum coherence for the amide hydrogen of Gly13 in ras p21.GDP were determined in the presence and absence of 17O labeling in the beta-phosphate of GDP. Guanosine Diphosphate 98-101 H3 histone pseudogene 16 Homo sapiens 94-97 7733887-0 1995 Mutation-deletion analysis of a Ca(2+)-dependent phospholipid binding (CaLB) domain within p120 GAP, a GTPase-activating protein for p21 ras. Phospholipids 49-61 H3 histone pseudogene 16 Homo sapiens 133-136 7706235-2 1995 Here, we report that nitric oxide (NO) activates p21ras in human T cells as evidenced by an increase in GTP-bound p21ras. Nitric Oxide 21-33 H3 histone pseudogene 16 Homo sapiens 49-52 7706235-2 1995 Here, we report that nitric oxide (NO) activates p21ras in human T cells as evidenced by an increase in GTP-bound p21ras. Guanosine Triphosphate 104-107 H3 histone pseudogene 16 Homo sapiens 49-52 7706235-8 1995 These studies identify p21ras as a target of NO in T cells and suggest that NO activates p21ras by an action which mimics that of guanine nucleotide exchange factors. Guanine Nucleotides 130-148 H3 histone pseudogene 16 Homo sapiens 23-26 7880841-0 1995 Mutagenesis of the H-ras p21 at glycine-60 residue disrupts GTP-induced conformational change. Guanosine Triphosphate 60-63 H3 histone pseudogene 16 Homo sapiens 25-28 7762999-8 1995 Thus, farnesylation of G proteins and ras oncoprotein P21 underscores the importance of the cholesterol biosynthetic pathway in cell growth and carcinogenesis. Cholesterol 92-103 H3 histone pseudogene 16 Homo sapiens 54-57 7898933-1 1995 Association of the p21ras guanine nucleotide exchange factor mSOS with tyrosine-phosphorylated Shc has been implicated in the activation of p21ras. Tyrosine 71-79 H3 histone pseudogene 16 Homo sapiens 19-22 18475641-6 1995 When the in vitro results are transferred to live animals using the same inducing agents and pathway inhibitors, it is found that theophylline (Ca(2+)/CaM inhibitor) and anti-p21(ras) are the most potent suppressors of the IFN-gamma- and 5-azaC-induced side effects during pregnancy. Azacitidine 238-244 H3 histone pseudogene 16 Homo sapiens 175-178 7728775-0 1995 CD8+ T cells from a patient with colon carcinoma, specific for a mutant p21-Ras-derived peptide (Gly13-->Asp), are cytotoxic towards a carcinoma cell line harbouring the same mutation. Aspartic Acid 108-111 H3 histone pseudogene 16 Homo sapiens 72-75 7576949-0 1995 Effect of retinoic acid on p21ras and regulators of its activity in neuroblastoma. Tretinoin 10-23 H3 histone pseudogene 16 Homo sapiens 27-30 7576949-3 1995 Therefore, the aim of the present study was to examine the role of p21ras and regulators of its activity in the differentiation of neuroblastoma cells induced by retinoic acid (RA). Tretinoin 162-175 H3 histone pseudogene 16 Homo sapiens 67-70 7576949-3 1995 Therefore, the aim of the present study was to examine the role of p21ras and regulators of its activity in the differentiation of neuroblastoma cells induced by retinoic acid (RA). Tretinoin 177-179 H3 histone pseudogene 16 Homo sapiens 67-70 7762999-11 1995 The activation of p21 would then be aided by continuous farnesylation due to stimulation of the cholesterol biosynthetic pathway in tumors. Cholesterol 96-107 H3 histone pseudogene 16 Homo sapiens 18-21 7819254-0 1995 Substrate and product structural requirements for binding of nucleotides to H-ras p21: the mechanism of discrimination between guanosine and adenosine nucleotides. Guanosine 127-136 H3 histone pseudogene 16 Homo sapiens 82-85 7819254-0 1995 Substrate and product structural requirements for binding of nucleotides to H-ras p21: the mechanism of discrimination between guanosine and adenosine nucleotides. adenosine nucleotides 141-162 H3 histone pseudogene 16 Homo sapiens 82-85 7851434-3 1995 The highly purified (greater than 95%) stable fusion protein, obtained by affinity chromatography, was very active in enhancing the dissociation rate or the GDP/GTP exchange of the GDP complex of Ras2p or human H-ras p21. Guanosine Triphosphate 161-164 H3 histone pseudogene 16 Homo sapiens 217-220 7851434-3 1995 The highly purified (greater than 95%) stable fusion protein, obtained by affinity chromatography, was very active in enhancing the dissociation rate or the GDP/GTP exchange of the GDP complex of Ras2p or human H-ras p21. Guanosine Diphosphate 181-184 H3 histone pseudogene 16 Homo sapiens 217-220 7851434-10 1995 On gel filtration, truncated Sdc25p-C and nucleotide-free Ras2p (or p21) formed a stable 1:1 stoichiometric complex that was dissociated by increasing concentrations of GDP. Guanosine Diphosphate 169-172 H3 histone pseudogene 16 Homo sapiens 68-71 7971997-7 1994 Deletion analysis of p21 indicated that the sequences essential for inhibition of RSV LTR function include the previously identified ARg/Ser-rich region and zinc finger-like motif. Arginine 133-136 H3 histone pseudogene 16 Homo sapiens 21-24 7799925-4 1995 By using the yeast two-hybrid system, we identified p62, a tyrosine-phosphorylated protein that associates with p21ras GTPase-activating protein, as a src family kinase SH3-domain-binding protein. Tyrosine 59-67 H3 histone pseudogene 16 Homo sapiens 112-115 7819095-0 1994 Haemoglobin inhibits GTP-hydrolysis and GDP/GTP-exchange activities of a low M(r) GTP-binding protein, ras p21. Guanosine Triphosphate 21-24 H3 histone pseudogene 16 Homo sapiens 107-110 7819095-0 1994 Haemoglobin inhibits GTP-hydrolysis and GDP/GTP-exchange activities of a low M(r) GTP-binding protein, ras p21. Guanosine Diphosphate 40-43 H3 histone pseudogene 16 Homo sapiens 107-110 7819095-0 1994 Haemoglobin inhibits GTP-hydrolysis and GDP/GTP-exchange activities of a low M(r) GTP-binding protein, ras p21. Guanosine Triphosphate 44-47 H3 histone pseudogene 16 Homo sapiens 107-110 7819095-0 1994 Haemoglobin inhibits GTP-hydrolysis and GDP/GTP-exchange activities of a low M(r) GTP-binding protein, ras p21. (r) gtp 78-85 H3 histone pseudogene 16 Homo sapiens 107-110 7819095-1 1994 Haemoglobin was observed to inhibit the GDP/GTP-exchange activity of ras protein (ras p21) by measurement of [3H]GDP-dissociation activity in time- and dose-dependent manners. Guanosine Diphosphate 40-43 H3 histone pseudogene 16 Homo sapiens 86-89 7819095-1 1994 Haemoglobin was observed to inhibit the GDP/GTP-exchange activity of ras protein (ras p21) by measurement of [3H]GDP-dissociation activity in time- and dose-dependent manners. Guanosine Triphosphate 44-47 H3 histone pseudogene 16 Homo sapiens 86-89 7819095-1 1994 Haemoglobin was observed to inhibit the GDP/GTP-exchange activity of ras protein (ras p21) by measurement of [3H]GDP-dissociation activity in time- and dose-dependent manners. Tritium 110-112 H3 histone pseudogene 16 Homo sapiens 86-89 7819095-2 1994 Haemoglobin also inhibited the [32P]GTP-hydrolysis activity of ras p21 time- and dose-dependently. Phosphorus-32 32-35 H3 histone pseudogene 16 Homo sapiens 67-70 7819095-2 1994 Haemoglobin also inhibited the [32P]GTP-hydrolysis activity of ras p21 time- and dose-dependently. Guanosine Triphosphate 36-39 H3 histone pseudogene 16 Homo sapiens 67-70 7819095-4 1994 Globin showed limited inhibition on the [32P]GTP-hydrolysis activity of ras p21, and haemin had no effect, indicating that the ternary tetrameric structure of haemoglobin is essential for the inhibitory effects on ras p21 activities. Phosphorus-32 41-44 H3 histone pseudogene 16 Homo sapiens 76-79 7819095-4 1994 Globin showed limited inhibition on the [32P]GTP-hydrolysis activity of ras p21, and haemin had no effect, indicating that the ternary tetrameric structure of haemoglobin is essential for the inhibitory effects on ras p21 activities. Guanosine Triphosphate 45-48 H3 histone pseudogene 16 Homo sapiens 76-79 7819095-5 1994 Methaemoglobin also inhibited both [3H]GDP-dissociation and [32P]GTP-hydrolysis activities of ras p21 in a very similar manner to that by haemoglobin. Tritium 36-38 H3 histone pseudogene 16 Homo sapiens 98-101 7819095-5 1994 Methaemoglobin also inhibited both [3H]GDP-dissociation and [32P]GTP-hydrolysis activities of ras p21 in a very similar manner to that by haemoglobin. Guanosine Diphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 98-101 7819095-5 1994 Methaemoglobin also inhibited both [3H]GDP-dissociation and [32P]GTP-hydrolysis activities of ras p21 in a very similar manner to that by haemoglobin. Phosphorus-32 61-64 H3 histone pseudogene 16 Homo sapiens 98-101 7819095-5 1994 Methaemoglobin also inhibited both [3H]GDP-dissociation and [32P]GTP-hydrolysis activities of ras p21 in a very similar manner to that by haemoglobin. Guanosine Triphosphate 65-68 H3 histone pseudogene 16 Homo sapiens 98-101 7819095-6 1994 The obtained results strongly suggest that haemoglobin suppresses the physiological function(s) of ras p21 in vivo inhibiting both [32P]GTP-hydrolysis and GDP/GTP-dissociation of ras p21 in erythrocytes. Phosphorus-32 132-135 H3 histone pseudogene 16 Homo sapiens 103-106 7819095-6 1994 The obtained results strongly suggest that haemoglobin suppresses the physiological function(s) of ras p21 in vivo inhibiting both [32P]GTP-hydrolysis and GDP/GTP-dissociation of ras p21 in erythrocytes. Guanosine Triphosphate 136-139 H3 histone pseudogene 16 Homo sapiens 103-106 7819095-6 1994 The obtained results strongly suggest that haemoglobin suppresses the physiological function(s) of ras p21 in vivo inhibiting both [32P]GTP-hydrolysis and GDP/GTP-dissociation of ras p21 in erythrocytes. Guanosine Diphosphate 155-158 H3 histone pseudogene 16 Homo sapiens 103-106 7819095-6 1994 The obtained results strongly suggest that haemoglobin suppresses the physiological function(s) of ras p21 in vivo inhibiting both [32P]GTP-hydrolysis and GDP/GTP-dissociation of ras p21 in erythrocytes. Guanosine Triphosphate 159-162 H3 histone pseudogene 16 Homo sapiens 103-106 7819095-6 1994 The obtained results strongly suggest that haemoglobin suppresses the physiological function(s) of ras p21 in vivo inhibiting both [32P]GTP-hydrolysis and GDP/GTP-dissociation of ras p21 in erythrocytes. Guanosine Triphosphate 159-162 H3 histone pseudogene 16 Homo sapiens 183-186 7960106-10 1994 Introduction of ras p21 into digitonin-permeabilized PMNs was without effect on subsequent Luk-PV stimulation. Digitonin 29-38 H3 histone pseudogene 16 Homo sapiens 20-23 7802640-6 1994 Therefore, we investigated the role of p21 in cAMP metabolism and PLC activity. Cyclic AMP 46-50 H3 histone pseudogene 16 Homo sapiens 39-42 7802640-7 1994 We demonstrated that after p21 reached maximal level of expression, cAMP synthesis was reduced to 45% of the control. Cyclic AMP 68-72 H3 histone pseudogene 16 Homo sapiens 27-30 7881906-7 1994 The presence of sulphate ions in the crystals and comparisons with the related Ha-ras-p21 oncogene product are used to infer the ATP-binding site, corroborated by the difference electron density for the ATP analogue AMP-PNP. Sulfates 16-24 H3 histone pseudogene 16 Homo sapiens 86-89 7881906-7 1994 The presence of sulphate ions in the crystals and comparisons with the related Ha-ras-p21 oncogene product are used to infer the ATP-binding site, corroborated by the difference electron density for the ATP analogue AMP-PNP. Adenosine Triphosphate 129-132 H3 histone pseudogene 16 Homo sapiens 86-89 7881906-7 1994 The presence of sulphate ions in the crystals and comparisons with the related Ha-ras-p21 oncogene product are used to infer the ATP-binding site, corroborated by the difference electron density for the ATP analogue AMP-PNP. Adenosine Triphosphate 203-206 H3 histone pseudogene 16 Homo sapiens 86-89 7881906-7 1994 The presence of sulphate ions in the crystals and comparisons with the related Ha-ras-p21 oncogene product are used to infer the ATP-binding site, corroborated by the difference electron density for the ATP analogue AMP-PNP. Adenylyl Imidodiphosphate 216-223 H3 histone pseudogene 16 Homo sapiens 86-89 7971997-7 1994 Deletion analysis of p21 indicated that the sequences essential for inhibition of RSV LTR function include the previously identified ARg/Ser-rich region and zinc finger-like motif. Serine 137-140 H3 histone pseudogene 16 Homo sapiens 21-24 21607514-1 1994 We examined the possible implication of ras in the regulation of the activity of several metabolic enzymes by employing an inducible H-ras expression system (RFLSVrasLAP cell line), in which the addition of IPTG decreases the levels of ras p21 3-fold. Isopropyl Thiogalactoside 207-211 H3 histone pseudogene 16 Homo sapiens 240-243 7853016-2 1994 Like other guanine nucleotide-binding proteins p21ras is active when GTP bound and inactive when GDP bound. Guanine Nucleotides 11-29 H3 histone pseudogene 16 Homo sapiens 47-50 7853016-2 1994 Like other guanine nucleotide-binding proteins p21ras is active when GTP bound and inactive when GDP bound. Guanosine Triphosphate 69-72 H3 histone pseudogene 16 Homo sapiens 47-50 7853016-2 1994 Like other guanine nucleotide-binding proteins p21ras is active when GTP bound and inactive when GDP bound. Guanosine Diphosphate 97-100 H3 histone pseudogene 16 Homo sapiens 47-50 7935463-8 1994 ralGDS interacted with the GTP-bound form of ras p21 but not with the GDP-bound form in vitro. Guanosine Triphosphate 27-30 H3 histone pseudogene 16 Homo sapiens 49-52 7935423-9 1994 We observed that calcium treatment inhibited EGF-induced p21ras activation. Calcium 17-24 H3 histone pseudogene 16 Homo sapiens 57-60 21607461-5 1994 Given that this interaction is inhibited by IPTG, such a cell line overexpresses the H-ras gene encoded protein ras p21 and the addition of isopropyl beta-D-thiogalactopyranoside (IPTG) into the culture medium diminishes overexpression. Isopropyl Thiogalactoside 44-48 H3 histone pseudogene 16 Homo sapiens 116-119 8208513-2 1994 For biological activity the gene product p21 ras needs to be bound to the cell membrane by a farnesyl residue. FARNESYL 93-101 H3 histone pseudogene 16 Homo sapiens 41-44 8076673-1 1994 In contrast to the previous topological model of the ATP binding domain of the F1-ATPase beta subunit based on analogies to those of ras p21 and adenylate kinase, a more consistent model can be constructed with the known structure of the recA protein as a reference. Adenosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 137-140 15299412-1 1994 The parameters affecting the crystal quality of complexes between p21(H-ras) and caged GTP have been investigated. Guanosine Triphosphate 87-90 H3 histone pseudogene 16 Homo sapiens 66-69 15299412-2 1994 The use of pure diastereomers of caged GTP complexed to the more stable p21(G12P)" mutant of p21 and the addition of n-octyl-beta-D-glucopyranoside improved the reproducibility and decreased the mosaicity of the crystals significantly. Guanosine Triphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 72-75 15299412-2 1994 The use of pure diastereomers of caged GTP complexed to the more stable p21(G12P)" mutant of p21 and the addition of n-octyl-beta-D-glucopyranoside improved the reproducibility and decreased the mosaicity of the crystals significantly. Guanosine Triphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 93-96 15299412-5 1994 A structure of p21(G12P)":GTP could be obtained 2 min after photolytic removal of the cage group and led to the identification of a previously unidentified conformation for the so-called catalytically active loop L4. Guanosine Triphosphate 26-29 H3 histone pseudogene 16 Homo sapiens 15-18 15299413-0 1994 Crystallization and preliminary X-ray structure analysis of thermally unstable p21(H-ras) guanosine complexes. Guanosine 90-99 H3 histone pseudogene 16 Homo sapiens 79-82 15299413-1 1994 p21 is a small guanine nucleotide binding protein that is involved in intracellular signal transduction. Guanine Nucleotides 15-33 H3 histone pseudogene 16 Homo sapiens 0-3 15299413-3 1994 Guanosine or GMP bind six orders of magnitude more weakly to p21 than GDP or GTP. Guanosine 0-9 H3 histone pseudogene 16 Homo sapiens 61-64 15299413-3 1994 Guanosine or GMP bind six orders of magnitude more weakly to p21 than GDP or GTP. guanosine 5'-monophosphorothioate 13-16 H3 histone pseudogene 16 Homo sapiens 61-64 15299413-5 1994 We have crystallized C-terminally truncated forms of p21(H-ras), with guanosine or GMP bound, in the space groups P4(3)2(1)2, P2(1)2(1)2 and P2(1). Guanosine 70-79 H3 histone pseudogene 16 Homo sapiens 53-56 15299413-5 1994 We have crystallized C-terminally truncated forms of p21(H-ras), with guanosine or GMP bound, in the space groups P4(3)2(1)2, P2(1)2(1)2 and P2(1). guanosine 5'-monophosphorothioate 83-86 H3 histone pseudogene 16 Homo sapiens 53-56 8020607-4 1994 Furthermore, activity of Ki-ras p21 2 h prior to TPA exposure enhanced the inhibitory effect of TPA in quiescent cells. Tetradecanoylphorbol Acetate 49-52 H3 histone pseudogene 16 Homo sapiens 32-35 8020607-4 1994 Furthermore, activity of Ki-ras p21 2 h prior to TPA exposure enhanced the inhibitory effect of TPA in quiescent cells. Tetradecanoylphorbol Acetate 96-99 H3 histone pseudogene 16 Homo sapiens 32-35 8020607-6 1994 The suppression of junctional communication by TPA was completely prevented if the oncogenic p21 had been active for a longer period of time (48 h). Tetradecanoylphorbol Acetate 47-50 H3 histone pseudogene 16 Homo sapiens 93-96 8020607-8 1994 From these results we conclude that there is a cell-state dependence of junctional sensitivity to TPA in NRK cells and that ras p21 activity potentiates the junctional response to TPA. Tetradecanoylphorbol Acetate 180-183 H3 histone pseudogene 16 Homo sapiens 128-131 8175645-9 1994 Furthermore, Cys-3-AMBA-Met and Cys-4-ABA-Met are true inhibitors of p21ras FTase since they are not farnesylated by this enzyme, in contrast to Cys-Val-Ile-Met, which inhibits the enzyme by acting as alternative substrate. cys-3-amba 13-23 H3 histone pseudogene 16 Homo sapiens 69-72 8061177-0 1994 Mutant c-Ki-ras p21 protein in chemical carcinogenesis in humans exposed to vinyl chloride. Vinyl Chloride 76-90 H3 histone pseudogene 16 Homo sapiens 16-19 7961601-0 1994 The hydration of Ras p21 in solution during GTP hydrolysis based on solution X-ray scattering profile. Guanosine Triphosphate 44-47 H3 histone pseudogene 16 Homo sapiens 21-24 7961601-2 1994 In the presence of GDP, the radius of gyration, Rg, determined for wild type ras p21 was 16.89 +/- 0.01 A, while the wild type ras p21 bound to the GTP analogue GDPNHP (5"-guanyl imido diphosphate beta-gamma-imidoguanosine 5"-triphosphate) showed an Rg value of 17.46 +/- 0.01 A, which is 3.3% larger. Guanosine Diphosphate 19-22 H3 histone pseudogene 16 Homo sapiens 81-84 7961601-2 1994 In the presence of GDP, the radius of gyration, Rg, determined for wild type ras p21 was 16.89 +/- 0.01 A, while the wild type ras p21 bound to the GTP analogue GDPNHP (5"-guanyl imido diphosphate beta-gamma-imidoguanosine 5"-triphosphate) showed an Rg value of 17.46 +/- 0.01 A, which is 3.3% larger. Guanosine Diphosphate 19-22 H3 histone pseudogene 16 Homo sapiens 131-134 7961601-2 1994 In the presence of GDP, the radius of gyration, Rg, determined for wild type ras p21 was 16.89 +/- 0.01 A, while the wild type ras p21 bound to the GTP analogue GDPNHP (5"-guanyl imido diphosphate beta-gamma-imidoguanosine 5"-triphosphate) showed an Rg value of 17.46 +/- 0.01 A, which is 3.3% larger. Guanosine Triphosphate 148-151 H3 histone pseudogene 16 Homo sapiens 131-134 7961601-2 1994 In the presence of GDP, the radius of gyration, Rg, determined for wild type ras p21 was 16.89 +/- 0.01 A, while the wild type ras p21 bound to the GTP analogue GDPNHP (5"-guanyl imido diphosphate beta-gamma-imidoguanosine 5"-triphosphate) showed an Rg value of 17.46 +/- 0.01 A, which is 3.3% larger. gdpnhp 161-167 H3 histone pseudogene 16 Homo sapiens 131-134 7961601-2 1994 In the presence of GDP, the radius of gyration, Rg, determined for wild type ras p21 was 16.89 +/- 0.01 A, while the wild type ras p21 bound to the GTP analogue GDPNHP (5"-guanyl imido diphosphate beta-gamma-imidoguanosine 5"-triphosphate) showed an Rg value of 17.46 +/- 0.01 A, which is 3.3% larger. 5"-guanyl imido diphosphate 169-196 H3 histone pseudogene 16 Homo sapiens 131-134 7961601-2 1994 In the presence of GDP, the radius of gyration, Rg, determined for wild type ras p21 was 16.89 +/- 0.01 A, while the wild type ras p21 bound to the GTP analogue GDPNHP (5"-guanyl imido diphosphate beta-gamma-imidoguanosine 5"-triphosphate) showed an Rg value of 17.46 +/- 0.01 A, which is 3.3% larger. beta-gamma-imidoguanosine 5"-triphosphate 197-238 H3 histone pseudogene 16 Homo sapiens 131-134 7961601-3 1994 The result shows that ras p21 expands upon GTP binding. Guanosine Triphosphate 43-46 H3 histone pseudogene 16 Homo sapiens 26-29 7961601-5 1994 The scattering profiles were analyzed by simulation of hydrated ras p21, based on the crystal atomic coordinates, and it was concluded that the ras p21 molecule incorporates 20% more bulk water upon GTP binding. Water 188-193 H3 histone pseudogene 16 Homo sapiens 148-151 7961601-5 1994 The scattering profiles were analyzed by simulation of hydrated ras p21, based on the crystal atomic coordinates, and it was concluded that the ras p21 molecule incorporates 20% more bulk water upon GTP binding. Guanosine Triphosphate 199-202 H3 histone pseudogene 16 Homo sapiens 148-151 8190099-10 1994 In vitro assembly/co-sedimentation experiments in the presence of GTP gamma S revealed a 2-fold increase in a small cytosolic G protein with a molecular mass of 21 kDa (p21) in pelleted membranes, as detected by [35S]GTP gamma S protein blot probing, that was not affected by B-003. Guanosine Triphosphate 66-69 H3 histone pseudogene 16 Homo sapiens 169-172 8190099-10 1994 In vitro assembly/co-sedimentation experiments in the presence of GTP gamma S revealed a 2-fold increase in a small cytosolic G protein with a molecular mass of 21 kDa (p21) in pelleted membranes, as detected by [35S]GTP gamma S protein blot probing, that was not affected by B-003. Sulfur 76-77 H3 histone pseudogene 16 Homo sapiens 169-172 8190099-10 1994 In vitro assembly/co-sedimentation experiments in the presence of GTP gamma S revealed a 2-fold increase in a small cytosolic G protein with a molecular mass of 21 kDa (p21) in pelleted membranes, as detected by [35S]GTP gamma S protein blot probing, that was not affected by B-003. Sulfur-35 213-216 H3 histone pseudogene 16 Homo sapiens 169-172 8190099-10 1994 In vitro assembly/co-sedimentation experiments in the presence of GTP gamma S revealed a 2-fold increase in a small cytosolic G protein with a molecular mass of 21 kDa (p21) in pelleted membranes, as detected by [35S]GTP gamma S protein blot probing, that was not affected by B-003. Guanosine Triphosphate 217-220 H3 histone pseudogene 16 Homo sapiens 169-172 8190099-10 1994 In vitro assembly/co-sedimentation experiments in the presence of GTP gamma S revealed a 2-fold increase in a small cytosolic G protein with a molecular mass of 21 kDa (p21) in pelleted membranes, as detected by [35S]GTP gamma S protein blot probing, that was not affected by B-003. Sulfur 215-216 H3 histone pseudogene 16 Homo sapiens 169-172 8175645-9 1994 Furthermore, Cys-3-AMBA-Met and Cys-4-ABA-Met are true inhibitors of p21ras FTase since they are not farnesylated by this enzyme, in contrast to Cys-Val-Ile-Met, which inhibits the enzyme by acting as alternative substrate. Methionine 24-27 H3 histone pseudogene 16 Homo sapiens 69-72 8175645-9 1994 Furthermore, Cys-3-AMBA-Met and Cys-4-ABA-Met are true inhibitors of p21ras FTase since they are not farnesylated by this enzyme, in contrast to Cys-Val-Ile-Met, which inhibits the enzyme by acting as alternative substrate. cys-4-aba 32-41 H3 histone pseudogene 16 Homo sapiens 69-72 8175645-9 1994 Furthermore, Cys-3-AMBA-Met and Cys-4-ABA-Met are true inhibitors of p21ras FTase since they are not farnesylated by this enzyme, in contrast to Cys-Val-Ile-Met, which inhibits the enzyme by acting as alternative substrate. Cysteine 13-16 H3 histone pseudogene 16 Homo sapiens 69-72 8139548-0 1994 rac p21 is involved in insulin-induced membrane ruffling and rho p21 is involved in hepatocyte growth factor- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced membrane ruffling in KB cells. Tetradecanoylphorbol Acetate 114-150 H3 histone pseudogene 16 Homo sapiens 65-68 8142406-0 1994 Characterization of the active site of p21 ras by electron spin-echo envelope modulation spectroscopy with selective labeling: comparisons between GDP and GTP forms. Guanosine Diphosphate 147-150 H3 histone pseudogene 16 Homo sapiens 39-42 8142406-0 1994 Characterization of the active site of p21 ras by electron spin-echo envelope modulation spectroscopy with selective labeling: comparisons between GDP and GTP forms. Guanosine Triphosphate 155-158 H3 histone pseudogene 16 Homo sapiens 39-42 8142406-2 1994 We incorporated [4-13C]-labeled Asx into p21.MnIIGDP and found that the distance from the carboxyl 13C of Asp57 to MnII is approximately 4.1 A. 4-13c 17-22 H3 histone pseudogene 16 Homo sapiens 41-44 8142406-2 1994 We incorporated [4-13C]-labeled Asx into p21.MnIIGDP and found that the distance from the carboxyl 13C of Asp57 to MnII is approximately 4.1 A. asx 32-35 H3 histone pseudogene 16 Homo sapiens 41-44 8142406-14 1994 The ESEEM spectrum of p21.MnIIGMPPNP labeled with [2-2H]Thr yields a MnII-2H distance of 4.9 A, a distance inconsistent with strong coordination. mniigmppnp 26-36 H3 histone pseudogene 16 Homo sapiens 22-25 8142406-14 1994 The ESEEM spectrum of p21.MnIIGMPPNP labeled with [2-2H]Thr yields a MnII-2H distance of 4.9 A, a distance inconsistent with strong coordination. [2-2h]thr 50-59 H3 histone pseudogene 16 Homo sapiens 22-25 8142406-14 1994 The ESEEM spectrum of p21.MnIIGMPPNP labeled with [2-2H]Thr yields a MnII-2H distance of 4.9 A, a distance inconsistent with strong coordination. Deuterium 53-55 H3 histone pseudogene 16 Homo sapiens 22-25 8142406-15 1994 A sample of p21 in which the Thr residues were fully labeled with 13C and 15N yielded a value of 5.0 A for the distance from MnII to the amide nitrogen of Thr35, while the 13C signal is much smaller than expected if Thr35 were coordinated. Threonine 29-32 H3 histone pseudogene 16 Homo sapiens 12-15 8142406-15 1994 A sample of p21 in which the Thr residues were fully labeled with 13C and 15N yielded a value of 5.0 A for the distance from MnII to the amide nitrogen of Thr35, while the 13C signal is much smaller than expected if Thr35 were coordinated. 13c 66-69 H3 histone pseudogene 16 Homo sapiens 12-15 8142406-15 1994 A sample of p21 in which the Thr residues were fully labeled with 13C and 15N yielded a value of 5.0 A for the distance from MnII to the amide nitrogen of Thr35, while the 13C signal is much smaller than expected if Thr35 were coordinated. 15n 74-77 H3 histone pseudogene 16 Homo sapiens 12-15 8142406-15 1994 A sample of p21 in which the Thr residues were fully labeled with 13C and 15N yielded a value of 5.0 A for the distance from MnII to the amide nitrogen of Thr35, while the 13C signal is much smaller than expected if Thr35 were coordinated. Amides 137-142 H3 histone pseudogene 16 Homo sapiens 12-15 8142406-15 1994 A sample of p21 in which the Thr residues were fully labeled with 13C and 15N yielded a value of 5.0 A for the distance from MnII to the amide nitrogen of Thr35, while the 13C signal is much smaller than expected if Thr35 were coordinated. Nitrogen 143-151 H3 histone pseudogene 16 Homo sapiens 12-15 8142406-15 1994 A sample of p21 in which the Thr residues were fully labeled with 13C and 15N yielded a value of 5.0 A for the distance from MnII to the amide nitrogen of Thr35, while the 13C signal is much smaller than expected if Thr35 were coordinated. 