PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11314025-5 2001 Inhibition of focal contacts development by plating of cells onto poly-L-lysine abrogated both Erk1/2 and p53 activations in colcemid-treated cells, while plating of cells onto fibronectin caused transient up-regulation of p53 even in the absence of colcemid. Lysine 66-79 tumor protein p53 Homo sapiens 106-109 11495913-4 2001 Furthermore, interaction of p53 with the transcriptional coactivator p300 was induced, and Lys(382) of p53 was acetylated. Lysine 91-94 tumor protein p53 Homo sapiens 28-31 11495913-4 2001 Furthermore, interaction of p53 with the transcriptional coactivator p300 was induced, and Lys(382) of p53 was acetylated. Lysine 91-94 tumor protein p53 Homo sapiens 103-106 11481424-7 2001 Furthermore, p33ING2 expression increases the acetylation of p53 at Lys-382. Lysine 68-71 tumor protein p53 Homo sapiens 61-64 10910364-6 2000 p53 is acetylated at lysine 382 upon Ras expression, an event that is essential for its biological function. Lysine 21-27 tumor protein p53 Homo sapiens 0-3 11046142-0 2000 Multiple C-terminal lysine residues target p53 for ubiquitin-proteasome-mediated degradation. Lysine 20-26 tumor protein p53 Homo sapiens 43-46 11046142-6 2000 Simultaneous mutation of lysine residues 370, 372, 373, 381, 382, and 386 to arginine residues (6KR p53 mutant) generates a p53 molecule with potent transcriptional activity that is resistant to Mdm2-induced degradation and is refractory to Mdm2-mediated ubiquitination. Lysine 25-31 tumor protein p53 Homo sapiens 100-103 11046142-6 2000 Simultaneous mutation of lysine residues 370, 372, 373, 381, 382, and 386 to arginine residues (6KR p53 mutant) generates a p53 molecule with potent transcriptional activity that is resistant to Mdm2-induced degradation and is refractory to Mdm2-mediated ubiquitination. Lysine 25-31 tumor protein p53 Homo sapiens 124-127 11046142-8 2000 Those differences are also manifest in HeLa cells which express the human papillomavirus E6 protein, suggesting that p53 C-terminal lysine residues are also implicated in E6-AP-mediated ubiquitination. Lysine 132-138 tumor protein p53 Homo sapiens 117-120 11046142-9 2000 These data suggest that p53 C-terminal lysine residues are the main sites of ubiquitin ligation, which target p53 for proteasome-mediated degradation. Lysine 39-45 tumor protein p53 Homo sapiens 24-27 11046142-9 2000 These data suggest that p53 C-terminal lysine residues are the main sites of ubiquitin ligation, which target p53 for proteasome-mediated degradation. Lysine 39-45 tumor protein p53 Homo sapiens 110-113 10891493-6 2000 PCAF binds to the E1B 55-kDa protein and to a region near the C terminus of p53 encompassing Lys-320, the specific PCAF acetylation site. Lysine 93-96 tumor protein p53 Homo sapiens 76-79 11094089-0 2000 Multiple lysine mutations in the C-terminal domain of p53 interfere with MDM2-dependent protein degradation and ubiquitination. Lysine 9-15 tumor protein p53 Homo sapiens 54-57 10562558-3 1999 A lysine residue at amino acid position 386 of p53 is required for this previously undescribed modification, strongly suggesting that this lysine residue serves as the major attachment site for SUMO-1. Lysine 2-8 tumor protein p53 Homo sapiens 47-50 10788439-9 2000 The SUMO-1 attachment site in p53 (Lys-386) resides within a region known to regulate the DNA binding activity of the protein. Lysine 35-38 tumor protein p53 Homo sapiens 30-33 10600518-1 1999 Recent studies have implicated acetylation of several nuclear proteins such as histones and p53 on their epsilon-portion of lysine residues in eukaryotic transcription. Lysine 124-130 tumor protein p53 Homo sapiens 92-95 10562558-3 1999 A lysine residue at amino acid position 386 of p53 is required for this previously undescribed modification, strongly suggesting that this lysine residue serves as the major attachment site for SUMO-1. Lysine 139-145 tumor protein p53 Homo sapiens 47-50 10321742-1 1999 It has been reported that Lysine-305 is needed for the nuclear import of the p53 protein (Liang et al., 1998). Lysine 26-32 tumor protein p53 Homo sapiens 77-80 10207063-6 1999 Lys residues within the peptide were critical for both p53 activation and core domain binding. Lysine 0-3 tumor protein p53 Homo sapiens 55-58 10551826-4 1999 To characterize further the function of these two domains, we demonstrate in this report that the previously described major nuclear localization signal works together with Lys(305)-Arg(306) to form a bipartite and functional nuclear localization sequence (NLS) for p53 nuclear import. Lysine 173-176 tumor protein p53 Homo sapiens 266-269 10321742-2 1999 In the present study, further mutagenesis analyses were carried out between Lys-305 and the major nuclear localization signal (NLS I) of p53. Lysine 76-79 tumor protein p53 Homo sapiens 137-140 9677415-0 1998 Cooperation of a single lysine mutation and a C-terminal domain in the cytoplasmic sequestration of the p53 protein. Lysine 24-30 tumor protein p53 Homo sapiens 104-107 9891054-5 1999 In this study, we demonstrate that PCAF also acetylates p53 in vitro at a lysine residue distinct from that acetylated by p300 and thereby increases p53"s ability to bind to its cognate DNA site. Lysine 74-80 tumor protein p53 Homo sapiens 56-59 9891054-5 1999 In this study, we demonstrate that PCAF also acetylates p53 in vitro at a lysine residue distinct from that acetylated by p300 and thereby increases p53"s ability to bind to its cognate DNA site. Lysine 74-80 tumor protein p53 Homo sapiens 149-152 9891054-6 1999 We have generated antibodies to acetylated p53 peptides at either of the two lysine residues that are targeted by PCAF or p300 and have demonstrated that these antibodies are highly specific for both acetylation and the particular site. Lysine 77-83 tumor protein p53 Homo sapiens 43-46 9744860-4 1998 p300 acetylates Lys-382 in the carboxy-terminal region of p53, whereas PCAF acetylates Lys-320 in the nuclear localization signal. Lysine 16-19 tumor protein p53 Homo sapiens 58-61 9744860-6 1998 Using a polyclonal antisera specific for p53 that is phosphorylated or acetylated at specific residues, we show that Lys-382 of human p53 becomes acetylated and Ser-33 and Ser-37 become phosphorylated in vivo after exposing cells to UV light or ionizing radiation. Lysine 117-120 tumor protein p53 Homo sapiens 41-44 9744860-6 1998 Using a polyclonal antisera specific for p53 that is phosphorylated or acetylated at specific residues, we show that Lys-382 of human p53 becomes acetylated and Ser-33 and Ser-37 become phosphorylated in vivo after exposing cells to UV light or ionizing radiation. Lysine 117-120 tumor protein p53 Homo sapiens 134-137 12953991-0 1999 P53 gene of chang-liver cells (Atcc-Ccl13) exposed to aflatoxin B1 (Afb): the effect of lysine on mutation at codon 249 of exon 7. Lysine 88-94 tumor protein p53 Homo sapiens 0-3 12953991-1 1999 The effect of different regimes of lysine-pre treatment on mutation at the 3rd nucleotide base of codon 249 which is located at the 7th exon of p53 gene of Chang-liver cells (CCIL13) exposed to aflatoxin B1 (AFB1) has been investigated. Lysine 35-41 tumor protein p53 Homo sapiens 144-147 9677415-6 1998 Mutagenesis analysis demonstrated that a single amino acid mutation of Lys-305 (mt p53) caused cytoplasmic sequestration of the p53 protein in the MCF-7 and RKO cells, whereas the fusion protein was distributed in both the cytoplasm and the nucleus of SAOS-2 cells. Lysine 71-74 tumor protein p53 Homo sapiens 83-86 9677415-6 1998 Mutagenesis analysis demonstrated that a single amino acid mutation of Lys-305 (mt p53) caused cytoplasmic sequestration of the p53 protein in the MCF-7 and RKO cells, whereas the fusion protein was distributed in both the cytoplasm and the nucleus of SAOS-2 cells. Lysine 71-74 tumor protein p53 Homo sapiens 128-131 9677415-10 1998 Lys-305 is needed for nuclear import of p53 protein, and amino acid residues 326-355 can sequester mt p53 in the cytoplasm. Lysine 0-3 tumor protein p53 Homo sapiens 40-43 9677415-10 1998 Lys-305 is needed for nuclear import of p53 protein, and amino acid residues 326-355 can sequester mt p53 in the cytoplasm. Lysine 0-3 tumor protein p53 Homo sapiens 102-105 8649776-2 1996 By using recombination PCR in vitro mutagenesis, we introduced point mutations into the codon 273 of wild-type (wt) p53 (pC53-SN3) from Arg to His (pC53-273H [273H]), Asp (273D), Pro (273P), Lys (273K), Leu (273L) or Thr (273T), and compared their biological and biochemical activities with wt p53 and cancer-derived 175H, 248W and 273H/309S. Lysine 191-194 tumor protein p53 Homo sapiens 116-119 9530523-8 1998 The results of these experiments demonstrate that: (1) there were mutations in p53 exon 5 and 8 in 35% (14 out of 40 samples) of human renal cancer tissues as revealed by PCR-SSCP analysis; (2) DNA sequencing of samples showing frame-shift have hot spot of p53 mutation on exon 8 at codon 244 (GGC-->TGC) and exon 5 at codon 132 [AAG (Lys)-->AGG (Arg)]. Lysine 338-341 tumor protein p53 Homo sapiens 79-82 8275497-1 1994 We investigated the expression of p53 in paraformaldehyde-lysine-periodate fixed normal and chronic myelogenous leukemia (CML) hemopoietic cells with flow cytometry and two monoclonal antibodies, PAb1801 and the mutant-conformation-associated PAb240. Lysine 58-64 tumor protein p53 Homo sapiens 34-37 8599213-5 1996 Mutation of lysine residues within the C-terminus of p53 resulted in resistance to E6-mediated degradation in vitro, although the ability of the two proteins to form a complex was not affected. Lysine 12-18 tumor protein p53 Homo sapiens 53-56 1406679-5 1992 Phosphorylation of the conserved serine 15 in human p53 peptides depended on the presence of an adjacent glutamine, and phosphorylation was inhibited by the presence of a nearby lysine. Lysine 178-184 tumor protein p53 Homo sapiens 52-55 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. Lysine 30-33 tumor protein p53 Homo sapiens 48-51 34270461-7 2021 Mechanically, upon interaction with p53, BMI1 was recruited on the promoter of miR-3682-3p gene concomitant with an increase in the mono-ubiquitination of histone H2A lysine 119, leading to transcription repression of miR-3682-3p gene followed by derepression of ABCB1 (ATP binding cassette subfamily B member 1) gene. Lysine 167-173 tumor protein p53 Homo sapiens 36-39 34928233-4 2022 AIMS: To explore whether homebox D3 binding to lysine (K)-specific demethylase 5C promoted malignant progression of diffuse large B-cell lymphoma by decreasing p53 expression. Lysine 47-53 tumor protein p53 Homo sapiens 160-163 34928233-16 2022 CONCLUSION: Homebox D3 up-regulating lysine (K)-specific demethylase 5C promotes malignant progression of diffuse large B-cell lymphoma by decreasing p53 expression. Lysine 37-43 tumor protein p53 Homo