PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32098913-8 2020 We further identified Ser15, Thr18 and Ser20 of p53 are critical to the beta-actin: p53 interaction, which upon mutation into alanine abrogates the binding. Alanine 126-133 tumor protein p53 Homo sapiens 48-51 32098913-8 2020 We further identified Ser15, Thr18 and Ser20 of p53 are critical to the beta-actin: p53 interaction, which upon mutation into alanine abrogates the binding. Alanine 126-133 tumor protein p53 Homo sapiens 84-87 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 tumor protein p53 Homo sapiens 171-174 31592145-7 2019 We found 0.5 mmol/L of ALA and 3 J/cm2 of red light did not affect the vitality of cells, and could reduce UVB induced apoptosis, accelerate the clearance of CPDs, inhibit proliferation and activate p53. Alanine 23-26 tumor protein p53 Homo sapiens 199-202 27777309-5 2016 Remarkably, inhibition of Ser-314 phosphorylation either with Ser-to-Ala substitution or with a specific inhibitor of CDK4/6 kinase blocked Her4-induced stabilization of MDMX-MDM2 and rescued p53 activity. Alanine 69-72 tumor protein p53 Homo sapiens 192-195 23388716-6 2013 These results indicated that the mutations created by substitution of residues 443 to 448 for alanine (Sub19) impair repression of transcription of IFN-inducible genes, by the E1B, 55-kDa protein, consistent with their location in a segment required for repression of p53-dependent transcription. Alanine 94-101 tumor protein p53 Homo sapiens 268-271 23897481-7 2013 Pro184 makes a ring-to-ring interaction with Trp53 of Cul5, which is substituted by alanine in Cul2. Alanine 84-91 tumor protein p53 Homo sapiens 45-50 25244701-4 2014 Using the intrinsically disordered N-terminal region of the p53 protein as an experimental model, a set of proline (PRO) and alanine (ALA) to glycine (GLY) substitution variants were designed to modulate backbone conformational propensities without introducing non-native intramolecular interactions. Alanine 125-132 tumor protein p53 Homo sapiens 60-63 23667851-5 2013 Germline TP53 mutation c.566C>T results in the missense mutation GCC (Ala) to GTC (Val) at codon 189 (A189V) and has been reported in a case of multiple primary colon tumors. Alanine 73-76 tumor protein p53 Homo sapiens 9-13 20847049-8 2010 However, the double mutant p53(S215A/S269A) was transcriptionally inactive and more thermally unstable than either individual Ser-Ala loop mutant. Alanine 130-133 tumor protein p53 Homo sapiens 27-30 21737649-4 2011 In three mutant forms of p53--S15A, S20A and S46A--serine was converted to alanine at these sites to prevent phosphorylation, and in two other mutant forms, S15D and S20D, serine was converted to aspartic acid to mimic phosphorylation. Alanine 75-82 tumor protein p53 Homo sapiens 25-28 22862424-5 2013 Thus, the decrease of the expression of frataxin unregulated by p53 in tumor cells enhances ALA-induced photo-damage, by down-regulation of mitochondrial functions. Alanine 92-95 tumor protein p53 Homo sapiens 64-67 19331830-4 2009 Two human p14ARF residues (Ala(14) and Thr(31)) were found to destabilize the protein while two others (Val(24) and Ala(41)) promoted more efficient p53 stabilization and activation. Alanine 116-119 tumor protein p53 Homo sapiens 149-152 21103216-5 2010 Proline to alanine substitutions at P53, P481, P484, and P485 in the V42C background, as well as P53, P481, and P484 in the G489C background, exhibited decreased nucleotidase activities. Alanine 11-18 tumor protein p53 Homo sapiens 36-39 21103216-6 2010 More importantly, alanine substitutions at P53 and P481 in the V42C background and P481 in the G489C background no longer exhibited the ATP-induced decrease in transmembrane cross-linking efficiency. Alanine 18-25 tumor protein p53 Homo sapiens 43-46 19766654-6 2009 In fact, substitution of this Asn to Ala of CHC diminished its ability to interact with p53, leading