13c 172-175 H3 histone pseudogene 16 Homo sapiens 12-15 8142406-16 1994 A [15N]serine/glycine-labeled sample gives a distance to the amide 15N of Ser17 of 3.9 A, consistent with the X-ray structure; a [4-13C]-labeled Asx sample of p21 gives a distance of approximately 4 A between MnII and the label of Asp57, again implying indirect coordination. asx 145-148 H3 histone pseudogene 16 Homo sapiens 159-162 8139548-9 1994 The phorbol ester-induced membrane ruffling was morphologically similar to the rhoA p21-induced kind and inhibited by microinjection of rho GDI or C3. Phorbol Esters 4-17 H3 histone pseudogene 16 Homo sapiens 84-87 8139548-10 1994 These results indicate that rac p21 and rho GDI are involved in insulin-induced membrane ruffling and that rho p21 and rho GDI are involved in HGF- and phorbol ester-induced membrane rufflings. Phorbol Esters 152-165 H3 histone pseudogene 16 Homo sapiens 111-114 8139548-0 1994 rac p21 is involved in insulin-induced membrane ruffling and rho p21 is involved in hepatocyte growth factor- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced membrane ruffling in KB cells. Tetradecanoylphorbol Acetate 152-155 H3 histone pseudogene 16 Homo sapiens 4-7 8139548-0 1994 rac p21 is involved in insulin-induced membrane ruffling and rho p21 is involved in hepatocyte growth factor- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced membrane ruffling in KB cells. Tetradecanoylphorbol Acetate 152-155 H3 histone pseudogene 16 Homo sapiens 65-68 8139548-2 1994 Insulin-induced membrane ruffling was inhibited by microinjection of rho GDI, an inhibitory GDP/GTP exchange regulator for both rho p21 and rac p21 small GTP-binding proteins, but not inhibited by microinjection of botulinum exoenzyme C3, known to selectively ADP-ribosylate rho p21 and to impair its function. Guanosine Diphosphate 92-95 H3 histone pseudogene 16 Homo sapiens 132-135 8139548-2 1994 Insulin-induced membrane ruffling was inhibited by microinjection of rho GDI, an inhibitory GDP/GTP exchange regulator for both rho p21 and rac p21 small GTP-binding proteins, but not inhibited by microinjection of botulinum exoenzyme C3, known to selectively ADP-ribosylate rho p21 and to impair its function. Guanosine Diphosphate 92-95 H3 histone pseudogene 16 Homo sapiens 144-147 8139548-2 1994 Insulin-induced membrane ruffling was inhibited by microinjection of rho GDI, an inhibitory GDP/GTP exchange regulator for both rho p21 and rac p21 small GTP-binding proteins, but not inhibited by microinjection of botulinum exoenzyme C3, known to selectively ADP-ribosylate rho p21 and to impair its function. Guanosine Diphosphate 92-95 H3 histone pseudogene 16 Homo sapiens 144-147 8139548-2 1994 Insulin-induced membrane ruffling was inhibited by microinjection of rho GDI, an inhibitory GDP/GTP exchange regulator for both rho p21 and rac p21 small GTP-binding proteins, but not inhibited by microinjection of botulinum exoenzyme C3, known to selectively ADP-ribosylate rho p21 and to impair its function. Guanosine Triphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 132-135 8139548-2 1994 Insulin-induced membrane ruffling was inhibited by microinjection of rho GDI, an inhibitory GDP/GTP exchange regulator for both rho p21 and rac p21 small GTP-binding proteins, but not inhibited by microinjection of botulinum exoenzyme C3, known to selectively ADP-ribosylate rho p21 and to impair its function. Guanosine Triphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 144-147 8139548-2 1994 Insulin-induced membrane ruffling was inhibited by microinjection of rho GDI, an inhibitory GDP/GTP exchange regulator for both rho p21 and rac p21 small GTP-binding proteins, but not inhibited by microinjection of botulinum exoenzyme C3, known to selectively ADP-ribosylate rho p21 and to impair its function. Guanosine Triphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 144-147 8139548-3 1994 This rho GDI action was prevented by comicroinjection with guanosine 5"-(3-O-thio)triphosphate (GTP gamma S)-bound rac1 p21. Guanosine 5'-O-(3-Thiotriphosphate) 59-94 H3 histone pseudogene 16 Homo sapiens 120-123 8139548-3 1994 This rho GDI action was prevented by comicroinjection with guanosine 5"-(3-O-thio)triphosphate (GTP gamma S)-bound rac1 p21. Guanosine Triphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 120-123 8139548-3 1994 This rho GDI action was prevented by comicroinjection with guanosine 5"-(3-O-thio)triphosphate (GTP gamma S)-bound rac1 p21. Sulfur 106-107 H3 histone pseudogene 16 Homo sapiens 120-123 8139548-5 1994 This rho GDI action was prevented by comicroinjection with GTP gamma S-bound rhoA p21, and this C3 action was prevented by comicroinjection with GTP gamma S-bound rhoAIle-41 p21, which is resistant to C3. Guanosine 5'-O-(3-Thiotriphosphate) 59-70 H3 histone pseudogene 16 Homo sapiens 82-85 8139548-6 1994 Microinjection of either GTP gamma S-bound rac1 p21 or rhoA p21 alone induced membrane ruffling in the absence of the growth factors. Guanosine Triphosphate 25-28 H3 histone pseudogene 16 Homo sapiens 48-51 8139548-8 1994 Membrane ruffling was also induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C-activating phorbol ester, but not by Ca2+ ionophore or microinjection of a dominant active Ki-ras p21 mutant (Ki-rasVal-12 p21). Tetradecanoylphorbol Acetate 76-79 H3 histone pseudogene 16 Homo sapiens 199-202 8139548-8 1994 Membrane ruffling was also induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C-activating phorbol ester, but not by Ca2+ ionophore or microinjection of a dominant active Ki-ras p21 mutant (Ki-rasVal-12 p21). Tetradecanoylphorbol Acetate 76-79 H3 histone pseudogene 16 Homo sapiens 224-227 8142349-1 1994 A high-resolution solution structure of the GDP form of a truncated version of the ras p21 protein (residues 1-166) has been determined using NMR spectroscopy. Guanosine Diphosphate 44-47 H3 histone pseudogene 16 Homo sapiens 87-90 8136358-2 1994 The side chain of the amino acid at position 61 may play a key role in this hydrolysis of GTP by p21. Guanosine Triphosphate 90-93 H3 histone pseudogene 16 Homo sapiens 97-100 8144884-6 1994 In contrast, cross-linked anti-CD3 or the combination of phorbol ester and ionomycin were found to activate p21ras equally in both T cell subsets. Phorbol Esters 57-70 H3 histone pseudogene 16 Homo sapiens 108-111 8137813-8 1994 A different mutant, rab5 S34N, was found, like the inhibitory p21-ras S17N mutant, to have a preferential affinity for GDP. Guanosine Diphosphate 119-122 H3 histone pseudogene 16 Homo sapiens 62-65 8144884-6 1994 In contrast, cross-linked anti-CD3 or the combination of phorbol ester and ionomycin were found to activate p21ras equally in both T cell subsets. Ionomycin 75-84 H3 histone pseudogene 16 Homo sapiens 108-111 8116235-4 1994 Domain-swapping and site-directed mutagenesis experiments indicated that codon 9 of the core protein coding sequence played a crucial role on the synthesis of the core protein: a lysine codon at this position led to the synthesis of P16 and an arginine codon at this position led to the synthesis of P21. Lysine 179-185 H3 histone pseudogene 16 Homo sapiens 300-303 8114695-7 1994 Furthermore, Shc immune complexes contained guanine nucleotide exchange activity toward p21ras in vitro. Guanine Nucleotides 44-62 H3 histone pseudogene 16 Homo sapiens 88-91 8144711-5 1994 The first demonstrates the ability of the program to generate candidate inhibitors for a receptor site of known 3D structure, specifically the GDP binding site of p21. Guanosine Diphosphate 143-146 H3 histone pseudogene 16 Homo sapiens 163-166 8107774-3 1994 The kinase complexes specifically with activated (GTP-bound) p21, inhibiting p21 GTPase activity and leading to kinase autophosphorylation and activation. Guanosine Triphosphate 50-53 H3 histone pseudogene 16 Homo sapiens 61-64 8107774-3 1994 The kinase complexes specifically with activated (GTP-bound) p21, inhibiting p21 GTPase activity and leading to kinase autophosphorylation and activation. Guanosine Triphosphate 50-53 H3 histone pseudogene 16 Homo sapiens 77-80 8270251-2 1994 Biochemically, these mutations result in the ras gene product (p21) being constitutively activated in its GTP-bound form and insensitive to the hydrolytic action of the ras-specific GTPase-activating protein (ras GAP). Guanosine Triphosphate 106-109 H3 histone pseudogene 16 Homo sapiens 63-66 8270251-3 1994 We hypothesized that, if tumor development is related to the p21 ras being in the active GTP-bound state, then a similar malignant phenotype may result from an inactivating mutation in the ras GAP gene in the region that interacts with ras p21 (so-called catalytic domain). Guanosine Triphosphate 89-92 H3 histone pseudogene 16 Homo sapiens 61-64 8060496-0 1994 Comparison of the low energy conformations of an oncogenic and a non-oncogenic p21 protein, neither of which binds GTP or GDP. Guanosine Triphosphate 115-118 H3 histone pseudogene 16 Homo sapiens 79-82 8060496-0 1994 Comparison of the low energy conformations of an oncogenic and a non-oncogenic p21 protein, neither of which binds GTP or GDP. Guanosine Diphosphate 122-125 H3 histone pseudogene 16 Homo sapiens 79-82 8060496-1 1994 Oncogenic p21 protein, encoded by the ras-oncogene, that causes malignant transformation of normal cells and many human tumors, is almost identical in sequence to its normal protooncogene-encoded counterpart protein, except for the substitution of arbitrary amino acids for the normally occurring amino acids at critical positions such as Gly 12 and Gln 61. Glycine 339-342 H3 histone pseudogene 16 Homo sapiens 10-13 8060496-1 1994 Oncogenic p21 protein, encoded by the ras-oncogene, that causes malignant transformation of normal cells and many human tumors, is almost identical in sequence to its normal protooncogene-encoded counterpart protein, except for the substitution of arbitrary amino acids for the normally occurring amino acids at critical positions such as Gly 12 and Gln 61. Glutamine 350-353 H3 histone pseudogene 16 Homo sapiens 10-13 8060496-2 1994 Since p21 is normally activated by the binding of GTP in place of GDP, it has been postulated that oncogenic forms must retain bound GTP for prolonged time periods. Guanosine Triphosphate 50-53 H3 histone pseudogene 16 Homo sapiens 6-9 8060496-2 1994 Since p21 is normally activated by the binding of GTP in place of GDP, it has been postulated that oncogenic forms must retain bound GTP for prolonged time periods. Guanosine Diphosphate 66-69 H3 histone pseudogene 16 Homo sapiens 6-9 8060496-2 1994 Since p21 is normally activated by the binding of GTP in place of GDP, it has been postulated that oncogenic forms must retain bound GTP for prolonged time periods. Guanosine Triphosphate 133-136 H3 histone pseudogene 16 Homo sapiens 6-9 8060496-3 1994 However, two multiply substituted p21 proteins have been cloned, neither of which binds GDP or GTP. Guanosine Diphosphate 88-91 H3 histone pseudogene 16 Homo sapiens 34-37 8060496-3 1994 However, two multiply substituted p21 proteins have been cloned, neither of which binds GDP or GTP. Guanosine Triphosphate 95-98 H3 histone pseudogene 16 Homo sapiens 34-37 8060496-11 1994 These regions have been found to be the most flexible in the p21 protein bound to GDP from prior molecular dynamics calculations (Dykes et al., 1993). Guanosine Diphosphate 82-85 H3 histone pseudogene 16 Homo sapiens 61-64 8226937-3 1993 Here, we examined whether rho GDI interacts with the GTP-bound form of rho p21 and rac p21 and inhibits their basal and rho GAP-stimulated GTPase activity, rho GDI interacted with both the GDP- and GTP-bound forms of rhoA p21 and rac1 p21 as estimated by measuring its ability to form a complex with both forms and to inhibit the membrane-binding activity of both forms. Guanosine Diphosphate 189-192 H3 histone pseudogene 16 Homo sapiens 87-90 8142894-1 1994 We have utilized Raman difference spectroscopy to investigate hydrogen bonding interactions of the guanine moiety in guanine nucleotides with the binding site of two G proteins, EF-Tu (elongation factor Tu from Escherichia coli) and the c-Harvey ras protein, p21 (the gene product of the human c-H-ras proto-oncogene). Guanine 99-106 H3 histone pseudogene 16 Homo sapiens 259-262 8142894-1 1994 We have utilized Raman difference spectroscopy to investigate hydrogen bonding interactions of the guanine moiety in guanine nucleotides with the binding site of two G proteins, EF-Tu (elongation factor Tu from Escherichia coli) and the c-Harvey ras protein, p21 (the gene product of the human c-H-ras proto-oncogene). Guanine Nucleotides 117-136 H3 histone pseudogene 16 Homo sapiens 259-262 8142894-7 1994 In general, the spectral shifts provide a rationale for the stronger binding of GDP and IDP with p21 compared to EF-Tu. Guanosine Diphosphate 80-83 H3 histone pseudogene 16 Homo sapiens 97-100 8142894-8 1994 Despite the structural similarity of the binding sites of EF-Tu and p21, the strengths of the observed hydrogen bonds at the 6-keto and 2-amino positions vary substantially, by up to a factor of 2. Hydrogen 103-111 H3 histone pseudogene 16 Homo sapiens 68-71 8257693-7 1993 The p21-bound fluorescein and aminocoumarin nucleotide derivatives reported correlation times of 19 and 29 ns, respectively. Fluorescein 14-25 H3 histone pseudogene 16 Homo sapiens 4-7 8244990-0 1993 Comparison of kinetic properties between two mammalian ras p21 GDP/GTP exchange proteins, ras guanine nucleotide-releasing factor and smg GDP dissociation stimulation. Guanosine Diphosphate 63-66 H3 histone pseudogene 16 Homo sapiens 59-62 8244990-1 1993 The mammalian counterpart of the yeast ras p21 GDP/GTP exchange protein CDC25, ras GRF, was expressed in Escherichia coli and purified, and its kinetic properties were compared with those of another mammalian ras p21 GDP/GTP exchange protein, smg GDS. Guanosine Triphosphate 51-54 H3 histone pseudogene 16 Homo sapiens 43-46 8246952-7 1993 In contrast to the results obtained with p120GAP, the Pro-34-->Arg p21 species is effectively coupled to the raf-1 product, as judged from electrophoretic mobility shifts of the Raf-1 phosphoprotein. Proline 54-57 H3 histone pseudogene 16 Homo sapiens 70-73 8246952-7 1993 In contrast to the results obtained with p120GAP, the Pro-34-->Arg p21 species is effectively coupled to the raf-1 product, as judged from electrophoretic mobility shifts of the Raf-1 phosphoprotein. Arginine 66-69 H3 histone pseudogene 16 Homo sapiens 70-73 8226937-0 1993 Consequences of weak interaction of rho GDI with the GTP-bound forms of rho p21 and rac p21. Guanosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 76-79 8226937-0 1993 Consequences of weak interaction of rho GDI with the GTP-bound forms of rho p21 and rac p21. Guanosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 88-91 8226937-2 1993 Recently, rho GDI has been reported to interact with the GTP-bound form of G25K and rac1 p21 and to inhibit their basal and GTPase-activating protein (GAP)-stimulated GTPase activity. Guanosine Triphosphate 57-60 H3 histone pseudogene 16 Homo sapiens 89-92 8226937-3 1993 Here, we examined whether rho GDI interacts with the GTP-bound form of rho p21 and rac p21 and inhibits their basal and rho GAP-stimulated GTPase activity, rho GDI interacted with both the GDP- and GTP-bound forms of rhoA p21 and rac1 p21 as estimated by measuring its ability to form a complex with both forms and to inhibit the membrane-binding activity of both forms. Guanosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 75-78 8226937-3 1993 Here, we examined whether rho GDI interacts with the GTP-bound form of rho p21 and rac p21 and inhibits their basal and rho GAP-stimulated GTPase activity, rho GDI interacted with both the GDP- and GTP-bound forms of rhoA p21 and rac1 p21 as estimated by measuring its ability to form a complex with both forms and to inhibit the membrane-binding activity of both forms. Guanosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 87-90 8226937-3 1993 Here, we examined whether rho GDI interacts with the GTP-bound form of rho p21 and rac p21 and inhibits their basal and rho GAP-stimulated GTPase activity, rho GDI interacted with both the GDP- and GTP-bound forms of rhoA p21 and rac1 p21 as estimated by measuring its ability to form a complex with both forms and to inhibit the membrane-binding activity of both forms. Guanosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 87-90 8226937-3 1993 Here, we examined whether rho GDI interacts with the GTP-bound form of rho p21 and rac p21 and inhibits their basal and rho GAP-stimulated GTPase activity, rho GDI interacted with both the GDP- and GTP-bound forms of rhoA p21 and rac1 p21 as estimated by measuring its ability to form a complex with both forms and to inhibit the membrane-binding activity of both forms. Guanosine Triphosphate 53-56 H3 histone pseudogene 16 Homo sapiens 87-90 8226937-3 1993 Here, we examined whether rho GDI interacts with the GTP-bound form of rho p21 and rac p21 and inhibits their basal and rho GAP-stimulated GTPase activity, rho GDI interacted with both the GDP- and GTP-bound forms of rhoA p21 and rac1 p21 as estimated by measuring its ability to form a complex with both forms and to inhibit the membrane-binding activity of both forms. Guanosine Diphosphate 189-192 H3 histone pseudogene 16 Homo sapiens 87-90 8262955-1 1993 Rabphilin-3A is a putative target molecule for rab3A p25/smg p25A, which is a member of a ras p21-related small GTP-binding protein and implicated in neurotransmitter release from the synapse. Guanosine Triphosphate 112-115 H3 histone pseudogene 16 Homo sapiens 94-97 8129867-1 1993 We previously reported a complete computer-based three-dimensional structure for residues 1-171 of the Gly 12-containing ras-gene-encoded p21 protein complexed with GDP. Glycine 103-106 H3 histone pseudogene 16 Homo sapiens 138-141 8129867-1 1993 We previously reported a complete computer-based three-dimensional structure for residues 1-171 of the Gly 12-containing ras-gene-encoded p21 protein complexed with GDP. Guanosine Diphosphate 165-168 H3 histone pseudogene 16 Homo sapiens 138-141 8226937-3 1993 Here, we examined whether rho GDI interacts with the GTP-bound form of rho p21 and rac p21 and inhibits their basal and rho GAP-stimulated GTPase activity, rho GDI interacted with both the GDP- and GTP-bound forms of rhoA p21 and rac1 p21 as estimated by measuring its ability to form a complex with both forms and to inhibit the membrane-binding activity of both forms. Guanosine Diphosphate 189-192 H3 histone pseudogene 16 Homo sapiens 87-90 7693851-7 1993 Finally, we also show that a 62-kD protein coimmunoprecipitating with the p21ras GTPase activating protein (GAP) is heavily tyrosine phosphorylated only after CD2 stimulation. Tyrosine 124-132 H3 histone pseudogene 16 Homo sapiens 74-77 7691613-0 1993 Overlapping epitopes encompassing a point mutation (12 Gly-->Arg) in p21 ras can be recognized by HLA-DR, -DP and -DQ restricted T cells. Glycine 55-58 H3 histone pseudogene 16 Homo sapiens 72-75 8409414-13 1993 Finally, under conditions in which the PKC inhibitor calphostin C blocks PMA-induced p21ras activation, it does not inhibit Ag-induced p21ras activation. Tetradecanoylphorbol Acetate 73-76 H3 histone pseudogene 16 Homo sapiens 85-88 7691613-0 1993 Overlapping epitopes encompassing a point mutation (12 Gly-->Arg) in p21 ras can be recognized by HLA-DR, -DP and -DQ restricted T cells. Arginine 64-67 H3 histone pseudogene 16 Homo sapiens 72-75 7691613-5 1993 By repeated in vitro stimulation of peripheral blood mononuclear cells, several T cells clones could be generated which recognized a p21 ras derived peptide carrying a position 12 Gly-->Arg substitution. Glycine 180-183 H3 histone pseudogene 16 Homo sapiens 133-136 7691613-5 1993 By repeated in vitro stimulation of peripheral blood mononuclear cells, several T cells clones could be generated which recognized a p21 ras derived peptide carrying a position 12 Gly-->Arg substitution. Arginine 189-192 H3 histone pseudogene 16 Homo sapiens 133-136 8223583-10 1993 Treatment of the sigma 1 heterodimer with 1% sodium cholate, followed by gel filtration or anion-exchange chromatography in the presence of 1% sodium cholate, effectively separated rac1 p21 from rho GDI. Sodium Cholate 45-59 H3 histone pseudogene 16 Homo sapiens 186-189 8223583-10 1993 Treatment of the sigma 1 heterodimer with 1% sodium cholate, followed by gel filtration or anion-exchange chromatography in the presence of 1% sodium cholate, effectively separated rac1 p21 from rho GDI. Sodium Cholate 143-157 H3 histone pseudogene 16 Homo sapiens 186-189 8406231-6 1993 The GTP gamma S-induced Ca2+ sensitization seems to be mediated by rho A p21, a small G protein. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 73-76 8223583-11 1993 Monomeric rac1 p21, obtained by these procedures, was able to stimulate cell-free O2- generation. Superoxides 82-84 H3 histone pseudogene 16 Homo sapiens 15-18 8223583-13 1993 Monomeric rac1 p21 exhibited an almost absolute dependence on exogenous GTP following removal of the endogenous nucleotide in low Mg2+ solution. Guanosine Triphosphate 72-75 H3 histone pseudogene 16 Homo sapiens 15-18 8223583-13 1993 Monomeric rac1 p21 exhibited an almost absolute dependence on exogenous GTP following removal of the endogenous nucleotide in low Mg2+ solution. magnesium ion 130-134 H3 histone pseudogene 16 Homo sapiens 15-18 8406231-6 1993 The GTP gamma S-induced Ca2+ sensitization seems to be mediated by rho A p21, a small G protein. Sulfur 14-15 H3 histone pseudogene 16 Homo sapiens 73-76 8338843-3 1993 All assays gave good agreement except the filter binding assay of [3H]-GDP bound to p21, which gave values of 35-40% compared to the other methods. Tritium 67-69 H3 histone pseudogene 16 Homo sapiens 84-87 8395827-0 1993 Combination of arachidonic acid and guanosine 5"-O-(3-thiotriphosphate) induce translocation of rac p21s to membrane and activation of NADPH oxidase in a cell-free system. guanosine 5"-o- 36-51 H3 histone pseudogene 16 Homo sapiens 100-103 8395827-0 1993 Combination of arachidonic acid and guanosine 5"-O-(3-thiotriphosphate) induce translocation of rac p21s to membrane and activation of NADPH oxidase in a cell-free system. 3-thiotriphosphate 52-70 H3 histone pseudogene 16 Homo sapiens 100-103 8395827-5 1993 However, GTP gamma S in combination with AA markedly augmented rac p21s translocation to the membrane. Guanosine Triphosphate 9-12 H3 histone pseudogene 16 Homo sapiens 67-70 8395827-5 1993 However, GTP gamma S in combination with AA markedly augmented rac p21s translocation to the membrane. Sulfur 19-20 H3 histone pseudogene 16 Homo sapiens 67-70 8395827-7 1993 These results indicate that the GTP-bound active form of rac p21s is the entity that is translocated to the membrane by the action of AA. Guanosine Triphosphate 32-35 H3 histone pseudogene 16 Homo sapiens 61-64 8352776-1 1993 Rho p21 and rac p21 small GTP-binding proteins are regulated by the same inhibitory and stimulatory GDP/GTP exchange proteins termed rho GDI and smg GDS, respectively. Guanosine Triphosphate 26-29 H3 histone pseudogene 16 Homo sapiens 4-7 8352776-1 1993 Rho p21 and rac p21 small GTP-binding proteins are regulated by the same inhibitory and stimulatory GDP/GTP exchange proteins termed rho GDI and smg GDS, respectively. Guanosine Triphosphate 26-29 H3 histone pseudogene 16 Homo sapiens 16-19 8352776-1 1993 Rho p21 and rac p21 small GTP-binding proteins are regulated by the same inhibitory and stimulatory GDP/GTP exchange proteins termed rho GDI and smg GDS, respectively. Guanosine Diphosphate 100-103 H3 histone pseudogene 16 Homo sapiens 4-7 8352776-1 1993 Rho p21 and rac p21 small GTP-binding proteins are regulated by the same inhibitory and stimulatory GDP/GTP exchange proteins termed rho GDI and smg GDS, respectively. Guanosine Diphosphate 100-103 H3 histone pseudogene 16 Homo sapiens 16-19 8352776-1 1993 Rho p21 and rac p21 small GTP-binding proteins are regulated by the same inhibitory and stimulatory GDP/GTP exchange proteins termed rho GDI and smg GDS, respectively. Guanosine Triphosphate 104-107 H3 histone pseudogene 16 Homo sapiens 4-7 8352776-1 1993 Rho p21 and rac p21 small GTP-binding proteins are regulated by the same inhibitory and stimulatory GDP/GTP exchange proteins termed rho GDI and smg GDS, respectively. Guanosine Triphosphate 104-107 H3 histone pseudogene 16 Homo sapiens 16-19 8352776-3 1993 RhoA p21 and rac1 p21 have similar GDP/GTP exchange rates in the absence of rho GDI and smg GDS. Guanosine Diphosphate 35-38 H3 histone pseudogene 16 Homo sapiens 5-8 8352776-3 1993 RhoA p21 and rac1 p21 have similar GDP/GTP exchange rates in the absence of rho GDI and smg GDS. Guanosine Diphosphate 35-38 H3 histone pseudogene 16 Homo sapiens 18-21 8352776-3 1993 RhoA p21 and rac1 p21 have similar GDP/GTP exchange rates in the absence of rho GDI and smg GDS. Guanosine Triphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 5-8 8352776-3 1993 RhoA p21 and rac1 p21 have similar GDP/GTP exchange rates in the absence of rho GDI and smg GDS. Guanosine Triphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 18-21 8352776-4 1993 The velocity of the GDP/GTP exchange reaction for rhoA p21 was enhanced much more by smg GDS than was the velocity of nucleotide exchange for rac1 p21. Guanosine Diphosphate 20-23 H3 histone pseudogene 16 Homo sapiens 55-58 8352776-4 1993 The velocity of the GDP/GTP exchange reaction for rhoA p21 was enhanced much more by smg GDS than was the velocity of nucleotide exchange for rac1 p21. Guanosine Triphosphate 24-27 H3 histone pseudogene 16 Homo sapiens 55-58 8352776-4 1993 The velocity of the GDP/GTP exchange reaction for rhoA p21 was enhanced much more by smg GDS than was the velocity of nucleotide exchange for rac1 p21. Guanosine Triphosphate 24-27 H3 histone pseudogene 16 Homo sapiens 147-150 8395827-0 1993 Combination of arachidonic acid and guanosine 5"-O-(3-thiotriphosphate) induce translocation of rac p21s to membrane and activation of NADPH oxidase in a cell-free system. Arachidonic Acid 15-31 H3 histone pseudogene 16 Homo sapiens 100-103 8357792-1 1993 The three-dimensional structures and biochemical properties of two mutants of the G-domain (residues 1-166) of p21H-ras, p21 (G12D) and p21 (G12P), have been determined in the triphosphate-bound form using guanosine 5"-(beta,gamma-imido)triphosphate (GppNHp). triphosphoric acid 176-188 H3 histone pseudogene 16 Homo sapiens 111-114 8357792-1 1993 The three-dimensional structures and biochemical properties of two mutants of the G-domain (residues 1-166) of p21H-ras, p21 (G12D) and p21 (G12P), have been determined in the triphosphate-bound form using guanosine 5"-(beta,gamma-imido)triphosphate (GppNHp). triphosphoric acid 176-188 H3 histone pseudogene 16 Homo sapiens 121-124 8357792-1 1993 The three-dimensional structures and biochemical properties of two mutants of the G-domain (residues 1-166) of p21H-ras, p21 (G12D) and p21 (G12P), have been determined in the triphosphate-bound form using guanosine 5"-(beta,gamma-imido)triphosphate (GppNHp). Guanylyl Imidodiphosphate 206-249 H3 histone pseudogene 16 Homo sapiens 111-114 8357792-1 1993 The three-dimensional structures and biochemical properties of two mutants of the G-domain (residues 1-166) of p21H-ras, p21 (G12D) and p21 (G12P), have been determined in the triphosphate-bound form using guanosine 5"-(beta,gamma-imido)triphosphate (GppNHp). Guanylyl Imidodiphosphate 206-249 H3 histone pseudogene 16 Homo sapiens 121-124 8357792-1 1993 The three-dimensional structures and biochemical properties of two mutants of the G-domain (residues 1-166) of p21H-ras, p21 (G12D) and p21 (G12P), have been determined in the triphosphate-bound form using guanosine 5"-(beta,gamma-imido)triphosphate (GppNHp). Guanylyl Imidodiphosphate 251-257 H3 histone pseudogene 16 Homo sapiens 111-114 8357792-1 1993 The three-dimensional structures and biochemical properties of two mutants of the G-domain (residues 1-166) of p21H-ras, p21 (G12D) and p21 (G12P), have been determined in the triphosphate-bound form using guanosine 5"-(beta,gamma-imido)triphosphate (GppNHp). Guanylyl Imidodiphosphate 251-257 H3 histone pseudogene 16 Homo sapiens 121-124 8357792-6 1993 The structure of p21 (G12P) is remarkably similar to that of wild-type p21 in the active site, including the position of the nucleophilic water. Water 138-143 H3 histone pseudogene 16 Homo sapiens 17-20 8338843-3 1993 All assays gave good agreement except the filter binding assay of [3H]-GDP bound to p21, which gave values of 35-40% compared to the other methods. Guanosine Diphosphate 71-74 H3 histone pseudogene 16 Homo sapiens 84-87 8338843-4 1993 Concentrations of p21 were thus based on the absorbance of the mant-chromophore of the p21-mant-nucleotide complexes. mant 63-67 H3 histone pseudogene 16 Homo sapiens 18-21 8338843-4 1993 Concentrations of p21 were thus based on the absorbance of the mant-chromophore of the p21-mant-nucleotide complexes. mant 63-67 H3 histone pseudogene 16 Homo sapiens 87-90 8338843-5 1993 The rate constants of the elementary steps of the p21 intrinsic GTPase activity and the GAP activated activity were similar between GTP and mantGTP. Guanosine Triphosphate 64-67 H3 histone pseudogene 16 Homo sapiens 50-53 8338843-6 1993 Incubation of a stoichiometric complex of p21.mantGTP results in a biphasic decrease in fluorescence. 2'(3')-O-(N-methyl)anthraniloylguanosine 5'-triphosphate 46-53 H3 histone pseudogene 16 Homo sapiens 42-45 8338843-10 1993 This is interpreted that the cleavage step of p21.GTP is preceded by and controlled by an isomerization of the p21.GTP complex. Guanosine Triphosphate 50-53 H3 histone pseudogene 16 Homo sapiens 46-49 8338843-10 1993 This is interpreted that the cleavage step of p21.GTP is preceded by and controlled by an isomerization of the p21.GTP complex. Guanosine Triphosphate 50-53 H3 histone pseudogene 16 Homo sapiens 111-114 8338843-10 1993 This is interpreted that the cleavage step of p21.GTP is preceded by and controlled by an isomerization of the p21.GTP complex. Guanosine Triphosphate 115-118 H3 histone pseudogene 16 Homo sapiens 46-49 8338843-10 1993 This is interpreted that the cleavage step of p21.GTP is preceded by and controlled by an isomerization of the p21.GTP complex. Guanosine Triphosphate 115-118 H3 histone pseudogene 16 Homo sapiens 111-114 8338843-11 1993 GAP accelerates the rate constant of the second fluorescence phase occurring with p21.mantGpp[NH]p. This result shows that GAP accelerates the proposed isomerization which limits GTP cleavage rather than the cleavage step itself. Guanosine Triphosphate 179-182 H3 histone pseudogene 16 Homo sapiens 82-85 8329399-1 1993 Heteronuclear-edited proton-detected NMR methods are used to study the nucleotide-dependent conformational change between GDP- and GTP gamma S-bound forms of human N-ras p21. Guanosine Diphosphate 122-125 H3 histone pseudogene 16 Homo sapiens 170-173 8393791-0 1993 Affinity labeling of c-H-ras p21 consensus elements with periodate-oxidized GDP and GTP. metaperiodate 57-66 H3 histone pseudogene 16 Homo sapiens 29-32 8393791-0 1993 Affinity labeling of c-H-ras p21 consensus elements with periodate-oxidized GDP and GTP. Guanosine Diphosphate 76-79 H3 histone pseudogene 16 Homo sapiens 29-32 8393791-0 1993 Affinity labeling of c-H-ras p21 consensus elements with periodate-oxidized GDP and GTP. Guanosine Triphosphate 84-87 H3 histone pseudogene 16 Homo sapiens 29-32 8393791-1 1993 The amino acid sequence motifs of human c-H-ras p21 involved in the interaction with guanosine nucleotides were cross-linked to in situ periodate-oxidized [alpha-32P]GDP or [alpha-32P]GTP. guanosine nucleotides 85-106 H3 histone pseudogene 16 Homo sapiens 48-51 8393791-1 1993 The amino acid sequence motifs of human c-H-ras p21 involved in the interaction with guanosine nucleotides were cross-linked to in situ periodate-oxidized [alpha-32P]GDP or [alpha-32P]GTP. metaperiodate 136-145 H3 histone pseudogene 16 Homo sapiens 48-51 8393791-1 1993 The amino acid sequence motifs of human c-H-ras p21 involved in the interaction with guanosine nucleotides were cross-linked to in situ periodate-oxidized [alpha-32P]GDP or [alpha-32P]GTP. alpha-32p 156-165 H3 histone pseudogene 16 Homo sapiens 48-51 8393791-1 1993 The amino acid sequence motifs of human c-H-ras p21 involved in the interaction with guanosine nucleotides were cross-linked to in situ periodate-oxidized [alpha-32P]GDP or [alpha-32P]GTP. Guanosine Diphosphate 166-169 H3 histone pseudogene 16 Homo sapiens 48-51 8393791-1 1993 The amino acid sequence motifs of human c-H-ras p21 involved in the interaction with guanosine nucleotides were cross-linked to in situ periodate-oxidized [alpha-32P]GDP or [alpha-32P]GTP. alpha-32p 174-183 H3 histone pseudogene 16 Homo sapiens 48-51 8393791-1 1993 The amino acid sequence motifs of human c-H-ras p21 involved in the interaction with guanosine nucleotides were cross-linked to in situ periodate-oxidized [alpha-32P]GDP or [alpha-32P]GTP. Guanosine Triphosphate 184-187 H3 histone pseudogene 16 Homo sapiens 48-51 8393791-2 1993 Site-specific reaction was achieved by cross-linking conserved lysine residues close to the G-nucleotide binding site of p21 with the 2",3"-dialdehyde derivatives of GDP or GTP under kinetically controlled conditions. Lysine 63-69 H3 histone pseudogene 16 Homo sapiens 121-124 8393791-2 1993 Site-specific reaction was achieved by cross-linking conserved lysine residues close to the G-nucleotide binding site of p21 with the 2",3"-dialdehyde derivatives of GDP or GTP under kinetically controlled conditions. 2",3"-dialdehyde 134-150 H3 histone pseudogene 16 Homo sapiens 121-124 8393791-2 1993 Site-specific reaction was achieved by cross-linking conserved lysine residues close to the G-nucleotide binding site of p21 with the 2",3"-dialdehyde derivatives of GDP or GTP under kinetically controlled conditions. Guanosine Diphosphate 166-169 H3 histone pseudogene 16 Homo sapiens 121-124 8329399-1 1993 Heteronuclear-edited proton-detected NMR methods are used to study the nucleotide-dependent conformational change between GDP- and GTP gamma S-bound forms of human N-ras p21. Guanosine Triphosphate 131-134 H3 histone pseudogene 16 Homo sapiens 170-173 8393791-2 1993 Site-specific reaction was achieved by cross-linking conserved lysine residues close to the G-nucleotide binding site of p21 with the 2",3"-dialdehyde derivatives of GDP or GTP under kinetically controlled conditions. Guanosine Triphosphate 173-176 H3 histone pseudogene 16 Homo sapiens 121-124 8329399-3 1993 When GTP gamma S is substituted for GDP in cellular N-ras p21, the chemical shifts of resonances Asp-47, -126, -154, and Asn-172, as well as Gly-77 and -151, are not sensitive to nucleotide exchange, whereas Asp-30, -33, -38, -54, -57, -69, -92, -105, and -119 are affected. Guanosine Triphosphate 5-8 H3 histone pseudogene 16 Homo sapiens 58-61 8329399-3 1993 When GTP gamma S is substituted for GDP in cellular N-ras p21, the chemical shifts of resonances Asp-47, -126, -154, and Asn-172, as well as Gly-77 and -151, are not sensitive to nucleotide exchange, whereas Asp-30, -33, -38, -54, -57, -69, -92, -105, and -119 are affected. Guanosine Diphosphate 36-39 H3 histone pseudogene 16 Homo sapiens 58-61 8329399-3 1993 When GTP gamma S is substituted for GDP in cellular N-ras p21, the chemical shifts of resonances Asp-47, -126, -154, and Asn-172, as well as Gly-77 and -151, are not sensitive to nucleotide exchange, whereas Asp-30, -33, -38, -54, -57, -69, -92, -105, and -119 are affected. Aspartic Acid 97-100 H3 histone pseudogene 16 Homo sapiens 58-61 8329399-3 1993 When GTP gamma S is substituted for GDP in cellular N-ras p21, the chemical shifts of resonances Asp-47, -126, -154, and Asn-172, as well as Gly-77 and -151, are not sensitive to nucleotide exchange, whereas Asp-30, -33, -38, -54, -57, -69, -92, -105, and -119 are affected. Asparagine 121-124 H3 histone pseudogene 16 Homo sapiens 58-61 8329399-3 1993 When GTP gamma S is substituted for GDP in cellular N-ras p21, the chemical shifts of resonances Asp-47, -126, -154, and Asn-172, as well as Gly-77 and -151, are not sensitive to nucleotide exchange, whereas Asp-30, -33, -38, -54, -57, -69, -92, -105, and -119 are affected. Glycine 141-144 H3 histone pseudogene 16 Homo sapiens 58-61 8329399-3 1993 When GTP gamma S is substituted for GDP in cellular N-ras p21, the chemical shifts of resonances Asp-47, -126, -154, and Asn-172, as well as Gly-77 and -151, are not sensitive to nucleotide exchange, whereas Asp-30, -33, -38, -54, -57, -69, -92, -105, and -119 are affected. Aspartic Acid 208-211 H3 histone pseudogene 16 Homo sapiens 58-61 8508922-2 1993 Here we show that in beta-escin skinned mesenteric microarteries, H-ras p21 proteins, preactivated with GTP or GTP gamma S, increase force at constant submaximal Ca2+ (pCa 6.3) concentration dependently. Escin 21-31 H3 histone pseudogene 16 Homo sapiens 72-75 8508922-3 1993 The GTP-bound form of the wild-type H-ras p21 and the oncogenic mutant (p21[G12V]) were equally effective. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 42-45 8508922-2 1993 Here we show that in beta-escin skinned mesenteric microarteries, H-ras p21 proteins, preactivated with GTP or GTP gamma S, increase force at constant submaximal Ca2+ (pCa 6.3) concentration dependently. Guanosine Triphosphate 104-107 H3 histone pseudogene 16 Homo sapiens 72-75 8508922-3 1993 The GTP-bound form of the wild-type H-ras p21 and the oncogenic mutant (p21[G12V]) were equally effective. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 72-75 8508922-4 1993 The nucleotide-free and the inactive GDP-bound form of ras p21 had no effect on force. Guanosine Diphosphate 37-40 H3 histone pseudogene 16 Homo sapiens 59-62 8508922-2 1993 Here we show that in beta-escin skinned mesenteric microarteries, H-ras p21 proteins, preactivated with GTP or GTP gamma S, increase force at constant submaximal Ca2+ (pCa 6.3) concentration dependently. Guanosine 5'-O-(3-Thiotriphosphate) 111-122 H3 histone pseudogene 16 Homo sapiens 72-75 21573584-9 1993 None of the tumors had mutations in K-ras codons 12 or 13 (Gly-->Asp) It is suggested that the ras p21 oncoprotein may be involved in the pathogenesis and H-ras mutations and be a molecular genetic marker in small intestinal tumors. Aspartic Acid 68-71 H3 histone pseudogene 16 Homo sapiens 102-105 8512342-4 1993 The gene product, ras p21, binds to GDP or GTP, and hydrolyzes GTP to GDP and Pi. Guanosine Diphosphate 36-39 H3 histone pseudogene 16 Homo sapiens 22-25 8512342-4 1993 The gene product, ras p21, binds to GDP or GTP, and hydrolyzes GTP to GDP and Pi. Guanosine Triphosphate 43-46 H3 histone pseudogene 16 Homo sapiens 22-25 8512342-4 1993 The gene product, ras p21, binds to GDP or GTP, and hydrolyzes GTP to GDP and Pi. Guanosine Triphosphate 63-66 H3 histone pseudogene 16 Homo sapiens 22-25 8512342-4 1993 The gene product, ras p21, binds to GDP or GTP, and hydrolyzes GTP to GDP and Pi. Guanosine Diphosphate 70-73 H3 histone pseudogene 16 Homo sapiens 22-25 8496156-9 1993 In the course of these studies, we found, in contrast to previous observations, that both GAP and NF1-GRD can weakly activate the GTPase of Leu-61 mutant p21, showing that Gln-61 is not absolutely required for the stimulation of GTPase activity by GAPs. Leucine 140-143 H3 histone pseudogene 16 Homo sapiens 154-157 8496156-9 1993 In the course of these studies, we found, in contrast to previous observations, that both GAP and NF1-GRD can weakly activate the GTPase of Leu-61 mutant p21, showing that Gln-61 is not absolutely required for the stimulation of GTPase activity by GAPs. Glutamine 172-175 H3 histone pseudogene 16 Homo sapiens 154-157 8496156-11 1993 These data suggest a direct role for this residue in catalyzing GTP hydrolysis on p21ras, possibly by contributing a catalytic group to the p21 active site. Guanosine Triphosphate 64-67 H3 histone pseudogene 16 Homo sapiens 82-85 8318164-2 1993 Comparison of the computed and high-resolution x-ray crystallographic structures of Gly-12 p21. Glycine 84-87 H3 histone pseudogene 16 Homo sapiens 91-94 8318164-4 1993 p21 is thought to be activated by the binding of GTP in place of GDP to the protein. Guanosine Triphosphate 49-52 H3 histone pseudogene 16 Homo sapiens 0-3 8318164-4 1993 p21 is thought to be activated by the binding of GTP in place of GDP to the protein. Guanosine Diphosphate 65-68 H3 histone pseudogene 16 Homo sapiens 0-3 8497321-3 1993 We have previously shown that there is a diversity of GAPs that recognize this subfamily, including n-chimaerin, which is enriched in the hippocampus; we also detected proteins that bind these p21 proteins and seem to inhibit GTP hydrolysis. Guanosine Triphosphate 226-229 H3 histone pseudogene 16 Homo sapiens 193-196 8357627-2 1993 The mutated products of ras oncogenes (p21 protein) exhibit a decreased ability to hydrolyze GTP that lead to the stabilization of ras proteins in their active state and cause a continuous flow of signal transduction which may result in malignant transformation. Guanosine Triphosphate 93-96 H3 histone pseudogene 16 Homo sapiens 39-42 8386636-1 1993 Proton-NMR signals in the downfield region (below approximately 10 ppm) have been shown to provide a useful spectroscopic window to monitor the binding of guanine nucleotides to the active site of GTP/GDP-binding proteins via H-bonds, as specified here by the 21-kDa product of the c-H-ras gene (p21). Guanine Nucleotides 155-174 H3 histone pseudogene 16 Homo sapiens 296-299 8386636-1 1993 Proton-NMR signals in the downfield region (below approximately 10 ppm) have been shown to provide a useful spectroscopic window to monitor the binding of guanine nucleotides to the active site of GTP/GDP-binding proteins via H-bonds, as specified here by the 21-kDa product of the c-H-ras gene (p21). Guanosine Triphosphate 197-200 H3 histone pseudogene 16 Homo sapiens 296-299 8386636-1 1993 Proton-NMR signals in the downfield region (below approximately 10 ppm) have been shown to provide a useful spectroscopic window to monitor the binding of guanine nucleotides to the active site of GTP/GDP-binding proteins via H-bonds, as specified here by the 21-kDa product of the c-H-ras gene (p21). Guanosine Diphosphate 201-204 H3 histone pseudogene 16 Homo sapiens 296-299 8386636-2 1993 The time course of the intensity change of certain peaks upon addition of GTP to nucleotide-free p21 corresponds to the GTP hydrolysis rate as determined by HPLC. Guanosine Triphosphate 74-77 H3 histone pseudogene 16 Homo sapiens 97-100 8386636-2 1993 The time course of the intensity change of certain peaks upon addition of GTP to nucleotide-free p21 corresponds to the GTP hydrolysis rate as determined by HPLC. Guanosine Triphosphate 120-123 H3 histone pseudogene 16 Homo sapiens 97-100 21573584-2 1993 The level of ras p21 was analysed using the monoclonal antibody Y13-259 and the biotin-streptavidin-peroxidace-DAB technique. Biotin 80-86 H3 histone pseudogene 16 Homo sapiens 17-20 21573584-2 1993 The level of ras p21 was analysed using the monoclonal antibody Y13-259 and the biotin-streptavidin-peroxidace-DAB technique. diazobenzenesulfonic acid 111-114 H3 histone pseudogene 16 Homo sapiens 17-20 8318164-5 1993 We have previously constructed the three-dimensional structure of the p21 protein bound to GDP from an available alpha-carbon tracing of this protein using a combination of molecular dynamics and energy minimization (Dykes, et al., J. Biomol. Guanosine Diphosphate 91-94 H3 histone pseudogene 16 Homo sapiens 70-73 8318164-5 1993 We have previously constructed the three-dimensional structure of the p21 protein bound to GDP from an available alpha-carbon tracing of this protein using a combination of molecular dynamics and energy minimization (Dykes, et al., J. Biomol. Carbon 119-125 H3 histone pseudogene 16 Homo sapiens 70-73 8429832-0 1993 Effects of brefeldin A on cleavage of invariant chain to p21 and p10 and the appearance of Ii-freed class II MHC dimers. Brefeldin A 11-22 H3 histone pseudogene 16 Homo sapiens 57-60 8318164-8 1993 Until the recent publication of the all-heavy-atom x-ray crystallographic molecular coordinates of p21 residues 1-166 bound to a non-hydrolyzable GTP derivative (GppNp), no all-atom structure of the p21 protein has been available in the Brookhaven National Laboratories Protein Data Bank (PDB). Guanosine Triphosphate 146-149 H3 histone pseudogene 16 Homo sapiens 99-102 8318164-9 1993 In this communication we compare our computed structure for the p21-GDP complex to this x-ray crystal structure. Guanosine Diphosphate 68-71 H3 histone pseudogene 16 Homo sapiens 64-67 8318164-15 1993 Both of these regions have been found in x-ray crystallographic studies of p21-GDP and p21-GTP complexes to undergo significant changes in conformation upon the binding of GTP in place of GDP to the protein. Guanosine Diphosphate 79-82 H3 histone pseudogene 16 Homo sapiens 75-78 8318164-15 1993 Both of these regions have been found in x-ray crystallographic studies of p21-GDP and p21-GTP complexes to undergo significant changes in conformation upon the binding of GTP in place of GDP to the protein. Guanosine Triphosphate 91-94 H3 histone pseudogene 16 Homo sapiens 75-78 8318164-15 1993 Both of these regions have been found in x-ray crystallographic studies of p21-GDP and p21-GTP complexes to undergo significant changes in conformation upon the binding of GTP in place of GDP to the protein. Guanosine Triphosphate 91-94 H3 histone pseudogene 16 Homo sapiens 87-90 8318164-15 1993 Both of these regions have been found in x-ray crystallographic studies of p21-GDP and p21-GTP complexes to undergo significant changes in conformation upon the binding of GTP in place of GDP to the protein. Guanosine Triphosphate 172-175 H3 histone pseudogene 16 Homo sapiens 75-78 8318164-15 1993 Both of these regions have been found in x-ray crystallographic studies of p21-GDP and p21-GTP complexes to undergo significant changes in conformation upon the binding of GTP in place of GDP to the protein. Guanosine Triphosphate 172-175 H3 histone pseudogene 16 Homo sapiens 87-90 8318164-15 1993 Both of these regions have been found in x-ray crystallographic studies of p21-GDP and p21-GTP complexes to undergo significant changes in conformation upon the binding of GTP in place of GDP to the protein. Guanosine Diphosphate 188-191 H3 histone pseudogene 16 Homo sapiens 75-78 8318164-15 1993 Both of these regions have been found in x-ray crystallographic studies of p21-GDP and p21-GTP complexes to undergo significant changes in conformation upon the binding of GTP in place of GDP to the protein. Guanosine Diphosphate 188-191 H3 histone pseudogene 16 Homo sapiens 87-90 8462668-3 1993 Based on the similarities of ras-p21 and elongation factor Tu we propose here a model of the GDP state of ras-p21 that is in agreement with all relevant experimental evidence. Guanosine Diphosphate 93-96 H3 histone pseudogene 16 Homo sapiens 33-36 8462668-3 1993 Based on the similarities of ras-p21 and elongation factor Tu we propose here a model of the GDP state of ras-p21 that is in agreement with all relevant experimental evidence. Guanosine Diphosphate 93-96 H3 histone pseudogene 16 Homo sapiens 110-113 8429689-2 1993 The expression level of smg p21A and ras p21s during phorbol ester-induced differentiation of HL-60 and MEG-01 cell lines was analyzed by immuno- and Northern blotting. Phorbol Esters 53-66 H3 histone pseudogene 16 Homo sapiens 28-31 8095334-6 1993 In situ hybridization of a 3H-labeled probe to human metaphase spreads localized the NDF gene to the short arm of chromosome 8 at bands p12-p21. Tritium 27-29 H3 histone pseudogene 16 Homo sapiens 140-143 7679495-5 1993 LPA- and peptide-induced p21ras activation is inhibited by the tyrosine kinase inhibitor genistein, at doses that do not affect epidermal growth factor-induced p21ras activation. Genistein 89-98 H3 histone pseudogene 16 Homo sapiens 25-28 8429832-4 1993 Cell treatment with Brefeldin A (BFA) was associated with a decrease in Ii-freed alpha, beta dimers, with inhibition of leupeptin-revealed cleavage of Ii to p21 and p10, and with persistence of endoglycosidase H susceptibility of Ii and class II alpha, beta chains. leupeptin 120-129 H3 histone pseudogene 16 Homo sapiens 157-160 8429832-3 1993 The cleavage of Ii to p21 and p10 was revealed in leupeptin-treated cells. leupeptin 50-59 H3 histone pseudogene 16 Homo sapiens 22-25 8429832-4 1993 Cell treatment with Brefeldin A (BFA) was associated with a decrease in Ii-freed alpha, beta dimers, with inhibition of leupeptin-revealed cleavage of Ii to p21 and p10, and with persistence of endoglycosidase H susceptibility of Ii and class II alpha, beta chains. Brefeldin A 20-31 H3 histone pseudogene 16 Homo sapiens 157-160 8429832-4 1993 Cell treatment with Brefeldin A (BFA) was associated with a decrease in Ii-freed alpha, beta dimers, with inhibition of leupeptin-revealed cleavage of Ii to p21 and p10, and with persistence of endoglycosidase H susceptibility of Ii and class II alpha, beta chains. Brefeldin A 33-36 H3 histone pseudogene 16 Homo sapiens 157-160 8419371-1 1993 The coordination and binding of the Mg2+ ion in the nucleotide-binding site of p21 have been investigated using site-directed mutagenesis, kinetic methods, and phosphorous NMR. magnesium ion 36-40 H3 histone pseudogene 16 Homo sapiens 79-82 8425769-5 1993 Under the experimental conditions used, lovastatin prevented the membrane association, but not the biosynthesis, of p21. Lovastatin 40-50 H3 histone pseudogene 16 Homo sapiens 116-119 8419371-1 1993 The coordination and binding of the Mg2+ ion in the nucleotide-binding site of p21 have been investigated using site-directed mutagenesis, kinetic methods, and phosphorous NMR. Phosphinidene 160-171 H3 histone pseudogene 16 Homo sapiens 79-82 8419371-2 1993 Mg2+ in the p21.nucleotide.Mg2+ complex appears to be in fast equilibrium with the solvent. magnesium ion 0-4 H3 histone pseudogene 16 Homo sapiens 12-15 8419371-2 1993 Mg2+ in the p21.nucleotide.Mg2+ complex appears to be in fast equilibrium with the solvent. magnesium ion 27-31 H3 histone pseudogene 16 Homo sapiens 12-15 8419371-3 1993 The dissociation constant between Mg2+ and the p21.GDP complex was determined to be 2.8 microM. magnesium ion 34-38 H3 histone pseudogene 16 Homo sapiens 47-50 8419371-3 1993 The dissociation constant between Mg2+ and the p21.GDP complex was determined to be 2.8 microM. Guanosine Diphosphate 51-54 H3 histone pseudogene 16 Homo sapiens 47-50 8419371-5 1993 All three mutations influence the dissociation constants and the association and dissociation rate constants of the interaction between guanine nucleotides and p21, but to a different degree. Guanine Nucleotides 136-155 H3 histone pseudogene 16 Homo sapiens 160-163 8419371-7 1993 31P NMR spectra of the GDP and Gpp(NH)p (guanosine-5"-(beta,gamma-imido)triphosphate) complexes of mutated p21 show a remarkable perturbation of the guanine nucleotide-binding site compared to wild-type protein. Guanosine Diphosphate 23-26 H3 histone pseudogene 16 Homo sapiens 107-110 8419371-7 1993 31P NMR spectra of the GDP and Gpp(NH)p (guanosine-5"-(beta,gamma-imido)triphosphate) complexes of mutated p21 show a remarkable perturbation of the guanine nucleotide-binding site compared to wild-type protein. Guanylyl Imidodiphosphate 31-39 H3 histone pseudogene 16 Homo sapiens 107-110 8419371-7 1993 31P NMR spectra of the GDP and Gpp(NH)p (guanosine-5"-(beta,gamma-imido)triphosphate) complexes of mutated p21 show a remarkable perturbation of the guanine nucleotide-binding site compared to wild-type protein. Guanylyl Imidodiphosphate 41-84 H3 histone pseudogene 16 Homo sapiens 107-110 8419371-7 1993 31P NMR spectra of the GDP and Gpp(NH)p (guanosine-5"-(beta,gamma-imido)triphosphate) complexes of mutated p21 show a remarkable perturbation of the guanine nucleotide-binding site compared to wild-type protein. Guanine Nucleotides 149-167 H3 histone pseudogene 16 Homo sapiens 107-110 8353139-10 1993 The protein encoded by NF1 contains a GAP homology region, binds p21ras-GTP, and stimulates the hydrolysis of p21ras-bound GTP. Guanosine Triphosphate 72-75 H3 histone pseudogene 16 Homo sapiens 65-68 8232104-4 1993 Farnesyl can be used to synthesize cholesterol and can also bind covalently to several low molecular mass GTP-binding proteins such as p21 ras. FARNESYL 0-8 H3 histone pseudogene 16 Homo sapiens 135-138 8232104-4 1993 Farnesyl can be used to synthesize cholesterol and can also bind covalently to several low molecular mass GTP-binding proteins such as p21 ras. Guanosine Triphosphate 106-109 H3 histone pseudogene 16 Homo sapiens 135-138 1337001-0 1992 Sequential assignment of the backbone nuclei (1H, 15N and 13C) of c-H-ras p21 (1-166).GDP using a novel 4D NMR strategy. Hydrogen 46-48 H3 histone pseudogene 16 Homo sapiens 74-77 1464587-0 1992 Post-translational processing of rac p21s is important both for their interaction with the GDP/GTP exchange proteins and for their activation of NADPH oxidase. Guanosine Triphosphate 95-98 H3 histone pseudogene 16 Homo sapiens 37-40 1464587-1 1992 rac1 and rac2 p21s are ras p21-like small GTP-binding proteins which are implicated in the NADPH oxidase-catalyzed superoxide generation in phagocytes. Guanosine Triphosphate 42-45 H3 histone pseudogene 16 Homo sapiens 14-17 1464587-1 1992 rac1 and rac2 p21s are ras p21-like small GTP-binding proteins which are implicated in the NADPH oxidase-catalyzed superoxide generation in phagocytes. Superoxides 115-125 H3 histone pseudogene 16 Homo sapiens 14-17 1464587-3 1992 We studied the function of this post-translational processing of rac p21s in their interaction with the stimulatory and inhibitory GDP/GTP exchange proteins for rac p21s, named smg GDS and rho GDI, and in their NADPH oxidase activation. Guanosine Diphosphate 131-134 H3 histone pseudogene 16 Homo sapiens 69-72 1464587-3 1992 We studied the function of this post-translational processing of rac p21s in their interaction with the stimulatory and inhibitory GDP/GTP exchange proteins for rac p21s, named smg GDS and rho GDI, and in their NADPH oxidase activation. Guanosine Triphosphate 135-138 H3 histone pseudogene 16 Homo sapiens 69-72 1282032-1 1992 Point mutations in ras genes resulting in substitutions of amino acid Gly in positions 12 and 13, and Gln in position 61 of the ras gene product p21, are commonly found in human tumors. Glutamine 102-105 H3 histone pseudogene 16 Homo sapiens 145-148 1282032-3 1992 Here we report that CD4+ T cells of memory type (CD45RO+) from a patient with a follicular thyroid carcinoma respond against a synthetic peptide derived from aberrant p21 ras having a Gln-->Leu substitution at position 61. Glutamine 184-187 H3 histone pseudogene 16 Homo sapiens 167-170 1282032-3 1992 Here we report that CD4+ T cells of memory type (CD45RO+) from a patient with a follicular thyroid carcinoma respond against a synthetic peptide derived from aberrant p21 ras having a Gln-->Leu substitution at position 61. Leucine 193-196 H3 histone pseudogene 16 Homo sapiens 167-170 7999142-7 1993 We have demonstrated that the SDC25 C-terminus domain promotes GTP binding to Ras p21 in CHO cells. Guanosine Triphosphate 63-66 H3 histone pseudogene 16 Homo sapiens 82-85 7999142-11 1993 These results imply that, in subsets of human tumours, cellular Ras p21 might be found in its GTP-bound active form as a consequence of an oncogenic activation of a mammalian Ras guanine nucleotide exchange factor. Guanosine Triphosphate 94-97 H3 histone pseudogene 16 Homo sapiens 68-71 1447167-0 1992 A mouse CDC25-like product enhances the formation of the active GTP complex of human ras p21 and Saccharomyces cerevisiae RAS2 proteins. Guanosine Triphosphate 64-67 H3 histone pseudogene 16 Homo sapiens 89-92 1447167-4 1992 We show that the product of a recently isolated mouse CDC25-like gene (CDC25Mm) can strongly enhance (more than 1000 times) the GDP release from both human c-Ha-ras p21 and yeast RAS2 in vitro. Guanosine Diphosphate 128-131 H3 histone pseudogene 16 Homo sapiens 165-168 1459198-1 1992 We have recently shown that a peptide (residues 35-47) from a functional region of the ras p21 protein, thought to be involved in the binding of p21 to GTPase activating protein, the antibiotic azatyrosine, known to induce the ras-recision gene, and the selective protein kinase C inhibitor, CGP 41,251, all inhibit oncogenic p21 protein-induced maturation of oocytes in a dose-dependent manner. beta-(5-hydroxy-2-pyridyl)alanine 194-205 H3 histone pseudogene 16 Homo sapiens 91-94 1459198-1 1992 We have recently shown that a peptide (residues 35-47) from a functional region of the ras p21 protein, thought to be involved in the binding of p21 to GTPase activating protein, the antibiotic azatyrosine, known to induce the ras-recision gene, and the selective protein kinase C inhibitor, CGP 41,251, all inhibit oncogenic p21 protein-induced maturation of oocytes in a dose-dependent manner. beta-(5-hydroxy-2-pyridyl)alanine 194-205 H3 histone pseudogene 16 Homo sapiens 145-148 1459198-1 1992 We have recently shown that a peptide (residues 35-47) from a functional region of the ras p21 protein, thought to be involved in the binding of p21 to GTPase activating protein, the antibiotic azatyrosine, known to induce the ras-recision gene, and the selective protein kinase C inhibitor, CGP 41,251, all inhibit oncogenic p21 protein-induced maturation of oocytes in a dose-dependent manner. beta-(5-hydroxy-2-pyridyl)alanine 194-205 H3 histone pseudogene 16 Homo sapiens 145-148 1337001-0 1992 Sequential assignment of the backbone nuclei (1H, 15N and 13C) of c-H-ras p21 (1-166).GDP using a novel 4D NMR strategy. 15n 50-53 H3 histone pseudogene 16 Homo sapiens 74-77 1337001-0 1992 Sequential assignment of the backbone nuclei (1H, 15N and 13C) of c-H-ras p21 (1-166).GDP using a novel 4D NMR strategy. 13c 58-61 H3 histone pseudogene 16 Homo sapiens 74-77 1337001-0 1992 Sequential assignment of the backbone nuclei (1H, 15N and 13C) of c-H-ras p21 (1-166).GDP using a novel 4D NMR strategy. Guanosine Diphosphate 86-89 H3 histone pseudogene 16 Homo sapiens 74-77 1406640-3 1992 We have previously reported that the posttranslational processing of Ki-ras p21 is essential for its interaction with one of its GDP/GTP exchange proteins named smg GDS. Guanosine Diphosphate 129-132 H3 histone pseudogene 16 Homo sapiens 76-79 1429539-2 1992 The model is based on analogies to the known structures of the MgATP site on adenylate kinase and the guanine nucleotide sites on elongation factor Tu (Ef-Tu) and the ras p21 protein. Adenosine Triphosphate 63-68 H3 histone pseudogene 16 Homo sapiens 171-174 1429539-2 1992 The model is based on analogies to the known structures of the MgATP site on adenylate kinase and the guanine nucleotide sites on elongation factor Tu (Ef-Tu) and the ras p21 protein. Guanine Nucleotides 102-120 H3 histone pseudogene 16 Homo sapiens 171-174 1406640-3 1992 We have previously reported that the posttranslational processing of Ki-ras p21 is essential for its interaction with one of its GDP/GTP exchange proteins named smg GDS. Guanosine Triphosphate 133-136 H3 histone pseudogene 16 Homo sapiens 76-79 1390653-0 1992 On the mechanism of guanosine triphosphate hydrolysis in ras p21 proteins. Guanosine Triphosphate 20-42 H3 histone pseudogene 16 Homo sapiens 61-64 1390653-2 1992 Such mutations lead to a major reduction in the rate of GTP hydrolysis by the complex of ras p21 and the GTPase activating protein (GAP) and lock the protein in a growth-promoting state. Guanosine Triphosphate 56-59 H3 histone pseudogene 16 Homo sapiens 93-96 1524403-4 1992 In oocyte microinjection experiments, it was found that this peptide strongly inhibits the mitogenic effects of oncogenic (Val 12-containing)p21 but does not inhibit the cellular effects of activation of normal p21 protein. val 12 123-129 H3 histone pseudogene 16 Homo sapiens 141-144 1325460-3 1992 To test this hypothesis, we examined the ability of NDK to catalyze the phosphorylation of the GDP bound to the following three members of the superfamily of regulatory GTP-binding proteins: Gt, Ha-ras p21, and ARF. Guanosine Diphosphate 95-98 H3 histone pseudogene 16 Homo sapiens 202-205 1524403-5 1992 Furthermore, it has been shown that the cellular effects of oncogenic p21 protein can be completely inhibited by selectively blocking protein kinase C (PKC) with a highly specific inhibitor of this protein, CGP 41 251, a staurosporine derivative. Staurosporine 221-234 H3 histone pseudogene 16 Homo sapiens 70-73 1501882-2 1992 The GDP/GTP exchange reaction of smg p21 is regulated by smg GDS, which is also active on Ki-ras p21 and rho p21. Guanosine Triphosphate 8-11 H3 histone pseudogene 16 Homo sapiens 97-100 1501280-4 1992 Fractionation of radiolabeled oocyte extracts on 10 to 60% sucrose gradients revealed that Cys-minus core proteins resolved into the nonparticulate and capsid forms seen for wild-type p21.5. Cysteine 91-94 H3 histone pseudogene 16 Homo sapiens 184-187 1501280-8 1992 However, Cys residues stabilize isolated p21.5 structures, as evidenced by the marked reduction in stability of Cys-minus dimers and capsids (i) in nonreducing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and (ii) upon protease digestion. Cysteine 9-12 H3 histone pseudogene 16 Homo sapiens 41-44 1501882-1 1992 rap1/Krev-1/smg p21 (smg p21), a member of the small GTP-binding protein (G protein) superfamily, has a geranylgeranylated cysteine residue and clustered basic amino acids in the C-terminal region. Cysteine 123-131 H3 histone pseudogene 16 Homo sapiens 16-19 1501882-1 1992 rap1/Krev-1/smg p21 (smg p21), a member of the small GTP-binding protein (G protein) superfamily, has a geranylgeranylated cysteine residue and clustered basic amino acids in the C-terminal region. Cysteine 123-131 H3 histone pseudogene 16 Homo sapiens 25-28 1501882-1 1992 rap1/Krev-1/smg p21 (smg p21), a member of the small GTP-binding protein (G protein) superfamily, has a geranylgeranylated cysteine residue and clustered basic amino acids in the C-terminal region. Amino Acids, Basic 154-171 H3 histone pseudogene 16 Homo sapiens 16-19 1501882-2 1992 The GDP/GTP exchange reaction of smg p21 is regulated by smg GDS, which is also active on Ki-ras p21 and rho p21. Guanosine Triphosphate 8-11 H3 histone pseudogene 16 Homo sapiens 97-100 1501882-1 1992 rap1/Krev-1/smg p21 (smg p21), a member of the small GTP-binding protein (G protein) superfamily, has a geranylgeranylated cysteine residue and clustered basic amino acids in the C-terminal region. Amino Acids, Basic 154-171 H3 histone pseudogene 16 Homo sapiens 25-28 1501882-4 1992 Moreover, smg p21 is phosphorylated by cyclic AMP- and cyclic GMP-dependent protein kinases at the serine residue between the polybasic region and the prenylated cysteine residue, and this phosphorylation initiates the smg GDS-induced smg p21 activation. Cyclic AMP 39-49 H3 histone pseudogene 16 Homo sapiens 14-17 1501882-2 1992 The GDP/GTP exchange reaction of smg p21 is regulated by smg GDS, which is also active on Ki-ras p21 and rho p21. Guanosine Diphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 37-40 1501882-2 1992 The GDP/GTP exchange reaction of smg p21 is regulated by smg GDS, which is also active on Ki-ras p21 and rho p21. Guanosine Diphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 97-100 1501882-4 1992 Moreover, smg p21 is phosphorylated by cyclic AMP- and cyclic GMP-dependent protein kinases at the serine residue between the polybasic region and the prenylated cysteine residue, and this phosphorylation initiates the smg GDS-induced smg p21 activation. Cyclic AMP 39-49 H3 histone pseudogene 16 Homo sapiens 239-242 1501882-2 1992 The GDP/GTP exchange reaction of smg p21 is regulated by smg GDS, which is also active on Ki-ras p21 and rho p21. Guanosine Diphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 97-100 1501882-4 1992 Moreover, smg p21 is phosphorylated by cyclic AMP- and cyclic GMP-dependent protein kinases at the serine residue between the polybasic region and the prenylated cysteine residue, and this phosphorylation initiates the smg GDS-induced smg p21 activation. Serine 99-105 H3 histone pseudogene 16 Homo sapiens 14-17 1501882-2 1992 The GDP/GTP exchange reaction of smg p21 is regulated by smg GDS, which is also active on Ki-ras p21 and rho p21. Guanosine Triphosphate 8-11 H3 histone pseudogene 16 Homo sapiens 37-40 1501882-4 1992 Moreover, smg p21 is phosphorylated by cyclic AMP- and cyclic GMP-dependent protein kinases at the serine residue between the polybasic region and the prenylated cysteine residue, and this phosphorylation initiates the smg GDS-induced smg p21 activation. Cysteine 162-170 H3 histone pseudogene 16 Homo sapiens 14-17 1432605-1 1992 Isomers of ursodeoxycholic acid, 3 beta,7 alpha- and 3 beta,7 beta-dihydroxy-5 beta-cholan-24-oic acids (3 beta 7 alpha U and 3 beta 7 beta U) crystallize in the orthorhombic space group P2(1)2(1)2(1) containing one molecule and in the monoclinic group P2(1) containing two independent molecules in an asymmetric unit. Ursodeoxycholic Acid 11-31 H3 histone pseudogene 16 Homo sapiens 187-192 14731519-3 1992 A model is presented in which the GTP-binding protein p21(ras) acts as an integrator of the signal transduction pathways controlled by the T-cell antigen receptor. Guanosine Triphosphate 34-37 H3 histone pseudogene 16 Homo sapiens 54-57 1421163-1 1992 The three-dimensional structure of the H-ras oncogene product p21 has been determined in both its active, GTP-bound and its inactive, GDP-bound forms. Guanosine Triphosphate 106-109 H3 histone pseudogene 16 Homo sapiens 62-65 1421163-1 1992 The three-dimensional structure of the H-ras oncogene product p21 has been determined in both its active, GTP-bound and its inactive, GDP-bound forms. Guanosine Diphosphate 134-137 H3 histone pseudogene 16 Homo sapiens 62-65 1432605-1 1992 Isomers of ursodeoxycholic acid, 3 beta,7 alpha- and 3 beta,7 beta-dihydroxy-5 beta-cholan-24-oic acids (3 beta 7 alpha U and 3 beta 7 beta U) crystallize in the orthorhombic space group P2(1)2(1)2(1) containing one molecule and in the monoclinic group P2(1) containing two independent molecules in an asymmetric unit. cholanic acid 76-103 H3 histone pseudogene 16 Homo sapiens 187-192 1377053-10 1992 Epo was also able to activate p21ras as measured by exchange of guanosine diphosphate for guanosine triphosphate. Guanosine Diphosphate 64-85 H3 histone pseudogene 16 Homo sapiens 30-33 1634508-1 1992 smg GDS and rho GDI are stimulatory and inhibitory GDP/GTP exchange proteins, respectively, for a group of ras p21-related small GTP-binding proteins (G proteins). Guanosine Diphosphate 51-54 H3 histone pseudogene 16 Homo sapiens 111-114 1634508-1 1992 smg GDS and rho GDI are stimulatory and inhibitory GDP/GTP exchange proteins, respectively, for a group of ras p21-related small GTP-binding proteins (G proteins). Guanosine Triphosphate 55-58 H3 histone pseudogene 16 Homo sapiens 111-114 1634508-1 1992 smg GDS and rho GDI are stimulatory and inhibitory GDP/GTP exchange proteins, respectively, for a group of ras p21-related small GTP-binding proteins (G proteins). Guanosine Triphosphate 129-132 H3 histone pseudogene 16 Homo sapiens 111-114 1634508-2 1992 rho p21 is a common substrate small G protein for both GDP/GTP exchange proteins. Guanosine Triphosphate 59-62 H3 histone pseudogene 16 Homo sapiens 4-7 1634508-3 1992 We examined here the functional interactions of these GDP/GTP exchange proteins with rho p21 as a substrate. Guanosine Diphosphate 54-57 H3 histone pseudogene 16 Homo sapiens 89-92 1634508-3 1992 We examined here the functional interactions of these GDP/GTP exchange proteins with rho p21 as a substrate. Guanosine Triphosphate 58-61 H3 histone pseudogene 16 Homo sapiens 89-92 1634508-4 1992 smg GDS and rho GDI interacted with the GDP-bound form of rho p21 and thereby stimulated and inhibited, respectively, the dissociation of GDP. Guanosine Diphosphate 40-43 H3 histone pseudogene 16 Homo sapiens 62-65 1634508-4 1992 smg GDS and rho GDI interacted with the GDP-bound form of rho p21 and thereby stimulated and inhibited, respectively, the dissociation of GDP. Guanosine Diphosphate 138-141 H3 histone pseudogene 16 Homo sapiens 62-65 1634508-6 1992 The GDP-bound form of rho p21 formed a complex with rho GDI but not with smg GDS in their simultaneous presence. Guanosine Diphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 26-29 1634508-7 1992 Since the content of smg GDS was generally less than that of rho GDI in cells, these results suggest that there is some mechanism to release the inhibitory action of rho GDI and to make rho p21 sensitive to the smg GDS action during the conversion of rhoA p21 from the GDP-bound inactive form to the GTP-bound active form in intact cells. Guanosine Diphosphate 269-272 H3 histone pseudogene 16 Homo sapiens 190-193 1634508-7 1992 Since the content of smg GDS was generally less than that of rho GDI in cells, these results suggest that there is some mechanism to release the inhibitory action of rho GDI and to make rho p21 sensitive to the smg GDS action during the conversion of rhoA p21 from the GDP-bound inactive form to the GTP-bound active form in intact cells. Guanosine Triphosphate 300-303 H3 histone pseudogene 16 Homo sapiens 190-193 1379346-7 1992 This portion of Ras-GRF accelerated the release of GDP from RasH and RasN p21 in vitro, but not from the related RalA, or CDC42Hs GTP-binding proteins. Guanosine Diphosphate 51-54 H3 histone pseudogene 16 Homo sapiens 74-77 1377053-10 1992 Epo was also able to activate p21ras as measured by exchange of guanosine diphosphate for guanosine triphosphate. Guanosine Triphosphate 90-112 H3 histone pseudogene 16 Homo sapiens 30-33 1620132-5 1992 Thus, in the absence of PKC stimulation, the TCR was still able to induce accumulation of p21ras-GTP complexes, and this stimulation correlated with an inactivation of p21ras GTPase-activating proteins. Guanosine Triphosphate 97-100 H3 histone pseudogene 16 Homo sapiens 90-93 1506429-2 1992 The v-H-ras monoclonal antibody (mAb) against the c-ras protein, p21, reacted specifically with the acrosomal region of methanol-fixed as well as unfixed-live capacitated and non-capacitated human sperm cell in the indirect immunofluorescence technique. Methanol 120-128 H3 histone pseudogene 16 Homo sapiens 65-68 1316893-11 1992 These results indicate that the superoxide-generating NADPH oxidase system is regulated by both smg GDS and rho GDI through rac2 p21 or the rac2-related small G protein in phagocytes. Superoxides 32-42 H3 histone pseudogene 16 Homo sapiens 129-132 1599919-0 1992 Simulation of the solution structure of the H-ras p21-GTP complex. Guanosine Triphosphate 54-57 H3 histone pseudogene 16 Homo sapiens 50-53 1599919-1 1992 An unconstrained simulation of the GTP-bound form of the H-ras protein p21 is performed in an aqueous environment with charge-neutralizing counterions. Guanosine Triphosphate 35-38 H3 histone pseudogene 16 Homo sapiens 71-74 1402877-5 1992 The crystal of [PdCl2(sperH)]2[PdCl4] x 2H2O (II) is monoclinic, P2(1)/n, with a = 7.023(1) A, b = 12.662(1) A, c = 18.435(3) A, and beta = 99.95(1) degrees, Z = 4, R = 0.051, and Rw = 0.058 on the basis of 2690 independent reflections. pdcl4 31-36 H3 histone pseudogene 16 Homo sapiens 65-70 1318075-1 1992 The number of water molecules bound to Mn2+ in the complex with a variant of Ha ras p21 and GDP has been determined by electron paramagnetic resonance (EPR) measurements in 17O-enriched water. Water 14-19 H3 histone pseudogene 16 Homo sapiens 84-87 1318075-1 1992 The number of water molecules bound to Mn2+ in the complex with a variant of Ha ras p21 and GDP has been determined by electron paramagnetic resonance (EPR) measurements in 17O-enriched water. Manganese(2+) 39-43 H3 histone pseudogene 16 Homo sapiens 84-87 1318075-1 1992 The number of water molecules bound to Mn2+ in the complex with a variant of Ha ras p21 and GDP has been determined by electron paramagnetic resonance (EPR) measurements in 17O-enriched water. 