sapiens 150-153 34880421-6 2021 Once freed from PEPD, p53 mutants undergo multiple posttranslational modifications, especially lysine 373 acetylation, which cause them to refold and regain tumor suppressor activities that are typically displayed by p53. Lysine 95-101 tumor protein p53 Homo sapiens 22-25 34880421-6 2021 Once freed from PEPD, p53 mutants undergo multiple posttranslational modifications, especially lysine 373 acetylation, which cause them to refold and regain tumor suppressor activities that are typically displayed by p53. Lysine 95-101 tumor protein p53 Homo sapiens 217-220 34947995-3 2021 In this study, we investigated the posttranslationally modified p53, including p53 acetylated at lysine 382 (K382), p53 phosphorylated at serine 46 (S46), and the p53 cofactor TTC5/STRAP (Tetratricopeptide repeat domain 5/ Stress-responsive activator of p300-TTC5) proteins in lung cancer. Lysine 97-103 tumor protein p53 Homo sapiens 79-82 34255515-3 2021 The bromodomains of CREBBP and EP300 enable the binding of acetylated lysine residues from histones and a number of other important proteins, including p53, p73, E2F, and GATA1. Lysine 70-76 tumor protein p53 Homo sapiens 152-155 27452519-3 2017 Among different covalent modifications found on p53 the most controversial one is lysine methylation. Lysine 82-88 tumor protein p53 Homo sapiens 48-51 35025136-4 2022 Similarly, since p53 can be ubiquitylated at different lysine residues, it remains unclear if the eventual effect depends on the position of the lysine modified. Lysine 55-61 tumor protein p53 Homo sapiens 17-20 34335587-12 2021 In the mechanistic study, we found that the induction of p53 deacetylation, due to either the resveratrol/quercetin -induced activation of the deacetylase Sirtuin 1 (Sirt1) or the mutation of the acetylated lysine site in p53, promoted RTEC autophagy and alleviated SAKI. Lysine 207-213 tumor protein p53 Homo sapiens 57-60 34335587-12 2021 In the mechanistic study, we found that the induction of p53 deacetylation, due to either the resveratrol/quercetin -induced activation of the deacetylase Sirtuin 1 (Sirt1) or the mutation of the acetylated lysine site in p53, promoted RTEC autophagy and alleviated SAKI. Lysine 207-213 tumor protein p53 Homo sapiens 222-225 33546767-7 2021 We found that inhibition of NAMPT or SIRT2 in iPS cells induces p53 protein by promoting its lysine acetylation. Lysine 93-99 tumor protein p53 Homo sapiens 64-67 35204825-8 2022 The p53 complexes with SIRT2, MUL1, USP7, TXN, PIN1 and PPIF control regulation of p53 function through post-translational modifications, such as lysine acetylation or ubiquitination, cysteine/cystine redox transformation and peptidyl-prolyl cis-trans isomerization. Lysine 146-152 tumor protein p53 Homo sapiens 4-7 35204825-8 2022 The p53 complexes with SIRT2, MUL1, USP7, TXN, PIN1 and PPIF control regulation of p53 function through post-translational modifications, such as lysine acetylation or ubiquitination, cysteine/cystine redox transformation and peptidyl-prolyl cis-trans isomerization. Lysine 146-152 tumor protein p53 Homo sapiens 83-86 33966047-1 2021 Role of p53 lysine 120 NEDDylation. Lysine 12-18 tumor protein p53 Homo sapiens 8-11 33256840-5 2020 Moreover, MEG3 increases the methylation modification of histone H3 at the 27th lysine via P53. Lysine 80-86 tumor protein p53 Homo sapiens 91-94 33160987-5 2021 However, transfection with adenoviral construct including SIRT3 significantly inhibited HG-induced SA-gal activity, decreased p53 acetylation level at the site Lys 320 (k320), and overexpression of SIRT3 antagonized high glucose-induced angiogenic dysfunction. Lysine 160-163 tumor protein p53 Homo sapiens 126-129 33339442-1 2020 The histone methyltransferase SETD8, which methylates the lysine 20 of histone H4 (H4K20), is reportedly involved in human carcinogenesis along with nonhistone proteins such as p53. Lysine 58-64 tumor protein p53 Homo sapiens 177-180 32093281-7 2020 Additionally, the protein stability and transcriptional activity of p53 in TFAM knockdown tumor cells was attenuated, and this was associated with decreased acetylation, especially the acetylation of lysine 382 of p53. Lysine 200-206 tumor protein p53 Homo sapiens 68-71 32527012-4 2020 Hypo- or hyperacetylation mutations of STRAP at lysines 147, 148, and 156 (3KR or 3KQ) influence its activation and stabilization of p53. Lysine 48-55 tumor protein p53 Homo sapiens 133-136 32061389-2 2020 Lysine acetylation is required to mediate activation of p53. Lysine 0-6 tumor protein p53 Homo sapiens 56-59 32061389-6 2020 We found that not all lysine residues are equally capable of promoting p53"s functions. Lysine 22-28 tumor protein p53 Homo sapiens 71-74 32831651-11 2020 Results: Here, using a panel of OSCC cell lines with wild type or mutant p53, we show that p33ING1b expression is correlated to acetylation of p53 at lysine 382 residue. Lysine 150-156 tumor protein p53 Homo sapiens 143-146 32093281-7 2020 Additionally, the protein stability and transcriptional activity of p53 in TFAM knockdown tumor cells was attenuated, and this was associated with decreased acetylation, especially the acetylation of lysine 382 of p53. Lysine 200-206 tumor protein p53 Homo sapiens 214-217 31002112-10 2019 Further analysis confirmed that lysines 381, 382, 386 of p53 are the key sites for the ubiquitination modification of SMYD3 to p53. Lysine 32-39 tumor protein p53 Homo sapiens 57-60 31642121-5 2020 Using this tool, we have identified a putative domain enriched in hydrophilic and disorder-promoting residues (Pro, Ser, and Thr) and depleted in positive charges (Arg and Lys) bordering the folded DNA-binding domains of several transcription factors (p53, GCR, NAC46, MYB28, and MYB29). Lysine 172-175 tumor protein p53 Homo sapiens 252-255 31002112-10 2019 Further analysis confirmed that lysines 381, 382, 386 of p53 are the key sites for the ubiquitination modification of SMYD3 to p53. Lysine 32-39 tumor protein p53 Homo sapiens 127-130 31885199-7 2019 Instead, we provide evidence that the time-varying acetylation state of p53"s C-terminal lysine residues is critical for gene-specific regulation of stochastic bursting. Lysine 89-95 tumor protein p53 Homo sapiens 72-75 31328874-4 2019 Lysine-to-methionine point mutations at amino acid 27 (H3K27M) co-occur with alterations in signaling genes, including the receptor tyrosine kinases (PDGFR/KIT/VEGFR/MET/EGFR), activin A receptor (ACVR1), intracellular kinases (PI3K/AKT/mTOR), cyclin-dependent kinases (CDKs1/4/6), transcriptional regulators (MYCN), and tumor suppressors (PTEN/TP53). Lysine 0-6 tumor protein p53 Homo sapiens 345-349 31346036-6 2019 The polyubiquitylation of p53 occurred via Lys-48 linkage and involved phosphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and DNA-dependent protein kinase (DNA-PK), respectively. Lysine 43-46 tumor protein p53 Homo sapiens 26-29 31492752-4 2019 Mass spectrometry and biochemical analysis of the reaction products identified lysine residues as p53 ubiquitination sites. Lysine 79-85 tumor protein p53 Homo sapiens 98-101 31492752-5 2019 A p53 mutant with arginine substitutions of its 18 lysine residues was not ubiquitinated. Lysine 51-57 tumor protein p53 Homo sapiens 2-5 31346036-7 2019 These phosphorylation events created a phosphodegron that enhanced p53 binding to FBW7alpha, allowing for the attachment of polyubiquitin moieties at Lys-132 in p53. Lysine 150-153 tumor protein p53 Homo sapiens 67-70 31346036-7 2019 These phosphorylation events created a phosphodegron that enhanced p53 binding to FBW7alpha, allowing for the attachment of polyubiquitin moieties at Lys-132 in p53. Lysine 150-153 tumor protein p53 Homo sapiens 161-164 31346036-10 2019 Phosphodegron-mediated polyubiquitylation of p53 on Lys-132 had functional consequences, with cells in which FBW7alpha-mediated p53 degradation was abrogated exhibiting enhancement of their tumorigenic potential. Lysine 52-55 tumor protein p53 Homo sapiens 45-48 30623565-4 2019 Based on the reported prerequisite role of nucleolar stress response in stress-induced p53 protein accumulation, we have also provided evidence suggesting that Sirt1-mediated inhibition on nucleolar stress response may represent a novel mechanism by which Sirt1 can modulate intracellular p53 accumulation independent of lysine deacetylation. Lysine 321-327 tumor protein p53 Homo sapiens 87-90 31388677-9 2019 A weak transcription activity of Cr(VI)-upregulated p53 was associated with its low lysine acetylation in the regulatory C-terminal domain, resulting from the inability of Cr(VI) to activate ATM in ascorbate-restored cells. Lysine 84-90 tumor protein p53 Homo sapiens 52-55 30623565-4 2019 Based on the reported prerequisite role of nucleolar stress response in stress-induced p53 protein accumulation, we have also provided evidence suggesting that Sirt1-mediated inhibition on nucleolar stress response may represent a novel mechanism by which Sirt1 can modulate intracellular p53 accumulation independent of lysine deacetylation. Lysine 321-327 tumor protein p53 Homo sapiens 289-292 30643005-3 2019 These characteristics are typically associated with regulation through chromatin acetylation by binding histone H3 trimethylated at lysine 4 (H3K4me3) and through transcriptional activity of transcription factor P53 and NF-kappaB. Lysine 132-138 tumor protein p53 Homo sapiens 212-215 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. Lysine 263-266 tumor protein p53 Homo sapiens 124-127 30710424-9 2019 The marked reduction in SIRT1 expression by combination of metformin and tenovin-6 increased acetylation of p53 at lysine 382 and enhanced p53 stability in LKB1-deficient A549 cells. Lysine 115-121 tumor protein p53 Homo sapiens 108-111 30881498-6 2019 Furthermore, treating cells with resveratrol upregulated SET domain containing lysine methyltransferase 7/9 (SET7/9) expression, which positively regulates p53 through its mono-methylation at lysine 372, compared with untreated cells. Lysine 79-85 tumor protein p53 Homo sapiens 156-159 30925159-7 2019 Finally, lysine residue 358 was the key site for p53 K63-linked ubiquitination by the N and P proteins. Lysine 9-15 tumor protein p53 Homo sapiens 49-52 29631413-6 2019 Augmented PPARalpha in hypertrophied myocytes revealed downregulated p53 acetylation (lys 382), leading to reduced apoptosis. Lysine 86-89 tumor protein p53 Homo sapiens 69-72 31087303-3 2019 Much like nucleosomal histones, the tumor suppressor protein p53 is acetylated on a number of distinct lysine residues, often with distinct functional consequences. Lysine 103-109 tumor protein p53 Homo sapiens 61-64 30409904-3 2019 Here, using Bcl6 -/- knockout mice, HEK293A and HCT116 p53 -/- cells, and site-directed mutagenesis, we found that BCL6 interacts with p53 and thereby inhibits acetylation of Lys-132 in p53 by E1A-binding