to reduced activity to transactivate p53. Alanine 37-40 tumor protein p53 Homo sapiens 88-91 19766654-6 2009 In fact, substitution of this Asn to Ala of CHC diminished its ability to interact with p53, leading to reduced activity to transactivate p53. Alanine 37-40 tumor protein p53 Homo sapiens 138-141 19816404-7 2009 Blocking MDM2 phosphorylation by alanine substitution of all six phosphorylation sites results in constitutive degradation of p53 after DNA damage. Alanine 33-40 tumor protein p53 Homo sapiens 126-129 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 tumor protein p53 Homo sapiens 36-39 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 tumor protein p53 Homo sapiens 53-56 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 tumor protein p53 Homo sapiens 53-56 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 tumor protein p53 Homo sapiens 53-56 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 tumor protein p53 Homo sapiens 53-56 15946545-2 2005 METHODS: Plasmid containing mutant p53-GFP was constructed by site-directed mutagenesis by which 5 amino scid residues in the nuclear localization signal (NLS) were replaced by alanine to produce mutant p53KRKKK-GFP. Alanine 177-184 tumor protein p53 Homo sapiens 35-38 17467838-6 2007 In addition, alanine substitution at the residues Trp53, Glu55, and Arg56 in NS2B significantly reduced the cis- and trans-cleavage activities of the NS3 protease. Alanine 13-20 tumor protein p53 Homo sapiens 50-55 16940182-5 2006 Compared to the wild-type form, Chk2 with alanine substitutions at S19, S33, and S35 (Chk2(S3A)) showed impaired dimerization, defective auto- and trans-phosphorylation activities, and reduced ability to promote degradation of Hdmx, a phosphorylation target of Chk2 and regulator of p53 activity. Alanine 42-49 tumor protein p53 Homo sapiens 283-286 16457841-0 2006 Kinetic computational alanine scanning: application to p53 oligomerization. Alanine 22-29 tumor protein p53 Homo sapiens 55-58 16291740-5 2006 Mechanistically, we showed that conversion of a minimal four of these lysines to alanines but not arginines mimics p300-mediated p53 nuclear export, and these lysine-neutralizing mutations effectively prevent p53 tetramerization, thus exposing the oligomerization-regulated nuclear export signal. Alanine 81-89 tumor protein p53 Homo sapiens 129-132 16291740-5 2006 Mechanistically, we showed that conversion of a minimal four of these lysines to alanines but not arginines mimics p300-mediated p53 nuclear export, and these lysine-neutralizing mutations effectively prevent p53 tetramerization, thus exposing the oligomerization-regulated nuclear export signal. Alanine 81-89 tumor protein p53 Homo sapiens 209-212 15879716-7 2005 The alanine-replaced BAF53 mutants also stimulated p53-dependent transcription, in which the SWI/SNF and TRRAP complexes are involved. Alanine 4-11 tumor protein p53 Homo sapiens 51-54 14701864-1 2004 C-terminal truncation of ADAMTS-4 from the p68 form to the p53 form is required for activation of its capacity to cleave the Glu(373)-Ala(374) interglobular domain bond of aggrecan. Alanine 134-137 tumor protein p53 Homo sapiens 59-62 15364927-2 2004 Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction. Alanine 192-195 tumor protein p53 Homo sapiens 83-86 15364927-2 2004 Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction. Alanine 192-195 tumor protein p53 Homo sapiens 235-238 15381086-0 2004 Stabilization of alanine substituted p53 protein at Ser15, Thr18, and Ser20 in response to ionizing radiation. Alanine 17-24 tumor protein p53 Homo sapiens 37-40 15381086-2 2004 In the present study, we examined the X-ray-induced stabilization of Ala-substituted p53 protein at Ser15, Thr18, and Ser20, whose gene expression was controlled under an ecdyson-inducible promoter. Alanine 69-72 tumor protein p53 Homo sapiens 85-88 15381086-3 2004 We found that all