17o 173-176 H3 histone pseudogene 16 Homo sapiens 84-87 1318075-1 1992 The number of water molecules bound to Mn2+ in the complex with a variant of Ha ras p21 and GDP has been determined by electron paramagnetic resonance (EPR) measurements in 17O-enriched water. Water 186-191 H3 histone pseudogene 16 Homo sapiens 84-87 1318075-7 1992 The resolution enhancement method has also been applied in a measurement of the 17O-Mn2+ superhyperfine coupling constant of 17O in the beta-phosphate of the GDP in the ras p21 complex. 17o 80-83 H3 histone pseudogene 16 Homo sapiens 173-176 1318075-7 1992 The resolution enhancement method has also been applied in a measurement of the 17O-Mn2+ superhyperfine coupling constant of 17O in the beta-phosphate of the GDP in the ras p21 complex. beta-phosphate 136-150 H3 histone pseudogene 16 Homo sapiens 173-176 1318075-7 1992 The resolution enhancement method has also been applied in a measurement of the 17O-Mn2+ superhyperfine coupling constant of 17O in the beta-phosphate of the GDP in the ras p21 complex. Guanosine Diphosphate 158-161 H3 histone pseudogene 16 Homo sapiens 173-176 1318075-8 1992 The intrinsically narrow EPR signals of Mn2+ in the complex with ras p21 and GDP in 2H2O respond to resolution enhancement such that the superhyperfine splitting from the 17O nuclear spin (I = 5/2) becomes visible in the EPR signals. Manganese(2+) 40-44 H3 histone pseudogene 16 Homo sapiens 69-72 21584509-1 1992 Ras p21 expression was investigated in 28 cases of neuroblastomas and 12 cases of ganglio-neuroblastomas by the biotin-streptavidin immunoperoxidase method using the anti-ras p21 rat monoclonal antibody Y13-259. Biotin 112-118 H3 histone pseudogene 16 Homo sapiens 4-7 1637501-2 1992 An energy-refined structure for the normal p21 protein complexed with GDP. Guanosine Diphosphate 70-73 H3 histone pseudogene 16 Homo sapiens 43-46 1637501-3 1992 A complete three-dimensional structure for the ras-gene-encoded p21 protein with Gly 12 and Gln 61, bound to GDP, has been constructed in four stages using the available alpha-carbon coordinates as deposited in the Brookhaven National Laboratories Protein Data Bank. Glycine 81-84 H3 histone pseudogene 16 Homo sapiens 64-67 1637501-3 1992 A complete three-dimensional structure for the ras-gene-encoded p21 protein with Gly 12 and Gln 61, bound to GDP, has been constructed in four stages using the available alpha-carbon coordinates as deposited in the Brookhaven National Laboratories Protein Data Bank. Glutamine 92-95 H3 histone pseudogene 16 Homo sapiens 64-67 1637501-3 1992 A complete three-dimensional structure for the ras-gene-encoded p21 protein with Gly 12 and Gln 61, bound to GDP, has been constructed in four stages using the available alpha-carbon coordinates as deposited in the Brookhaven National Laboratories Protein Data Bank. Guanosine Diphosphate 109-112 H3 histone pseudogene 16 Homo sapiens 64-67 1637501-3 1992 A complete three-dimensional structure for the ras-gene-encoded p21 protein with Gly 12 and Gln 61, bound to GDP, has been constructed in four stages using the available alpha-carbon coordinates as deposited in the Brookhaven National Laboratories Protein Data Bank. Carbon 176-182 H3 histone pseudogene 16 Homo sapiens 64-67 1592117-4 1992 In addition cross-linking of [alpha-32P]GTP with GTP-binding proteins was demonstrated in model systems using different purified GTPases, human c-H-ras p21, transducin from bovine retina, polypeptide elongation factor Tu (EF-Tu) from T. thermophilus and initiation factor 2 (IF2) from T. thermophilus. [alpha-32p]gtp 29-43 H3 histone pseudogene 16 Homo sapiens 152-155 1592117-4 1992 In addition cross-linking of [alpha-32P]GTP with GTP-binding proteins was demonstrated in model systems using different purified GTPases, human c-H-ras p21, transducin from bovine retina, polypeptide elongation factor Tu (EF-Tu) from T. thermophilus and initiation factor 2 (IF2) from T. thermophilus. Guanosine Triphosphate 40-43 H3 histone pseudogene 16 Homo sapiens 152-155 1513332-3 1992 Artemia p21 was unable to hydrolyze Gp4G, although this dinucleotide exhibits high affinity for the protein. Dinucleoside Phosphates 56-68 H3 histone pseudogene 16 Homo sapiens 8-11 1533366-6 1992 The results of this analysis have indicated two distinct interactive regions in p21, one associated with the guanine-nucleotide-binding site, whilst the second is proposed to be associated with a binding site for an activator protein. Guanine Nucleotides 109-127 H3 histone pseudogene 16 Homo sapiens 80-83 1569940-2 1992 Mutations of residues in loop L1 (Gly-12 and Gly-13), in loop L2 (Thr-35 and Asp-38), and in loop L4 (Gln-61 and Glu-63) influence the reaction in different ways, but all of these mutant p21 proteins still form complexes with GAP. Threonine 66-69 H3 histone pseudogene 16 Homo sapiens 187-190 1569940-2 1992 Mutations of residues in loop L1 (Gly-12 and Gly-13), in loop L2 (Thr-35 and Asp-38), and in loop L4 (Gln-61 and Glu-63) influence the reaction in different ways, but all of these mutant p21 proteins still form complexes with GAP. Glutamine 102-105 H3 histone pseudogene 16 Homo sapiens 187-190 1569940-2 1992 Mutations of residues in loop L1 (Gly-12 and Gly-13), in loop L2 (Thr-35 and Asp-38), and in loop L4 (Gln-61 and Glu-63) influence the reaction in different ways, but all of these mutant p21 proteins still form complexes with GAP. Glutamic Acid 113-116 H3 histone pseudogene 16 Homo sapiens 187-190 1351291-0 1992 The role of nucleoside triphosphate hydrolysis in transducing systems: p21ras and muscle. [[(2R,3S,4R,5S)-3,4-dihydroxy-5-methyloxolan-2-yl]methoxy-hydroxyphosphoryl] phosphono hydrogen phosphate 12-35 H3 histone pseudogene 16 Homo sapiens 71-74 1351293-1 1992 Current knowledge of the structure of H-ras p21 is reviewed with particular emphasis on the interaction between guanine nucleotides and the active site of the protein. Guanine Nucleotides 112-131 H3 histone pseudogene 16 Homo sapiens 44-47 1351295-1 1992 Ras p21 proteins cycle between inactive, GDP-bound forms and active GTP-bound forms. Guanosine Diphosphate 41-44 H3 histone pseudogene 16 Homo sapiens 4-7 1351295-1 1992 Ras p21 proteins cycle between inactive, GDP-bound forms and active GTP-bound forms. Guanosine Triphosphate 68-71 H3 histone pseudogene 16 Homo sapiens 4-7 1351295-5 1992 This is a protein of 325,000 Da that is defective in patients with NF1; NF1-GAP is regulated by signalling lipids, and may serve to connect ras p21 with phospholipid second messenger systems. Phospholipids 153-165 H3 histone pseudogene 16 Homo sapiens 144-147 1351296-1 1992 Guanine nucleotides modified by acetylation of the ribose moiety with the small fluorophore N-methylanthranilic acid(mant) have been shown to bind to p21 ras with similar equilibrium and kinetic rate constants as the parent nucleotides. Guanine Nucleotides 0-19 H3 histone pseudogene 16 Homo sapiens 150-153 1351296-1 1992 Guanine nucleotides modified by acetylation of the ribose moiety with the small fluorophore N-methylanthranilic acid(mant) have been shown to bind to p21 ras with similar equilibrium and kinetic rate constants as the parent nucleotides. Ribose 51-57 H3 histone pseudogene 16 Homo sapiens 150-153 1351296-1 1992 Guanine nucleotides modified by acetylation of the ribose moiety with the small fluorophore N-methylanthranilic acid(mant) have been shown to bind to p21 ras with similar equilibrium and kinetic rate constants as the parent nucleotides. N-Methylanthranilic acid 92-116 H3 histone pseudogene 16 Homo sapiens 150-153 1351296-1 1992 Guanine nucleotides modified by acetylation of the ribose moiety with the small fluorophore N-methylanthranilic acid(mant) have been shown to bind to p21 ras with similar equilibrium and kinetic rate constants as the parent nucleotides. mant 117-121 H3 histone pseudogene 16 Homo sapiens 150-153 1351296-4 1992 The fluorescence change with p21.mantGMP.PNP is accelerated in the presence of the C-terminal catalytic domain of GAP, which is consistent with this mechanism. mantgmp 33-40 H3 histone pseudogene 16 Homo sapiens 29-32 1351296-7 1992 These data imply a rapidly reversible formation of the p21.mantGTP complex with GAP followed by the isomerization of this complex. 2'(3')-O-(N-methyl)anthraniloylguanosine 5'-triphosphate 59-66 H3 histone pseudogene 16 Homo sapiens 55-58 1569940-2 1992 Mutations of residues in loop L1 (Gly-12 and Gly-13), in loop L2 (Thr-35 and Asp-38), and in loop L4 (Gln-61 and Glu-63) influence the reaction in different ways, but all of these mutant p21 proteins still form complexes with GAP. Glycine 34-37 H3 histone pseudogene 16 Homo sapiens 187-190 1569940-2 1992 Mutations of residues in loop L1 (Gly-12 and Gly-13), in loop L2 (Thr-35 and Asp-38), and in loop L4 (Gln-61 and Glu-63) influence the reaction in different ways, but all of these mutant p21 proteins still form complexes with GAP. Glycine 45-48 H3 histone pseudogene 16 Homo sapiens 187-190 1533366-7 1992 These studies indicate that the p21 protein, besides the ability to function as a plasma-membrane-associated guanine-nucleotide-binding regulatory protein and bind free guanine nucleotides in the cytoplasm, has the structural ability to bind guanine incorporated in DNA. Guanine Nucleotides 169-188 H3 histone pseudogene 16 Homo sapiens 32-35 1533366-7 1992 These studies indicate that the p21 protein, besides the ability to function as a plasma-membrane-associated guanine-nucleotide-binding regulatory protein and bind free guanine nucleotides in the cytoplasm, has the structural ability to bind guanine incorporated in DNA. Guanine 109-116 H3 histone pseudogene 16 Homo sapiens 32-35 1540187-1 1992 A stimulatory GDP/GTP exchange protein for smg p21 (smg GDS) stimulated the binding of guanosine 5"-(3-0-thio) triphosphate (GTP gamma S) to smg p21B. Guanosine Diphosphate 14-17 H3 histone pseudogene 16 Homo sapiens 47-50 1371879-0 1992 p21ras activation via hemopoietin receptors and c-kit requires tyrosine kinase activity but not tyrosine phosphorylation of p21ras GTPase-activating protein. Tyrosine 63-71 H3 histone pseudogene 16 Homo sapiens 0-3 1740128-6 1992 The concentrations of Mg2+ influencing the dissociation rate of the p21.GDP complex are much higher than for the intrinsic GTPase activity, an effect also observed for EF-Tu. Guanosine Diphosphate 72-75 H3 histone pseudogene 16 Homo sapiens 68-71 1639630-0 1992 T-cell responses against products of oncogenes: generation and characterization of human T-cell clones specific for p21 ras-derived synthetic peptides. Peptides 142-150 H3 histone pseudogene 16 Homo sapiens 116-119 1639630-8 1992 TCC B and I were restricted by HLA-DR molecules, and recognized the mutated p21 ras-derived peptide carrying Arg and Lys at residue 12, respectively. Arginine 109-112 H3 histone pseudogene 16 Homo sapiens 76-79 1639630-8 1992 TCC B and I were restricted by HLA-DR molecules, and recognized the mutated p21 ras-derived peptide carrying Arg and Lys at residue 12, respectively. Lysine 117-120 H3 histone pseudogene 16 Homo sapiens 76-79 1639630-9 1992 TCC E and F were restricted by HLA-DQ molecules, the former being specific for a mutated p21 ras-derived peptide with Val in position 13 and the latter more broadly reactive. Valine 118-121 H3 histone pseudogene 16 Homo sapiens 89-92 1371879-7 1992 Activation of p21ras was also observed in response to Steel factor, which stimulates the endogenous tyrosine kinase activity of the c-kit receptor, as well as with phorbol esters, which activate protein kinase C. Experiments with protein kinase inhibitors implicated tyrosine kinase activity, but not protein kinase C activity, as the upstream signal in p21ras activation via these growth factor receptors. Phorbol Esters 164-178 H3 histone pseudogene 16 Homo sapiens 14-17 1740128-2 1992 The influence of the ionic environment on the intrinsic GTPase activity and the guanine-nucleotide interaction of Ha-ras protein p21 were studied in various experimental conditions and compared with the behaviour of elongation factor (EF) Tu. Guanine Nucleotides 80-98 H3 histone pseudogene 16 Homo sapiens 129-132 1740128-4 1992 Specific differences between p21 and EF-Tu were found in the action of divalent anions which strongly enhance the dissociation rate of p21.GDP without affecting that of EF-Tu. Guanosine Diphosphate 139-142 H3 histone pseudogene 16 Homo sapiens 29-32 1740128-4 1992 Specific differences between p21 and EF-Tu were found in the action of divalent anions which strongly enhance the dissociation rate of p21.GDP without affecting that of EF-Tu. Guanosine Diphosphate 139-142 H3 histone pseudogene 16 Homo sapiens 135-138 1740128-6 1992 The concentrations of Mg2+ influencing the dissociation rate of the p21.GDP complex are much higher than for the intrinsic GTPase activity, an effect also observed for EF-Tu. magnesium ion 22-26 H3 histone pseudogene 16 Homo sapiens 68-71 1540187-1 1992 A stimulatory GDP/GTP exchange protein for smg p21 (smg GDS) stimulated the binding of guanosine 5"-(3-0-thio) triphosphate (GTP gamma S) to smg p21B. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 47-50 1540187-1 1992 A stimulatory GDP/GTP exchange protein for smg p21 (smg GDS) stimulated the binding of guanosine 5"-(3-0-thio) triphosphate (GTP gamma S) to smg p21B. guanosine 5"-(3-0-thio) triphosphate 87-123 H3 histone pseudogene 16 Homo sapiens 47-50 1540187-1 1992 A stimulatory GDP/GTP exchange protein for smg p21 (smg GDS) stimulated the binding of guanosine 5"-(3-0-thio) triphosphate (GTP gamma S) to smg p21B. Guanosine Triphosphate 125-128 H3 histone pseudogene 16 Homo sapiens 47-50 1540187-1 1992 A stimulatory GDP/GTP exchange protein for smg p21 (smg GDS) stimulated the binding of guanosine 5"-(3-0-thio) triphosphate (GTP gamma S) to smg p21B. Sulfur 58-59 H3 histone pseudogene 16 Homo sapiens 47-50 1613976-4 1992 There are two regulatory proteins for smg p21, smg p21 GTPase activating protein (GAP) and smg GDP dissociation stimulator (GDS). Guanosine Diphosphate 95-98 H3 histone pseudogene 16 Homo sapiens 42-45 1733958-12 1992 Kinetic studies of the ADP-ribosylation and peptide mapping of the reaction products of rhoB p21 by EDIN and C3 suggest that the mode of action of the ADP-ribosylation by EDIN is quite similar to that by C3 and that the ADP-ribosylation site of rhoB p21 by EDIN is presumably the same as that by C3. Adenosine Diphosphate 23-26 H3 histone pseudogene 16 Homo sapiens 93-96 1733958-12 1992 Kinetic studies of the ADP-ribosylation and peptide mapping of the reaction products of rhoB p21 by EDIN and C3 suggest that the mode of action of the ADP-ribosylation by EDIN is quite similar to that by C3 and that the ADP-ribosylation site of rhoB p21 by EDIN is presumably the same as that by C3. edin 100-104 H3 histone pseudogene 16 Homo sapiens 93-96 1733958-12 1992 Kinetic studies of the ADP-ribosylation and peptide mapping of the reaction products of rhoB p21 by EDIN and C3 suggest that the mode of action of the ADP-ribosylation by EDIN is quite similar to that by C3 and that the ADP-ribosylation site of rhoB p21 by EDIN is presumably the same as that by C3. Adenosine Diphosphate 151-154 H3 histone pseudogene 16 Homo sapiens 93-96 1733958-12 1992 Kinetic studies of the ADP-ribosylation and peptide mapping of the reaction products of rhoB p21 by EDIN and C3 suggest that the mode of action of the ADP-ribosylation by EDIN is quite similar to that by C3 and that the ADP-ribosylation site of rhoB p21 by EDIN is presumably the same as that by C3. Adenosine Diphosphate 151-154 H3 histone pseudogene 16 Homo sapiens 250-253 1733958-12 1992 Kinetic studies of the ADP-ribosylation and peptide mapping of the reaction products of rhoB p21 by EDIN and C3 suggest that the mode of action of the ADP-ribosylation by EDIN is quite similar to that by C3 and that the ADP-ribosylation site of rhoB p21 by EDIN is presumably the same as that by C3. edin 171-175 H3 histone pseudogene 16 Homo sapiens 93-96 1733958-12 1992 Kinetic studies of the ADP-ribosylation and peptide mapping of the reaction products of rhoB p21 by EDIN and C3 suggest that the mode of action of the ADP-ribosylation by EDIN is quite similar to that by C3 and that the ADP-ribosylation site of rhoB p21 by EDIN is presumably the same as that by C3. edin 171-175 H3 histone pseudogene 16 Homo sapiens 250-253 1733958-12 1992 Kinetic studies of the ADP-ribosylation and peptide mapping of the reaction products of rhoB p21 by EDIN and C3 suggest that the mode of action of the ADP-ribosylation by EDIN is quite similar to that by C3 and that the ADP-ribosylation site of rhoB p21 by EDIN is presumably the same as that by C3. edin 171-175 H3 histone pseudogene 16 Homo sapiens 93-96 1733958-12 1992 Kinetic studies of the ADP-ribosylation and peptide mapping of the reaction products of rhoB p21 by EDIN and C3 suggest that the mode of action of the ADP-ribosylation by EDIN is quite similar to that by C3 and that the ADP-ribosylation site of rhoB p21 by EDIN is presumably the same as that by C3. edin 171-175 H3 histone pseudogene 16 Homo sapiens 250-253 1733441-1 1992 Immunocytochemistry with monoclonal antibody Y13-259 demonstrated p21 ras in paraffin sections of breast tissue from 171 women: 85 with invasive breast carcinoma, 14 with non-invasive carcinoma and 72 with benign changes only. Paraffin 77-85 H3 histone pseudogene 16 Homo sapiens 66-69 1549353-0 1992 Induction of smg p21/rap1A p21/krev-1 p21 gene expression during phorbol ester-induced differentiation of a human megakaryocytic leukemia cell line. Phorbol Esters 65-78 H3 histone pseudogene 16 Homo sapiens 17-20 1549353-0 1992 Induction of smg p21/rap1A p21/krev-1 p21 gene expression during phorbol ester-induced differentiation of a human megakaryocytic leukemia cell line. Phorbol Esters 65-78 H3 histone pseudogene 16 Homo sapiens 27-30 1549353-0 1992 Induction of smg p21/rap1A p21/krev-1 p21 gene expression during phorbol ester-induced differentiation of a human megakaryocytic leukemia cell line. Phorbol Esters 65-78 H3 histone pseudogene 16 Homo sapiens 27-30 1549353-1 1992 smg p21A and -B (smg p21s) are ras p21-like small GTP-binding proteins (G proteins) with the same putative effector domain as ras p21s. Guanosine Triphosphate 50-53 H3 histone pseudogene 16 Homo sapiens 4-7 1549353-3 1992 The smg p21 protein molecules also increased during the TPA-induced differentiation of CMK cells. Tetradecanoylphorbol Acetate 56-59 H3 histone pseudogene 16 Homo sapiens 8-11 1549353-5 1992 Ha-ras p21 mRNA was undetectable, but both Ki- and N-ras p21 mRNAs were detected in CMK cells and their levels were also increased during TPA-induced differentiation of CMK cells, although to a lesser extent than those of smg p21 mRNAs. Tetradecanoylphorbol Acetate 138-141 H3 histone pseudogene 16 Homo sapiens 7-10 1549353-5 1992 Ha-ras p21 mRNA was undetectable, but both Ki- and N-ras p21 mRNAs were detected in CMK cells and their levels were also increased during TPA-induced differentiation of CMK cells, although to a lesser extent than those of smg p21 mRNAs. Tetradecanoylphorbol Acetate 138-141 H3 histone pseudogene 16 Homo sapiens 57-60 1549353-5 1992 Ha-ras p21 mRNA was undetectable, but both Ki- and N-ras p21 mRNAs were detected in CMK cells and their levels were also increased during TPA-induced differentiation of CMK cells, although to a lesser extent than those of smg p21 mRNAs. Tetradecanoylphorbol Acetate 138-141 H3 histone pseudogene 16 Homo sapiens 57-60 1549353-9 1992 A dramatic increase in the smg p21 mRNA levels was also observed in other leukemia cell lines during TPA-induced differentiation. Tetradecanoylphorbol Acetate 101-104 H3 histone pseudogene 16 Homo sapiens 31-34 1734890-2 1992 smg GDS, previously thought to be a stimulatory GDP/GTP exchange protein for smg p21, Ki-ras p21, and rho p21, but not for Ha-ras p21 or smg p25A, was also active on rac1 p21. Guanosine Triphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 81-84 1734890-2 1992 smg GDS, previously thought to be a stimulatory GDP/GTP exchange protein for smg p21, Ki-ras p21, and rho p21, but not for Ha-ras p21 or smg p25A, was also active on rac1 p21. Guanosine Triphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 93-96 1734890-2 1992 smg GDS, previously thought to be a stimulatory GDP/GTP exchange protein for smg p21, Ki-ras p21, and rho p21, but not for Ha-ras p21 or smg p25A, was also active on rac1 p21. Guanosine Triphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 93-96 1734890-2 1992 smg GDS, previously thought to be a stimulatory GDP/GTP exchange protein for smg p21, Ki-ras p21, and rho p21, but not for Ha-ras p21 or smg p25A, was also active on rac1 p21. Guanosine Triphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 93-96 1734890-2 1992 smg GDS, previously thought to be a stimulatory GDP/GTP exchange protein for smg p21, Ki-ras p21, and rho p21, but not for Ha-ras p21 or smg p25A, was also active on rac1 p21. Guanosine Triphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 93-96 1734890-3 1992 rho GDI, previously thought to be an inhibitory GDP/GTP exchange protein specific for rho p21, was also active on rac1 p21. Guanosine Triphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 90-93 1734890-3 1992 rho GDI, previously thought to be an inhibitory GDP/GTP exchange protein specific for rho p21, was also active on rac1 p21. Guanosine Triphosphate 52-55 H3 histone pseudogene 16 Homo sapiens 119-122 1610210-0 1992 Immunohistological localization of smg p25A, a ras p21-like guanosine 5"-triphosphate (GTP)-binding protein in human skin. Guanosine Triphosphate 87-90 H3 histone pseudogene 16 Homo sapiens 51-54 1549351-0 1992 Molecular cloning of the human cDNA for a stimulatory GDP/GTP exchange protein for c-Ki-ras p21 and smg p21. Guanosine Diphosphate 54-57 H3 histone pseudogene 16 Homo sapiens 92-95 1549351-0 1992 Molecular cloning of the human cDNA for a stimulatory GDP/GTP exchange protein for c-Ki-ras p21 and smg p21. Guanosine Diphosphate 54-57 H3 histone pseudogene 16 Homo sapiens 104-107 1549351-0 1992 Molecular cloning of the human cDNA for a stimulatory GDP/GTP exchange protein for c-Ki-ras p21 and smg p21. Guanosine Triphosphate 58-61 H3 histone pseudogene 16 Homo sapiens 92-95 1549351-0 1992 Molecular cloning of the human cDNA for a stimulatory GDP/GTP exchange protein for c-Ki-ras p21 and smg p21. Guanosine Triphosphate 58-61 H3 histone pseudogene 16 Homo sapiens 104-107 1731253-7 1992 We propose that recA protein may change its conformation upon ATP hydrolysis in a manner analogous to one such protein, the p21 protein from the ras oncogene. Adenosine Triphosphate 62-65 H3 histone pseudogene 16 Homo sapiens 124-127 1731253-9 1992 The mechanism by which nucleoside triphosphate hydrolysis is coupled to the binding of another ligand in recA protein and p21 may be typical of the large class of NTPases containing this conserved motif. [[(2R,3S,4R,5S)-3,4-dihydroxy-5-methyloxolan-2-yl]methoxy-hydroxyphosphoryl] phosphono hydrogen phosphate 23-46 H3 histone pseudogene 16 Homo sapiens 122-125 1516585-4 1992 P21 product of H-ras and P62 product of c-myc genes were detected in paraffin embedded parallel tissue sections. Paraffin 69-77 H3 histone pseudogene 16 Homo sapiens 0-3 1386285-6 1992 This competition for binding to GAP, or other proteins that interact with the effector site of ras p21, may explain the ability of Ki-rev1 to suppress cellular transformation by ras oncogenes. ki-rev1 131-138 H3 histone pseudogene 16 Homo sapiens 99-102 1959989-1 1991 A novel 21-kDa protein (p21) was isolated from auto-immune complexes, found in sera of 14 patients with malignant urogenital tumors and isolated on Protein A-Sepharose. Sepharose 158-167 H3 histone pseudogene 16 Homo sapiens 24-27 1469896-5 1992 This upregulation was manifested as persistent Ras p21-GTP binding, altered C16 alpha/C2 hydroxylation of estradiol, and hyperplasia preceding tumorigenesis. Guanosine Triphosphate 55-58 H3 histone pseudogene 16 Homo sapiens 51-54 1779468-9 1991 These findings suggest that smg p21s play an important role during the TPA-induced differentiation of CMK cells. Tetradecanoylphorbol Acetate 71-74 H3 histone pseudogene 16 Homo sapiens 32-35 1932038-0 1991 Is there a rate-limiting step before GTP cleavage by H-ras p21? Guanosine Triphosphate 37-40 H3 histone pseudogene 16 Homo sapiens 59-62 1932038-1 1991 A slow fluorescence change of the complex between ras p21 and the fluorescent GTP analogue 2"(3")-O-(N-methylanthraniloyl)guanosine 5"-triphosphate (mGTP) has been postulated to be a signal arising from a step which is rate limiting and precedes the actual GTP hydrolysis reaction [Neal, S. E., Eccleston, J. F., & Webb, M. R. (1990) Proc. Guanosine Triphosphate 78-81 H3 histone pseudogene 16 Homo sapiens 54-57 1932038-1 1991 A slow fluorescence change of the complex between ras p21 and the fluorescent GTP analogue 2"(3")-O-(N-methylanthraniloyl)guanosine 5"-triphosphate (mGTP) has been postulated to be a signal arising from a step which is rate limiting and precedes the actual GTP hydrolysis reaction [Neal, S. E., Eccleston, J. F., & Webb, M. R. (1990) Proc. 2'(3')-O-(N-methyl)anthraniloylguanosine 5'-triphosphate 91-147 H3 histone pseudogene 16 Homo sapiens 54-57 1932038-1 1991 A slow fluorescence change of the complex between ras p21 and the fluorescent GTP analogue 2"(3")-O-(N-methylanthraniloyl)guanosine 5"-triphosphate (mGTP) has been postulated to be a signal arising from a step which is rate limiting and precedes the actual GTP hydrolysis reaction [Neal, S. E., Eccleston, J. F., & Webb, M. R. (1990) Proc. 2'(3')-O-(N-methyl)anthraniloylguanosine 5'-triphosphate 149-153 H3 histone pseudogene 16 Homo sapiens 54-57 1932038-1 1991 A slow fluorescence change of the complex between ras p21 and the fluorescent GTP analogue 2"(3")-O-(N-methylanthraniloyl)guanosine 5"-triphosphate (mGTP) has been postulated to be a signal arising from a step which is rate limiting and precedes the actual GTP hydrolysis reaction [Neal, S. E., Eccleston, J. F., & Webb, M. R. (1990) Proc. Guanosine Triphosphate 150-153 H3 histone pseudogene 16 Homo sapiens 54-57 1932038-7 1991 In contrast, a faster fluorescence change of smaller amplitude seen in the complex between p21 and the uncleavable 2"(3")-O-(N-methylanthraniloyl)guanosine 5"-O-(beta,gamma-imidotriphosphate) (mGppNHp) is not affected by GAP. 2"(3")-o-(n-methylanthraniloyl)guanosine 5"-o-(beta,gamma-imidotriphosphate 115-190 H3 histone pseudogene 16 Homo sapiens 91-94 1932038-7 1991 In contrast, a faster fluorescence change of smaller amplitude seen in the complex between p21 and the uncleavable 2"(3")-O-(N-methylanthraniloyl)guanosine 5"-O-(beta,gamma-imidotriphosphate) (mGppNHp) is not affected by GAP. mgppnhp 193-200 H3 histone pseudogene 16 Homo sapiens 91-94 1932038-8 1991 The corresponding fluorescent derivative of guanosine 5"-O-(gamma-thiotriphosphate) (mGTP gamma S) shows a very slow fluorescence change after binding to p21, and this rate is also accelerated significantly by GAP. guanosine 5"-o-(gamma-thiotriphosphate) 44-83 H3 histone pseudogene 16 Homo sapiens 154-157 1939160-3 1991 Activation of p21ras was not observed when the cells were stimulated with the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and pretreatment with TPA for 16 h, sufficient to down-regulate PKC activity, did not abolish p21ras activation by insulin. Tetradecanoylphorbol Acetate 131-134 H3 histone pseudogene 16 Homo sapiens 14-17 1932015-0 1991 An isotope edited classical Raman difference spectroscopic study of the interactions of guanine nucleotides with elongation factor Tu and H-ras p21. Guanine Nucleotides 88-107 H3 histone pseudogene 16 Homo sapiens 144-147 1932015-1 1991 We have measured the Raman spectrum of GDP bound to the elongation factor protein, EF-Tu, and the c-Harvey-ras protein, p21, two proteins of the guanine nucleotide binding family. Guanine Nucleotides 145-163 H3 histone pseudogene 16 Homo sapiens 120-123 1932015-5 1991 The data show that the guanine amino group of the nucleotide interacts differently with both EF-Tu and p21 than it does with water, showing a change in hydrogen-bonding properties upon binding. Guanine 23-30 H3 histone pseudogene 16 Homo sapiens 103-106 1932015-5 1991 The data show that the guanine amino group of the nucleotide interacts differently with both EF-Tu and p21 than it does with water, showing a change in hydrogen-bonding properties upon binding. Water 125-130 H3 histone pseudogene 16 Homo sapiens 103-106 1932015-5 1991 The data show that the guanine amino group of the nucleotide interacts differently with both EF-Tu and p21 than it does with water, showing a change in hydrogen-bonding properties upon binding. Hydrogen 152-160 H3 histone pseudogene 16 Homo sapiens 103-106 1932015-7 1991 The data strongly suggest that the conformation of the nucleotide when bound to EF-Tu and that p21 is the C2" endo pucker of the ribose ring and anti about the glycosidic bond. Ribose 129-135 H3 histone pseudogene 16 Homo sapiens 95-98 1939160-3 1991 Activation of p21ras was not observed when the cells were stimulated with the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and pretreatment with TPA for 16 h, sufficient to down-regulate PKC activity, did not abolish p21ras activation by insulin. Tetradecanoylphorbol Acetate 158-161 H3 histone pseudogene 16 Homo sapiens 14-17 1744743-2 1991 Polycyclic aromatic hydrocarbons are important respiratory carcinogens and have been shown to cause specific mutational lesions that can lead to the activation of the ras oncogene and expression of its p21 protein product; ras oncogene activation and p21 expression frequently are detected in human lung cancers. Polycyclic Aromatic Hydrocarbons 0-32 H3 histone pseudogene 16 Homo sapiens 202-205 1820685-4 1991 Other cellular factors can positively regulate p21ras by stimulating GDP/GTP exchange. Guanosine Diphosphate 69-72 H3 histone pseudogene 16 Homo sapiens 47-50 1820685-4 1991 Other cellular factors can positively regulate p21ras by stimulating GDP/GTP exchange. Guanosine Triphosphate 73-76 H3 histone pseudogene 16 Homo sapiens 47-50 1924354-0 1991 Posttranslational modification of Ha-ras p21 by farnesyl versus geranylgeranyl isoprenoids is determined by the COOH-terminal amino acid. FARNESYL 48-56 H3 histone pseudogene 16 Homo sapiens 41-44 1924354-0 1991 Posttranslational modification of Ha-ras p21 by farnesyl versus geranylgeranyl isoprenoids is determined by the COOH-terminal amino acid. geranylgeranyl isoprenoids 64-90 H3 histone pseudogene 16 Homo sapiens 41-44 1924354-0 1991 Posttranslational modification of Ha-ras p21 by farnesyl versus geranylgeranyl isoprenoids is determined by the COOH-terminal amino acid. Carbonic Acid 112-116 H3 histone pseudogene 16 Homo sapiens 41-44 1924354-3 1991 We changed the terminal Ser-189 of Ha-ras p21 to Leu-189 by site-directed mutagenesis and found that the protein was modified by [3H]geranylgeranyl instead of [3H]farnesyl in an in vitro assay. Serine 24-27 H3 histone pseudogene 16 Homo sapiens 42-45 1924354-3 1991 We changed the terminal Ser-189 of Ha-ras p21 to Leu-189 by site-directed mutagenesis and found that the protein was modified by [3H]geranylgeranyl instead of [3H]farnesyl in an in vitro assay. Leucine 49-52 H3 histone pseudogene 16 Homo sapiens 42-45 1924354-3 1991 We changed the terminal Ser-189 of Ha-ras p21 to Leu-189 by site-directed mutagenesis and found that the protein was modified by [3H]geranylgeranyl instead of [3H]farnesyl in an in vitro assay. [3h]geranylgeranyl 129-147 H3 histone pseudogene 16 Homo sapiens 42-45 1924354-3 1991 We changed the terminal Ser-189 of Ha-ras p21 to Leu-189 by site-directed mutagenesis and found that the protein was modified by [3H]geranylgeranyl instead of [3H]farnesyl in an in vitro assay. 