protein p300 (p300), a modification that normally occurs upon DNA damage-induced cellular stress and whose abrogation by BCL6 diminished transcriptional activation of p53 target genes, including that encoding caspase-1. Lysine 175-178 tumor protein p53 Homo sapiens 135-138 30409904-3 2019 Here, using Bcl6 -/- knockout mice, HEK293A and HCT116 p53 -/- cells, and site-directed mutagenesis, we found that BCL6 interacts with p53 and thereby inhibits acetylation of Lys-132 in p53 by E1A-binding protein p300 (p300), a modification that normally occurs upon DNA damage-induced cellular stress and whose abrogation by BCL6 diminished transcriptional activation of p53 target genes, including that encoding caspase-1. Lysine 175-178 tumor protein p53 Homo sapiens 135-138 30409904-3 2019 Here, using Bcl6 -/- knockout mice, HEK293A and HCT116 p53 -/- cells, and site-directed mutagenesis, we found that BCL6 interacts with p53 and thereby inhibits acetylation of Lys-132 in p53 by E1A-binding protein p300 (p300), a modification that normally occurs upon DNA damage-induced cellular stress and whose abrogation by BCL6 diminished transcriptional activation of p53 target genes, including that encoding caspase-1. Lysine 175-178 tumor protein p53 Homo sapiens 135-138 29954944-4 2018 We further reveal that mutant p53 forms physiological associations and direct interactions with MLL4 and promotes the enhancer binding of MLL4, which is required for TNFalpha-inducible H3K4me1 and histone H3 lysine 27 acetylation (H3K27ac) levels, enhancer-derived transcript (eRNA) synthesis, and mutant p53-dependent target gene activation. Lysine 208-214 tumor protein p53 Homo sapiens 30-33 29633022-6 2018 Moreover, mutant IDH1 can drive the immortalization and transformation of p53-/pRb-deficient astrocytes by reactivating telomerase and stabilizing telomeres in combination with increased histone lysine methylation and c-Myc/Max binding at the TERT promoter. Lysine 195-201 tumor protein p53 Homo sapiens 74-77 29954944-4 2018 We further reveal that mutant p53 forms physiological associations and direct interactions with MLL4 and promotes the enhancer binding of MLL4, which is required for TNFalpha-inducible H3K4me1 and histone H3 lysine 27 acetylation (H3K27ac) levels, enhancer-derived transcript (eRNA) synthesis, and mutant p53-dependent target gene activation. Lysine 208-214 tumor protein p53 Homo sapiens 305-308 29233643-4 2018 Here, we report that SIRT6 deacetylates lysine 382 of p53 in short synthetic peptide sequence and in full length p53. Lysine 40-46 tumor protein p53 Homo sapiens 54-57 30072621-0 2018 Inhibitor of CBP Histone Acetyltransferase Downregulates p53 Activation and Facilitates Methylation at Lysine 27 on Histone H3. Lysine 103-109 tumor protein p53 Homo sapiens 57-60 30057418-13 2018 Instead, p53 acetylation at lysine 382 was unexpectedly upregulated. Lysine 28-34 tumor protein p53 Homo sapiens 9-12 29233643-4 2018 Here, we report that SIRT6 deacetylates lysine 382 of p53 in short synthetic peptide sequence and in full length p53. Lysine 40-46 tumor protein p53 Homo sapiens 113-116 29774081-10 2018 G9a dimethylated p53 at lysine 373, which in turn increased Plk1 expression and promoted CRC cell growth. Lysine 24-30 tumor protein p53 Homo sapiens 17-20 29174981-7 2018 Excitingly, Lys-104 (K104), a previously identified lysine acetylation site of TIP60 with unknown function, was observed to be indispensable for inducing p53-mediated apoptosis under low glucose condition. Lysine 12-15 tumor protein p53 Homo sapiens 154-157 29174981-7 2018 Excitingly, Lys-104 (K104), a previously identified lysine acetylation site of TIP60 with unknown function, was observed to be indispensable for inducing p53-mediated apoptosis under low glucose condition. Lysine 52-58 tumor protein p53 Homo sapiens 154-157 29054408-3 2017 Here, we show HDAC6 negatively regulates pro-apoptotic acetylation of p53 at lysine residue 120 (K120) in mesenchymal stem cells (MSCs). Lysine 77-83 tumor protein p53 Homo sapiens 70-73 27735058-1 2016 The C-terminal domain (CTD) of tumor suppressor protein p53 is an intrinsically disordered region that binds to various partner proteins, where lysine of CTD is acetylated/nonacetylated and histidine neutralized/non-neutralized. Lysine 144-150 tumor protein p53 Homo sapiens 56-59 28655792-4 2017 C646 treatment blocked acetylation of specific lysine residues that regulate p53 activity. Lysine 47-53 tumor protein p53 Homo sapiens 77-80 28542145-7 2017 TRIM45 conjugates K63-linked polyubiquitin chain to the C-terminal six lysine residues of p53, thereby inhibiting the availability of these residues to the K48-linked polyubiquitination that targets p53 for degradation. Lysine 71-77 tumor protein p53 Homo sapiens 90-93 28542145-7 2017 TRIM45 conjugates K63-linked polyubiquitin chain to the C-terminal six lysine residues of p53, thereby inhibiting the availability of these residues to the K48-linked polyubiquitination that targets p53 for degradation. Lysine 71-77 tumor protein p53 Homo sapiens 199-202 29029401-2 2017 Lysine methylation of histones such as H4K20 and non-histone proteins including p53 has been shown to be essential for the mounting of the DDR. Lysine 0-6 tumor protein p53 Homo sapiens 80-83 28189587-7 2017 In addition, deacetylation of p53 is required to make lysine residues accessible to ubiquitin ligases. Lysine 54-60 tumor protein p53 Homo sapiens 30-33 28153791-0 2017 HDAC6 deacetylates p53 at lysines 381/382 and differentially coordinates p53-induced apoptosis. Lysine 26-33 tumor protein p53 Homo sapiens 19-22 28153791-4 2017 Interestingly, HDAC6 levels inversely correlated with p53 acetylation at lysines 381/382 associated with p53 functional activation. Lysine 73-80 tumor protein p53 Homo sapiens 54-57 28153791-4 2017 Interestingly, HDAC6 levels inversely correlated with p53 acetylation at lysines 381/382 associated with p53 functional activation. Lysine 73-80 tumor protein p53 Homo sapiens 105-108 27911860-3 2017 Recently, studies have focused on physiological mechanisms such as acetylation of lysine residues to rescue the wild type activity of mutant p53. Lysine 82-88 tumor protein p53 Homo sapiens 141-144 27270439-2 2017 Here we identified that the lysine-specific demethylase KDM3A played a dual role in breast cancer cell invasion and apoptosis by demethylating histone and the non-histone protein p53, respectively. Lysine 28-34 tumor protein p53 Homo sapiens 179-182 26183023-2 2015 Previously, we found that p53 interacts with KAISO, and acetylation of p53 lysine residues by p300 is modulated by KAISO. Lysine 75-81 tumor protein p53 Homo sapiens 71-74 27688818-2 2016 Lysine residues of non-histone proteins including proliferating cell nuclear antigen (PCNA) and p53 are also monomethylated. Lysine 0-6 tumor protein p53 Homo sapiens 96-99 27695348-8 2016 Mechanistic studies revealed that HOTAIR modified the promoter of p53 and enhanced histone H3 lysine 27 trimethylation (H3K27me3). Lysine 94-100 tumor protein p53 Homo sapiens 66-69 27226597-4 2016 We used the genetic code expansion concept to produce natively folded, site-specific, and lysine-acetylated Sirt1-3 substrate proteins, namely Ras-related nuclear, p53, PEPCK1, superoxide dismutase, cyclophilin D, and Hsp10, and analyzed the deacetylation reaction. Lysine 90-96 tumor protein p53 Homo sapiens 164-167 27210019-0 2016 Lysines in the tetramerization domain of p53 selectively modulate G1 arrest. Lysine 0-7 tumor protein p53 Homo sapiens 41-44 27210019-4 2016 By changing lysines 351 and 357 to arginine, thereby blocking all post-translational modifications of these residues, DNA binding and transcriptional regulation by p53 remain virtually unchanged. Lysine 12-19 tumor protein p53 Homo sapiens 164-167 27210019-5 2016 On the other hand, by changing these lysines to glutamine (2KQ-p53), thereby neutralizing their positive charge and potentially mimicking acetylation, p53 is impaired in the induction of cell cycle arrest and yet can still effectively induce cell death. Lysine 37-44 tumor protein p53 Homo sapiens 63-66 27210019-5 2016 On the other hand, by changing these lysines to glutamine (2KQ-p53), thereby neutralizing their positive charge and potentially mimicking acetylation, p53 is impaired in the induction of cell cycle arrest and yet can still effectively induce cell death. Lysine 37-44 tumor protein p53 Homo sapiens 151-154 27210019-7 2016 Our findings show that strong induction of p21 is not sufficient to block H1299 cells in G1, and imply that modification of one or both of the lysines within the tetramerization domain may serve as a mechanism to shunt p53 from inducing cell cycle arrest. Lysine 143-150 tumor protein p53 Homo sapiens 219-222 26596838-2 2016 We previously demonstrated that aspirin acetylated the tumor suppressor protein p53 at lysine 382 in MDA-MB-231 human breast cancer cells. Lysine 87-93 tumor protein p53 Homo sapiens 80-83 26851285-0 2016 Acetylation of p53 Protein at Lysine 120 Up-regulates Apaf-1 Protein and Sensitizes the Mitochondrial Apoptotic Pathway. Lysine 30-36 tumor protein p53 Homo sapiens 15-18 26851285-3 2016 Here we demonstrate that acetylation of p53 at Lys-120 up-regulates its transcriptional activity toward Apaf-1, a core component in the mitochondrial apoptotic pathway, and thus sensitizes caspase activation and apoptosis. Lysine 47-50 tumor protein p53 Homo sapiens 40-43 26851285-4 2016 We found that histone deacetylase (HDAC) inhibitors, including butyrate, augment Lys-120 acetylation of p53 and thus Apaf-1 expression by inhibiting HDAC1. Lysine 81-84 tumor protein p53 Homo sapiens 104-107 26986569-13 2016 In the same cells, the amide also increased the acetylation of lysine (K382) in p53, but not (K305). Lysine 63-69 tumor protein p53 Homo sapiens 80-83 26505788-1 2015 Lysine acetyltransferase 8 (KAT8) is a histone acetyltransferase (HAT) responsible for acetylating lysine 16 on histone H4 (H4K16) and plays a role in cell cycle progression as well as acetylation of the tumor suppressor protein p53. Lysine 99-105 tumor protein p53 Homo sapiens 229-232 27535933-0 2016 Lysine methylation represses p53 activity in teratocarcinoma cancer cells. Lysine 0-6 tumor protein p53 Homo sapiens 29-32 27535933-3 2016 Here we report that in the teratocarcinoma cell line NTera2, p53 is subject to lysine methylation at its carboxyl terminus, which has been shown to repress p53"s transcriptional activity. Lysine 79-85 tumor protein p53 Homo sapiens 61-64 27535933-3 2016 Here we report that in the teratocarcinoma cell line NTera2, p53 is subject to lysine methylation at its carboxyl terminus, which has been shown to repress p53"s transcriptional activity. Lysine 79-85 tumor protein p53 Homo sapiens 156-159 27535933-6 2016 Our results provide evidence that lysine methylation of endogenous wild-type p53 represses its activity in