single-, double-, or triple-Ala-substituted p53 at Ser15, Yhr18, and Ser20 were accumulated in the nucleus similarly to wild-type p53 after X-irradiation. Alanine 46-49 tumor protein p53 Homo sapiens 62-65 15116093-5 2004 MCF55a cells were established by transfection of full-length p53 carrying Thr55 mutation (Thr to Ala) into MCF7 cells. Alanine 97-100 tumor protein p53 Homo sapiens 61-64 15464845-7 2004 The over-expressed B1R protein induces the degradation of p53 in a concentration-dependent manner and is lost when Ser15 and Th18 are changed to alanine or when the B1R kinase is inactivated by introducing the K149Q substitution. Alanine 145-152 tumor protein p53 Homo sapiens 58-61 12706118-5 2003 We have found up-regulated levels of the cyclin-dependent kinase 2 (cdk2) protein in HDF expressing 143(ala) mutant p53 as compared to senescent controls, together with an increase in p21-free cdk2 which, in conjunction with cyclin E, is able to form an active kinase which can phosphorylate the retinoblastoma protein. Alanine 104-107 tumor protein p53 Homo sapiens 116-119 12167711-4 2002 Mutants with serine-to-alanine substitutions between residues 244 and 260 abolished or at least reduced the capacity of Mdm2 to promote p53 degradation. Alanine 23-30 tumor protein p53 Homo sapiens 136-139 12670900-0 2003 Fas-mediated apoptosis is dependent on wild-type p53 status in human cancer cells expressing a temperature-sensitive p53 mutant alanine-143. Alanine 128-135 tumor protein p53 Homo sapiens 117-120 12524418-1 2003 During a search for causative genes in patients with concurrent multiple primary colon tumours, we found a novel case with a germline mutation of the p53 gene, from GCC (Ala) to GTC (Val) at codon 189. Alanine 170-173 tumor protein p53 Homo sapiens 150-153 11971195-2 2002 In the present study, we showed that when lysine residues 372, 373, 381, and 382 of p53 were substituted with alanine, the resulting A4 protein was resistant to MDM2-mediated proteosomal degradation but was highly sensitive to human papillomavirus E6-mediated proteolysis. Alanine 110-117 tumor protein p53 Homo sapiens 84-87 11925449-7 2002 Introducing an Ala(19) mutation into the p53(F270A) protein abolished both RNA.MDM2 complex binding and hyper-ubiquitination in vivo, thus indicating that p53(F270A) protein hyper-ubiquitination depends upon MDM2 binding to its primary site in the BOX-I domain. Alanine 15-18 tumor protein p53 Homo sapiens 41-46 11925449-7 2002 Introducing an Ala(19) mutation into the p53(F270A) protein abolished both RNA.MDM2 complex binding and hyper-ubiquitination in vivo, thus indicating that p53(F270A) protein hyper-ubiquitination depends upon MDM2 binding to its primary site in the BOX-I domain. Alanine 15-18 tumor protein p53 Homo sapiens 155-160 11960383-3 2002 In this study, we demonstrated that p53 with lysine residues 372, 373, 381, and 382 mutated to alanine (the A4 mutant) retained the transactivation activity of wild-type p53, although the transactivation activity of p21 promoter by the A4 mutant was slightly reduced. Alanine 95-102 tumor protein p53 Homo sapiens 36-39 11960383-3 2002 In this study, we demonstrated that p53 with lysine residues 372, 373, 381, and 382 mutated to alanine (the A4 mutant) retained the transactivation activity of wild-type p53, although the transactivation activity of p21 promoter by the A4 mutant was slightly reduced. Alanine 95-102 tumor protein p53 Homo sapiens 170-173 11078726-5 2001 Transfection of the p53 gene with an alanine mutation at the Ser(315) site into Saos-2 cells gave rise to a form of p53 protein with a substantially reduced specific activity as a transcription factor. Alanine 37-44 tumor protein p53 Homo sapiens 20-23 11854596-7 2002 In addition, a new p53 mutation not previously reported in ET/pPNET involving exon 5 codon 138: GCC to GAC (Ala/Asp) was detected. Alanine 108-111 tumor protein p53 Homo sapiens 19-22 