3h]farnesyl 160-171 H3 histone pseudogene 16 Homo sapiens 42-45 1924354-4 1991 Gel-permeation chromatography of [3H]mevalonate-labeled hydrocarbons released from immunoprecipitated ras proteins overexpressed in COS cells indicated that Ha-ras p21(Leu-189) was also a substrate for 20-carbon isoprenyl modification in vivo. [3h]mevalonate 33-47 H3 histone pseudogene 16 Homo sapiens 164-167 1924354-4 1991 Gel-permeation chromatography of [3H]mevalonate-labeled hydrocarbons released from immunoprecipitated ras proteins overexpressed in COS cells indicated that Ha-ras p21(Leu-189) was also a substrate for 20-carbon isoprenyl modification in vivo. Hydrocarbons 56-68 H3 histone pseudogene 16 Homo sapiens 164-167 1924354-4 1991 Gel-permeation chromatography of [3H]mevalonate-labeled hydrocarbons released from immunoprecipitated ras proteins overexpressed in COS cells indicated that Ha-ras p21(Leu-189) was also a substrate for 20-carbon isoprenyl modification in vivo. Leucine 168-171 H3 histone pseudogene 16 Homo sapiens 164-167 1924354-4 1991 Gel-permeation chromatography of [3H]mevalonate-labeled hydrocarbons released from immunoprecipitated ras proteins overexpressed in COS cells indicated that Ha-ras p21(Leu-189) was also a substrate for 20-carbon isoprenyl modification in vivo. Carbon 61-67 H3 histone pseudogene 16 Homo sapiens 164-167 1924354-5 1991 Additional steps in Ha-ras p21 processing, normally initiated by farnesylation, appear to be supported by geranylgeranylation, based on metabolic labeling of Ha-ras p21(Leu-189) with [3H]palmitate and its subcellular localization in a particulate fraction from COS cells. Leucine 169-172 H3 histone pseudogene 16 Homo sapiens 27-30 1924354-5 1991 Additional steps in Ha-ras p21 processing, normally initiated by farnesylation, appear to be supported by geranylgeranylation, based on metabolic labeling of Ha-ras p21(Leu-189) with [3H]palmitate and its subcellular localization in a particulate fraction from COS cells. Leucine 169-172 H3 histone pseudogene 16 Homo sapiens 165-168 1924354-5 1991 Additional steps in Ha-ras p21 processing, normally initiated by farnesylation, appear to be supported by geranylgeranylation, based on metabolic labeling of Ha-ras p21(Leu-189) with [3H]palmitate and its subcellular localization in a particulate fraction from COS cells. Tritium 184-186 H3 histone pseudogene 16 Homo sapiens 27-30 1924354-5 1991 Additional steps in Ha-ras p21 processing, normally initiated by farnesylation, appear to be supported by geranylgeranylation, based on metabolic labeling of Ha-ras p21(Leu-189) with [3H]palmitate and its subcellular localization in a particulate fraction from COS cells. Tritium 184-186 H3 histone pseudogene 16 Homo sapiens 165-168 1924354-6 1991 These observations indicate that the amino acid occupying the terminal position (Xaa) in the Cys-Ali-Ali-Xaa motif constitutes a key structural feature by which Ha-ras p21 and other proteins with ras-like COOH-terminal isoprenylation sites are distinguished as substrates for farnesyl- or geranylgeranyltransferases. Cysteine 93-96 H3 histone pseudogene 16 Homo sapiens 168-171 1939117-0 1991 Inhibition of the action of the stimulatory GDP/GTP exchange protein for smg p21 by the geranylgeranylated synthetic peptides designed from its C-terminal region. Guanosine Diphosphate 44-47 H3 histone pseudogene 16 Homo sapiens 77-80 1939117-0 1991 Inhibition of the action of the stimulatory GDP/GTP exchange protein for smg p21 by the geranylgeranylated synthetic peptides designed from its C-terminal region. Guanosine Triphosphate 48-51 H3 histone pseudogene 16 Homo sapiens 77-80 1939117-0 1991 Inhibition of the action of the stimulatory GDP/GTP exchange protein for smg p21 by the geranylgeranylated synthetic peptides designed from its C-terminal region. Peptides 117-125 H3 histone pseudogene 16 Homo sapiens 77-80 1939117-1 1991 smg p21B, a member of the ras p21-like small GTP-binding protein superfamily, undergoes post-translational modifications, which are geranylgeranylation of the cysteine residue in the C-terminal region followed by removal of the three C-terminal amino acids (QLL) and the subsequent carboxyl methylation of the exposed prenylated cysteine residue. Cysteine 159-167 H3 histone pseudogene 16 Homo sapiens 4-7 1939117-1 1991 smg p21B, a member of the ras p21-like small GTP-binding protein superfamily, undergoes post-translational modifications, which are geranylgeranylation of the cysteine residue in the C-terminal region followed by removal of the three C-terminal amino acids (QLL) and the subsequent carboxyl methylation of the exposed prenylated cysteine residue. qll 258-261 H3 histone pseudogene 16 Homo sapiens 4-7 1939117-1 1991 smg p21B, a member of the ras p21-like small GTP-binding protein superfamily, undergoes post-translational modifications, which are geranylgeranylation of the cysteine residue in the C-terminal region followed by removal of the three C-terminal amino acids (QLL) and the subsequent carboxyl methylation of the exposed prenylated cysteine residue. Cysteine 329-337 H3 histone pseudogene 16 Homo sapiens 4-7 1939117-6 1991 The results indicate that the phosphorylated form of PGKARKKSSC-geranylgeranyl stoichiometrically interacts with smg p21 GDS, that the presence of the geranylgeranyl moiety is essential for, but not sufficient for, the smg p21 GDS action, and that the presence of the methyl moiety, removal of the three C-terminal amino acids, and the presence of the polybasic amino acids also affect the smg p21 GDS action. -geranylgeranyl 63-78 H3 histone pseudogene 16 Homo sapiens 117-120 1939117-6 1991 The results indicate that the phosphorylated form of PGKARKKSSC-geranylgeranyl stoichiometrically interacts with smg p21 GDS, that the presence of the geranylgeranyl moiety is essential for, but not sufficient for, the smg p21 GDS action, and that the presence of the methyl moiety, removal of the three C-terminal amino acids, and the presence of the polybasic amino acids also affect the smg p21 GDS action. -geranylgeranyl 63-78 H3 histone pseudogene 16 Homo sapiens 223-226 1939117-6 1991 The results indicate that the phosphorylated form of PGKARKKSSC-geranylgeranyl stoichiometrically interacts with smg p21 GDS, that the presence of the geranylgeranyl moiety is essential for, but not sufficient for, the smg p21 GDS action, and that the presence of the methyl moiety, removal of the three C-terminal amino acids, and the presence of the polybasic amino acids also affect the smg p21 GDS action. -geranylgeranyl 63-78 H3 histone pseudogene 16 Homo sapiens 223-226 1939117-6 1991 The results indicate that the phosphorylated form of PGKARKKSSC-geranylgeranyl stoichiometrically interacts with smg p21 GDS, that the presence of the geranylgeranyl moiety is essential for, but not sufficient for, the smg p21 GDS action, and that the presence of the methyl moiety, removal of the three C-terminal amino acids, and the presence of the polybasic amino acids also affect the smg p21 GDS action. geranylgeranyl 64-78 H3 histone pseudogene 16 Homo sapiens 117-120 1939117-6 1991 The results indicate that the phosphorylated form of PGKARKKSSC-geranylgeranyl stoichiometrically interacts with smg p21 GDS, that the presence of the geranylgeranyl moiety is essential for, but not sufficient for, the smg p21 GDS action, and that the presence of the methyl moiety, removal of the three C-terminal amino acids, and the presence of the polybasic amino acids also affect the smg p21 GDS action. geranylgeranyl 64-78 H3 histone pseudogene 16 Homo sapiens 223-226 1939117-6 1991 The results indicate that the phosphorylated form of PGKARKKSSC-geranylgeranyl stoichiometrically interacts with smg p21 GDS, that the presence of the geranylgeranyl moiety is essential for, but not sufficient for, the smg p21 GDS action, and that the presence of the methyl moiety, removal of the three C-terminal amino acids, and the presence of the polybasic amino acids also affect the smg p21 GDS action. geranylgeranyl 64-78 H3 histone pseudogene 16 Homo sapiens 223-226 1744743-2 1991 Polycyclic aromatic hydrocarbons are important respiratory carcinogens and have been shown to cause specific mutational lesions that can lead to the activation of the ras oncogene and expression of its p21 protein product; ras oncogene activation and p21 expression frequently are detected in human lung cancers. Polycyclic Aromatic Hydrocarbons 0-32 H3 histone pseudogene 16 Homo sapiens 251-254 1883816-3 1991 Antisense oligonucleoside methylphosphonates and their psoralen derivatives directed at either normal human Ha-ras p21 or ras p21 that is mutated at a single base in codon 61 have been examined for their efficacy and specificity as inhibitors of p21 expression. oligonucleoside methylphosphonates 10-44 H3 histone pseudogene 16 Homo sapiens 126-129 1883816-3 1991 Antisense oligonucleoside methylphosphonates and their psoralen derivatives directed at either normal human Ha-ras p21 or ras p21 that is mutated at a single base in codon 61 have been examined for their efficacy and specificity as inhibitors of p21 expression. oligonucleoside methylphosphonates 10-44 H3 histone pseudogene 16 Homo sapiens 126-129 1883817-0 1991 GTP hydrolysis mechanisms in ras p21 and in the ras-GAP complex studied by fluorescence measurements on tryptophan mutants. Guanosine Triphosphate 0-3 H3 histone pseudogene 16 Homo sapiens 33-36 1883817-1 1991 We have substituted leucine 56 or tyrosine 64 of p21 ras with a tryptophan. Tyrosine 34-42 H3 histone pseudogene 16 Homo sapiens 49-52 1883817-1 1991 We have substituted leucine 56 or tyrosine 64 of p21 ras with a tryptophan. Tryptophan 64-74 H3 histone pseudogene 16 Homo sapiens 49-52 1907371-0 1991 A stimulatory GDP/GTP exchange protein for smg p21 is active on the post-translationally processed form of c-Ki-ras p21 and rhoA p21. Guanosine Diphosphate 14-17 H3 histone pseudogene 16 Homo sapiens 47-50 1907371-0 1991 A stimulatory GDP/GTP exchange protein for smg p21 is active on the post-translationally processed form of c-Ki-ras p21 and rhoA p21. Guanosine Diphosphate 14-17 H3 histone pseudogene 16 Homo sapiens 116-119 1907371-1 1991 We have purified a stimulatory GDP/GTP exchange protein for smg p21A and -B, ras p21-like small GTP-binding proteins (G proteins), cloned its cDNA, and named it GDP dissociation stimulator (smg p21 GDS). Guanosine Diphosphate 31-34 H3 histone pseudogene 16 Homo sapiens 81-84 1907371-0 1991 A stimulatory GDP/GTP exchange protein for smg p21 is active on the post-translationally processed form of c-Ki-ras p21 and rhoA p21. Guanosine Diphosphate 14-17 H3 histone pseudogene 16 Homo sapiens 116-119 1907371-1 1991 We have purified a stimulatory GDP/GTP exchange protein for smg p21A and -B, ras p21-like small GTP-binding proteins (G proteins), cloned its cDNA, and named it GDP dissociation stimulator (smg p21 GDS). Guanosine Triphosphate 35-38 H3 histone pseudogene 16 Homo sapiens 64-67 1907371-1 1991 We have purified a stimulatory GDP/GTP exchange protein for smg p21A and -B, ras p21-like small GTP-binding proteins (G proteins), cloned its cDNA, and named it GDP dissociation stimulator (smg p21 GDS). Guanosine Triphosphate 35-38 H3 histone pseudogene 16 Homo sapiens 81-84 1907371-0 1991 A stimulatory GDP/GTP exchange protein for smg p21 is active on the post-translationally processed form of c-Ki-ras p21 and rhoA p21. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 47-50 1907371-1 1991 We have purified a stimulatory GDP/GTP exchange protein for smg p21A and -B, ras p21-like small GTP-binding proteins (G proteins), cloned its cDNA, and named it GDP dissociation stimulator (smg p21 GDS). Guanosine Triphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 64-67 1907371-1 1991 We have purified a stimulatory GDP/GTP exchange protein for smg p21A and -B, ras p21-like small GTP-binding proteins (G proteins), cloned its cDNA, and named it GDP dissociation stimulator (smg p21 GDS). Guanosine Triphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 81-84 1907371-0 1991 A stimulatory GDP/GTP exchange protein for smg p21 is active on the post-translationally processed form of c-Ki-ras p21 and rhoA p21. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 116-119 1907371-0 1991 A stimulatory GDP/GTP exchange protein for smg p21 is active on the post-translationally processed form of c-Ki-ras p21 and rhoA p21. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 116-119 1907371-1 1991 We have purified a stimulatory GDP/GTP exchange protein for smg p21A and -B, ras p21-like small GTP-binding proteins (G proteins), cloned its cDNA, and named it GDP dissociation stimulator (smg p21 GDS). Guanosine Diphosphate 31-34 H3 histone pseudogene 16 Homo sapiens 64-67 1773783-1 1991 The three-dimensional structure of the active guanosine triphosphate (GTP)-analogue-containing complex of the H-ras-encoded p21 has been determined. Guanosine Triphosphate 46-68 H3 histone pseudogene 16 Homo sapiens 124-127 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Guanosine Triphosphate 203-206 H3 histone pseudogene 16 Homo sapiens 270-273 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Guanosine Triphosphate 203-206 H3 histone pseudogene 16 Homo sapiens 307-310 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Arginine 245-248 H3 histone pseudogene 16 Homo sapiens 270-273 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Arginine 245-248 H3 histone pseudogene 16 Homo sapiens 307-310 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Arginine 311-314 H3 histone pseudogene 16 Homo sapiens 270-273 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Arginine 311-314 H3 histone pseudogene 16 Homo sapiens 307-310 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Lysine 320-323 H3 histone pseudogene 16 Homo sapiens 270-273 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Lysine 320-323 H3 histone pseudogene 16 Homo sapiens 307-310 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Leucine 333-336 H3 histone pseudogene 16 Homo sapiens 270-273 2052624-7 1991 (iii) Identification of sequence regions, other than the effector loop and the nucleotide binding site, that may be involved in the functional cycle: they are loop L4, known to change conformation after GTP hydrolysis; helix alpha 2, especially Arg-73 and Met-67 in ras p21; loops L8 and L10, including ras p21 Arg-123, Lys-147, and Leu-120; and residues located spatially near the N and C termini. Leucine 333-336 H3 histone pseudogene 16 Homo sapiens 307-310 2026138-3 1991 It is shown that all fatty acids and acidic phospholipids tested, provided the critical micellar concentration and the critical micellar temperature are reached, inhibit the GAP stimulated p21 GTPase activity. Fatty Acids 21-32 H3 histone pseudogene 16 Homo sapiens 189-192 2026138-3 1991 It is shown that all fatty acids and acidic phospholipids tested, provided the critical micellar concentration and the critical micellar temperature are reached, inhibit the GAP stimulated p21 GTPase activity. Phospholipids 44-57 H3 histone pseudogene 16 Homo sapiens 189-192 1746900-1 1991 In the present work, we studied the expression of the c-myc oncoprotein p-62 and the ras oncoprotein p-21 in the dermal cellular infiltrate of paraffin embedded skin specimens, obtained from patients suffering from Mycosis Fungoides and Sezary syndrome. Paraffin 143-151 H3 histone pseudogene 16 Homo sapiens 101-105 1908842-0 1991 Inhibition of the action of a stimulatory GDP/GTP exchange protein for smg p21 by acidic membrane phospholipids. Guanosine Diphosphate 42-45 H3 histone pseudogene 16 Homo sapiens 75-78 1908842-0 1991 Inhibition of the action of a stimulatory GDP/GTP exchange protein for smg p21 by acidic membrane phospholipids. Guanosine Triphosphate 46-49 H3 histone pseudogene 16 Homo sapiens 75-78 1908842-0 1991 Inhibition of the action of a stimulatory GDP/GTP exchange protein for smg p21 by acidic membrane phospholipids. Phospholipids 98-111 H3 histone pseudogene 16 Homo sapiens 75-78 1908842-1 1991 A stimulatory GDP/GTP exchange protein for smg p21 (smg p21 GDS) stimulated the dissociation of GDP from smg p21B. Guanosine Diphosphate 14-17 H3 histone pseudogene 16 Homo sapiens 47-50 1908842-1 1991 A stimulatory GDP/GTP exchange protein for smg p21 (smg p21 GDS) stimulated the dissociation of GDP from smg p21B. Guanosine Diphosphate 14-17 H3 histone pseudogene 16 Homo sapiens 56-59 1908842-1 1991 A stimulatory GDP/GTP exchange protein for smg p21 (smg p21 GDS) stimulated the dissociation of GDP from smg p21B. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 47-50 1908842-1 1991 A stimulatory GDP/GTP exchange protein for smg p21 (smg p21 GDS) stimulated the dissociation of GDP from smg p21B. Guanosine Triphosphate 18-21 H3 histone pseudogene 16 Homo sapiens 56-59 1908842-1 1991 A stimulatory GDP/GTP exchange protein for smg p21 (smg p21 GDS) stimulated the dissociation of GDP from smg p21B. Guanosine Diphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 47-50 1908842-1 1991 A stimulatory GDP/GTP exchange protein for smg p21 (smg p21 GDS) stimulated the dissociation of GDP from smg p21B. Guanosine Diphosphate 96-99 H3 histone pseudogene 16 Homo sapiens 56-59 1908842-3 1991 These acidic phospholipids inhibited the smg p21 GDS action in a manner competitive with both smg p21 GDS and smg p21B. Phospholipids 13-26 H3 histone pseudogene 16 Homo sapiens 45-48 1908842-3 1991 These acidic phospholipids inhibited the smg p21 GDS action in a manner competitive with both smg p21 GDS and smg p21B. Phospholipids 13-26 H3 histone pseudogene 16 Homo sapiens 98-101 1908842-5 1991 The acidic phospholipids also inhibited these two actions of smg p21 GDS. Phospholipids 11-24 H3 histone pseudogene 16 Homo sapiens 65-68 1908842-6 1991 smg p21B has a polybasic region and an isoprenoid moiety in its C-terminal region which are necessary for its membrane-binding activity and its sensitivity to the smg p21 GDS actions. Terpenes 39-49 H3 histone pseudogene 16 Homo sapiens 4-7 1908842-7 1991 Therefore, it is possible that acidic membrane phospholipids interact with this polybasic region and thereby inhibit the smg p21 GDS actions. Phospholipids 47-60 H3 histone pseudogene 16 Homo sapiens 125-128 1773783-1 1991 The three-dimensional structure of the active guanosine triphosphate (GTP)-analogue-containing complex of the H-ras-encoded p21 has been determined. Guanosine Triphosphate 70-73 H3 histone pseudogene 16 Homo sapiens 124-127 1826565-2 1991 The ras gene product (p21) is a GTP-binding protein, and the activity of the protein is regulated by bound GDP/GTP. Guanosine Triphosphate 32-35 H3 histone pseudogene 16 Homo sapiens 22-25 1674518-6 1991 In the present report, we demonstrate that the TCR/CD3 complex and the CD2 Ag control the accumulation of p21ras-GTP complexes via a regulatory effect on p21ras GTPase activity. Guanosine Triphosphate 113-116 H3 histone pseudogene 16 Homo sapiens 106-109 1901241-1 1991 We prepared monoclonal antibodies specific for smg p21A, one of the low molecular weight GTP-binding proteins and possibly a suppressor molecule for ras p21. Guanosine Triphosphate 89-92 H3 histone pseudogene 16 Homo sapiens 51-54 1826565-2 1991 The ras gene product (p21) is a GTP-binding protein, and the activity of the protein is regulated by bound GDP/GTP. Guanosine Diphosphate 107-110 H3 histone pseudogene 16 Homo sapiens 22-25 1826565-2 1991 The ras gene product (p21) is a GTP-binding protein, and the activity of the protein is regulated by bound GDP/GTP. Guanosine Triphosphate 111-114 H3 histone pseudogene 16 Homo sapiens 22-25 1826565-3 1991 Recent studies have shown that a certain class of growth factors stimulates the formation of active p21-GTP complexes in fibroblasts and that oncogene products with enhanced tyrosine kinase activities have a similar effect on ras p21. Guanosine Triphosphate 104-107 H3 histone pseudogene 16 Homo sapiens 100-103 1826565-4 1991 We have measured the ratio of active GTP-bound p21 to total p21 in several lymphoid and myeloid cell lines in order to understand the role of ras in the proliferation of these cells. Guanosine Triphosphate 37-40 H3 histone pseudogene 16 Homo sapiens 47-50 1826565-5 1991 Interleukin 2 (IL-2), IL-3, and granulocyte/macrophage colony-stimulating factor (GM-CSF) enhance the formation of the active p21.GTP, whereas IL-4 has no effect on p21-bound GDP/GTP. Guanosine Triphosphate 130-133 H3 histone pseudogene 16 Homo sapiens 126-129 1889625-1 1991 The use of ribose-modified guanine nucleotides and tryptophan mutants of p21ras, neither of which have significant effect on the kinetic mechanism of the p21ras GTPase and the GAP-activated p21ras GTPase, will now allow a detailed kinetic study of how GAP and other regulatory proteins interact with p21ras. Tryptophan 51-61 H3 histone pseudogene 16 Homo sapiens 73-76 1810347-0 1991 "Hot spot" amino acid distribution in Ha-ras oncogene product p21: relationship to guanine binding site. Guanine 83-90 H3 histone pseudogene 16 Homo sapiens 62-65 1901412-5 1991 Other low molecular weight GTP-binding proteins belonging to the Ras superfamily, including Rab-3A, Rap-2b, and c-Ha-ras p21, are not phosphorylated by CaM kinase Gr. Guanosine Triphosphate 27-30 H3 histone pseudogene 16 Homo sapiens 121-124 1899665-0 1991 Role of the C-terminal region of smg p21, a ras p21-like small GTP-binding protein, in membrane and smg p21 GDP/GTP exchange protein interactions. Guanosine Triphosphate 112-115 H3 histone pseudogene 16 Homo sapiens 37-40 1900364-3 1991 Two ras-related human genes rap1A and rap1B encode 95% homologous 21-kDa proteins that share with Ras p21 the same effector domain and a similar C-terminal Cys-Ali-Ali-Xaa sequence (where Ali is an aliphatic amino acid; also known as a CAAX sequence). Cysteine 156-159 H3 histone pseudogene 16 Homo sapiens 102-105 1899665-0 1991 Role of the C-terminal region of smg p21, a ras p21-like small GTP-binding protein, in membrane and smg p21 GDP/GTP exchange protein interactions. Guanosine Triphosphate 63-66 H3 histone pseudogene 16 Homo sapiens 37-40 1899665-0 1991 Role of the C-terminal region of smg p21, a ras p21-like small GTP-binding protein, in membrane and smg p21 GDP/GTP exchange protein interactions. Guanosine Triphosphate 63-66 H3 histone pseudogene 16 Homo sapiens 48-51 1899665-0 1991 Role of the C-terminal region of smg p21, a ras p21-like small GTP-binding protein, in membrane and smg p21 GDP/GTP exchange protein interactions. Guanosine Triphosphate 112-115 H3 histone pseudogene 16 Homo sapiens 48-51 1899665-0 1991 Role of the C-terminal region of smg p21, a ras p21-like small GTP-binding protein, in membrane and smg p21 GDP/GTP exchange protein interactions. Guanosine Triphosphate 63-66 H3 histone pseudogene 16 Homo sapiens 48-51 1899665-0 1991 Role of the C-terminal region of smg p21, a ras p21-like small GTP-binding protein, in membrane and smg p21 GDP/GTP exchange protein interactions. Guanosine Triphosphate 112-115 H3 histone pseudogene 16 Homo sapiens 48-51 1899665-1 1991 Limited proteolysis with trypsin of smg p21B, a ras p21-like small GTP-binding protein having the same putative effector domain as ras p21s, produced the N-terminal fragment and the C-terminal tail of Lys-Lys-Ser-Ser-geranylgeranyl-Cys methyl ester. Guanosine Triphosphate 67-70 H3 histone pseudogene 16 Homo sapiens 40-43 1899665-1 1991 Limited proteolysis with trypsin of smg p21B, a ras p21-like small GTP-binding protein having the same putative effector domain as ras p21s, produced the N-terminal fragment and the C-terminal tail of Lys-Lys-Ser-Ser-geranylgeranyl-Cys methyl ester. lys-lys-ser-ser-geranylgeranyl-cys methyl ester 201-248 H3 histone pseudogene 16 Homo sapiens 40-43 1900001-0 1991 Stoichiometric interaction of smg p21 with its GDP/GTP exchange protein and its novel action to regulate the translocation of smg p21 between membrane and cytoplasm. Guanosine Triphosphate 51-54 H3 histone pseudogene 16 Homo sapiens 34-37 1899665-8 1991 In contrast, a GDP/GTP exchange protein for smg p21, named GDP dissociation stimulator, stimulated the GDP/GTP exchange reaction of the intact smg p21B but not that of the N-terminal fragment. Guanosine Diphosphate 15-18 H3 histone pseudogene 16 Homo sapiens 48-51 1900001-0 1991 Stoichiometric interaction of smg p21 with its GDP/GTP exchange protein and its novel action to regulate the translocation of smg p21 between membrane and cytoplasm. Guanosine Triphosphate 51-54 H3 histone pseudogene 16 Homo sapiens 130-133 1899665-8 1991 In contrast, a GDP/GTP exchange protein for smg p21, named GDP dissociation stimulator, stimulated the GDP/GTP exchange reaction of the intact smg p21B but not that of the N-terminal fragment. Guanosine Triphosphate 19-22 H3 histone pseudogene 16 Homo sapiens 48-51 1900001-1 1991 We have previously purified a GDP/GTP exchange protein for smg p21A and -B, members of a ras p21/ras p21-like small GTP-binding protein superfamily. Guanosine Diphosphate 30-33 H3 histone pseudogene 16 Homo sapiens 63-66 1900001-1 1991 We have previously purified a GDP/GTP exchange protein for smg p21A and -B, members of a ras p21/ras p21-like small GTP-binding protein superfamily. Guanosine Diphosphate 30-33 H3 histone pseudogene 16 Homo sapiens 93-96 1900001-1 1991 We have previously purified a GDP/GTP exchange protein for smg p21A and -B, members of a ras p21/ras p21-like small GTP-binding protein superfamily. Guanosine Triphosphate 34-37 H3 histone pseudogene 16 Homo sapiens 63-66 1900001-1 1991 We have previously purified a GDP/GTP exchange protein for smg p21A and -B, members of a ras p21/ras p21-like small GTP-binding protein superfamily. Guanosine Triphosphate 34-37 H3 histone pseudogene 16 Homo sapiens 93-96 1900001-1 1991 We have previously purified a GDP/GTP exchange protein for smg p21A and -B, members of a ras p21/ras p21-like small GTP-binding protein superfamily. Guanosine Triphosphate 116-119 H3 histone pseudogene 16 Homo sapiens 63-66 1900001-1 1991 We have previously purified a GDP/GTP exchange protein for smg p21A and -B, members of a ras p21/ras p21-like small GTP-binding protein superfamily. Guanosine Triphosphate 116-119 H3 histone pseudogene 16 Homo sapiens 93-96 1900001-2 1991 This regulatory protein, named smg p21 GDP dissociation stimulator (GDS), stimulates the dissociation of both GDP and GTP from and the subsequent binding of both GDP and GTP to smg p21s. Guanosine Diphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 35-38 1899665-8 1991 In contrast, a GDP/GTP exchange protein for smg p21, named GDP dissociation stimulator, stimulated the GDP/GTP exchange reaction of the intact smg p21B but not that of the N-terminal fragment. Guanosine Diphosphate 59-62 H3 histone pseudogene 16 Homo sapiens 48-51 1900001-2 1991 This regulatory protein, named smg p21 GDP dissociation stimulator (GDS), stimulates the dissociation of both GDP and GTP from and the subsequent binding of both GDP and GTP to smg p21s. Guanosine Diphosphate 110-113 H3 histone pseudogene 16 Homo sapiens 35-38 1899665-8 1991 In contrast, a GDP/GTP exchange protein for smg p21, named GDP dissociation stimulator, stimulated the GDP/GTP exchange reaction of the intact smg p21B but not that of the N-terminal fragment. Guanosine Diphosphate 59-62 H3 histone pseudogene 16 Homo sapiens 48-51 1900001-2 1991 This regulatory protein, named smg p21 GDP dissociation stimulator (GDS), stimulates the dissociation of both GDP and GTP from and the subsequent binding of both GDP and GTP to smg p21s. Guanosine Triphosphate 118-121 H3 histone pseudogene 16 Homo sapiens 35-38 1900001-2 1991 This regulatory protein, named smg p21 GDP dissociation stimulator (GDS), stimulates the dissociation of both GDP and GTP from and the subsequent binding of both GDP and GTP to smg p21s. Guanosine Diphosphate 110-113 H3 histone pseudogene 16 Homo sapiens 35-38 1899665-8 1991 In contrast, a GDP/GTP exchange protein for smg p21, named GDP dissociation stimulator, stimulated the GDP/GTP exchange reaction of the intact smg p21B but not that of the N-terminal fragment. Guanosine Triphosphate 107-110 H3 histone pseudogene 16 Homo sapiens 48-51 1900001-2 1991 This regulatory protein, named smg p21 GDP dissociation stimulator (GDS), stimulates the dissociation of both GDP and GTP from and the subsequent binding of both GDP and GTP to smg p21s. Guanosine Triphosphate 170-173 H3 histone pseudogene 16 Homo sapiens 35-38 1900001-3 1991 We show here that smg p21 GDS forms a complex with both the GDP- and GTP-bound forms of smg p21B at a molar ratio of about 1:1. Guanosine Diphosphate 60-63 H3 histone pseudogene 16 Homo sapiens 22-25 1899665-9 1991 These results indicate 1) that smg p21B is composed of at least two functionally different domains, the N-terminal GDP/GTP-binding and GTPase domain and the C-terminal membrane-binding domain, 2) that smg p21B binds to membranes through its C-terminal hydrophobic and basic domain, and 3) that this C-terminal domain is also essential for the smg p21 GDP dissociation stimulator action but not for the smg p21 GTPase-activating protein action. Guanosine Diphosphate 115-118 H3 histone pseudogene 16 Homo sapiens 35-38 1900001-3 1991 We show here that smg p21 GDS forms a complex with both the GDP- and GTP-bound forms of smg p21B at a molar ratio of about 1:1. Guanosine Triphosphate 69-72 H3 histone pseudogene 16 Homo sapiens 22-25 1899665-9 1991 These results indicate 1) that smg p21B is composed of at least two functionally different domains, the N-terminal GDP/GTP-binding and GTPase domain and the C-terminal membrane-binding domain, 2) that smg p21B binds to membranes through its C-terminal hydrophobic and basic domain, and 3) that this C-terminal domain is also essential for the smg p21 GDP dissociation stimulator action but not for the smg p21 GTPase-activating protein action. Guanosine Triphosphate 119-122 H3 histone pseudogene 16 Homo sapiens 35-38 1900001-6 1991 These results indicate that smg p21 GDS stoichiometrically interacts with smg p21B and thereby regulates its GDP/GTP exchange reaction and its translocation between membranes and cytoplasm. Guanosine Diphosphate 109-112 H3 histone pseudogene 16 Homo sapiens 32-35 1900001-6 1991 These results indicate that smg p21 GDS stoichiometrically interacts with smg p21B and thereby regulates its GDP/GTP exchange reaction and its translocation between membranes and cytoplasm. Guanosine Triphosphate 113-116 H3 histone pseudogene 16 Homo sapiens 32-35 1899665-9 1991 These results indicate 1) that smg p21B is composed of at least two functionally different domains, the N-terminal GDP/GTP-binding and GTPase domain and the C-terminal membrane-binding domain, 2) that smg p21B binds to membranes through its C-terminal hydrophobic and basic domain, and 3) that this C-terminal domain is also essential for the smg p21 GDP dissociation stimulator action but not for the smg p21 GTPase-activating protein action. Guanosine Diphosphate 351-354 H3 histone pseudogene 16 Homo sapiens 35-38 1899665-9 1991 These results indicate 1) that smg p21B is composed of at least two functionally different domains, the N-terminal GDP/GTP-binding and GTPase domain and the C-terminal membrane-binding domain, 2) that smg p21B binds to membranes through its C-terminal hydrophobic and basic domain, and 3) that this C-terminal domain is also essential for the smg p21 GDP dissociation stimulator action but not for the smg p21 GTPase-activating protein action. Guanosine Diphosphate 351-354 H3 histone pseudogene 16 Homo sapiens 205-208 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Diphosphate 207-210 H3 histone pseudogene 16 Homo sapiens 106-109 1652268-2 1991 Here we present evidence that c-Ha-ras (p21(Gly-12)) and its oncogenic mutant T24-ras (p21(Val-12)) selectively induce omega-conotoxin and dihydropyridine-sensitive Ca2+ currents within a few hours after introduction into the cytoplasm of neuroblastoma x glioma hybrid cells. Glycine 44-47 H3 histone pseudogene 16 Homo sapiens 40-43 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Diphosphate 207-210 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-2 1991 Here we present evidence that c-Ha-ras (p21(Gly-12)) and its oncogenic mutant T24-ras (p21(Val-12)) selectively induce omega-conotoxin and dihydropyridine-sensitive Ca2+ currents within a few hours after introduction into the cytoplasm of neuroblastoma x glioma hybrid cells. Glycine 44-47 H3 histone pseudogene 16 Homo sapiens 87-90 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Diphosphate 207-210 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-2 1991 Here we present evidence that c-Ha-ras (p21(Gly-12)) and its oncogenic mutant T24-ras (p21(Val-12)) selectively induce omega-conotoxin and dihydropyridine-sensitive Ca2+ currents within a few hours after introduction into the cytoplasm of neuroblastoma x glioma hybrid cells. val-12 91-97 H3 histone pseudogene 16 Homo sapiens 40-43 1652268-2 1991 Here we present evidence that c-Ha-ras (p21(Gly-12)) and its oncogenic mutant T24-ras (p21(Val-12)) selectively induce omega-conotoxin and dihydropyridine-sensitive Ca2+ currents within a few hours after introduction into the cytoplasm of neuroblastoma x glioma hybrid cells. val-12 91-97 H3 histone pseudogene 16 Homo sapiens 87-90 1652268-2 1991 Here we present evidence that c-Ha-ras (p21(Gly-12)) and its oncogenic mutant T24-ras (p21(Val-12)) selectively induce omega-conotoxin and dihydropyridine-sensitive Ca2+ currents within a few hours after introduction into the cytoplasm of neuroblastoma x glioma hybrid cells. 