cancer cells and suggest new therapeutic possibilities of targeting testicular teratocarcinoma. Lysine 34-40 tumor protein p53 Homo sapiens 77-80 26851285-7 2016 Therefore, HDAC inhibitors can induce p53 acetylation at lysine 120, which in turn enhances mitochondrion-mediated apoptosis through transcriptional up-regulation of Apaf-1. Lysine 57-63 tumor protein p53 Homo sapiens 38-41 26227335-4 2015 We will use p53 and nuclear receptors, especially estrogen receptor alpha, as examples to discuss the dynamic nature of non-histone protein lysine methylation, the writers, erasers, and readers of these modifications, and the crosstalk between lysine methylation and other PTMs in regulating the functions of the modified proteins. Lysine 140-146 tumor protein p53 Homo sapiens 12-15 25014164-4 2014 Here we show that the histone 3 lysine 4- and lysine 36-specific methyltransferase Smyd2 acts as an endogenous antagonistic player of p53-dependent cardiomyocyte apoptosis. Lysine 32-38 tumor protein p53 Homo sapiens 134-137 25825497-8 2015 LLY-507 is active in cells as measured by reduction of SMYD2-induced monomethylation of p53 Lys(370) at submicromolar concentrations. Lysine 92-95 tumor protein p53 Homo sapiens 88-91 26030124-5 2015 Here, we examined the effect of a novel protein assembly modulator, the lysine (Lys)-specific molecular tweezer, CLR01, on different aggregation stages of misfolded mutant p53 in vitro and on the cytotoxicity of the resulting p53 aggregates in cell culture. Lysine 72-78 tumor protein p53 Homo sapiens 172-175 26030124-5 2015 Here, we examined the effect of a novel protein assembly modulator, the lysine (Lys)-specific molecular tweezer, CLR01, on different aggregation stages of misfolded mutant p53 in vitro and on the cytotoxicity of the resulting p53 aggregates in cell culture. Lysine 80-83 tumor protein p53 Homo sapiens 172-175 25815376-1 2015 SIRT1 regulates p53 transcriptional activation in response to genotoxic insult by deacetylating key lysine residues. Lysine 100-106 tumor protein p53 Homo sapiens 16-19 26021170-4 2015 NaBu activated the TP53 protein via hyper acetylation at lysine residue K382, without significant changes in the level of protein expression. Lysine 57-63 tumor protein p53 Homo sapiens 19-23 25521755-7 2014 Rg3 also decreased the expression of HDAC3 and increased the acetylation of p53 on lysine (k373/k382). Lysine 83-89 tumor protein p53 Homo sapiens 76-79 25014164-4 2014 Here we show that the histone 3 lysine 4- and lysine 36-specific methyltransferase Smyd2 acts as an endogenous antagonistic player of p53-dependent cardiomyocyte apoptosis. Lysine 46-52 tumor protein p53 Homo sapiens 134-137 24667498-5 2014 We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53. Lysine 110-116 tumor protein p53 Homo sapiens 14-17 25156493-4 2014 ArhGAP30 binds to p53 C-terminal domain and P300, facilitating P300-mediated acetylation of p53 at lysine 382. Lysine 99-105 tumor protein p53 Homo sapiens 18-21 25156493-4 2014 ArhGAP30 binds to p53 C-terminal domain and P300, facilitating P300-mediated acetylation of p53 at lysine 382. Lysine 99-105 tumor protein p53 Homo sapiens 92-95 24845634-10 2014 RESULTS: Pulsed H2O2 exposure triggered the acetylation of p53 at lysine 382 (K382) and subsequent increase in its target p21(Waf1/Cip1). Lysine 66-72 tumor protein p53 Homo sapiens 59-62 25288756-6 2014 Ras signaling selectively inactivates p53-mediated induction of p21Cip1 expression by inhibiting acetylation of specific lysine residues in the p53 DNA binding domain. Lysine 121-127 tumor protein p53 Homo sapiens 38-41 25288756-6 2014 Ras signaling selectively inactivates p53-mediated induction of p21Cip1 expression by inhibiting acetylation of specific lysine residues in the p53 DNA binding domain. Lysine 121-127 tumor protein p53 Homo sapiens 144-147 25288756-7 2014 Proliferation of cells lacking both Ras proteins and p53 can be prevented by reexpression of the human p53 ortholog, provided that it retains an active DNA binding domain and an intact lysine residue at position 164. Lysine 185-191 tumor protein p53 Homo sapiens 53-56 25288756-7 2014 Proliferation of cells lacking both Ras proteins and p53 can be prevented by reexpression of the human p53 ortholog, provided that it retains an active DNA binding domain and an intact lysine residue at position 164. Lysine 185-191 tumor protein p53 Homo sapiens 103-106 24691905-5 2014 By employing homologous recombination, we introduced various combinations of missense mutations (lysine to arginine) into eight acetylation sites of the endogenous p53 gene in human embryonic stem cells (hESCs). Lysine 97-103 tumor protein p53 Homo sapiens 164-167 24151879-1 2014 Protein lysine methyltransferase G9a, which catalyzes methylation of lysine 9 of histone H3 (H3K9) and lysine 373 (K373) of p53, is overexpressed in human cancers. Lysine 8-14 tumor protein p53 Homo sapiens 124-127 24151879-1 2014 Protein lysine methyltransferase G9a, which catalyzes methylation of lysine 9 of histone H3 (H3K9) and lysine 373 (K373) of p53, is overexpressed in human cancers. Lysine 69-75 tumor protein p53 Homo sapiens 124-127 24633296-5 2014 We describe here an MHC class II binding peptide from the tumor protein p53, which possesses an acetylated lysine at position 120 (p53110-124/AcK120) that is effective in eliciting CD4(+) T cell responses specific for the acetylated peptide. Lysine 107-113 tumor protein p53 Homo sapiens 72-75 24528089-6 2014 By employing the quantitative chromatin immunoprecipitation assay in detecting specific histone modifications in senescence-related genes including p53 and p16, it was demonstrated that the mRNA expression of p53 was associated with increased H4 acetylation in replicative senescence and increased H4 acetylation and trimethylation of histone H3 at lysine 4 (H3K4me3) in premature senescence. Lysine 349-355 tumor protein p53 Homo sapiens 148-151 24528089-6 2014 By employing the quantitative chromatin immunoprecipitation assay in detecting specific histone modifications in senescence-related genes including p53 and p16, it was demonstrated that the mRNA expression of p53 was associated with increased H4 acetylation in replicative senescence and increased H4 acetylation and trimethylation of histone H3 at lysine 4 (H3K4me3) in premature senescence. Lysine 349-355 tumor protein p53 Homo sapiens 209-212 24667498-5 2014 We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53. Lysine 110-116 tumor protein p53 Homo sapiens 124-127 24403071-8 2014 Adding either Lys-59 or Lys-109 back to the Otub1(K0) mutant restores the monoubiquitination of Otub1 and its function to stabilize and activate p53. Lysine 24-27 tumor protein p53 Homo sapiens 145-148 24375404-5 2014 We found that MYBBP1A has two regions that directly bind to lysine residues of the p53 C-terminal regulatory domain. Lysine 60-66 tumor protein p53 Homo sapiens 83-86 24403071-8 2014 Adding either Lys-59 or Lys-109 back to the Otub1(K0) mutant restores the monoubiquitination of Otub1 and its function to stabilize and activate p53. Lysine 14-17 tumor protein p53 Homo sapiens 145-148 24761888-6 2014 Further, significant differences were observed in the p53 exon 8 mutations for the genetic polymorphisms of Lys/Arg for AhR (p=0.02, 95%CI: 0.70-15.86), Val/Val for CYP1A1 (p=0.04, 95%CI: 0.98-19.09) and null for GSTM1 (p=0.02, 95%CI: 1.19-6.26), respectively. Lysine 108-111 tumor protein p53 Homo sapiens 54-57 24330748-5 2013 Immuno-precipitation/-blot studies were performed to demonstrate interactions between Id4, p53 and CBP/p300 and acetylation of specific lysine residues within p53. Lysine 136-142 tumor protein p53 Homo sapiens 159-162 24899917-1 2014 The latest experimental evidence indicates that acetylation of p53 at K164 (lysine 164) and K120 may induce directly cell apoptosis under severe DNA damage. Lysine 76-82 tumor protein p53 Homo sapiens 63-66 24038750-3 2014 We further discovered that the silencing of Oct4 significantly reduces the expression of Sirt1, a deacetylase known to inhibit p53 activity and the differentiation of ESCs, leading to increased acetylation of p53 at lysine 120 and 164. Lysine 216-222 tumor protein p53 Homo sapiens 209-212 24038750-5 2014 In addition, using knock-in approach, we revealed that the acetylation of p53 at lysine 120 and 164 is required for both stabilization and activity of p53 in hESCs. Lysine 81-87 tumor protein p53 Homo sapiens 74-77 24038750-5 2014 In addition, using knock-in approach, we revealed that the acetylation of p53 at lysine 120 and 164 is required for both stabilization and activity of p53 in hESCs. Lysine 81-87 tumor protein p53 Homo sapiens 151-154 24621507-3 2014 Conversely, Tip60 activates p53 through direct association on target promoters as well as acetylation of p53 at lysine 120 (K120). Lysine 112-118 tumor protein p53 Homo sapiens 105-108 24096875-6 2013 The inhibition of Lys(118) acetylation promoted the generation of NOS3-promoting prosurvival form of p53. Lysine 18-21 tumor protein p53 Homo sapiens 101-104 24032713-6 2013 Enhancer of zeste homologue 2 (EZH2), an important histone-modifying enzyme, is able to trimethylate histone 3 on lysine 27 (H3K27Me3), consequently leading to gene silencing, especially silencing of tumor suppressor genes such as p53. Lysine 114-120 tumor protein p53 Homo sapiens 231-234 24298606-0 2013 Lysine-specific modifications of p53: a matter of life and death? Lysine 0-6 tumor protein p53 Homo sapiens 33-36 24298606-3 2013 In this review, we focus on the role of recently discovered lysine-specific modifications of p53, methylation and acetylation in particular, and their effects on p53 activity in damaged cells. Lysine 60-66 tumor protein p53 Homo sapiens 93-96 24298606-3 2013 In this review, we focus on the role of recently discovered lysine-specific modifications of p53, methylation and acetylation in particular, and their effects on p53 activity in damaged cells. Lysine 60-66 tumor protein p53 Homo sapiens 162-165 24096875-0 2013 p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation. Lysine 142-145 tumor protein p53 Homo sapiens 0-3 24096875-0 2013 p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation. Lysine 142-145 tumor protein p53 Homo sapiens 95-98 24096875-0 2013 p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation. Lysine 142-145 tumor protein p53 Homo sapiens 95-98 24096875-5 2013 In the infarct heart, p53 was heavily acetylated at Lys(118) residue, which was exclusively reversed in the oxygenated heart, apparently regulated by oxygen-dependent expression of TIP60. Lysine 52-55 tumor protein p53 Homo sapiens 22-25 24194938-0 2013 Acetylation of lysine 382 and phosphorylation of serine 392 in p53 modulate the interaction between p53 and MDC1 in vitro. Lysine 15-21 tumor protein p53 Homo sapiens 100-103 24194938-5 2013 We further show that both acetylation of lysine 