11805282-0 2002 Functional p53 chimeras containing the Epstein-Barr virus Gly-Ala repeat are protected from Mdm2- and HPV-E6-induced proteolysis. Alanine 62-65 tumor protein p53 Homo sapiens 11-14 11713288-6 2001 The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA). Alanine 319-327 tumor protein p53 Homo sapiens 26-29 11713288-6 2001 The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA). Alanine 319-327 tumor protein p53 Homo sapiens 126-129 11713288-6 2001 The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA). Alanine 319-327 tumor protein p53 Homo sapiens 126-129 11521201-4 2001 We observed that an unmodified C-terminus was required for the suppression of apoptosis by the p53 135(Ala to Val) oncogenic p53 mutant. Alanine 103-106 tumor protein p53 Homo sapiens 95-98 11521201-4 2001 We observed that an unmodified C-terminus was required for the suppression of apoptosis by the p53 135(Ala to Val) oncogenic p53 mutant. Alanine 103-106 tumor protein p53 Homo sapiens 125-128 11358908-11 2001 The distal portion of the duodenal tumour showed an additional point mutation in p53 gene at exon 5 (GCC (alanine)-->GTC (valine) at codon 129). Alanine 106-113 tumor protein p53 Homo sapiens 81-84 11078726-5 2001 Transfection of the p53 gene with an alanine mutation at the Ser(315) site into Saos-2 cells gave rise to a form of p53 protein with a substantially reduced specific activity as a transcription factor. Alanine 37-44 tumor protein p53 Homo sapiens 116-119 11483158-9 2001 Mutation of either serine 33 or serine 37 of p53 to alanine blocked the ability of GSK3beta to regulate p53 transcriptional activity. Alanine 52-59 tumor protein p53 Homo sapiens 45-48 11483158-9 2001 Mutation of either serine 33 or serine 37 of p53 to alanine blocked the ability of GSK3beta to regulate p53 transcriptional activity. Alanine 52-59 tumor protein p53 Homo sapiens 104-107 11080808-12 2000 In addition, mutation of p53 at Ser-15 and Ser-392 to alanines renders p53 resistant to Tax inhibition. Alanine 54-62 tumor protein p53 Homo sapiens 25-28 11016934-6 2000 Using a combination of alanine scanning, polymer blot analysis, and photoaffinity labeling, we have identified poly(ADP-ribose)-binding sites in the following proteins: p53, p21(CIP1/WAF1), xeroderma pigmentosum group A complementing protein, MSH6, DNA ligase III, XRCC1, DNA polymerase epsilon, DNA-PK(CS), Ku70, NF-kappaB, inducible nitric-oxide synthase, caspase-activated DNase, and telomerase. Alanine 23-30 tumor protein p53 Homo sapiens 169-172 11080808-12 2000 In addition, mutation of p53 at Ser-15 and Ser-392 to alanines renders p53 resistant to Tax inhibition. Alanine 54-62 tumor protein p53 Homo sapiens 71-74 10660538-4 2000 Contrary to bax, another known pro-apoptotic p53-target gene, both mouse and human FAS p53REs are still activated by the discriminatory p53 mutants Pro-175 and Ala-143, a class of mutants unable to induce apoptosis. Alanine 160-163 tumor protein p53 Homo sapiens 87-90 10884347-5 2000 An alanine mutation at any one of four key positions abrogates the efficacy of a synthetic peptide containing this motif as an inhibitor of cyclin A-cdk2 phosphorylation of p53 protein. Alanine 3-10 tumor protein p53 Homo sapiens 173-176 11033015-4 2000 For each of these mAbs we localized the epitope recognized on human p53 by the Spot method of multiple peptide synthesis, defined critical residues on p53 involved in the interaction by alanine scanning replacement experiments and determined kinetic parameters using real-time interaction analysis. Alanine 186-193 tumor protein p53 Homo sapiens 68-71 11033015-4 2000 For each of these mAbs we localized the epitope recognized on human p53 by the Spot method of multiple peptide synthesis, defined critical residues on p53 involved in the interaction by alanine scanning replacement experiments and determined kinetic parameters using real-time interaction analysis. Alanine 