1,4-dihydropyridine 139-154 H3 histone pseudogene 16 Homo sapiens 40-43 1652268-2 1991 Here we present evidence that c-Ha-ras (p21(Gly-12)) and its oncogenic mutant T24-ras (p21(Val-12)) selectively induce omega-conotoxin and dihydropyridine-sensitive Ca2+ currents within a few hours after introduction into the cytoplasm of neuroblastoma x glioma hybrid cells. 1,4-dihydropyridine 139-154 H3 histone pseudogene 16 Homo sapiens 87-90 1652268-4 1991 In cells loaded with p21(Gly-12), the effect occurred after 2 hours and was terminated after 8 hours. Glycine 25-28 H3 histone pseudogene 16 Homo sapiens 21-24 1652268-5 1991 In contrast, introduction of p21(Val-12) resulted in a prolonged delay (6 hours) of the effect which lasted for more than 24 hours. val-12 33-39 H3 histone pseudogene 16 Homo sapiens 29-32 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Diphosphate 207-210 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 62-65 H3 histone pseudogene 16 Homo sapiens 106-109 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 62-65 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Diphosphate 207-210 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 62-65 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 62-65 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 211-214 H3 histone pseudogene 16 Homo sapiens 106-109 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 62-65 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 110-113 H3 histone pseudogene 16 Homo sapiens 106-109 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 211-214 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 126-129 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 211-214 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 126-129 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 126-129 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 211-214 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 126-129 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Guanosine Triphosphate 211-214 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 106-109 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 266-269 H3 histone pseudogene 16 Homo sapiens 106-109 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 266-269 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 266-269 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 266-269 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Valine 266-269 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 106-109 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 122-125 1652268-6 1991 When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. Glycine 242-245 H3 histone pseudogene 16 Homo sapiens 122-125 1793483-5 1991 It leads to the substitution of glycine by aspartic acid in the resulting p21 protein, a consistent amino acid substitution found so far in all types of human cancer exhibiting a codon 13-mutated Ki-ras gene. Aspartic Acid 43-56 H3 histone pseudogene 16 Homo sapiens 74-77 1793483-5 1991 It leads to the substitution of glycine by aspartic acid in the resulting p21 protein, a consistent amino acid substitution found so far in all types of human cancer exhibiting a codon 13-mutated Ki-ras gene. Glycine 32-39 H3 histone pseudogene 16 Homo sapiens 74-77 1814747-2 1991 Using an ABC immunoencymatic staining technique and a P21-specific monoclonal antibody, SCI-Oncogema I, we have detected the expression of P21 in formalin-fixed, paraffin-embedded samples from 53 bladder tumors and 7 normal bladder mucosae. Formaldehyde 146-154 H3 histone pseudogene 16 Homo sapiens 139-142 1814747-2 1991 Using an ABC immunoencymatic staining technique and a P21-specific monoclonal antibody, SCI-Oncogema I, we have detected the expression of P21 in formalin-fixed, paraffin-embedded samples from 53 bladder tumors and 7 normal bladder mucosae. Paraffin 162-170 H3 histone pseudogene 16 Homo sapiens 139-142 1652685-5 1991 Clonal analysis of this population demonstrated that the increased NAb binding was associated with tumorigenic conversion and ras-p21 expression. nab 67-70 H3 histone pseudogene 16 Homo sapiens 130-133 2245170-5 1990 The p21 expression was greater in patients with advanced (stage III) than in earlier MM (stages I + II) (P less than 0.005), and it was directly related to the BMPC infiltration (r = 0.7; P less than 0.005). Dimethylol-p-kresol 160-164 H3 histone pseudogene 16 Homo sapiens 4-7 2014702-1 1991 A hypothesis presented in the paper discusses the role of valine substitution in p21 protein of H-ras, a product of ras family oncogene. Valine 58-64 H3 histone pseudogene 16 Homo sapiens 81-84 2014702-5 1991 Based on similarity of valine substitution in p21 protein and hemoglobin, a relationship between certain forms of malignant transformation and malaria at molecular level is suggested. Valine 23-29 H3 histone pseudogene 16 Homo sapiens 46-49 2085809-2 1990 The crystal structure of neocarrabiose monohydrate, 3-O-(3,6-anhydro-alpha-D-galactopyranosyl)-beta-D-galactopyranose (C12H20O10.H2O) belongs to the monoclinic space group P2(1), and has a unit cell of dimensions a = 6.351(1), b = 7.675(2), c = 15.096(8) A, and beta = 91.11(1) degree. neocarrabiose monohydrate 25-50 H3 histone pseudogene 16 Homo sapiens 172-177 2085809-2 1990 The crystal structure of neocarrabiose monohydrate, 3-O-(3,6-anhydro-alpha-D-galactopyranosyl)-beta-D-galactopyranose (C12H20O10.H2O) belongs to the monoclinic space group P2(1), and has a unit cell of dimensions a = 6.351(1), b = 7.675(2), c = 15.096(8) A, and beta = 91.11(1) degree. neocarrabiose 52-117 H3 histone pseudogene 16 Homo sapiens 172-177 2199064-1 1990 The X-ray structures of the guanine nucleotide binding domains (amino acids 1-166) of five mutants of the H-ras oncogene product p21 were determined. Guanine Nucleotides 28-46 H3 histone pseudogene 16 Homo sapiens 129-132 2278880-3 1990 Lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, may prevent the farnesylation of de novo synthesized ras p21. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 145-148 2085379-1 1990 The predicted conformation and position of the central transforming region (residues 55-67) of the p21 protein are compared with the conformation and position of this segment in a recently determined X-ray crystal structure of residues 1-166 of this protein in the activated state bound to a nonhydrolyzable GTP derivative. Guanosine Triphosphate 308-311 H3 histone pseudogene 16 Homo sapiens 99-102 2146678-1 1990 The ras gene product (p21) is a GTP-binding protein and has been thought to transduce signals regulating proliferation or differentiation of cells. Guanosine Triphosphate 32-35 H3 histone pseudogene 16 Homo sapiens 22-25 2146678-2 1990 Like other GTP-binding proteins, p21.GTP is an active conformation, which can transduce the signals downstream, whereas p21.GDP is an inactive one. Guanosine Triphosphate 11-14 H3 histone pseudogene 16 Homo sapiens 33-36 2146678-2 1990 Like other GTP-binding proteins, p21.GTP is an active conformation, which can transduce the signals downstream, whereas p21.GDP is an inactive one. Guanosine Triphosphate 11-14 H3 histone pseudogene 16 Homo sapiens 120-123 2146678-2 1990 Like other GTP-binding proteins, p21.GTP is an active conformation, which can transduce the signals downstream, whereas p21.GDP is an inactive one. Guanosine Triphosphate 37-40 H3 histone pseudogene 16 Homo sapiens 33-36 2146678-2 1990 Like other GTP-binding proteins, p21.GTP is an active conformation, which can transduce the signals downstream, whereas p21.GDP is an inactive one. Guanosine Diphosphate 124-127 H3 histone pseudogene 16 Homo sapiens 33-36 2146678-2 1990 Like other GTP-binding proteins, p21.GTP is an active conformation, which can transduce the signals downstream, whereas p21.GDP is an inactive one. Guanosine Diphosphate 124-127 H3 histone pseudogene 16 Homo sapiens 120-123 2146678-3 1990 Recently, we have shown that p21.GTP levels increased in cells treated with fetal bovine serum or platelet-derived growth factor to initiate DNA synthesis. Guanosine Triphosphate 33-36 H3 histone pseudogene 16 Homo sapiens 29-32 2146678-4 1990 In this paper, we report that epidermal growth factor can also increase the amounts of p21.GTP in the cells. Guanosine Triphosphate 91-94 H3 histone pseudogene 16 Homo sapiens 87-90 2146678-7 1990 We also found that the ratio of p21.GTP to p21.GDP increased 3- to 4-fold in transformants carrying activated erbB-2/neu or v-src oncogenes. Guanosine Triphosphate 36-39 H3 histone pseudogene 16 Homo sapiens 32-35 2146678-7 1990 We also found that the ratio of p21.GTP to p21.GDP increased 3- to 4-fold in transformants carrying activated erbB-2/neu or v-src oncogenes. Guanosine Triphosphate 36-39 H3 histone pseudogene 16 Homo sapiens 43-46 2146678-7 1990 We also found that the ratio of p21.GTP to p21.GDP increased 3- to 4-fold in transformants carrying activated erbB-2/neu or v-src oncogenes. Guanosine Diphosphate 47-50 H3 histone pseudogene 16 Homo sapiens 32-35 2146678-7 1990 We also found that the ratio of p21.GTP to p21.GDP increased 3- to 4-fold in transformants carrying activated erbB-2/neu or v-src oncogenes. Guanosine Diphosphate 47-50 H3 histone pseudogene 16 Homo sapiens 43-46 2279848-1 1990 The GTP-binding p21 protein, encoded by the ras-oncogene, becomes transforming if amino acid substitutions are made at critical positions in the polypeptide chain, e.g., at Gly 12, Gly 13, Ala 59, Gln 61 and Glu 63. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 16-19 2279848-1 1990 The GTP-binding p21 protein, encoded by the ras-oncogene, becomes transforming if amino acid substitutions are made at critical positions in the polypeptide chain, e.g., at Gly 12, Gly 13, Ala 59, Gln 61 and Glu 63. Glycine 173-176 H3 histone pseudogene 16 Homo sapiens 16-19 2279848-1 1990 The GTP-binding p21 protein, encoded by the ras-oncogene, becomes transforming if amino acid substitutions are made at critical positions in the polypeptide chain, e.g., at Gly 12, Gly 13, Ala 59, Gln 61 and Glu 63. Glycine 181-184 H3 histone pseudogene 16 Homo sapiens 16-19 2279848-1 1990 The GTP-binding p21 protein, encoded by the ras-oncogene, becomes transforming if amino acid substitutions are made at critical positions in the polypeptide chain, e.g., at Gly 12, Gly 13, Ala 59, Gln 61 and Glu 63. Alanine 189-192 H3 histone pseudogene 16 Homo sapiens 16-19 2279848-1 1990 The GTP-binding p21 protein, encoded by the ras-oncogene, becomes transforming if amino acid substitutions are made at critical positions in the polypeptide chain, e.g., at Gly 12, Gly 13, Ala 59, Gln 61 and Glu 63. Glutamine 197-200 H3 histone pseudogene 16 Homo sapiens 16-19 2279848-1 1990 The GTP-binding p21 protein, encoded by the ras-oncogene, becomes transforming if amino acid substitutions are made at critical positions in the polypeptide chain, e.g., at Gly 12, Gly 13, Ala 59, Gln 61 and Glu 63. Glutamic Acid 208-211 H3 histone pseudogene 16 Homo sapiens 16-19 2199064-4 1990 Cellular and mutant p21 proteins are almost identical, and the only significant differences are seen in loop L4 and in the vicinity of the gamma-phosphate. gamma-phosphate 139-154 H3 histone pseudogene 16 Homo sapiens 20-23 2199064-6 1990 Gln-61 in cellular p21 adopts a conformation where it is able to catalyze GTP hydrolysis. Glutamine 0-3 H3 histone pseudogene 16 Homo sapiens 19-22 2199064-6 1990 Gln-61 in cellular p21 adopts a conformation where it is able to catalyze GTP hydrolysis. Guanosine Triphosphate 74-77 H3 histone pseudogene 16 Homo sapiens 19-22 2164357-0 1990 Electron paramagnetic resonance measurements of the hydration of Mn(II) in ternary complexes with GDP and ras p21 proteins. Manganese(2+) 65-71 H3 histone pseudogene 16 Homo sapiens 110-113 2164357-2 1990 EPR signals of Mn(II) in the GDP complex with viral-Harvey p21pRAS1 (Arg 12, Thr 59), p21EC (Gly 12, Thr 59), and p21EJ (Val 12, Thr 59) have narrow line-widths that permit ready observation of inhomogeneous broadening from unresolved superhyperfine coupling with the nuclear spin of 17O of directly coordinated oxygen ligands. Oxygen 312-318 H3 histone pseudogene 16 Homo sapiens 59-67 2164357-1 1990 Electron paramagnetic resonance (EPR) spectroscopy has been used to determine the hydration numbers of Mn(II) in complexes with GDP and three forms of ras p21. Manganese(2+) 103-109 H3 histone pseudogene 16 Homo sapiens 155-158 2164357-2 1990 EPR signals of Mn(II) in the GDP complex with viral-Harvey p21pRAS1 (Arg 12, Thr 59), p21EC (Gly 12, Thr 59), and p21EJ (Val 12, Thr 59) have narrow line-widths that permit ready observation of inhomogeneous broadening from unresolved superhyperfine coupling with the nuclear spin of 17O of directly coordinated oxygen ligands. Manganese(2+) 15-21 H3 histone pseudogene 16 Homo sapiens 59-67 2164357-2 1990 EPR signals of Mn(II) in the GDP complex with viral-Harvey p21pRAS1 (Arg 12, Thr 59), p21EC (Gly 12, Thr 59), and p21EJ (Val 12, Thr 59) have narrow line-widths that permit ready observation of inhomogeneous broadening from unresolved superhyperfine coupling with the nuclear spin of 17O of directly coordinated oxygen ligands. Guanosine Diphosphate 29-32 H3 histone pseudogene 16 Homo sapiens 59-67 2164357-2 1990 EPR signals of Mn(II) in the GDP complex with viral-Harvey p21pRAS1 (Arg 12, Thr 59), p21EC (Gly 12, Thr 59), and p21EJ (Val 12, Thr 59) have narrow line-widths that permit ready observation of inhomogeneous broadening from unresolved superhyperfine coupling with the nuclear spin of 17O of directly coordinated oxygen ligands. Arginine 69-72 H3 histone pseudogene 16 Homo sapiens 59-67 2096262-3 1990 ras p21 was overlaid on the vesicle proteins immobilized on a nitrocellulose sheet transferred from the gel of sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Sodium Dodecyl Sulfate 111-133 H3 histone pseudogene 16 Homo sapiens 4-7 2196171-0 1990 Refined crystal structure of the triphosphate conformation of H-ras p21 at 1.35 A resolution: implications for the mechanism of GTP hydrolysis. triphosphoric acid 33-45 H3 histone pseudogene 16 Homo sapiens 68-71 2196171-0 1990 Refined crystal structure of the triphosphate conformation of H-ras p21 at 1.35 A resolution: implications for the mechanism of GTP hydrolysis. Guanosine Triphosphate 128-131 H3 histone pseudogene 16 Homo sapiens 68-71 2196171-1 1990 The crystal structure of the H-ras oncogene protein p21 complexed to the slowly hydrolysing GTP analogue GppNp has been determined at 1.35 A resolution. Guanosine Triphosphate 92-95 H3 histone pseudogene 16 Homo sapiens 52-55 2096262-3 1990 ras p21 was overlaid on the vesicle proteins immobilized on a nitrocellulose sheet transferred from the gel of sodium dodecyl sulfate-polyacrylamide gel electrophoresis. polyacrylamide 134-148 H3 histone pseudogene 16 Homo sapiens 4-7 2157708-7 1990 Taken together, these results point out that Thr82 is in close proximity to the gamma-phosphate of GTP, as in the case of Thr59 in p21. gamma-phosphate 80-95 H3 histone pseudogene 16 Homo sapiens 131-134 2202949-0 1990 Characterization of monoclonal antibodies specific to the activated ras p21 with aspartic acid at position 13. Aspartic Acid 81-94 H3 histone pseudogene 16 Homo sapiens 72-75 2202949-6 1990 Western blot analysis demonstrates that D129 and D146 react specifically with p21 extracted from transformed NIH3T3 fibroblast lines containing aspartic acid at position 13. Aspartic Acid 144-157 H3 histone pseudogene 16 Homo sapiens 78-81 2202949-7 1990 These studies also demonstrate that D146 is able to detect the activated p21 with aspartic acid at position 13 that is shed into the culture media. d146 36-40 H3 histone pseudogene 16 Homo sapiens 73-76 2202949-7 1990 These studies also demonstrate that D146 is able to detect the activated p21 with aspartic acid at position 13 that is shed into the culture media. Aspartic Acid 82-95 H3 histone pseudogene 16 Homo sapiens 73-76 2202949-9 1990 Using a sandwich ELISA format, D146 is able to detect the p21 with position 13 aspartic acid from cell extracts and culture fluids. d146 31-35 H3 histone pseudogene 16 Homo sapiens 58-61 2202949-9 1990 Using a sandwich ELISA format, D146 is able to detect the p21 with position 13 aspartic acid from cell extracts and culture fluids. Aspartic Acid 79-92 H3 histone pseudogene 16 Homo sapiens 58-61 2202949-10 1990 The ability of D146 to function in the ELISA format raises the possibility that this assay maybe a quick and effective way of determining the presence of activated p21 with aspartic acid at position 13 in human fluids and tissues. d146 15-19 H3 histone pseudogene 16 Homo sapiens 164-167 2202949-10 1990 The ability of D146 to function in the ELISA format raises the possibility that this assay maybe a quick and effective way of determining the presence of activated p21 with aspartic acid at position 13 in human fluids and tissues. Aspartic Acid 173-186 H3 histone pseudogene 16 Homo sapiens 164-167 2115641-3 1990 The Gln 227 site of alpha s corresponds to the Gln 61 site in the low Mw G protein, p21 ras, where the Leu substitution had already been shown to be oncogenic. Glutamine 4-7 H3 histone pseudogene 16 Homo sapiens 84-87 2115641-3 1990 The Gln 227 site of alpha s corresponds to the Gln 61 site in the low Mw G protein, p21 ras, where the Leu substitution had already been shown to be oncogenic. Glutamine 47-50 H3 histone pseudogene 16 Homo sapiens 84-87 2115641-3 1990 The Gln 227 site of alpha s corresponds to the Gln 61 site in the low Mw G protein, p21 ras, where the Leu substitution had already been shown to be oncogenic. Leucine 103-106 H3 histone pseudogene 16 Homo sapiens 84-87 2188736-2 1990 Recombinant human ras p21 GAP (GTPase activating protein) at subnanomolar concentrations inhibited GTP-dependent channel opening in isolated atrial cell membranes. Guanosine Triphosphate 31-34 H3 histone pseudogene 16 Homo sapiens 22-25 2188736-5 1990 We therefore propose that ras p21 GTP complexed with GAP (ras p21-GAP) blocks K+[ACh] currents. Guanosine Triphosphate 34-37 H3 histone pseudogene 16 Homo sapiens 30-33 2188736-5 1990 We therefore propose that ras p21 GTP complexed with GAP (ras p21-GAP) blocks K+[ACh] currents. Guanosine Triphosphate 34-37 H3 histone pseudogene 16 Homo sapiens 62-65 2188736-5 1990 We therefore propose that ras p21 GTP complexed with GAP (ras p21-GAP) blocks K+[ACh] currents. Acetylcholine 81-84 H3 histone pseudogene 16 Homo sapiens 30-33 2188736-5 1990 We therefore propose that ras p21 GTP complexed with GAP (ras p21-GAP) blocks K+[ACh] currents. Acetylcholine 81-84 H3 histone pseudogene 16 Homo sapiens 62-65 2188736-6 1990 The channel block could be overcome by GTP gamma S activation of endogenous Gk; this indicates that ras p21-GAP does not interfere with interaction of Gk with the K+[ACh] channel directly, but prevents coupling of the muscarinic receptor to endogenous Gk. Guanosine Triphosphate 39-42 H3 histone pseudogene 16 Homo sapiens 104-107 2198577-1 1990 The ras gene product (p21) is a GTP-binding protein and is thought to play an important role in signal transduction of growth and differentiation in many types of mammalian cells. Guanosine Triphosphate 32-35 H3 histone pseudogene 16 Homo sapiens 22-25 2164710-6 1990 Binding of GAP to Rap1A-p21 was strictly guanosine triphosphate (GTP)-dependent. Guanosine Triphosphate 41-63 H3 histone pseudogene 16 Homo sapiens 24-27 2164710-6 1990 Binding of GAP to Rap1A-p21 was strictly guanosine triphosphate (GTP)-dependent. Guanosine Triphosphate 65-68 H3 histone pseudogene 16 Homo sapiens 24-27 2197592-0 1990 The Ha-ras protein, p21, is modified by a derivative of mevalonate and methyl-esterified when expressed in the insect/baculovirus system. Mevalonic Acid 56-66 H3 histone pseudogene 16 Homo sapiens 20-23 2197592-1 1990 Using the insect/baculovirus expression system, we demonstrate the incorporation of [3H]mevalonate and [3H]methyl groups into recombinant c-Ha-ras protein (p21). [3h]mevalonate 84-98 H3 histone pseudogene 16 Homo sapiens 156-159 2197592-1 1990 Using the insect/baculovirus expression system, we demonstrate the incorporation of [3H]mevalonate and [3H]methyl groups into recombinant c-Ha-ras protein (p21). Tritium 85-87 H3 histone pseudogene 16 Homo sapiens 156-159 2197592-3 1990 It is highly likely that the insect expression system recognizes the C-terminal CAAX Motif in p21, incorporates the mevalonate into the recently described polyisoprenylation modification and carboxyl-methylates the protein. Mevalonic Acid 116-126 H3 histone pseudogene 16 Homo sapiens 94-97 2200519-4 1990 By use of a nonequilibrium competition method, guanosine and GMP have been shown to interact weakly but significantly with p21 (dissociation constants of 153 and 29 microM, respectively). Guanosine 47-56 H3 histone pseudogene 16 Homo sapiens 123-126 2200519-4 1990 By use of a nonequilibrium competition method, guanosine and GMP have been shown to interact weakly but significantly with p21 (dissociation constants of 153 and 29 microM, respectively). guanosine 5'-monophosphorothioate 61-64 H3 histone pseudogene 16 Homo sapiens 123-126 2200519-5 1990 The presence of guanosine or GMP at the active site of p21 leads to a marked stabilization of p21 against spontaneous denaturation when compared with the nucleotide- and nucleoside-free protein. Guanosine 16-25 H3 histone pseudogene 16 Homo sapiens 55-58 2200519-5 1990 The presence of guanosine or GMP at the active site of p21 leads to a marked stabilization of p21 against spontaneous denaturation when compared with the nucleotide- and nucleoside-free protein. Guanosine 16-25 H3 histone pseudogene 16 Homo sapiens 94-97 2200519-5 1990 The presence of guanosine or GMP at the active site of p21 leads to a marked stabilization of p21 against spontaneous denaturation when compared with the nucleotide- and nucleoside-free protein. guanosine 5'-monophosphorothioate 29-32 H3 histone pseudogene 16 Homo sapiens 55-58 2200519-5 1990 The presence of guanosine or GMP at the active site of p21 leads to a marked stabilization of p21 against spontaneous denaturation when compared with the nucleotide- and nucleoside-free protein. guanosine 5'-monophosphorothioate 29-32 H3 histone pseudogene 16 Homo sapiens 94-97 2200519-5 1990 The presence of guanosine or GMP at the active site of p21 leads to a marked stabilization of p21 against spontaneous denaturation when compared with the nucleotide- and nucleoside-free protein. Nucleosides 170-180 H3 histone pseudogene 16 Homo sapiens 55-58 2200519-5 1990 The presence of guanosine or GMP at the active site of p21 leads to a marked stabilization of p21 against spontaneous denaturation when compared with the nucleotide- and nucleoside-free protein. Nucleosides 170-180 H3 histone pseudogene 16 Homo sapiens 94-97 2111463-0 1990 Time-resolved X-ray crystallographic study of the conformational change in Ha-Ras p21 protein on GTP hydrolysis. Guanosine Triphosphate 97-100 H3 histone pseudogene 16 Homo sapiens 82-85 2111463-1 1990 Crystals of Ha-Ras p21 with caged GTP at the active site have been used to investigate the conformational changes of p21 on GTP hydrolysis. Guanosine Triphosphate 34-37 H3 histone pseudogene 16 Homo sapiens 19-22 2111463-1 1990 Crystals of Ha-Ras p21 with caged GTP at the active site have been used to investigate the conformational changes of p21 on GTP hydrolysis. Guanosine Triphosphate 124-127 H3 histone pseudogene 16 Homo sapiens 19-22 2111463-1 1990 Crystals of Ha-Ras p21 with caged GTP at the active site have been used to investigate the conformational changes of p21 on GTP hydrolysis. Guanosine Triphosphate 124-127 H3 histone pseudogene 16 Homo sapiens 117-120 2111463-2 1990 The structure of the short-lived p21.GTP complex was determined by Laue diffraction methods. Guanosine Triphosphate 37-40 H3 histone pseudogene 16 Homo sapiens 33-36 2158984-4 1990 The GTP-bound form of smg p21, however, inhibited the ras p21 GAP-stimulated GTPase activity of c-Ha-ras p21 in a dose-dependent manner. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 26-29 2158984-4 1990 The GTP-bound form of smg p21, however, inhibited the ras p21 GAP-stimulated GTPase activity of c-Ha-ras p21 in a dose-dependent manner. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 58-61 2158984-4 1990 The GTP-bound form of smg p21, however, inhibited the ras p21 GAP-stimulated GTPase activity of c-Ha-ras p21 in a dose-dependent manner. Guanosine Triphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 58-61 2158984-6 1990 The GDP-bound form also inhibited the ras p21 GAP-stimulated GTPase activity of c-Ha-ras p21, but the efficiency was 40-50% that of the GTP-bound form. Guanosine Diphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 42-45 2158984-6 1990 The GDP-bound form also inhibited the ras p21 GAP-stimulated GTPase activity of c-Ha-ras p21, but the efficiency was 40-50% that of the GTP-bound form. Guanosine Diphosphate 4-7 H3 histone pseudogene 16 Homo sapiens 89-92 2158984-6 1990 The GDP-bound form also inhibited the ras p21 GAP-stimulated GTPase activity of c-Ha-ras p21, but the efficiency was 40-50% that of the GTP-bound form. Guanosine Triphosphate 61-64 H3 histone pseudogene 16 Homo sapiens 42-45 2158984-6 1990 The GDP-bound form also inhibited the ras p21 GAP-stimulated GTPase activity of c-Ha-ras p21, but the efficiency was 40-50% that of the GTP-bound form. Guanosine Triphosphate 61-64 H3 histone pseudogene 16 Homo sapiens 89-92 2157708-7 1990 Taken together, these results point out that Thr82 is in close proximity to the gamma-phosphate of GTP, as in the case of Thr59 in p21. Guanosine Triphosphate 99-102 H3 histone pseudogene 16 Homo sapiens 131-134 2157708-8 1990 These results are in agreement with the observations derived from x-ray diffraction analysis that the tertiary structure of the GTP-binding domain of elongation factor Tu and that of p21 are similar. Guanosine Triphosphate 128-131 H3 histone pseudogene 16 Homo sapiens 183-186 2108052-5 1990 Selective excitation of the single tryptophan in p21 produced a decrease in fluorescence intensity which was accompanied by a blue shift in the wavelength of maximum emission on nucleotide exchange. Tryptophan 35-45 H3 histone pseudogene 16 Homo sapiens 49-52 2235101-6 1990 p21 was examined with avidin-biotin linked immunoperoxidase visualization. avidin-biotin 22-35 H3 histone pseudogene 16 Homo sapiens 0-3 2191717-0 1990 NMR study of the phosphoryl binding loop in purine nucleotide proteins: evidence for strong hydrogen bonding in human N-ras p21. purine 44-50 H3 histone pseudogene 16 Homo sapiens 124-127 2191717-0 1990 NMR study of the phosphoryl binding loop in purine nucleotide proteins: evidence for strong hydrogen bonding in human N-ras p21. Hydrogen 92-100 H3 histone pseudogene 16 Homo sapiens 124-127 2405906-7 1990 In solution, the p21-bound GDP.Mg2+ has an anti conformation, and the phenyl ring of Phe28 is close to the ribose of the bound GDP.Mg2+. Guanosine Diphosphate 27-30 H3 histone pseudogene 16 Homo sapiens 17-20 2405906-7 1990 In solution, the p21-bound GDP.Mg2+ has an anti conformation, and the phenyl ring of Phe28 is close to the ribose of the bound GDP.Mg2+. magnesium ion 31-35 H3 histone pseudogene 16 Homo sapiens 17-20 2405906-7 1990 In solution, the p21-bound GDP.Mg2+ has an anti conformation, and the phenyl ring of Phe28 is close to the ribose of the bound GDP.Mg2+. Ribose 107-113 H3 histone pseudogene 16 Homo sapiens 17-20 2405906-7 1990 In solution, the p21-bound GDP.Mg2+ has an anti conformation, and the phenyl ring of Phe28 is close to the ribose of the bound GDP.Mg2+. Guanosine Diphosphate 127-130 H3 histone pseudogene 16 Homo sapiens 17-20 2405906-7 1990 In solution, the p21-bound GDP.Mg2+ has an anti conformation, and the phenyl ring of Phe28 is close to the ribose of the bound GDP.Mg2+. magnesium ion 131-135 H3 histone pseudogene 16 Homo sapiens 17-20 2180382-1 1990 The ras oncogene product, ras p21, is structurally homologous to guanine nucleotide-binding proteins, which play an important role in transmembrane signaling systems. Guanine Nucleotides 65-83 H3 histone pseudogene 16 Homo sapiens 30-33 2192633-3 1990 The newly developed assay for quantitative determination of ras protooncogene expression which utilizes affinity labeling of ras p21 with [alpha-32P]GTP can effectively demonstrate the presence of ras protooncogene expression in explant cultures of human mammary tissues. [alpha-32p]gtp 138-152 H3 histone pseudogene 16 Homo sapiens 129-132 34971958-8 2022 However, oridonin did not affect SA beta-gal activity and enhanced the expression of p21. oridonin 9-17 H3 histone pseudogene 16 Homo sapiens 85-88 33939887-10 2021 Breast tissue-occurring metabolites" antiproliferation was mainly exerted in p53-wild-type MCF-7 cells by curcuminoids through cell cycle arrest, senescence, and apoptosis induction via p53/p21 induction, while isoflavone-derived metabolites exerted estrogenic-like activity. Diarylheptanoids 106-118 H3 histone pseudogene 16 Homo sapiens 190-193 33939887-10 2021 Breast tissue-occurring metabolites" antiproliferation was mainly exerted in p53-wild-type MCF-7 cells by curcuminoids through cell cycle arrest, senescence, and apoptosis induction via p53/p21 induction, while isoflavone-derived metabolites exerted estrogenic-like activity. Isoflavones 211-221 H3 histone pseudogene 16 Homo sapiens 190-193 33821368-11 2021 Ozone induced G2/M phase cell cycle arrest, which could be elucidated by the change of protein levels of p53, p21, Cyclin D1, cyclin B1, cdc2, and CDK4. Ozone 0-5 H3 histone pseudogene 16 Homo sapiens 110-113 33799486-8 2021 Increased p21 expression was observed with both calcium and Aquamin . Calcium 48-55 H3 histone pseudogene 16 Homo sapiens 10-13 26628962-3 2015 To identify the detailed mechanism, we examined the functional importance of p21 and p53 in DPA-induced anticancer effect. dpa 92-95 H3 histone pseudogene 16 Homo sapiens 77-80 26628962-6 2015 Additionally, Western blot showed that DPA treatment induced the p21, p53, and cyclin-E protein expressions in HCT-116 cells. dpa 39-42 H3 histone pseudogene 16 Homo sapiens 65-68 26628962-7 2015 The p21 associated cell cycle regulatory protein such as cyclin D, CDK4, and pRb were decreased after DPA treatment in HCT-116 cells. dpa 102-105 H3 histone pseudogene 16 Homo sapiens 4-7 26628962-10 2015 We assumed that p21 was required for DPA-induced anti-colon cancer effect through the Erk and p38 pathway leading to cell cycle arrest and inhibition of cell motility. dpa 37-40 H3 histone pseudogene 16 Homo sapiens 16-19 26628962-13 2015 This is the first pharmacokinetic study of DPA, and indicated that anti-proliferation and the cell mobility inhibition effects of DPA in HCT116 WT cells may result from the induction of p21 through activation of ERK and p38 pathway. dpa 43-46 H3 histone pseudogene 16 Homo sapiens 186-189 26628962-13 2015 This is the first pharmacokinetic study of DPA, and indicated that anti-proliferation and the cell mobility inhibition effects of DPA in HCT116 WT cells may result from the induction of p21 through activation of ERK and p38 pathway. dpa 130-133 H3 histone pseudogene 16 Homo sapiens 186-189 22944197-9 2013 Vorinostat induced G2/M arrest, an increase in the sub-G1 fraction, up-regulation of p21, and down-regulation of TS in all UCC. Vorinostat 0-10 H3 histone pseudogene 16 Homo sapiens 85-88 34971743-7 2022 Upon exploring the underlying mechanism by which lincRNA-p21 mediates benzene-induced hematotoxicity, we observed that the negative regulation of 1,4-benzoquinone (1,4-BQ) on cell cycle arrest and inhibition of K562 cell proliferation was partially relieved by lincRNA-p21 knockdown, which can inhibit the expression of P21 and thereby suppress the toxic effects of 1,4-BQ. Benzene 70-77 H3 histone pseudogene 16 Homo sapiens 320-323 34971743-7 2022 Upon exploring the underlying mechanism by which lincRNA-p21 mediates benzene-induced hematotoxicity, we observed that the negative regulation of 1,4-benzoquinone (1,4-BQ) on cell cycle arrest and inhibition of K562 cell proliferation was partially relieved by lincRNA-p21 knockdown, which can inhibit the expression of P21 and thereby suppress the toxic effects of 1,4-BQ. quinone 146-162 H3 histone pseudogene 16 Homo sapiens 320-323 34971743-7 2022 Upon exploring the underlying mechanism by which lincRNA-p21 mediates benzene-induced hematotoxicity, we observed that the negative regulation of 1,4-benzoquinone (1,4-BQ) on cell cycle arrest and inhibition of K562 cell proliferation was partially relieved by lincRNA-p21 knockdown, which can inhibit the expression of P21 and thereby suppress the toxic effects of 1,4-BQ. quinone 164-170 H3 histone pseudogene 16 Homo sapiens 320-323 34971743-7 2022 Upon exploring the underlying mechanism by which lincRNA-p21 mediates benzene-induced hematotoxicity, we observed that the negative regulation of 1,4-benzoquinone (1,4-BQ) on cell cycle arrest and inhibition of K562 cell proliferation was partially relieved by lincRNA-p21 knockdown, which can inhibit the expression of P21 and thereby suppress the toxic effects of 1,4-BQ. quinone 366-372 H3 histone pseudogene 16 Homo sapiens 320-323 34971743-9 2022 In conclusion, our research suggested that benzene induces hematotoxicity via the lincRNA-p21/miRNA-17-5p/p21 signaling which might contribute to the underlying mechanism of lincRNA-p21 in benzene-induced hematotoxicity. Benzene 43-50 H3 histone pseudogene 16 Homo sapiens 106-109 34971743-9 2022 In conclusion, our research suggested that benzene induces hematotoxicity via the lincRNA-p21/miRNA-17-5p/p21 signaling which might contribute to the underlying mechanism of lincRNA-p21 in benzene-induced hematotoxicity. Benzene 189-196 H3 histone pseudogene 16 Homo sapiens 106-109 34800264-0 2022 Metoprolol Protects Against Arginine Vasopressin-Induced Cellular Senescence in H9C2 Cardiomyocytes by Regulating the Sirt1/p53/p21 Axis. Metoprolol 0-10 H3 histone pseudogene 16 Homo sapiens 128-131 34800264-9 2022 Finally, Metoprolol was able to downregulate the AVP-induced expression of acetylated p53 and p21. Metoprolol 9-19 H3 histone pseudogene 16 Homo sapiens 94-97 34697424-1 2022 The p21-Activated Kinases (PAKs) are a family of six serine/threonine kinases that were originally identified as downstream effectors of the Rho GTPases Cdc42 and Rac. Serine 53-59 H3 histone pseudogene 16 Homo sapiens 4-7 33941774-8 2021 By activating the P53/P21 pathway, APG-115 exhibited potent antiproliferative and apoptogenic activities, and induced cell cycle arrest, in TP53 wild-type AML lines. AA-115 35-42 H3 histone pseudogene 16 Homo sapiens 22-25 33817171-4 2019 The activation of AMPKalpha induced changes of downstream proteins, including increase of P53 phosphorylation and P21 production, as well as decrease of mTOR phosphorylation, that eventually inhibited C6 cells growth. ampkalpha 18-27 H3 histone pseudogene 16 Homo sapiens 114-117 16287099-8 2006 Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in elevated levels of active p53 as demonstrated by p53 small interfering RNA (siRNA) sensitive p21 upregulation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 57-62 H3 histone pseudogene 16 Homo sapiens 168-171 11931974-0 2002 Vanadate-induced cell growth arrest is p53-dependent through activation of p21 in C141 cells. Vanadates 0-8 H3 histone pseudogene 16 Homo sapiens 75-78 11931974-10 2002 Western blotting analysis demonstrated that vanadate caused a dose- and time-dependent increase of p21 level in C141 cells. Vanadates 44-52 H3 histone pseudogene 16 Homo sapiens 99-102 11931974-11 2002 Pretreatment of C141 cells with PFT decreased p21 expression induced by vanadate while the p21 expression did not vary in vanadate stimulated p53 -/- cells. Vanadates 72-80 H3 histone pseudogene 16 Homo sapiens 46-49 11931974-12 2002 The results obtained from the present study suggest that vanadate is able to induce S phase arrest through p53- and p21-dependent pathway. Vanadates 57-65 H3 histone pseudogene 16 Homo sapiens 116-119 34843865-1 2022 We report a novel topoisomerase IIalpha inhibitor, mercaptopyridine oxide (MPO), which induces G2/M arrest and senescence with distinctly different cell cycle regulators (p21 or p14ARF) in HCT116p 53WT and HCT116 p53-/- cells, respectively. mercaptopyridine oxide 51-73 H3 histone pseudogene 16 Homo sapiens 171-174 34843865-1 2022 We report a novel topoisomerase IIalpha inhibitor, mercaptopyridine oxide (MPO), which induces G2/M arrest and senescence with distinctly different cell cycle regulators (p21 or p14ARF) in HCT116p 53WT and HCT116 p53-/- cells, respectively. mpo 75-78 H3 histone pseudogene 16 Homo sapiens 171-174 34728235-3 2022 AZD2461/UCN-01 combination activated p53/p21 and downregulated c-Myc in these cells, leading to a reduced expression level of RAD51, molecule involved in DNA repair. AZD2461 0-7 H3 histone pseudogene 16 Homo sapiens 41-44 34856803-5 2022 SM in Xadago in the high-humidity environment undergoes phase transformation to the P21 form which can be easily reversed just by heating up to 80 C. For the commercial form of the API, there is also a reversible thermal transformation observed between Z" = 1 Z" = 3 crystallographic forms in the 0-20 C temperature range. safinamide 0-2 H3 histone pseudogene 16 Homo sapiens 84-87 34856803-5 2022 SM in Xadago in the high-humidity environment undergoes phase transformation to the P21 form which can be easily reversed just by heating up to 80 C. For the commercial form of the API, there is also a reversible thermal transformation observed between Z" = 1 Z" = 3 crystallographic forms in the 0-20 C temperature range. safinamide 6-12 H3 histone pseudogene 16 Homo sapiens 84-87 34772529-5 2022 Mechanistically, MIR002 and GEM144 induced acetylation of p53, activation of p21, G1/S cell cycle arrest, and apoptosis. gem144 28-34 H3 histone pseudogene 16 Homo sapiens 77-80 34728235-4 2022 The effect of AZD2461/UCN-01 on c-Myc and p53/p21 was inter-dependent and, besides impairing cell proliferation, contributed to the activation of the replicative cycle of KSHV, carried in a latent state in PEL cells. AZD2461 14-21 H3 histone pseudogene 16 Homo sapiens 46-49 34826438-9 2022 Moreover, veratramine was sufficient to affect the phosphatidylinositol-3-kinase/serine-threonine kinase/mechanistic target of rapamycin signaling pathway and its downstream Mdm2/p53/p21 pathway in human glioblastoma cell lines. veratramine 10-21 H3 histone pseudogene 16 Homo sapiens 183-186 34783124-8 2022 Moreover, ginsenoside Rg1 treatment before doxorubicin activates the DNA damage response elements (ATM, H2AX, RAD51, and XRCC1) and subsequent apoptosis-related gene expression (p21, TP53. Doxorubicin 43-54 H3 histone pseudogene 16 Homo sapiens 178-181 34826438-10 2022 SIGNIFICANCE: Antitumor effects of veratramine in suppression of glioma progression was mediated by the regulation of PI3K/Akt/mTOR and Mdm2/p53/p21 signaling pathway. veratramine 35-46 H3 histone pseudogene 16 Homo sapiens 145-148 34945706-7 2021 An increment in p53 and p21 expression stimulated by GTE was observed in MCF-7, and the opposite phenomenon was found in MDA-MB-231 cells, with a redistribution of mutant-p53 from the nucleus and no differences in p21 levels. epigallocatechin gallate 53-56 H3 histone pseudogene 16 Homo sapiens 24-27 34920321-6 2022 PURPOSE: To demonstrate the proliferative inhibitory potential of brazilin in human breast cancer cell line (MCF-7) with concurrent mitigation of DNMT1 functional expression and to understand its effect on downstream targets like cell cycle inhibitor p21. brazilin 66-74 H3 histone pseudogene 16 Homo sapiens 251-254 34920321-17 2022 Furthermore, the brazilin restored the p21 levels in the exposed cells as the CpGs in the p21 promoter (-128 bp/+17 bp) were significantly demethylated as observed in the methylation-specific PCR (MSP). brazilin 17-25 H3 histone pseudogene 16 Homo sapiens 39-42 34920321-17 2022 Furthermore, the brazilin restored the p21 levels in the exposed cells as the CpGs in the p21 promoter (-128 bp/+17 bp) were significantly demethylated as observed in the methylation-specific PCR (MSP). brazilin 17-25 H3 histone pseudogene 16 Homo sapiens 90-93 34820007-6 2022 Isoliensinine was found to induce cell cycle arrest at the G0/G1 phase by upregulating p21 expression and downregulating CDK2 and cyclin E in breast cancer cells. isoliensinine 0-13 H3 histone pseudogene 16 Homo sapiens 87-90 34932948-4 2021 The clearance of EpiSCs with DSBs is caused by selective differentiation and delamination through the DNA damage response (DDR)-p53-Notch/p21 axis, with the downregulation of ITGB1. dsbs 29-33 H3 histone pseudogene 16 Homo sapiens 138-141 34970530-8 2021 Mechanistically, 2b induced apoptosis-dependent anticancer effect (43%) higher than that of 5-fluorouracil (34.95%) in three studied cancer cell lines, activated p53 (47%), downregulated the Bcl2 gene (1.25-fold), and upregulated p21 (2-fold) in the treated cancer cells. Fluorouracil 92-106 H3 histone pseudogene 16 Homo sapiens 230-233 34921996-0 2022 Repurposing gestrinone for tumor suppressor through P21 reduction regulated by JNK in gynecological cancer. Gestrinone 12-22 H3 histone pseudogene 16 Homo sapiens 52-55 34921996-10 2022 Cellular experiments verified the anti-cancer effects of gestrinone, which effectively and specifically inhibited the growth of HeLa cervical cancer cells, decreased P21 expression via JNK phosphorylation, and induced apoptosis. Gestrinone 57-67 H3 histone pseudogene 16 Homo sapiens 166-169 34921996-11 2022 Combining the results of clinical database analysis and cell experiments, our findings prove that gestrinone has the potential to protect against cancer through regulation of the JNK-P21 axis. Gestrinone 98-108 H3 histone pseudogene 16 Homo sapiens 183-186 34923957-16 2021 GLA reduced the expression of cell cycle-related proteins CCNB1, CCND1, CCND2, and CCND3 and increased the expression of p21 in MM cell lines. glaucocalyxin A 0-3 H3 histone pseudogene 16 Homo sapiens 121-124 34912007-11 2021 The mRNA and protein levels of p73 target genes (PML, p21 and Bax) were all increased by UVB but decreased by silibinin co-treatment. Silybin 110-119 H3 histone pseudogene 16 Homo sapiens 54-57 34733363-6 2021 TMZ enhanced the autophagic response and senescence, which was mediated via the p53 and p21 pathways. Temozolomide 0-3 H3 histone pseudogene 16 Homo sapiens 88-91 34879876-12 2021 Furthermore, in an H2O2 stress-induced premature senescence condition, WNT16 treatment increased cell senescence in AS-osteoprogenitor cells and WNT16 treatment under the H2O2 stress condition showed an increase in p21 protein and SASP mRNA expression. Hydrogen Peroxide 19-23 H3 histone pseudogene 16 Homo sapiens 215-218 34879876-12 2021 Furthermore, in an H2O2 stress-induced premature senescence condition, WNT16 treatment increased cell senescence in AS-osteoprogenitor cells and WNT16 treatment under the H2O2 stress condition showed an increase in p21 protein and SASP mRNA expression. Hydrogen Peroxide 171-175 H3 histone pseudogene 16 Homo sapiens 215-218 34658297-0 2021 Polyphyllin I, a lethal partner of Palbociclib, suppresses non-small cell lung cancer through activation of p21/CDK2/Rb pathway in vitro and in vivo. polyphyllin I 0-13 H3 histone pseudogene 16 Homo sapiens 108-111 34658297-7 2021 Mechanistically, PPI can inhibit Rb through the p21/CDK2/Rb signaling pathway in NSCLC. Rubidium 33-35 H3 histone pseudogene 16 Homo sapiens 48-51 34855924-0 2021 Retraction: miR-24-3p Suppresses Malignant Behavior of Lacrimal Adenoid Cystic Carcinoma by Targeting PRKCH to Regulate p53/p21 Pathway. mir-24-3p 12-21 H3 histone pseudogene 16 Homo sapiens 124-127 34895043-9 2021 Lastly, the expression level of p21 and p53 was greatly elevated in chondrocytes by stimulation with TNF-alpha which was then pronouncedly repressed by treatment with Celecoxib. Celecoxib 167-176 H3 histone pseudogene 16 Homo sapiens 32-35 34288819-9 2021 Thirdly, Anagliptin dramatically reversed the upregulated p16, p21, and downregulated sirtuin1 (SIRT1) in IL-1beta-treated vascular smooth muscle cells. anagliptin 9-19 H3 histone pseudogene 16 Homo sapiens 63-66 33757397-4 2021 Our results suggested that aldosterone treatment increased the senescence and oxidative stress as evidenced by increased percent of SA-beta-Gal positive cells, reactive oxygen species level, expression of NADPH oxidase 4 (NOX4) rather than NOX2, and the up-regulation of p21 in cultured PTC. Aldosterone 27-38 H3 histone pseudogene 16 Homo sapiens 271-274 34663173-10 2021 Expressions of p16, p21, TXNIP, NLRP3, cleaved caspase-3 and cleaved caspase-1 in H2O2-treated HUVECs were inhibited by Gen, while the inhibition as such was partially reversed by overexpressed TXNIP. Hydrogen Peroxide 82-86 H3 histone pseudogene 16 Homo sapiens 20-23 34663173-10 2021 Expressions of p16, p21, TXNIP, NLRP3, cleaved caspase-3 and cleaved caspase-1 in H2O2-treated HUVECs were inhibited by Gen, while the inhibition as such was partially reversed by overexpressed TXNIP. Genistein 120-123 H3 histone pseudogene 16 Homo sapiens 20-23 34845672-9 2021 Enhanced MSC expansion with SB203580 therapy was associated with the lower expression of CDKIs like p15, p18, p19, p21, p27, and p57. SB 203580 28-36 H3 histone pseudogene 16 Homo sapiens 115-118 34853352-4 2021 H2O2 treated pre-adipocytes and adipocytes showed typical senescence-associated features including increased beta-galactosidase activity (SA-ss-gal) and p21, activation of ROS and increased expression of pro-inflammatory cytokines. Hydrogen Peroxide 0-4 H3 histone pseudogene 16 Homo sapiens 153-156 34730462-0 2021 Polymorphisms of the AS3MT gene are associated with arsenic methylation capacity and damage to the P21 gene in arsenic trioxide plant workers. Arsenic Trioxide 111-127 H3 histone pseudogene 16 Homo sapiens 99-102 34730462-7 2021 In our study, we investigate whether polymorphisms of the AS3MT gene alter As methylation capacity and adversely affect the P21 gene in arsenic trioxide plant workers. Arsenic Trioxide 136-152 H3 histone pseudogene 16 Homo sapiens 124-127 34730462-10 2021 The results showed that DNA damage in P21 gene fragments was greater in those individuals exposed to high levels of As. Arsenic 116-118 H3 histone pseudogene 16 Homo sapiens 38-41 34730462-11 2021 There was a strong positive correlation between the DNA damage to P21 gene fragments and the percentage of MMA in urine. mma 107-110 H3 histone pseudogene 16 Homo sapiens 66-69 34730462-12 2021 However, DNA damage in P21 gene fragments was negatively associated with the percentage of DMA in urine (%uDMA), primary methylation index (PMI), and secondary methylation index. dma 91-94 H3 histone pseudogene 16 Homo sapiens 23-26 34730462-12 2021 However, DNA damage in P21 gene fragments was negatively associated with the percentage of DMA in urine (%uDMA), primary methylation index (PMI), and secondary methylation index. UDMA 106-110 H3 histone pseudogene 16 Homo sapiens 23-26 34827693-10 2021 VIP116 and combination treatment increased p53 levels with subsequent induction of p21, Bax and cleaved caspase 3. vip116 0-6 H3 histone pseudogene 16 Homo sapiens 83-86 34856488-5 2021 The results showed that endosulfan significantly promoted cell proliferation, accompanied with the decrease of p27 mRNA expression and the increase in the mRNA expression levels of p21 and inflammatory factors IL-6/IL-8. Endosulfan 24-34 H3 histone pseudogene 16 Homo sapiens 181-184 34887234-5 2021 The prediction was that treated water would result in increased cell proliferation, that more cells would enter the cell cycle growth phase, and that there would be increased expression of genes (NANOG, OCT4 and SOX2) associated with improved cell growth and decreased expression of genes (p16, p21, and p53) associated with a decline in cell growth. Water 32-37 H3 histone pseudogene 16 Homo sapiens 295-298 34607979-6 2021 Accordingly, the p27 and p21 promoter activities were enhanced while Bcl-2 and IL-6 activities were significantly reduced by metformin treatment. Metformin 125-134 H3 histone pseudogene 16 Homo sapiens 25-28 34795783-6 2021 Low-dose oridonin induced GC cell cycle arrest at G0/G1 and cell senescence by suppressing the c-Myc-AP4 pathway and enhancing p53-p21 signaling. oridonin 9-17 H3 histone pseudogene 16 Homo sapiens 131-134 34722233-0 2021 CircFAM114A2 Promotes Cisplatin Sensitivity via miR-222-3p/P27 and miR-146a-5p/P21 Cascades in Urothelial Carcinoma. Cisplatin 22-31 H3 histone pseudogene 16 Homo sapiens 79-82 34233525-5 2021 The expression of cyclin D1 in megestrol acetate treated cells was downregulated, while the expressions of p21 and p16 were upregulated via PR-B isoform. Megestrol Acetate 31-48 H3 histone pseudogene 16 Homo sapiens 107-110 34912912-12 2021 Moreover, kombucha increased the expression levels of p21, p53, and B-cell leukemia/lymphoma 2 (Bcl-2)-associated X protein genes (2, 2.5, and 1.5 fold, respectively) while it decreased Bcl-2 gene expression level (5-8 fold) compared with doxorubicin alone. Doxorubicin 239-250 H3 histone pseudogene 16 Homo sapiens 54-57 34680153-9 2021 The IDO inhibitor 1-DL-methyl-tryptophan ameliorated the DDR; decreased p21, p16, and SA-beta-Gal activity; restored cell proliferation; and decreased IL-6 production. 1-dl-methyl-tryptophan 18-40 H3 histone pseudogene 16 Homo sapiens 72-75 34270989-6 2021 Consistent with the in vivo findings, high glucose induced endothelial senescence, impaired endothelial function and elevated DDR1 expression, accompanied by the elevation of senescence-related genes p53 and p21 expression, and these effects were reversed by DDR1 siRNA. Glucose 43-50 H3 histone pseudogene 16 Homo sapiens 208-211 34680118-7 2021 The phenolic acid induced modifications in levels of HO-1, non-proteic thiol groups, gamma-glutamylcysteine synthetase, reactive oxygen species, and p21. phenolic acid 4-17 H3 histone pseudogene 16 Homo sapiens 149-152 34680118-0 2021 Protocatechuic Acid, a Simple Plant Secondary Metabolite, Induced Apoptosis by Promoting Oxidative Stress through HO-1 Downregulation and p21 Upregulation in Colon Cancer Cells. protocatechuic acid 0-19 H3 histone pseudogene 16 Homo sapiens 138-141 34270989-9 2021 In conclusion, our data demonstrated that miR-199a-3p/DDR1/p53/p21 signaling pathway was involved in endothelial senescence under diabetic conditions, and therapeutic targeting DDR1 would be exploited to inhibit endothelial senescence owing to high glucose exposure. Glucose 249-256 H3 histone pseudogene 16 Homo sapiens 63-66 34303663-6 2021 Pimozide induced G1 cell cycle arrest concomitant with the upregulation of p21/p27/p53, and suppression of cyclin D2/E, cyclin-dependent kinase 2/4/6 and c-Myc expression, and pRb phosphorylation. Pimozide 0-8 H3 histone pseudogene 16 Homo sapiens 75-78 34411980-11 2021 Combination studies revealed that both compounds had synergistic effects (combination index CI < 1) on Cis and Eto through induction of apoptosis (p53 activation and up-regulation of BAX and p21 gene expression). Etoposide 111-114 H3 histone pseudogene 16 Homo sapiens 191-194 34639072-8 2021 Violacein induced nuclear condensation, dissipated mitochondrial membrane potential (MMP), increased generation of reactive oxygen species (ROS), activated the caspase cascade, and upregulated p53 and p21. violacein 0-9 H3 histone pseudogene 16 Homo sapiens 201-204 34255251-7 2021 Real-time RT-PCR indicated that the co-administration of Schiff base oxovanadium complex 40 microg/ml and arsenic trioxide 0.001 microM could increase the expression of P53 and P21 genes by 3.76 +- 0.19 and 6.57 +- 1.29 fold change, respectively to the control sample. schiff base oxovanadium complex 57-88 H3 histone pseudogene 16 Homo sapiens 177-180 34255251-7 2021 Real-time RT-PCR indicated that the co-administration of Schiff base oxovanadium complex 40 microg/ml and arsenic trioxide 0.001 microM could increase the expression of P53 and P21 genes by 3.76 +- 0.19 and 6.57 +- 1.29 fold change, respectively to the control sample. Arsenic Trioxide 106-122 H3 histone pseudogene 16 Homo sapiens 177-180 34669117-10 2021 In addition, genistein upregulated Phospho-cdc2, Myt1, Cyclin A, Cyclin E2, p21 and Phospho-histone H3, but downregulated Phospho-wee1. Genistein 13-22 H3 histone pseudogene 16 Homo sapiens 76-79 34638959-4 2021 Moreover, Morusin significantly increased G1 arrest, attenuated the expression of cyclin D1, cyclin D3, cyclin E, cyclin-dependent kinase 2 (CDK2), cyclin-dependent kinase 4 (CDK4), and cyclin-dependent kinase 6 (CDK6) and upregulated p21 and p27 in Hep3B and Huh7 cells. morusin 10-17 H3 histone pseudogene 16 Homo sapiens 235-238 34504568-12 2021 Furthermore, C5aRA prevented DOX-induced cellular senescence and decreased the levels of positive SA-beta-gal staining in H9c2 and AC16 cardiomyocytes, in addition to downregulating the expression levels of p53, p16, p21 and IGFBP3. Doxorubicin 29-32 H3 histone pseudogene 16 Homo sapiens 217-220 34638895-10 2021 In addition, BCP induced apoptosis through downregulation of HSP60, HTRA, survivin, and XIAP, along with the upregulation of p21 expressions. caryophyllene 13-16 H3 histone pseudogene 16 Homo sapiens 125-128 34284139-4 2021 IGFBP3 knockdown in MESCs committed to H2O2-induced senescence led to partial abrogation of p21/Rb axis, to elevated ERK phosphorylation and to increase in SA-beta-gal activity. Hydrogen Peroxide 39-43 H3 histone pseudogene 16 Homo sapiens 92-95 34698060-5 2021 The markers for apoptosis (Caspase3/9) and cell senescence (p21/p16), reported to be expressed in aged or resting phase follicles, were significantly reduced by D-panthenol. dexpanthenol 161-172 H3 histone pseudogene 16 Homo sapiens 60-63 34504274-4 2021 Treatment of cells with KS15 and SR8278 protected cells against the anti-proliferative effects of cisplatin and increased the expression of NER factor XPA and cell cycle regulators Wee1 and p21 at the mRNA and protein level. KS15 24-28 H3 histone pseudogene 16 Homo sapiens 190-193 34504274-4 2021 Treatment of cells with KS15 and SR8278 protected cells against the anti-proliferative effects of cisplatin and increased the expression of NER factor XPA and cell cycle regulators Wee1 and p21 at the mRNA and protein level. SR 8278 33-39 H3 histone pseudogene 16 Homo sapiens 190-193 34816661-9 2021 Inhibition of miR-670-5p decreased MMP-2 protein expression (P<0.05), increased P21 and E-cadherin expressions (P<0.05), and inhibited proliferation, migration and invasion of A549 cells (P<0.05). mir-670-5p 14-24 H3 histone pseudogene 16 Homo sapiens 80-83 34647281-7 2021 Furthermore, D-galactose increased the mRNA expression of p16, p21, and p53. Galactose 13-24 H3 histone pseudogene 16 Homo sapiens 63-66 34659819-12 2021 Similarly, the miR-488-5p inhibitor induced the expression of P53 and P21 than normal control (NC) group in which miR-488-5p expression was normal, while P53 KD prevented the effects of the miR-488-5p inhibitor in KYSE-150 cells. mir-488-5p 15-25 H3 histone pseudogene 16 Homo sapiens 70-73 34659819-12 2021 Similarly, the miR-488-5p inhibitor induced the expression of P53 and P21 than normal control (NC) group in which miR-488-5p expression was normal, while P53 KD prevented the effects of the miR-488-5p inhibitor in KYSE-150 cells. mir-488 190-197 H3 histone pseudogene 16 Homo sapiens 70-73 34659819-12 2021 Similarly, the miR-488-5p inhibitor induced the expression of P53 and P21 than normal control (NC) group in which miR-488-5p expression was normal, while P53 KD prevented the effects of the miR-488-5p inhibitor in KYSE-150 cells. CHEMBL3740941 198-200 H3 histone pseudogene 16 Homo sapiens 70-73 34478011-6 2021 Among tested cells, NALM-6 cells had the highest sensitivity to Britannin, and this agent was able to induce p21/p27-mediated G1 cell cycle arrest and Reactive Oxygen Specious (ROS)-mediated apoptotic cell death in this cell line. britannin 64-73 H3 histone pseudogene 16 Homo sapiens 109-112 34074418-2 2021 Herein, we reported a low cost and sensitive SERS sensing platform for simultaneous p21 mRNA and miRNA-21 detection based on duplex-specific nuclease signal amplification (DSNSA) plus multifunctional Fe3O4@SiO2 magnetic nanoparticles (Fe3O4@SiO2 MNPs). ferryl iron 200-205 H3 histone pseudogene 16 Homo sapiens 84-87 34074418-2 2021 Herein, we reported a low cost and sensitive SERS sensing platform for simultaneous p21 mRNA and miRNA-21 detection based on duplex-specific nuclease signal amplification (DSNSA) plus multifunctional Fe3O4@SiO2 magnetic nanoparticles (Fe3O4@SiO2 MNPs). Silicon Dioxide 206-210 H3 histone pseudogene 16 Homo sapiens 84-87 34074418-2 2021 Herein, we reported a low cost and sensitive SERS sensing platform for simultaneous p21 mRNA and miRNA-21 detection based on duplex-specific nuclease signal amplification (DSNSA) plus multifunctional Fe3O4@SiO2 magnetic nanoparticles (Fe3O4@SiO2 MNPs). ferryl iron 235-240 H3 histone pseudogene 16 Homo sapiens 84-87 34074418-5 2021 Under the assistance of the target p21 mRNA and miRNA-21, DNA (CP) of the DNA-RNA heteroduplexes could be specifically degraded by DSN and the SERS nanotags that were released from the surface of Fe3O4@SiO2 MNPs. ferryl iron 196-201 H3 histone pseudogene 16 Homo sapiens 35-38 34146926-7 2021 Delta9-THC and Delta8-THC also downregulated cyclin D1, p53, NOXA, PUMAalpha, and DRAM expressions but increased p21 and H2AX expression. Dronabinol 7-10 H3 histone pseudogene 16 Homo sapiens 113-116 34146926-7 2021 Delta9-THC and Delta8-THC also downregulated cyclin D1, p53, NOXA, PUMAalpha, and DRAM expressions but increased p21 and H2AX expression. Dronabinol 22-25 H3 histone pseudogene 16 Homo sapiens 113-116 34697742-5 2021 Phosphorylation of AMPKalpha, expression of p21 and replication of mtDNA was also promoted in MG-63 and U2-OS cells on treatment with IXNP. Magnesium 94-96 H3 histone pseudogene 16 Homo sapiens 44-47 34697742-5 2021 Phosphorylation of AMPKalpha, expression of p21 and replication of mtDNA was also promoted in MG-63 and U2-OS cells on treatment with IXNP. ixnp 134-138 H3 histone pseudogene 16 Homo sapiens 44-47 34298093-7 2021 Heme-iron induced lipid peroxidation and DNA oxidation by interacting with Nox4-independent mechanisms, promoting p53/p21 activity and cellular senescence. Heme 0-4 H3 histone pseudogene 16 Homo sapiens 118-121 34298093-7 2021 Heme-iron induced lipid peroxidation and DNA oxidation by interacting with Nox4-independent mechanisms, promoting p53/p21 activity and cellular senescence. Iron 5-9 H3 histone pseudogene 16 Homo sapiens 118-121 34353903-2 2021 Previous studies of human cells indicated that acute depletion of Ki-67 can elicit a delay at the G1/S boundary of the cell cycle, dependent on induction of the checkpoint protein p21. ki-67 66-71 H3 histone pseudogene 16 Homo sapiens 180-183 34540000-0 2021 Icaritin induces cellular senescence by accumulating the ROS production and regulation of the Jak2/Stat3/p21 pathway in imatinib-resistant, chronic myeloid leukemia cells. icaritin 0-8 H3 histone pseudogene 16 Homo sapiens 105-108 34160250-4 2021 Introduction of BRD4 inhibitor AZD5153 to senescent epithelial cells reversed this effect and reduced SASP related inflammatory molecule release in TMNK-1 or EAhy926 as representative human endothelial cell line, when exposed to cell culture medium (CM) derived from A549 cells expressing SARS-CoV-2 spike protein, also exhibited a senescence phenotype with enhanced p16, p21, SA-beta-galactosidase expression, and triggered SASP pathways. AZD5153 31-38 H3 histone pseudogene 16 Homo sapiens 372-375 34436310-0 2021 Largazole Inhibits Ocular Angiogenesis by Modulating the Expression of VEGFR2 and p21. largazole 0-9 H3 histone pseudogene 16 Homo sapiens 82-85 34436310-8 2021 Mechanistically, Largazole strongly inhibits the expression of VEGFR2 and leads to an increased expression of cell cycle inhibitor, p21. largazole 17-26 H3 histone pseudogene 16 Homo sapiens 132-135 34540000-8 2021 The results showed that icaritin inhibited cell growth and induced cell senescence in imatinib-resistant CML cells, which is associated with the regulation of the JAK2/STAT3/P21 axis and accompanied by the accumulation of ROS. icaritin 24-32 H3 histone pseudogene 16 Homo sapiens 174-177 34540000-8 2021 The results showed that icaritin inhibited cell growth and induced cell senescence in imatinib-resistant CML cells, which is associated with the regulation of the JAK2/STAT3/P21 axis and accompanied by the accumulation of ROS. Imatinib Mesylate 86-94 H3 histone pseudogene 16 Homo sapiens 174-177 34364983-10 2022 In addition, EZH2 was highly enriched in the promoter region of p21, and knockdown of p21 expression could rescue the effect of miR-144-3p on SMC proliferation and apoptosis. mir-144-3p 128-138 H3 histone pseudogene 16 Homo sapiens 64-67 34364983-10 2022 In addition, EZH2 was highly enriched in the promoter region of p21, and knockdown of p21 expression could rescue the effect of miR-144-3p on SMC proliferation and apoptosis. mir-144-3p 128-138 H3 histone pseudogene 16 Homo sapiens 86-89 34344977-6 2021 Our results showed an increase of both p16 and p21 mRNA restricted to the infarct area in the tMCAo brain. tmcao 94-99 H3 histone pseudogene 16 Homo sapiens 47-50 34296537-12 2021 It was also found that Ramelteon reduced the expressions of p21 and p53. ramelteon 23-32 H3 histone pseudogene 16 Homo sapiens 60-63 34294987-5 2021 The initial relaxation time of T21 was decreased significantly (P < 0.05), and the peak ration of P21 was increased significantly (P < 0.05) when treated at 200 and 300 MPa, that indicated the water was bound tightly and the ratio of immobilized water was increased. Water 193-198 H3 histone pseudogene 16 Homo sapiens 98-101 34190396-3 2021 The results confirmed that hepatocyte senescence occurred in HFD-fed Golden hamsters and PA-treated LO2 cells as manifested by increased levels of senescence marker SA-beta-gal, p16 and p21, heterochromatin marker H3K9me3, DNA damage marker gamma-H2AX and decreased activity of telomerase. Protactinium 89-91 H3 histone pseudogene 16 Homo sapiens 186-189 34164906-6 2021 In metformin-treated cells, MALAT1 knock-down increased the Bax/Bcl2 ratio and enhanced p21 but decreased cyclin B1 expression. Metformin 3-12 H3 histone pseudogene 16 Homo sapiens 88-91 34294987-5 2021 The initial relaxation time of T21 was decreased significantly (P < 0.05), and the peak ration of P21 was increased significantly (P < 0.05) when treated at 200 and 300 MPa, that indicated the water was bound tightly and the ratio of immobilized water was increased. Water 246-251 H3 histone pseudogene 16 Homo sapiens 98-101 34367464-10 2021 In conclusion, we provide mechanistic evidence that AOPPs may induce cell cycle arrest in granulosa cells via the ROS-JNK/p38 MAPK-p21 pathway and thus may be a novel biomarker of POI. Reactive Oxygen Species 114-117 H3 histone pseudogene 16 Homo sapiens 131-134 34316328-8 2021 Both H727 and H720 cells were associated with induction of apoptosis, upregulation of the p21 cell cycle inhibitor, and downregulation of the PI3K/Akt/mTOR pathway, suggesting that the PI3K/Akt/mTOR pathway is a primary target of the AZ+SFN combination therapy. Acetazolamide 234-236 H3 histone pseudogene 16 Homo sapiens 90-93 34285189-17 2021 Taken together, p21-mediated premature senescence might be used by tumor cells to escape from CIR-induced cytotoxicity, at least for a time. Citrulline 94-97 H3 histone pseudogene 16 Homo sapiens 16-19 34405017-0 2021 HOTAIR promotes gefitinib resistance through modification of EZH2 and silencing p16 and p21 in non-small cell lung cancer. Gefitinib 16-25 H3 histone pseudogene 16 Homo sapiens 88-91 34405020-8 2021 5-Aza also increased p53 and p21 transcription through promoter demethylation, and decreased the expression of oncogene c-Myc in 22RV1 and LNCaP cells. Azacitidine 0-5 H3 histone pseudogene 16 Homo sapiens 29-32 34405020-11 2021 Thus, in responsible for its apoptotic induction and DNA damage, the mechanism of the antitumor activities of 5-Aza may involve in an increase of tumor suppressive maspin, upregulation of wild type p53-mediated p21 expression and a decrease of oncogene c-Myc level in 22RV1 and LNCaP cells, and enhancing the tumor suppressive maspin expression in DU145 cells. Azacitidine 110-115 H3 histone pseudogene 16 Homo sapiens 211-214 34704055-3 2021 Here, we present studies on short analogues of p21 peptides (143-151) conformationally constrained with a covalent linker between i, i + 4 separated cysteine residues at positions 145 and 149 to access peptidomimetics that target PCNA. Peptides 51-59 H3 histone pseudogene 16 Homo sapiens 47-50 34230134-8 2021 Induction of p21, and caspase-3, -8, and -9 cleavages, while down-regulation of cyclin B1 and cyclin D1 were observed in TOFA-treated cells. 