382 and phosphorylation of serine 392 in p53 enhance the interaction between p53 and MDC1. Lysine 41-47 tumor protein p53 Homo sapiens 125-128 24088713-3 2013 SET7/9 (Setd7, KMT7) is a protein methyltransferase that catalyses lysine monomethylation of histones, but also methylates many non-histone target proteins such as p53 or DNMT1. Lysine 67-73 tumor protein p53 Homo sapiens 164-167 23775793-8 2013 Furthermore, both p53 binding and transactivation were associated with increased active histone modification histone H3 lysine 4 trimethylation. Lysine 120-126 tumor protein p53 Homo sapiens 18-21 23576563-2 2013 p53 is acetylated at lysine 120 (K120) by acetyltranferases Tip60 (KAT5) and hMOF (KAT8) in response to DNA damage. Lysine 21-27 tumor protein p53 Homo sapiens 0-3 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 tumor protein p53 Homo sapiens 14-17 23416275-1 2013 Acetylation of C-terminal lysine residues in the p53 tumor suppressor is associated with increased stability and transcription factor activity. Lysine 26-32 tumor protein p53 Homo sapiens 49-52 23416275-3 2013 Here, we show that p14(ARF) increases the level of p53 acetylated at lysine 382 in a nuclear chromatin-rich fraction. Lysine 69-75 tumor protein p53 Homo sapiens 51-54 23583237-4 2013 Here we demonstrate that MYBBP1A interacts with lysine residues in the C-terminal regulatory domain region of p53. Lysine 48-54 tumor protein p53 Homo sapiens 110-113 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 tumor protein p53 Homo sapiens 61-64 22493095-3 2012 Sumoylation of HDAC2 at lysine 462 allows binding of HDAC2 to p53. Lysine 24-30 tumor protein p53 Homo sapiens 62-65 22583696-9 2012 Since H4 and p53 both contain the target lysine in an unstructured part of the protein, we conclude that the long recognition sequence of SET8 makes it difficult to methylate a lysine in a folded region of a protein, because amino acid side chains essential for recognition will be buried. Lysine 41-47 tumor protein p53 Homo sapiens 13-16 23148227-8 2013 Furthermore, RUNX1 was associated with p300 histone acetyltransferase, and ADR-dependent acetylation of p53 at Lys-373/382 was markedly inhibited in RUNX1 knockdown cells. Lysine 111-114 tumor protein p53 Homo sapiens 104-107 22683437-2 2012 Other individual reports identified lysine acetylation as a PTM regulating transcription factors and co-activators including p53, c-Myc, PGC1alpha and Ku70. Lysine 36-42 tumor protein p53 Homo sapiens 125-128 22493095-5 2012 Deacetylation of p53 at lysine 320 by sumoylated HDAC2 blocks recruitment of p53 into promoter-associated complexes and p53-dependent expression of genes for cell cycle control and apoptosis. Lysine 24-30 tumor protein p53 Homo sapiens 17-20 22493095-5 2012 Deacetylation of p53 at lysine 320 by sumoylated HDAC2 blocks recruitment of p53 into promoter-associated complexes and p53-dependent expression of genes for cell cycle control and apoptosis. Lysine 24-30 tumor protein p53 Homo sapiens 77-80 22493095-5 2012 Deacetylation of p53 at lysine 320 by sumoylated HDAC2 blocks recruitment of p53 into promoter-associated complexes and p53-dependent expression of genes for cell cycle control and apoptosis. Lysine 24-30 tumor protein p53 Homo sapiens 77-80 22696202-0 2012 Increased acetylation of lysine 317/320 of p53 caused by BCR-ABL protects from cytoplasmic translocation of p53 and mitochondria-dependent apoptosis in response to DNA damage. Lysine 25-31 tumor protein p53 Homo sapiens 43-46 22696202-0 2012 Increased acetylation of lysine 317/320 of p53 caused by BCR-ABL protects from cytoplasmic translocation of p53 and mitochondria-dependent apoptosis in response to DNA damage. Lysine 25-31 tumor protein p53 Homo sapiens 108-111 22696202-6 2012 In this study we have investigated whether the expression of BCR-ABL could influence the acetylation of p53, specifically at lysine 317/320 (K317/K320), which has been shown to regulate nuclear export and transcription-independent apoptotic activity of p53. Lysine 125-131 tumor protein p53 Homo sapiens 104-107 22864287-0 2012 PHF20 is an effector protein of p53 double lysine methylation that stabilizes and activates p53. Lysine 43-49 tumor protein p53 Homo sapiens 32-35 22864287-0 2012 PHF20 is an effector protein of p53 double lysine methylation that stabilizes and activates p53. Lysine 43-49 tumor protein p53 Homo sapiens 92-95 22552582-1 2012 Acetylation of the tumor suppressor gene p53 at the carboxy-terminal lysine (Lys) residues enhances its transcriptional activity associated with cell cycle arrest and apoptosis. Lysine 69-75 tumor protein p53 Homo sapiens 41-44 22552582-1 2012 Acetylation of the tumor suppressor gene p53 at the carboxy-terminal lysine (Lys) residues enhances its transcriptional activity associated with cell cycle arrest and apoptosis. Lysine 77-80 tumor protein p53 Homo sapiens 41-44 21963854-6 2012 p53 pre-methylated at lysine-372 (p53K372 mono-methylation) by SET7 protects p53 from E6-induced degradation. Lysine 22-28 tumor protein p53 Homo sapiens 0-3 21963854-6 2012 p53 pre-methylated at lysine-372 (p53K372 mono-methylation) by SET7 protects p53 from E6-induced degradation. Lysine 22-28 tumor protein p53 Homo sapiens 34-37 21597459-5 2011 Hades polyubiquitinates p53 in vitro independent of Mdm2 and targets a critical lysine residue in p53 (lysine 24) distinct from those targeted by Mdm2. Lysine 80-86 tumor protein p53 Homo sapiens 24-27 22214662-3 2012 Here, we report that RAX/PACT interacts with the SUMO E2 ligase Ubc9 to stimulate p53-Ubc9 association and reversible p53 sumoylation on lysine 386. Lysine 137-143 tumor protein p53 Homo sapiens 118-121 22194015-1 2012 During the last decade, we saw an explosion of studies investigating the role of lysine methylation/demethylation of histones and non-histone proteins, such as p53, NF-kappaB, and E2F1. Lysine 81-87 tumor protein p53 Homo sapiens 160-163 22237799-6 2012 We show here that metanephric p53 is phosphorylated and acetylated on key serine and lysine residues, respectively, in a temporal profile which correlates with the maturational changes in total p53 levels and DNA-binding activity. Lysine 85-91 tumor protein p53 Homo sapiens 30-33 20978925-8 2012 CG200745 increased acetylation of p53 lysine residues K320, K373, and K382. Lysine 38-44 tumor protein p53 Homo sapiens 34-37 22285752-4 2012 In other cells without adenovirus expression, the C-terminal domain of WTX binds to the DNA-binding domain of p53, enhances its binding to CBP, and increases CBP/p300-mediated acetylation of p53 at Lys 373/382. Lysine 198-201 tumor protein p53 Homo sapiens 191-194 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. Lysine 106-112 tumor protein p53 Homo sapiens 58-61 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. Lysine 106-112 tumor protein p53 Homo sapiens 87-90 22389628-4 2012 In response to retinoic acid, CBP/p300 acetylates p53 at lysine 373, which leads to dissociation from E3-ubiquitin ligases HDM2 and TRIM24. Lysine 57-63 tumor protein p53 Homo sapiens 50-53 21597459-5 2011 Hades polyubiquitinates p53 in vitro independent of Mdm2 and targets a critical lysine residue in p53 (lysine 24) distinct from those targeted by Mdm2. Lysine 80-86 tumor protein p53 Homo sapiens 98-101 21597459-5 2011 Hades polyubiquitinates p53 in vitro independent of Mdm2 and targets a critical lysine residue in p53 (lysine 24) distinct from those targeted by Mdm2. Lysine 103-109 tumor protein p53 Homo sapiens 24-27 21597459-5 2011 Hades polyubiquitinates p53 in vitro independent of Mdm2 and targets a critical lysine residue in p53 (lysine 24) distinct from those targeted by Mdm2. Lysine 103-109 tumor protein p53 Homo sapiens 98-101 22033337-4 2011 Our results show that virus infection induces p53 acetylation at lysine 379, and that this modification is absolutely required for p53-dependent transcriptional transactivation of both, pro-apoptotic and IFN-stimulated genes induced by virus infection, and for p53-mediated control of virus replication. Lysine 65-71 tumor protein p53 Homo sapiens 46-49 21880715-2 2011 Here we report that SMYD2 prefers to methylate p53 Lys-370 over histone substrates in vitro. Lysine 51-54 tumor protein p53 Homo sapiens 47-50 21880715-3 2011 Consistently, the level of endogenous p53 Lys-370 monomethylation is significantly elevated when SMYD2 is overexpressed in vivo. Lysine 42-45 tumor protein p53 Homo sapiens 38-41 22033337-4 2011 Our results show that virus infection induces p53 acetylation at lysine 379, and that this modification is absolutely required for p53-dependent transcriptional transactivation of both, pro-apoptotic and IFN-stimulated genes induced by virus infection, and for p53-mediated control of virus replication. Lysine 65-71 tumor protein p53 Homo sapiens 131-134 22033337-4 2011 Our results show that virus infection induces p53 acetylation at lysine 379, and that this modification is absolutely required for p53-dependent transcriptional transactivation of both, pro-apoptotic and IFN-stimulated genes induced by virus infection, and for p53-mediated control of virus replication. Lysine 65-71 tumor protein p53 Homo sapiens 131-134 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 310-313 tumor protein p53 Homo sapiens 97-100 21880715-10 2011 Meanwhile, mutation of EDEE residues impairs both the binding and the enzymatic activity of SMYD2 to p53 Lys-370. Lysine 105-108 tumor protein p53 Homo sapiens 101-104 21880715-11 2011 These data together reveal the molecular basis of SMYD2 in specifically recognizing and regulating functions of p53 tumor suppressor through Lys-370 monomethylation. Lysine 141-144 tumor protein p53 Homo sapiens 112-115 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 310-313 tumor protein p53 Homo sapiens 97-100 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 310-313 tumor protein p53 Homo sapiens 97-100 21791603-4 2011 Specifically, we show that Pirh2, a target of the p53 tumor suppressor, monoubiquitinates PolH at one of multiple lysine residues. Lysine 114-120 tumor protein p53 Homo sapiens 50-53 21780790-1 2011 Protein lysine methyltransferase G9a plays key roles in the transcriptional repression of a variety of genes via dimethylation of lysine 9 on histone H3 (H3K9me2) of chromatin as well as dimethylation of nonhistone proteins including tumor suppressor p53. Lysine 8-14 tumor protein p53 Homo sapiens 251-254 21855805-2 2011 In particular, Set7/9 (KMT7)-mediated monomethylation of human p53 at lysine 372 (p53K372me1) was suggested to be essential for p53 activation in human cell lines. Lysine 70-76 tumor protein p53 Homo sapiens 63-66 21855805-2 2011 In particular, Set7/9 (KMT7)-mediated monomethylation of human p53 at lysine 372 (p53K372me1) was suggested to be essential for p53 activation in human cell lines. Lysine 70-76 tumor protein p53 Homo sapiens 82-85 21855806-3 