186-193 tumor protein p53 Homo sapiens 151-154 10660538-4 2000 Contrary to bax, another known pro-apoptotic p53-target gene, both mouse and human FAS p53REs are still activated by the discriminatory p53 mutants Pro-175 and Ala-143, a class of mutants unable to induce apoptosis. Alanine 160-163 tumor protein p53 Homo sapiens 87-90 9213246-1 1997 The human hepatocellular carcinoma (HCC) cell line, HLF, expresses only mutant-type p53 (mt-p53), which has an amino acid substitution at the 244th residue from glycine to alanine. Alanine 172-179 tumor protein p53 Homo sapiens 84-87 10484981-7 1999 In the analyses of tumor tissues from the propositus and his daughter, a P16INK4A codon 94 missense point mutation (GCG-->GAG; Ala-->Glu) was observed with the hereditary TP53 mutation. Alanine 127-130 tumor protein p53 Homo sapiens 171-175 9582268-1 1998 The contribution of almost each amino acid side chain to the thermodynamic stability of the tetramerization domain (residues 326-353) of human p53 has been quantitated using 25 mutants with single-residue truncations to alanine (or glycine). Alanine 220-227 tumor protein p53 Homo sapiens 143-146 9620557-4 1998 Moreover, a HeLa clone stably transfected with a temperature sensitive (ts) 143 Ala p53 mutant exhibited temperature-dependent regulation of H19 expression. Alanine 80-83 tumor protein p53 Homo sapiens 84-87 9213246-1 1997 The human hepatocellular carcinoma (HCC) cell line, HLF, expresses only mutant-type p53 (mt-p53), which has an amino acid substitution at the 244th residue from glycine to alanine. Alanine 172-179 tumor protein p53 Homo sapiens 92-95 8967975-1 1996 With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine. Alanine 188-195 tumor protein p53 Homo sapiens 67-70 8967975-1 1996 With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine. Alanine 188-195 tumor protein p53 Homo sapiens 157-160 8810317-1 1996 We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --> Ala, Arg-175 --> His, Arg-248 --> Trp, Arg-249 --> Ser, and Arg-273 --> His). Alanine 130-133 tumor protein p53 Homo sapiens 101-104 7624116-1 1995 A human p53 mutant, p53Val-138 (amino acid 138, Alanine-->Valine), generated by in vitro mutagenesis was introduced into Saos-2 human osteosarcoma and Jurkat acute T-lymphoblastic leukemia cell lines, both lacking p53 protein expression. Alanine 48-55 tumor protein p53 Homo sapiens 8-11 8756655-1 1996 Human wild-type (wt) p53 can induce apoptosis in transiently transfected H1299 cells maintained at 37 degrees C, whereas tumor-derived mutant forms of p53 (with the mutation Ala-143, His-175, or Trp-248) fail to do so. Alanine 174-177 tumor protein p53 Homo sapiens 151-154 8756655-2 1996 At 37 degrees C, p53 with a mutation to Ala at amino acid 143 (p53Ala143) was transcriptionally inactive. Alanine 40-43 tumor protein p53 Homo sapiens 17-20 7479838-3 1995 We show that alanine substitution mutations in a single loop of TBP can disrupt its association in vitro with the activation domains of the herpes simplex virus activator VP16 and of the human tumor suppressor protein p53; these mutations do not, however, disrupt the transcriptional response of TBP to either activation domain in vivo. Alanine 13-20 tumor protein p53 Homo sapiens 218-221 7657383-7 1995 In this case, we identified a mutation in the TP53 gene at codon 161 changing GCC to ACC and resulting in an alteration of alanine to threonine in this position. Alanine 123-130 tumor protein p53 Homo sapiens 46-50 8649799-3 1996 Here we address this question in an intact cell system using normal human diploid fibroblasts in which p53 function is manipulated by expression of a dominant-negative mutant (ala(143)) introduced by a retroviral vector. Alanine 176-179 tumor protein p53 Homo sapiens 103-106 7624116-1 1995 A human p53 mutant, p53Val-138 (amino acid 138, Alanine-->Valine), generated by in vitro mutagenesis was introduced into Saos-2 human osteosarcoma