5-(tetradecyloxy)-2-furancarboxylic acid 121-125 H3 histone pseudogene 16 Homo sapiens 13-16 34298945-6 2021 D-Gal treatment significantly increased the expression levels of senescence markers, such as p53 and p21, in the heart and hippocampal tissues, while this effect was reversed in the Lico D-treated animals. Galactose 0-5 H3 histone pseudogene 16 Homo sapiens 101-104 34277403-1 2021 Our previous studies have demonstrated that Enzalutamide-induced upregulation of long non-coding RNA p21 (lncRNA-p21) facilitates prostate cancer (PCa) neuroendocrine differentiation (NED). enzalutamide 44-56 H3 histone pseudogene 16 Homo sapiens 101-104 34105888-10 2021 Mechanistically, LINC00525 epigenetically suppressed p21 transcription by guiding Enhancer Of Zeste 2 Polycomb Repressive Complex 2 Subunit (EZH2) to the p21 promoter through an formation of RNA-DNA triplex with the p21 promoter, leading to increased trimethylation of lysine 27 on histone 3 (H3K27me3) of the p21 promoter. Lysine 269-275 H3 histone pseudogene 16 Homo sapiens 53-56 34105888-10 2021 Mechanistically, LINC00525 epigenetically suppressed p21 transcription by guiding Enhancer Of Zeste 2 Polycomb Repressive Complex 2 Subunit (EZH2) to the p21 promoter through an formation of RNA-DNA triplex with the p21 promoter, leading to increased trimethylation of lysine 27 on histone 3 (H3K27me3) of the p21 promoter. Lysine 269-275 H3 histone pseudogene 16 Homo sapiens 154-157 34105888-10 2021 Mechanistically, LINC00525 epigenetically suppressed p21 transcription by guiding Enhancer Of Zeste 2 Polycomb Repressive Complex 2 Subunit (EZH2) to the p21 promoter through an formation of RNA-DNA triplex with the p21 promoter, leading to increased trimethylation of lysine 27 on histone 3 (H3K27me3) of the p21 promoter. Lysine 269-275 H3 histone pseudogene 16 Homo sapiens 216-219 34105888-10 2021 Mechanistically, LINC00525 epigenetically suppressed p21 transcription by guiding Enhancer Of Zeste 2 Polycomb Repressive Complex 2 Subunit (EZH2) to the p21 promoter through an formation of RNA-DNA triplex with the p21 promoter, leading to increased trimethylation of lysine 27 on histone 3 (H3K27me3) of the p21 promoter. Lysine 269-275 H3 histone pseudogene 16 Homo sapiens 310-313 34196654-8 2021 Cell experiments further confirmed that H2 could reverse MNU damage to CECs by decreasing oxidative stress injury, interfering with the NF-kappaB/NLRP3 pathway and the FOXO3a/p53/p21 pathway. Deuterium 40-42 H3 histone pseudogene 16 Homo sapiens 179-182 34196654-8 2021 Cell experiments further confirmed that H2 could reverse MNU damage to CECs by decreasing oxidative stress injury, interfering with the NF-kappaB/NLRP3 pathway and the FOXO3a/p53/p21 pathway. Methylnitrosourea 57-60 H3 histone pseudogene 16 Homo sapiens 179-182 34386269-7 2021 In addition, GA arrested cell cycle at the S or G2 phase via p53-p21-Cdc2-cyclin B pathway in the same cells. Gallic Acid 13-15 H3 histone pseudogene 16 Homo sapiens 65-68 34251962-7 2021 Under TMZ treatment, JARID2 overexpression inhibited CCND1 expression, promoted glioma cell apoptosis, and increased p21, cleaved-PARP, and cleaved-caspase3 in glioma cells treated with TMZ; meanwhile, CCND1 overexpression exerted opposite effects on glioma cells treated with TMZ and partially reversed the effects of JARID2 overexpression. Temozolomide 6-9 H3 histone pseudogene 16 Homo sapiens 117-120 34251962-7 2021 Under TMZ treatment, JARID2 overexpression inhibited CCND1 expression, promoted glioma cell apoptosis, and increased p21, cleaved-PARP, and cleaved-caspase3 in glioma cells treated with TMZ; meanwhile, CCND1 overexpression exerted opposite effects on glioma cells treated with TMZ and partially reversed the effects of JARID2 overexpression. Temozolomide 186-189 H3 histone pseudogene 16 Homo sapiens 117-120 34060394-4 2022 Our results also showed that Britannin decreased the proliferation of MOLT-4 cells by preventing the transition of the cells from the S phase of the cell cycle through the up-regulation of p21 and p27. britannin 29-38 H3 histone pseudogene 16 Homo sapiens 189-192 34069970-5 2021 We also found that delta-catenin could regulate the interaction between AKT and p21, leading to phosphorylation of p21 at Thr-145 residue. Threonine 122-125 H3 histone pseudogene 16 Homo sapiens 80-83 34069970-5 2021 We also found that delta-catenin could regulate the interaction between AKT and p21, leading to phosphorylation of p21 at Thr-145 residue. Threonine 122-125 H3 histone pseudogene 16 Homo sapiens 115-118 34136185-6 2021 Furthermore, PPa extract caused the accumulation of a population of cells at G0/G1 phase via a reduction in p-Rb, increasing p21 expression, and downregulating cell cycle regulator protein expression. ppa 13-16 H3 histone pseudogene 16 Homo sapiens 125-128 34195076-5 2021 Mechanistic studies revealed that FCL-induced G1 phase cell-cycle arrest in ESCC which is dependent on p21 and p27. fangchinoline 34-37 H3 histone pseudogene 16 Homo sapiens 103-106 34063233-0 2021 The Impact of Chlorambucil and Valproic Acid on Cell Viability, Apoptosis and Expression of p21, HDM2, BCL2 and MCL1 Genes in Chronic Lymphocytic Leukemia. Valproic Acid 31-44 H3 histone pseudogene 16 Homo sapiens 92-95 34063233-5 2021 Under the treatment with the drug combination, the expression of p21 gene was visibly higher than under the treatment with CLB alone. Chlorambucil 123-126 H3 histone pseudogene 16 Homo sapiens 65-68 34602402-5 2021 The docetaxel with radiation group obtained a higher expression of p21 and bax protein than the docetaxel group and the radiation group (P<0.05), and a higher ratio of bcl-2/bax than the others (P<0.05). Docetaxel 4-13 H3 histone pseudogene 16 Homo sapiens 67-70 34749615-4 2021 RSV is thought to have an impressive outcome in colorectal cancer (CRC) treatment through the vital molecules and cancer signaling pathways, including SIRT1, P53, P21, AMPK, ROS, BMP7, COX-2, NO, Caspases, Wnt, TNFs, NF-kappaB, EMT, and pentose phosphate pathway. Resveratrol 0-3 H3 histone pseudogene 16 Homo sapiens 163-166 34435054-11 2021 In Skov3 cells, the expression levels of p53 and p21 were downregulated, while those of Cyclin E, vascular endothelial growth factor (VEGF), matrix metallopeptidase 2 (MMP2), MMP9, signal transducers and activators of transcription 3 (Stat3), and p-Stat3 were upregulated by ATZ treatment. Atrazine 275-278 H3 histone pseudogene 16 Homo sapiens 49-52 34602402-7 2021 p21, bax, bcl-2 and other related proteins can regulate cell cycle phase distribution and induce cell apoptosis, thereby increasing the radiosensitivity effect of docetaxel in ECA109 cell line. Docetaxel 163-172 H3 histone pseudogene 16 Homo sapiens 0-3 34141150-6 2021 Ursolic acid treatment downregulated the gene expression of survival factors BCL-2, SURVIVIN, NFKB and SP1, while upregulated the growth-restricting genes BAX, P21 and P53. ursolic acid 0-12 H3 histone pseudogene 16 Homo sapiens 160-163 35568224-6 2022 Expressions of genes responses to DNA damage, ATM, ATR, p53, p21, Bax, H2AX, and GADD45A were disturbed by NIT treatment. nitenpyram 107-110 H3 histone pseudogene 16 Homo sapiens 61-64 34137693-10 2021 In vitro, HCB increased PCNA, pSMAD 2/3, and TGF-beta1 protein levels and mRNA expression and decreased p21 and p27 protein levels. Hexachlorobenzene 10-13 H3 histone pseudogene 16 Homo sapiens 104-107 35489384-6 2022 In mechanism, KPT-8602 restored the localization of cytoplasmic FOXO3A, p27, p21, IkappaBalpha and PP2A into the nucleus, leading to AKT and NF-kappaB deactivation. Eltanexor 14-22 H3 histone pseudogene 16 Homo sapiens 77-80 35551917-6 2022 In human umbilical vein endothelial cells (HUVEC) cultures, Doxo (10-100 nM) increased the number of SA-beta-gal positive cells and the levels of gammaH2AX, p21 and p53, used as markers of senescence. Doxorubicin 60-64 H3 histone pseudogene 16 Homo sapiens 157-160 35405615-11 2022 Capsaicin upregulated SIRT1 expression and downregulated the senescence marker, p21, thereby protecting endothelial cells from IHG-induced senescence as indicated by relieved G0/G1 phase arrest, improved cell viabilities, and reduced counts of senescent cells and ROS production. Capsaicin 0-9 H3 histone pseudogene 16 Homo sapiens 80-83 35489818-0 2022 Corrigendum to "PEG-4000 formed polymeric nanoparticles loaded with cetuximab downregulate p21 & stathmin-1 gene expression in cancer cell lines" (Life Sci. Polyethylene Glycols 16-19 H3 histone pseudogene 16 Homo sapiens 91-94 35324521-7 2022 Interestingly, DHMBA increased the levels of cancer suppressor p53, p21, Rb, and regucalcin. 3,5-dihydroxy-4-methoxybenzyl alcohol 15-20 H3 histone pseudogene 16 Homo sapiens 68-71 35546176-5 2022 The levels of cellular senescence-associated p53 and p21 significantly increased in H2O2-induced senescent House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and cochlear explants. Hydrogen Peroxide 84-88 H3 histone pseudogene 16 Homo sapiens 53-56 35570522-11 2022 Additionally, the treatment of endometrial cancer with compound 968 downregulated the expression of GLS1 and cyclin D1, and upregulated the expression of P21 and E-cadherin. compound 968 55-67 H3 histone pseudogene 16 Homo sapiens 154-157 35546176-7 2022 UA significantly decreased the expression of senescence-associated p53 and p21, and increased the expression of mitophagy-related proteins, in H2O2-induced senescent cells and cochlear explants. 3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one 0-2 H3 histone pseudogene 16 Homo sapiens 75-78 35221291-13 2022 Our study confirms the protective role of RES as an anti-ROS agent and its ability to alleviate DNA damage through a pathway involving p53/p21 signaling. Resveratrol 42-45 H3 histone pseudogene 16 Homo sapiens 139-142 35421264-10 2022 MiR-26a-5p upregulation suppressed the NPC cell proliferation, migration, invasion, angiogenesis, N-cadherin and EZH2 expression, while it elevated apoptosis and p21, p27 and E-cadherin expressions, whereas miR-26a-5p downregulation performed conversely. mir-26a-5p 0-10 H3 histone pseudogene 16 Homo sapiens 162-165 35500745-5 2022 PRMT5 and symmetric dimethylation at histone H4 arginine 3 (H4R3me2s) directly associate with chromatin of P21 to suppress its transcription. Arginine 48-56 H3 histone pseudogene 16 Homo sapiens 107-110 35245520-3 2022 KEY FINDINGS: TQ monotherapy had greater anticancer effects to active VD3 or 5-FU, revealing higher expression of p21/p27/PTEN/BAX/Cyto-C/Casp-3 and increased levels of total glutathione, with inhibitions in CCND1/CCND3/BCL-2 and PI3K/AKT/mTOR molecules, alongside higher rates of apoptosis in HT29, SW480 and SW620 cells (P < 0.005 for all markers). Fluorouracil 77-81 H3 histone pseudogene 16 Homo sapiens 114-117 35398238-8 2022 In addition, ATA treatment increased the levels of p53 and p21 proteins, which blocked cell cycle progression in the G1/S phase. acetyltanshinone IIA 13-16 H3 histone pseudogene 16 Homo sapiens 59-62 35563820-11 2022 Each treatment initiated a stable growth arrest, enhanced SA-beta-gal activity, and-except palbociclib-increased the expression of p21. palbociclib 91-102 H3 histone pseudogene 16 Homo sapiens 131-134 35176277-0 2022 PEG-4000 formed polymeric nanoparticles loaded with cetuximab downregulate p21 &stathmin-1 gene expression in cancer cell lines. polyethylene glycol 4000 0-8 H3 histone pseudogene 16 Homo sapiens 75-78 35529455-9 2022 Moreover, TBs-C suppressed the PI3K/AKT/mTOR pathway activation, promoted autophagy, and increased the expression of p21 downstream of AKT, which resulted in G1 cell-cycle arrest. tbs-c 10-15 H3 histone pseudogene 16 Homo sapiens 117-120 35562984-8 2022 G2 phase arrest and apoptosis in VIC-fedratinib-co-treated cells resulted from the upregulation of p21 and the DNA damaging marker pH2AX. Vincristine 33-36 H3 histone pseudogene 16 Homo sapiens 99-102 35562984-8 2022 G2 phase arrest and apoptosis in VIC-fedratinib-co-treated cells resulted from the upregulation of p21 and the DNA damaging marker pH2AX. Fedratinib 37-47 H3 histone pseudogene 16 Homo sapiens 99-102 35176277-10 2022 The expression levels of p21 and stathmin-1 were significantly decreased in both cell lines treated with CTX-PEGNPs compared to CTX alone. ctx-pegnps 105-115 H3 histone pseudogene 16 Homo sapiens 25-28 35176277-12 2022 The results indicated that CTX-PEGNP was an improved formulation than CTX alone to induce apoptosis and DNA damage and inhibit cell proliferation through the downregulation of P21 and stathmin-1 expression. ctx-pegnp 27-36 H3 histone pseudogene 16 Homo sapiens 176-179 35219733-6 2022 RETRA-treated cells also displayed necroptotic morphology of disintegrated plasma membranes with intact nuclei and also showed cell cycle arrest at the S phase with the upregulation of p21 and downregulation of cyclin-D3. RETRA hydrochloride 0-5 H3 histone pseudogene 16 Homo sapiens 185-188 35404445-4 2022 Lastly, the inhibitory effects of ketorolac tromethamine on the activation of beta-galactosidase and the upregulation of p21 and p53 were greatly abolished by the overexpression of COX-2. Ketorolac Tromethamine 34-56 H3 histone pseudogene 16 Homo sapiens 121-124 35304440-9 2022 Taken together, our study reports a novel mechanism by which p21 can be stabilized by CMTM6 and pinpoints a crucial role of the CMTM6-p21 axis in suppressing the progression of HCC and sensitizing patients with postoperative recurrence to TACE treatment. Chlorotrianisene 239-243 H3 histone pseudogene 16 Homo sapiens 61-64 35298792-9 2022 Phoenixin-14 resolved the morphine-caused cell cycle arrest with significant changes in the expression levels of p21, cyclin-dependent kinases 6 (CDK6), and p-Rb. phoenixin-14 0-12 H3 histone pseudogene 16 Homo sapiens 113-116 35298792-9 2022 Phoenixin-14 resolved the morphine-caused cell cycle arrest with significant changes in the expression levels of p21, cyclin-dependent kinases 6 (CDK6), and p-Rb. Morphine 26-34 H3 histone pseudogene 16 Homo sapiens 113-116 35432205-16 2022 Importantly, in immune-deficient mice transplanted with fat from obese patients, dasatinib plus quercetin, a senolytic cocktail that reduces the number of both p21 high and p16 high cells, improves both glucose tolerance and insulin resistance. Dasatinib 81-90 H3 histone pseudogene 16 Homo sapiens 160-163 35432205-16 2022 Importantly, in immune-deficient mice transplanted with fat from obese patients, dasatinib plus quercetin, a senolytic cocktail that reduces the number of both p21 high and p16 high cells, improves both glucose tolerance and insulin resistance. Quercetin 96-105 H3 histone pseudogene 16 Homo sapiens 160-163 35354250-5 2022 Mechanismly, PFKFB3 facilitated pro-apoptotic transcription factor FOXO3A and its downstream gene expressions, including p21, p27, FAS after 5FU treatment in vitro. Fluorouracil 141-144 H3 histone pseudogene 16 Homo sapiens 121-124 35356984-5 2022 Moreover, MSX2 knockdown suppressed the transcription of NOP2/Sun domain family member 2 (NSUN2), which regulates the expression of p21 by binding to and causing the 5-methylcytidine methylation of the 3"- untranslated region of p21 mRNA. 5-methylcytidine 166-182 H3 histone pseudogene 16 Homo sapiens 132-135 35356984-5 2022 Moreover, MSX2 knockdown suppressed the transcription of NOP2/Sun domain family member 2 (NSUN2), which regulates the expression of p21 by binding to and causing the 5-methylcytidine methylation of the 3"- untranslated region of p21 mRNA. 5-methylcytidine 166-182 H3 histone pseudogene 16 Homo sapiens 229-232 35388306-4 2022 The experiment found that Rg1 plays an antiaging role in reversing the SA-beta-gal staining associated with LiCl-induced hematopoietic stem cell senescence, the increase in p53 and p21 proteins, and sustained DNA damage. Lithium Chloride 108-112 H3 histone pseudogene 16 Homo sapiens 181-184 35085768-9 2022 Moreover, propofol increases the expression of P21, decreases the expression of c-Myc and GSTM3 through elevating GAS5 expression. Propofol 10-18 H3 histone pseudogene 16 Homo sapiens 47-50 35085768-11 2022 One possible mechanism involved was preliminary revealed: propofol up-regulates the expression of GAS5, thus stimulating P21 pathway, blocking c-Myc and GSTM3 pathways. Propofol 58-66 H3 histone pseudogene 16 Homo sapiens 121-124 35304440-9 2022 Taken together, our study reports a novel mechanism by which p21 can be stabilized by CMTM6 and pinpoints a crucial role of the CMTM6-p21 axis in suppressing the progression of HCC and sensitizing patients with postoperative recurrence to TACE treatment. Chlorotrianisene 239-243 H3 histone pseudogene 16 Homo sapiens 134-137 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 H3 histone pseudogene 16 Homo sapiens 203-206 35356282-14 2022 Pre-treatment with rapamycin or PFT-alpha significantly down-regulated the levels of SA beta-Gal, SAHF, p-p53, p21, autophagy related protein p62, the percentage of cells in the G0/G1 phase, and significantly up-regulated DeltaPsim, autophagy related protein BECN1, autophagosomes and autolysosomes compared with cells only treated with AOPPs. Sirolimus 19-28 H3 histone pseudogene 16 Homo sapiens 111-114 35371279-10 2022 HDAC3 is indirectly involved in the cGMP-PKG signaling pathway, thereby indirectly regulating the expression levels of p53 and p21 genes in patients with LAML. Cyclic GMP 36-40 H3 histone pseudogene 16 Homo sapiens 127-130 35356282-14 2022 Pre-treatment with rapamycin or PFT-alpha significantly down-regulated the levels of SA beta-Gal, SAHF, p-p53, p21, autophagy related protein p62, the percentage of cells in the G0/G1 phase, and significantly up-regulated DeltaPsim, autophagy related protein BECN1, autophagosomes and autolysosomes compared with cells only treated with AOPPs. pifithrin 32-41 H3 histone pseudogene 16 Homo sapiens 111-114 35184641-6 2022 Butorphanol tartrate prevented TNF-alpha-caused cell cycle arrest in the G0/G1 phase in HC-A cells and decreased p21 expression. Butorphanol 0-20 H3 histone pseudogene 16 Homo sapiens 113-116 35085581-0 2022 Piperlongumine induces ROS mediated apoptosis by transcriptional regulation of SMAD4/P21/P53 genes and synergizes with doxorubicin in osteosarcoma cells. piperlonguminine 0-14 H3 histone pseudogene 16 Homo sapiens 85-88 35111249-13 2022 Concurrent inhibition of CD44v9 and Nrf2 may trigger apoptosis induction, potentiate chemosensitivity and enhance antitumor activities through the ROS-activated p38/p21 pathway. Reactive Oxygen Species 147-150 H3 histone pseudogene 16 Homo sapiens 165-168 35227162-0 2022 The role of p53 and p21 on 8-chloro-adenosine-induced cellular response. Adenosine 36-45 H3 histone pseudogene 16 Homo sapiens 20-23 35227162-4 2022 Following 30 microM 8-Cl-Ado treatment, RNA synthesis was inhibited, p53 protein was stabilized, and p21 expression was activated. 8-chloroadenosine 20-28 H3 histone pseudogene 16 Homo sapiens 101-104 35085581-0 2022 Piperlongumine induces ROS mediated apoptosis by transcriptional regulation of SMAD4/P21/P53 genes and synergizes with doxorubicin in osteosarcoma cells. Reactive Oxygen Species 23-26 H3 histone pseudogene 16 Homo sapiens 85-88 35085581-7 2022 Piperlongumine treatment significantly upregulated the expression of genes BAX, P21, P53, and SMAD4; while the BCL-2, SURVIVIN, TNFA, and NFKB genes expression was found down-regulated. piperlonguminine 0-14 H3 histone pseudogene 16 Homo sapiens 80-83 35105283-4 2022 Furthermore, aging-related marker molecules (such as p16 and p21) were also significantly down-regulated under uridine treatment. Uridine 111-118 H3 histone pseudogene 16 Homo sapiens 61-64 35204761-0 2022 Correlation of Occupational Exposure to Carcinogenic Polycyclic Aromatic Hydrocarbons (cPAHs) and Blood Levels of p53 and p21 Proteins. Polycyclic Aromatic Hydrocarbons 53-85 H3 histone pseudogene 16 Homo sapiens 122-125 35204761-0 2022 Correlation of Occupational Exposure to Carcinogenic Polycyclic Aromatic Hydrocarbons (cPAHs) and Blood Levels of p53 and p21 Proteins. cpahs 87-92 H3 histone pseudogene 16 Homo sapiens 122-125 34985067-8 2022 In the presence of p21 mRNA, the Cy5-modified recognition nucleic acid specifically bound to p21 mRNA to form a more stable double chain and escaped from the gold sphere, leading to the recovery of red fluorescence. cyanine dye 5 33-36 H3 histone pseudogene 16 Homo sapiens 19-22 34985067-8 2022 In the presence of p21 mRNA, the Cy5-modified recognition nucleic acid specifically bound to p21 mRNA to form a more stable double chain and escaped from the gold sphere, leading to the recovery of red fluorescence. cyanine dye 5 33-36 H3 histone pseudogene 16 Homo sapiens 93-96 34985067-10 2022 Particularly, the sticky-flare probe used in this assay could allow the visual evaluation of the tumor treatment effect and the determination of the tumor progression stage by enabling monitoring of the relative expression level of p21 mRNA in tumor cells after cisplatin treatment. Cisplatin 262-271 H3 histone pseudogene 16 Homo sapiens 232-235 35064206-8 2022 These findings indicate that alphaalpha-syn is a functional tumor suppressor that can inhibit the proliferation of BCa cells by activating the p53/p21 signaling pathway. -syn 39-43 H3 histone pseudogene 16 Homo sapiens 147-150 34986369-9 2022 Increased SA-betagal staining and p16 and p21 expression was observed after DOX- or H2O2-induced senescence and mini Cry significantly decreased senescence-positive cells. Doxorubicin 76-79 H3 histone pseudogene 16 Homo sapiens 42-45 34986369-9 2022 Increased SA-betagal staining and p16 and p21 expression was observed after DOX- or H2O2-induced senescence and mini Cry significantly decreased senescence-positive cells. Hydrogen Peroxide 84-88 H3 histone pseudogene 16 Homo sapiens 42-45 35042627-0 2022 The involvement of ERK1/2 and p38 MAPK in the premature senescence of melanocytes induced by H2O2 through a p53-independent p21 pathway. Hydrogen Peroxide 93-97 H3 histone pseudogene 16 Homo sapiens 124-127 35042627-9 2022 H2O2 treatment tended to induce premature senescence in melanocytes through a p53-independent p21 pathway. Hydrogen Peroxide 0-4 H3 histone pseudogene 16 Homo sapiens 94-97 35141433-9 2022 Melatonin suppressed cell proliferation in the G2/M phase of the cell cycle (34.97 +- 0.92%) and induced apoptosis (12.43 +- 0.73%) through up-regulating p21 and p53 that was confirmed by the reduction of PCNA and Ki-67 expressions. Melatonin 0-9 H3 histone pseudogene 16 Homo sapiens 154-157 35155257-8 2022 Mechanistically, pevonedistat treatment and the siRNA knockdown neddylation pathway were able to remarkably induce the accumulation of Wee1, p27, and p21. pevonedistat 17-29 H3 histone pseudogene 16 Homo sapiens 150-153 35155257-10 2022 Conclusions: Our results showed that pevonedistat targeted the overexpression of the neddylation pathway in pancreatic cancer to induce cell growth suppression by inducing the accumulation of the cell cycle regulators Wee1, p27, and p21, which provides sound evidence for the clinical trial of pevonedistat for pancreatic cancer therapy. pevonedistat 37-49 H3 histone pseudogene 16 Homo sapiens 233-236 35127290-6 2022 Results: SA-beta-gal staining, PCR, and western blot revealed that aspirin could alleviate the cellular expression of senescence-related indicators of BM-MSCs, including a decrease of SA-beta-gal-positive cells and staining intensity, and downregulation of p16, p21, and p53 expression after aspirin treatment. Aspirin 67-74 H3 histone pseudogene 16 Homo sapiens 262-265 35042627-15 2022 CONCLUSION: H2O2 increases ROS levels, which activates the ERK1/2 and p38 MAPK pathways to induce the premature senescence of melanocytes through p21 via a p53-independent pathway and consequently disrupts melanosome transfer. Hydrogen Peroxide 12-16 H3 histone pseudogene 16 Homo sapiens 146-149 35042627-15 2022 CONCLUSION: H2O2 increases ROS levels, which activates the ERK1/2 and p38 MAPK pathways to induce the premature senescence of melanocytes through p21 via a p53-independent pathway and consequently disrupts melanosome transfer. ros 27-30 H3 histone pseudogene 16 Homo sapiens 146-149 35121394-0 2022 Andrographolide, a diterpene lactone from the Traditional Chinese Medicine Andrographis paniculate, induces senescence in human lung adenocarcinoma via p53/p21 and Skp2/p27. andrographolide 0-15 H3 histone pseudogene 16 Homo sapiens 156-159 35111765-9 2021 Moreover, the results showed that the delivery of si-02569 significantly alleviated the inflammatory response in the nucleus pulposus cells via inhibiting P65 phosphorylation and preventing its transfer into the nucleus, and meanwhile alleviated cell senescence by decreasing the expression of P21. si-02569 50-58 H3 histone pseudogene 16 Homo sapiens 294-297 35022897-10 2022 DUB-IN-1, an USP8 inhibitor, caused DNA damage, led to G2/M phase block by p53-p21 axis, and triggered apoptosis by regulating the p53 target proteins including Bax, Noxa, and Puma. DUBs-IN-1 0-8 H3 histone pseudogene 16 Homo sapiens 79-82 35022897-14 2022 DUB-IN-1 treatment led to G2/M cell cycle arrest by upregulating the protein level of p21 and triggered apoptosis by modulating the p53 target proteins including Bax, Noxa, and Puma. DUBs-IN-1 0-8 H3 histone pseudogene 16 Homo sapiens 86-89 35096810-6 2021 Moreover, combination of HAUS6 knockdown and 5-FU treatment further enhanced the suppression of cell proliferation of CRC cells by increasing activation of the p53/p21 pathway. Fluorouracil 45-49 H3 histone pseudogene 16 Homo sapiens 164-167 35173828-7 2022 In contrast, several tumor suppressor proteins (p21 and p53) have been reported to be downregulated by miR-24. mir-24 103-109 H3 histone pseudogene 16 Homo sapiens 48-51 35056723-8 2022 The molecular mechanism of action of low-dose 7HF in TNBC cells primarily involved G2/M-phase arrest through upregulation of the expression of Bub3, cyclin B1, phosphorylated Cdk1 (Tyr 15) and p53-independent p21. 7alpha-hydroxyfrullanolide 46-49 H3 histone pseudogene 16 Homo sapiens 209-212 34969758-9 2022 Treatment with eupatilin induced p21 expression but inhibited the expression of mutated p53. eupatilin 15-24 H3 histone pseudogene 16 Homo sapiens 33-36 35056691-6 2022 In addition, naringenin induced cell cycle arrest in osteosarcoma cells by inhibiting cyclin B1 and cyclin-dependent kinase 1 expression and upregulating p21 expression. naringenin 13-23 H3 histone pseudogene 16 Homo sapiens 154-157 34338241-2 2022 Here, we used ACPP to carry anti-p21Ras scFv for Ras-driven cancer therapy. acpp 14-18 H3 histone pseudogene 16 Homo sapiens 33-36 34338241-3 2022 The ACPP-p21Ras scFv fusion protein was prepared by a prokaryotic expression system and Ni-NTA column purification. ni-nta 88-94 H3 histone pseudogene 16 Homo sapiens 9-12 35125711-4 2022 Moreover, BKM120 robustly enhanced the growth-suppressive effect of imatinib through p21-mediated induction of G2/M cell cycle arrest and induction of apoptotic cell death. NVP-BKM120 10-16 H3 histone pseudogene 16 Homo sapiens 85-88 35125711-4 2022 Moreover, BKM120 robustly enhanced the growth-suppressive effect of imatinib through p21-mediated induction of G2/M cell cycle arrest and induction of apoptotic cell death. Imatinib Mesylate 68-76 H3 histone pseudogene 16 Homo sapiens 85-88 35591840-13 2022 The expression of p21 protein in MKN28 cells was markedly promoted on exposure to THDMF. 3,5,8-Trihydroxy-7,4'-dimethoxyflavone 82-87 H3 histone pseudogene 16 Homo sapiens 18-21 35053211-5 2022 Our studies evidenced that both DOX and GCD@DOX induced p53 and p21 signalling resulting in G0/G1 cell cycle arrest. Doxorubicin 32-35 H3 histone pseudogene 16 Homo sapiens 64-67