2011 Originally defined as a critical layer of p53 regulation in human cell lines, p53 lysine methylation by Set7/9 (also called Setd7) was proposed to fulfill a similar function in vivo in the mouse, promoting p53 acetylation, stabilization, and activation upon DNA damage (Kurash et al., 2008). Lysine 82-88 tumor protein p53 Homo sapiens 42-45 21855806-3 2011 Originally defined as a critical layer of p53 regulation in human cell lines, p53 lysine methylation by Set7/9 (also called Setd7) was proposed to fulfill a similar function in vivo in the mouse, promoting p53 acetylation, stabilization, and activation upon DNA damage (Kurash et al., 2008). Lysine 82-88 tumor protein p53 Homo sapiens 78-81 21642861-8 2011 Interestingly, p53 acetylation at lysine 382 was significantly increased, and c-myc expression simultaneously down-regulated in cotreated cells. Lysine 34-40 tumor protein p53 Homo sapiens 15-18 21642861-10 2011 Furthermore, c-myc down-regulation and apoptotic cell death coinduced by IR and HDACI were suppressed in cells transfected with mutant K382R p53 and C135Y p53 displaying loss of acetylation at lysine 382 and DNA-binding activity, respectively. Lysine 193-199 tumor protein p53 Homo sapiens 141-144 21642861-10 2011 Furthermore, c-myc down-regulation and apoptotic cell death coinduced by IR and HDACI were suppressed in cells transfected with mutant K382R p53 and C135Y p53 displaying loss of acetylation at lysine 382 and DNA-binding activity, respectively. Lysine 193-199 tumor protein p53 Homo sapiens 155-158 21565980-3 2011 SIRT1, the main member of the sirtuin family, inactivates p53 by deacetylating a critical lysine residue. Lysine 90-96 tumor protein p53 Homo sapiens 58-61 21586571-0 2011 Peptide-protein interactions suggest that acetylation of lysines 381 and 382 of p53 is important for positive coactivator 4-p53 interaction. Lysine 57-64 tumor protein p53 Homo sapiens 80-83 21586571-0 2011 Peptide-protein interactions suggest that acetylation of lysines 381 and 382 of p53 is important for positive coactivator 4-p53 interaction. Lysine 57-64 tumor protein p53 Homo sapiens 124-127 21586571-9 2011 Intermolecular nuclear Overhauser effect placed aspartate 76 in the vicinity of lysine 381, indicating that the region around residues 73-76 of PC4 is important for p53 recognition. Lysine 80-86 tumor protein p53 Homo sapiens 165-168 21586571-10 2011 We conclude that the 380-386 region of p53 interacts with the region around residues 73-76 of PC4, and acetylation of lysine 382/381 of p53 may play an important role in modulating p53-PC4 interaction and as a consequence PC4 mediated activation of p53 target genes. Lysine 118-124 tumor protein p53 Homo sapiens 39-42 21586571-10 2011 We conclude that the 380-386 region of p53 interacts with the region around residues 73-76 of PC4, and acetylation of lysine 382/381 of p53 may play an important role in modulating p53-PC4 interaction and as a consequence PC4 mediated activation of p53 target genes. Lysine 118-124 tumor protein p53 Homo sapiens 136-139 21586571-10 2011 We conclude that the 380-386 region of p53 interacts with the region around residues 73-76 of PC4, and acetylation of lysine 382/381 of p53 may play an important role in modulating p53-PC4 interaction and as a consequence PC4 mediated activation of p53 target genes. Lysine 118-124 tumor protein p53 Homo sapiens 136-139 21586571-10 2011 We conclude that the 380-386 region of p53 interacts with the region around residues 73-76 of PC4, and acetylation of lysine 382/381 of p53 may play an important role in modulating p53-PC4 interaction and as a consequence PC4 mediated activation of p53 target genes. Lysine 118-124 tumor protein p53 Homo sapiens 136-139 21826189-0 2011 Regulation of p53 function by lysine methylation. Lysine 30-36 tumor protein p53 Homo sapiens 14-17 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 101-104 tumor protein p53 Homo sapiens 50-53 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 101-104 tumor protein p53 Homo sapiens 97-100 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 101-104 tumor protein p53 Homo sapiens 97-100 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 101-104 tumor protein p53 Homo sapiens 97-100 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 310-313 tumor protein p53 Homo sapiens 50-53 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 310-313 tumor protein p53 Homo sapiens 97-100 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 310-313 tumor protein p53 Homo sapiens 97-100 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 310-313 tumor protein p53 Homo sapiens 97-100 21724641-7 2011 Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370). Lysine 310-313 tumor protein p53 Homo sapiens 50-53 21463657-5 2011 Overexpression of TRIM29 promoted degradation and changed localization of Tip60 and reduced acetylation of p53 at lysine 120 by Tip60, resulting in enhancement of cell growth and transforming activity. Lysine 114-120 tumor protein p53 Homo sapiens 107-110 21826189-2 2011 In addition to histones, several other nuclear factors such as the tumor suppressor and transcription factor p53 undergo lysine methylation, suggesting that this modification may be a common mechanism for modulating protein-protein interactions and key cellular signaling pathways. Lysine 121-127 tumor protein p53 Homo sapiens 109-112 21826189-3 2011 This article focuses on how lysine methylation events on the C-terminal tail of p53 are generated, sensed and transduced to modulate p53 functions. Lysine 28-34 tumor protein p53 Homo sapiens 80-83 21826189-3 2011 This article focuses on how lysine methylation events on the C-terminal tail of p53 are generated, sensed and transduced to modulate p53 functions. Lysine 28-34 tumor protein p53 Homo sapiens 133-136 21525412-0 2011 Acetylation of lysine 120 of p53 endows DNA-binding specificity at effective physiological salt concentration. Lysine 15-21 tumor protein p53 Homo sapiens 29-32 21525412-3 2011 We prepared p53 specifically acetylated at Lys120, AcK120p53, by in vivo incorporation of acetylated lysine to study biophysical and structural consequences of acetylation that may shed light on its biological role. Lysine 101-107 tumor protein p53 Homo sapiens 12-15 21513889-3 2011 p53 activation is dependent on lysine acetylation by the lysine acetyltransferase and transcriptional coactivator CREB-binding protein (CBP) and on acetylation-directed CBP recruitment for p53 target gene expression. Lysine 31-37 tumor protein p53 Homo sapiens 0-3 21417280-1 2011 Proteins which bind methylated lysines ("readers" of the histone code) are important components in the epigenetic regulation of gene expression and can also modulate other proteins that contain methyl-lysine such as p53 and Rb. Lysine 31-38 tumor protein p53 Homo sapiens 216-219 21303901-4 2011 VPA seems to stabilize a specific acetyl modification (lysine 120) of the p53 tumor suppressor protein, resulting in an increase in its proapoptotic function at the mitochondrial membrane. Lysine 55-61 tumor protein p53 Homo sapiens 74-77 21057544-1 2011 Inducible acetylation of p53 at lysine residues has a great impact on regulating the transactivation of this protein, which is associated with cell growth arrest and/or apoptosis under various stress conditions. Lysine 32-38 tumor protein p53 Homo sapiens 25-28 21465572-2 2011 In response to oxidative, nitrosative, and electrophilic insults, p53 undergoes post-translational modifications, such as oxidation and covalent modification of cysteines, nitration of tyrosines, acetylation of lysines, phosphorylation of serine/threonine residues, etc. Lysine 211-218 tumor protein p53 Homo sapiens 66-69 21271695-6 2011 The best cyclopeptide of the series exhibited a K(d) of 8.0 muM, representing a 24-fold improvement in affinity over that of the linear lysine 382-acetylated p53 peptide. Lysine 136-142 tumor protein p53 Homo sapiens 158-161 21151202-1 2011 p53, NFkappaB, STAT3, and several other transcription factors are reversibly methylated on lysine residues by enzymes that also modify histones. Lysine 91-97 tumor protein p53 Homo sapiens 0-3 20368352-7 2010 Mechanistically, ATDC binds p53, and this interaction is potentially fine-tuned by posttranslational acetylation of lysine 116 on ATDC. Lysine 116-122 tumor protein p53 Homo sapiens 28-31 21148320-7 2011 Specifically, acetylation of p53 at lysine 120, a DNA-binding domain residue mutated in human cancer, is essential for triggering apoptosis. Lysine 36-42 tumor protein p53 Homo sapiens 29-32 20703075-4 2010 We previously reported that the highly conserved p53 Arg(R)-174 is substituted by lysine (K) in Spalax, identical to a tumor-associated mutation. Lysine 82-88 tumor protein p53 Homo sapiens 49-52 20639885-1 2010 The p53 tumor suppressor interacts with its negative regulator Mdm2 via the former"s N-terminal region and core domain, yet the extreme p53 C-terminal region contains lysine residues ubiquitinated by Mdm2 and can bear post-translational modifications that inhibit Mdm2-p53 association. Lysine 167-173 tumor protein p53 Homo sapiens 136-139 20639885-1 2010 The p53 tumor suppressor interacts with its negative regulator Mdm2 via the former"s N-terminal region and core domain, yet the extreme p53 C-terminal region contains lysine residues ubiquitinated by Mdm2 and can bear post-translational modifications that inhibit Mdm2-p53 association. Lysine 167-173 tumor protein p53 Homo sapiens 136-139 20931131-1 2011 Upon genomic insult, the tumor suppressor p53 is phosphorylated and acetylated at specific serine and lysine residues, increasing its stability and transactivation function. Lysine 102-108 tumor protein p53 Homo sapiens 42-45 20614940-1 2010 Protein lysine methyltransferase G9a, which catalyzes methylation of lysine 9 of histone H3 (H3K9) and lysine 373 (K373) of p53, is overexpressed in human cancers. Lysine 8-14 tumor protein p53 Homo sapiens 124-127 20614940-1 2010 Protein lysine methyltransferase G9a, which catalyzes methylation of lysine 9 of histone H3 (H3K9) and lysine 373 (K373) of p53, is overexpressed in human cancers. Lysine 69-75 tumor protein p53 Homo sapiens 124-127 20307547-7 2010 The signature HKKme2 motif of p53, which defines specificity, is identified through a combination of NMR resonance perturbations, mutagenesis, measurements of binding affinities and docking simulations, and analysis of the crystal structures of 53BP1 bound to p53 peptides containing other dimethyl-lysine marks, p53K370me2 (p53 dimethylated at Lys370) and p53K372me2 (p53 dimethylated at Lys372). Lysine 299-305 tumor protein p53 Homo sapiens 30-33 20307547-7 2010 The signature HKKme2 motif of p53, which defines specificity, is identified through a combination of NMR resonance perturbations, mutagenesis, measurements of binding affinities and docking simulations, and