and Jurkat acute T-lymphoblastic leukemia cell lines, both lacking p53 protein expression. Alanine 48-55 tumor protein p53 Homo sapiens 20-23 7624134-8 1995 Mutation of serine 315 of p53 to alanine (p53-S315A) abolished phosphorylation by cdk2 kinase. Alanine 33-40 tumor protein p53 Homo sapiens 26-29 7624134-8 1995 Mutation of serine 315 of p53 to alanine (p53-S315A) abolished phosphorylation by cdk2 kinase. Alanine 33-40 tumor protein p53 Homo sapiens 42-45 8502477-8 1993 Expression of p53-Ala-37 in stably transformed T98G cells blocked progression of the cells into S phase as well as did the expression of wild-type p53. Alanine 18-21 tumor protein p53 Homo sapiens 14-17 7539102-5 1995 Similarly, K562, cells stably transfected with a plasmid vector containing the temperature-sensitive human p53 mutant Ala-143 demonstrated a four- to sixfold upregulation of Fas/APO-1 by flow-cytometric analysis at the permissive temperature of 32.5 degrees C. Temperature-sensitive upregulation of Fas/APO-1 in K562 Ala-143 cells was verified by immunoprecipitation and demonstrated to result from enhanced mRNA production by nuclear run-on and Northern (RNA) analyses. Alanine 118-121 tumor protein p53 Homo sapiens 107-110 8033090-6 1994 Expression of a dominant-negative mutant of p53 (codon 143, Val to Ala) in transfectants of the radiosensitive human ovarian cell line A2780 abrogates the radiation-induced G1 arrest. Alanine 67-70 tumor protein p53 Homo sapiens 44-47 8152811-4 1994 We therefore introduced the pC53-SCX3 143 (Val-Ala) p53 mutation into a non tumorigenic adenoma derived cell line, AA/C1, which contained a truncating APC mutation, activating K-ras mutation but was wild-type for the p53 protein. Alanine 47-50 tumor protein p53 Homo sapiens 52-55 8406999-8 1993 Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells. Alanine 88-91 tumor protein p53 Homo sapiens 25-28 8406999-8 1993 Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells. Alanine 88-91 tumor protein p53 Homo sapiens 207-210 8502477-8 1993 Expression of p53-Ala-37 in stably transformed T98G cells blocked progression of the cells into S phase as well as did the expression of wild-type p53. Alanine 18-21 tumor protein p53 Homo sapiens 147-150 8502477-10 1993 Several cell clones transformed with the mutant p53-Ala-15 gene expressed normal levels of p53 mRNA but accumulated little or no detectable p53 protein. Alanine 52-55 tumor protein p53 Homo sapiens 48-51 8502477-10 1993 Several cell clones transformed with the mutant p53-Ala-15 gene expressed normal levels of p53 mRNA but accumulated little or no detectable p53 protein. Alanine 52-55 tumor protein p53 Homo sapiens 91-94 8502477-10 1993 Several cell clones transformed with the mutant p53-Ala-15 gene expressed normal levels of p53 mRNA but accumulated little or no detectable p53 protein. Alanine 52-55 tumor protein p53 Homo sapiens 91-94 8389256-6 1993 The p53 point mutations in the three HCC cell lines from Japan resulted in the amino acid changes of cysteine for tyrosine in cell line HuH 7 at codon 220 (A:T-->G:C), alanine for glycine in cell line HLF at codon 244 (G:C-->C:G), and serine for arginine in cell line HLE at codon 249 (G:C-->C:G). Alanine 171-178 tumor protein p53 Homo sapiens 4-7 1466808-3 1992 Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249). Alanine 290-293 tumor protein p53 Homo sapiens 233-236 1466808-3 1992 Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249). Alanine 290-293 tumor protein p53 Homo sapiens 276-279 1450522-2 1992 The sequence -Thr-Pro-Ala-Pro-Lys-, as found in p53 protein, was also phosphorylated by this enzyme, but less efficiently than in the sequence described above. Alanine 22-25 tumor protein p53 Homo sapiens 48-51 2052362-10 1991 A mutant p53 with a ser 389 to ala exchange was not phosphorylated in vitro by the p53 associated protein kinase. Alanine 31-34 tumor protein p53 Homo sapiens 9-12