analysis of the crystal structures of 53BP1 bound to p53 peptides containing other dimethyl-lysine marks, p53K370me2 (p53 dimethylated at Lys370) and p53K372me2 (p53 dimethylated at Lys372). Lysine 299-305 tumor protein p53 Homo sapiens 260-263 20307547-7 2010 The signature HKKme2 motif of p53, which defines specificity, is identified through a combination of NMR resonance perturbations, mutagenesis, measurements of binding affinities and docking simulations, and analysis of the crystal structures of 53BP1 bound to p53 peptides containing other dimethyl-lysine marks, p53K370me2 (p53 dimethylated at Lys370) and p53K372me2 (p53 dimethylated at Lys372). Lysine 299-305 tumor protein p53 Homo sapiens 260-263 20307547-7 2010 The signature HKKme2 motif of p53, which defines specificity, is identified through a combination of NMR resonance perturbations, mutagenesis, measurements of binding affinities and docking simulations, and analysis of the crystal structures of 53BP1 bound to p53 peptides containing other dimethyl-lysine marks, p53K370me2 (p53 dimethylated at Lys370) and p53K372me2 (p53 dimethylated at Lys372). Lysine 299-305 tumor protein p53 Homo sapiens 260-263 20118233-2 2010 Lysine methylation has recently emerged as a key post-translational modification that alters the activity of p53. Lysine 0-6 tumor protein p53 Homo sapiens 109-112 20118233-3 2010 Here, we describe a novel lysine methylation site in p53 that is carried out by two homologous histone methyltransferases, G9a and Glp. Lysine 26-32 tumor protein p53 Homo sapiens 53-56 20118233-4 2010 G9a and Glp specifically methylate p53 at Lys(373), resulting mainly in dimethylation. Lysine 42-45 tumor protein p53 Homo sapiens 35-38 20118233-5 2010 During DNA damage, the overall level of p53 modified at Lys(373)me2 does not increase, despite the dramatic increase in total p53, indicating that Lys(373)me2 correlates with inactive p53. Lysine 56-59 tumor protein p53 Homo sapiens 40-43 19927155-7 2010 We find that direct binding of p53 to importin-alpha3 depends on the positive charge contributed by lysine residues 319-321 within NLS I. Lysine 100-106 tumor protein p53 Homo sapiens 31-34 19927155-11 2010 Thus, under normal growth conditions, ubiquitination of Lys 319-321 negatively regulates p53-importin-alpha3 binding, thereby restraining p53 import. Lysine 56-59 tumor protein p53 Homo sapiens 89-92 19927155-11 2010 Thus, under normal growth conditions, ubiquitination of Lys 319-321 negatively regulates p53-importin-alpha3 binding, thereby restraining p53 import. Lysine 56-59 tumor protein p53 Homo sapiens 138-141 19861417-7 2009 Persistent DHCR24 overexpression did not alter the phosphorylation status of p53 but resulted in decreased acetylation of p53 at lysine residues 373 and 382 in the nucleus after treatment with hydrogen peroxide. Lysine 129-135 tumor protein p53 Homo sapiens 122-125 19857530-7 2010 Lys 305 of p53 was identified as one of the Ub acceptor sites using this strategy. Lysine 0-3 tumor protein p53 Homo sapiens 11-14 19617712-4 2009 Here we report that human double minute-2 protein (HDM2), a p53-specific E3 ubiquitin ligase, specifically ubiquitinates HEXIM1 through the lysine residues located within the basic region of HEXIM1. Lysine 140-146 tumor protein p53 Homo sapiens 60-63 20024960-6 2009 DEB increased the acetylation of p53 at lys-382, dramatically reduced complex formation between p53 and its regulator protein mdm2 and induced the phosphorylation of p53 at serines 15, 20, 37, 46, and 392 in human lymphoblasts. Lysine 40-43 tumor protein p53 Homo sapiens 33-36 19808967-5 2009 MDM2 blocks RUNX3 transcriptional activity by interacting with RUNX3 through an acidic domain adjacent to the p53-binding domain of MDM2 and ubiquitinates RUNX3 on key lysine residues to mediate nuclear export and proteasomal degradation. Lysine 168-174 tumor protein p53 Homo sapiens 110-113 19494119-3 2009 We and others identified acetylation of the p53 DNA binding domain at lysine 120 as a critical event in apoptosis induction. Lysine 70-76 tumor protein p53 Homo sapiens 44-47 19494119-4 2009 Although initial studies showed that Lys-120 acetylation plays a role in p53 function in the nucleus, we report here a role for Lys-120 acetylation in transcription-independent apoptosis. Lysine 37-40 tumor protein p53 Homo sapiens 73-76 19494119-5 2009 We demonstrate that the Lys-120-acetylated isoform of p53 is enriched at mitochondria. Lysine 24-27 tumor protein p53 Homo sapiens 54-57 19494119-9 2009 These data support a model whereby Lys-120 acetylation contributes to both the transcription-dependent and -independent apoptotic pathways induced by p53. Lysine 35-38 tumor protein p53 Homo sapiens 150-153 19642109-3 2009 The vertical dimension and the bearing volume of the DNA binding domain (DBD) of p53, anchored to functionalized gold substrate through exposed lysine residues, alone and after deposing AZ, have been measured by TM-AFM. Lysine 144-150 tumor protein p53 Homo sapiens 81-84 21475861-9 2009 In a recent study using protein-specific anti-acetyl lysine antibodies and immunological methods, we demonstrated the ability of aspirin to acetylate the tumor suppressor protein p53. Lysine 53-59 tumor protein p53 Homo sapiens 179-182 19432880-4 2009 In addition, the Mdmx mutant cooperates with Mdm2 to induce ubiquitination of p53 at C-terminal lysine residues, and the integrity of the C-terminal lysines was partly required for the cooperative inhibition. Lysine 96-102 tumor protein p53 Homo sapiens 78-81 19432880-4 2009 In addition, the Mdmx mutant cooperates with Mdm2 to induce ubiquitination of p53 at C-terminal lysine residues, and the integrity of the C-terminal lysines was partly required for the cooperative inhibition. Lysine 149-156 tumor protein p53 Homo sapiens 78-81 19416725-5 2009 This suggests that acetylation at Lys-120 of p53 negatively regulates a signaling pathway leading to NFAT activation. Lysine 34-37 tumor protein p53 Homo sapiens 45-48 18753126-3 2009 Here we report identification of the first three in vivo non-histone protein substrates of lysine propionylation in eukaryotic cells: p53, p300, and CREB-binding protein. Lysine 91-97 tumor protein p53 Homo sapiens 134-137 19334741-1 2009 Lysine methylation is an important post-translational modification that affects protein function; for example, the transcriptional activity of the p53 tumor suppressor protein. Lysine 0-6 tumor protein p53 Homo sapiens 147-150 19334741-3 2009 The method, which relies on the synthesis of (13)C-enriched alkylating agents, was applied to the production of 15-residue p53 peptides variously methylated at lysine analogue 370. Lysine 160-166 tumor protein p53 Homo sapiens 123-126 19265193-1 2009 Acetylation of p53 at carboxyl-terminal lysine residues enhances its transcriptional activity associated with cell cycle arrest and apoptosis. Lysine 40-46 tumor protein p53 Homo sapiens 15-18 19265193-2 2009 Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824. Lysine 44-47 tumor protein p53 Homo sapiens 25-28 19265193-2 2009 Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824. Lysine 52-55 tumor protein p53 Homo sapiens 25-28 19265193-2 2009 Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824. Lysine 52-55 tumor protein p53 Homo sapiens 25-28 19106109-0 2009 p53 Oligomerization is essential for its C-terminal lysine acetylation. Lysine 52-58 tumor protein p53 Homo sapiens 0-3 19106109-1 2009 Acetylation of multiple lysine residues in the p53 plays critical roles in the protein stability and transcriptional activity of p53. Lysine 24-30 tumor protein p53 Homo sapiens 47-50 19106109-1 2009 Acetylation of multiple lysine residues in the p53 plays critical roles in the protein stability and transcriptional activity of p53. Lysine 24-30 tumor protein p53 Homo sapiens 129-132 19106109-3 2009 We found that p53 mutants that are defective in tetramer formation are also defective in C-terminal lysine residue acetylation. Lysine 100-106 tumor protein p53 Homo sapiens 14-17 19106109-4 2009 Consistently, we found that several cancer-derived p53 mutants that bear mutations in the tetramerization domain cannot form oligomers and are defective in C-terminal lysine acetylation, and these mutants are inactive in p21 transactivation. Lysine 167-173 tumor protein p53 Homo sapiens 51-54 19179064-0 2009 Modifications of p53: competing for the lysines. Lysine 40-47 tumor protein p53 Homo sapiens 17-20 19179064-2 2009 In addition to a multitude of phosphorylated serines and threonines, many of the lysine residues in p53 can be modified to regulate activity, stability and subcellular localization of the protein. Lysine 81-87 tumor protein p53 Homo sapiens 100-103 19179064-3 2009 This complexity is amplified by the variety of modifications that can target the same lysine residue - often with opposing effects on p53 function. Lysine 86-92 tumor protein p53 Homo sapiens 134-137 19046801-12 2009 Mutations of p53 determined in NHL cases (30%) were of Arg-176 (1/20: 5%), Phe-238 (1/20: 5%), Ser-249 (2/20; 10%), Lys-249 (1/20: 5%) and Phe-250 (1/20: 5%). Lysine 116-119 tumor protein p53 Homo sapiens 13-16 19221494-4 2009 p53 activity is influenced by post-translational modifications, including phosphorylation and lysine methylation. Lysine 94-100 tumor protein p53 Homo sapiens 0-3 19201868-8 2009 p53 was processed to three cleavage products of p40, p35, and p13 fragments at Lys(24) and Lys(305). Lysine 79-82 tumor protein p53 Homo sapiens 0-3 19201868-8 2009 p53 was processed to three cleavage products of p40, p35, and p13 fragments at Lys(24) and Lys(305). Lysine 91-94 tumor protein p53 Homo sapiens 0-3 19085961-8 2009 Moreover, we found that ectopic overexpression of p33(ING1b) or p24(ING1c) significantly induced p53 protein acetylation at Lys-373/Lys-382 residue, but did not alter the phosphorylation status of p53. Lysine 124-127 tumor protein p53 Homo sapiens 97-100 19085961-8 2009 Moreover, we found that ectopic overexpression of p33(ING1b) or p24(ING1c) significantly induced p53 protein acetylation at Lys-373/Lys-382 residue, but did not alter the phosphorylation status of p53. Lysine 132-135 tumor protein p53 Homo sapiens 97-100 19595309-5 2009 There are, however, still many open questions regarding, for example, whether sirtuins deacetylate those lysine residues in p53 that are critical for its activity. Lysine 105-111 tumor protein p53 Homo sapiens 124-127 18840612-0 2008 Role for 53BP1 Tudor domain recognition of p53 dimethylated at lysine 382 in DNA damage signaling. Lysine 63-69 tumor protein p53 Homo sapiens 43-46 18840612-3 2008 Recently, lysine methylation has been shown also to play a role in regulating non-histone proteins, including the tumor suppressor protein p53 (Huang, J., and Berger, S. L. (2008) Curr. Lysine 10-16 tumor protein p53 Homo sapiens 139-142 18840612-8 2008 Here, we identify a novel p53 species that is dimethylated at lysine 382 (p53K382me2) and show that the tandem Tudor domain of the DNA damage response mediator 53BP1 acts as an "effector" for this mark. Lysine 62-68 tumor protein p53 Homo sapiens 26-29 18697203-7 2008 For the repression, acetylation of the C-terminal lysines of p53 is important, and both acetyl-K373p53 and methyl-K370p53 became bound to the promoter. Lysine 50-57 tumor protein p53 Homo sapiens 61-64 18581285-6 2008 Indeed, histone lysine methyltransferases KMT5 (Set9), KMT3C (Smyd2), and KMT5A (Set8) methylate p53 at specific C-terminal lysines. Lysine 124-131 tumor protein p53 Homo sapiens 97-100 18707164-3 2008 The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr. Lysine 117-120 tumor protein p53 Homo sapiens 75-78 18707164-3 2008 The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr. Lysine 162-165 tumor protein p53 Homo sapiens 75-78 18523266-7 2008 The protein stability, Ser(392) phosphorylation and Lys(373)/Lys(382) acetylation of p53 were enhanced by MG132. Lysine 52-55 tumor protein p53 Homo sapiens 85-88 18523266-7 2008 The protein stability, Ser(392) phosphorylation and Lys(373)/Lys(382) acetylation of p53 were enhanced by MG132. Lysine 61-64 tumor protein p53 Homo sapiens 85-88 18406507-7 2008 Activation of p53 was evidenced by its phosphorylation at serine 15 (Ser15) and acetylation at lysine 382 (Lys382). Lysine 95-101 tumor protein p53 Homo sapiens 14-17 18512960-13 2008 The average value of the experimental DeltaG(E)() for the six lysine methyl transfer reactions catalyzed by vSET, LSMT, and SET7/9 with p53 as a substrate is 22.1 +/- 1.0 kcal/mol, and the computed average (DeltaG(C)()) is 22.2 +/- 0.8 kcal/mol. Lysine 62-68 tumor protein p53 Homo sapiens 136-139 18406507-11 2008 Acetylation of p53 at Lys 382 was not affected by these inhibitors, suggesting that acetylation stabilizes p53 in response to DNA damage. Lysine 22-25 tumor protein p53 Homo sapiens 15-18 18305112-2 2008 Here, we report that ARF associates with COMMD1 and promotes Lys(63)-mediated polyubiquitination of COMMD1 in a p53-independent manner. Lysine 61-64 tumor protein p53 Homo sapiens 112-115 18305112-8 2008 Together, these data suggest that the ability to promote Lys(63)-mediated polyubiquitination of COMMD1 is a novel property of ARF independent of p53. Lysine 57-60 tumor protein p53 Homo sapiens 145-148 18339539-3 2008 In particular, the tumor suppressor and transcription factor p53 has provided a model for lysine methylation on a non-histone protein. Lysine 90-96 tumor protein p53 Homo sapiens 61-64 18581285-7 2008 Lysine methylation enhances or suppresses p53 transcriptional activity depending on the methylation site. Lysine 0-6 tumor protein p53 Homo sapiens 42-45 17977830-6 2008 This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively. Lysine 86-89 tumor protein p53 Homo sapiens 14-17 17977830-6 2008 This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively. Lysine 86-89 tumor protein p53 Homo sapiens 79-82 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 83-86 tumor protein p53 Homo sapiens 216-219 17977830-6 2008 This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively. Lysine 99-102 tumor protein p53 Homo sapiens 14-17 17977830-6 2008 This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively. Lysine 99-102 tumor protein p53 Homo sapiens 14-17 17977830-7 2008 These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment. Lysine 165-168 tumor protein p53 Homo sapiens 6-9 17977830-7 2008 These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment. Lysine 165-168 tumor protein p53 Homo sapiens 158-161 17977830-7 2008 These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment. Lysine 174-177 tumor protein p53 Homo sapiens 6-9 17977830-7 2008 These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment. Lysine 174-177 tumor protein p53 Homo sapiens 158-161 17977830-7 2008 These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment. Lysine 174-177 tumor protein p53 Homo sapiens 6-9 17977830-7 2008 These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment. Lysine 174-177 tumor protein p53 Homo sapiens 158-161 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 74-77 tumor protein p53 Homo sapiens 23-26 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 74-77 tumor protein p53 Homo sapiens 216-219 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 74-77 tumor protein p53 Homo sapiens 216-219 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 83-86 tumor protein p53 Homo sapiens 23-26 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 83-86 tumor protein p53 Homo sapiens 216-219 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 83-86 tumor protein p53 Homo sapiens 216-219 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 83-86 tumor protein p53 Homo sapiens 23-26 18231594-5 2008 We find that expression of the human p53-Mdm2 module in yeast is sufficient to faithfully recapitulate key aspects of p53 regulation in higher eukaryotes, such as Mdm2-dependent targeting of p53 for degradation, sumoylation at lysine 386 and further regulation of this process by p14(ARF). Lysine 227-233 tumor protein p53 Homo sapiens 37-40 18231594-5 2008 We find that expression of the human p53-Mdm2 module in yeast is sufficient to faithfully recapitulate key aspects of p53 regulation in higher eukaryotes, such as Mdm2-dependent targeting of p53 for degradation, sumoylation at lysine 386 and further regulation of this process by p14(ARF). Lysine 227-233 tumor protein p53 Homo sapiens 118-121 18231594-5 2008 We find that expression of the human p53-Mdm2 module in yeast is sufficient to faithfully recapitulate key aspects of p53 regulation in higher eukaryotes, such as Mdm2-dependent targeting of p53 for degradation, sumoylation at lysine 386 and further regulation of this process by p14(ARF). Lysine 227-233 tumor protein p53 Homo sapiens 118-121 17707234-0 2007 Modulation of p53 function by SET8-mediated methylation at lysine 382. Lysine 59-65 tumor protein p53 Homo sapiens 14-17 17898049-5 2007 Treatment of E7-expressing cells with interferon ultimately resulted in cellular senescence through a process that is dependent upon acetylation of p53 by p300/CBP at lysine 382. Lysine 167-173 tumor protein p53 Homo sapiens 148-151 17898049-8 2007 Finally, p53 acetylation at lysine 382 was found not to be an essential determinant of other types of senescence such as that induced by overexpression of Ras in human fibroblasts. Lysine 28-34 tumor protein p53 Homo sapiens 9-12 17923702-7 2007 Mutation of lysine 3016 does not affect unstimulated ATM kinase activity but does abolish upregulation of ATM"s kinase activity by DNA damage, inhibits the conversion of inactive ATM dimers to active ATM monomers, and prevents the ATM-dependent phosphorylation of the p53 and chk2 proteins. Lysine 12-18 tumor protein p53 Homo sapiens 268-271 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 tumor protein p53 Homo sapiens 60-63 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 tumor protein p53 Homo sapiens 37-40 17620057-8 2007 Deacetylated lysine residues within Rb formed a domain similar to the SIRT1-targeted domain of the p53 tumour suppressor protein. Lysine 13-19 tumor protein p53 Homo sapiens 99-102 17914575-6 2007 A comparison with the wild-type after 1 nano-second molecular dynamic simulation analysis revealed a significant structural change (over 4A displacement) in the contact loop Lys-Ser-Val which lies upstream and next to the mutated site in the TP53, that sterically prevents its DNA-binding activity. Lysine 174-177 tumor protein p53 Homo sapiens 242-246 17805299-1 2007 p53, the tumour suppressor and transcriptional activator, is regulated by numerous post-translational modifications, including lysine methylation. Lysine 127-133 tumor protein p53 Homo sapiens 0-3 17707234-4 2007 We find that SET8 specifically monomethylates p53 at lysine 382 (p53K382me1). Lysine 53-59 tumor protein p53 Homo sapiens 46-49 17977830-8 2008 It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. Lysine 83-86 tumor protein p53 Homo sapiens 216-219 17646389-2 2007 Recently, we discovered that lysine methylation of p53 at K372 by Set7/9 (also known as SET7 and Set9) is important for transcriptional activation and stabilization of p53. Lysine 29-35 tumor protein p53 Homo sapiens 51-54 17646389-2 2007 Recently, we discovered that lysine methylation of p53 at K372 by Set7/9 (also known as SET7 and Set9) is important for transcriptional activation and stabilization of p53. Lysine 29-35 tumor protein p53 Homo sapiens 168-171 17646389-5 2007 Significantly, we show that lysine methylation of p53 is important for its subsequent acetylation, resulting in stabilization of the p53 protein. Lysine 28-34 tumor protein p53 Homo sapiens 50-53 17646389-5 2007 Significantly, we show that lysine methylation of p53 is important for its subsequent acetylation, resulting in stabilization of the p53 protein. Lysine 28-34 tumor protein p53 Homo sapiens 133-136 17646389-8 2007 Collectively, these results suggest that the cross talk between lysine methylation and acetylation is critical for p53 activation in response to DNA damage and that Set7/9 may play an important role in tumor suppression. Lysine 64-70 tumor protein p53 Homo sapiens 115-118 17534149-6 2007 We and others have recently identified a novel modification on p53, acetylation of lysine 120 within the DNA binding domain. Lysine 83-89 tumor protein p53 Homo sapiens 63-66 17630506-1 2007 p53 ubiquitination at C-terminal lysines by MDM2 and other E3 ligases had been considered a straightforward negative regulation of p53 with only one function, that is marking the protein for proteasomal degradation. Lysine 33-40 tumor protein p53 Homo sapiens 0-3 17630506-1 2007 p53 ubiquitination at C-terminal lysines by MDM2 and other E3 ligases had been considered a straightforward negative regulation of p53 with only one function, that is marking the protein for proteasomal degradation. Lysine 33-40 tumor protein p53 Homo sapiens 131-134 17534149-8 2007 We demonstrate here that both the DNA damage response pathway and the p19ARF/oncogene stress pathway induce the acetylation of p53 at lysine 120. Lysine 134-140 tumor protein p53 Homo sapiens 127-130 17353187-6 2007 HSCO specifically associates with histone deacetylase 1 (HDAC1) independently of Mdm2 and facilitates deacetylation of p53 at Lys-373/382 by HDAC1. Lysine 126-129 tumor protein p53 Homo sapiens 119-122 17371868-5 2007 Mutant p53 ubiquitination occurred at lysines in both the DNA-binding domain (DBD) and C terminus. Lysine 38-45 tumor protein p53 Homo sapiens 7-10 17371868-6 2007 Interestingly, Lys to Arg mutations that inhibited ubiquitination restored nuclear localization to mutant p53 but had no apparent effect on p53 conformation. Lysine 15-18 tumor protein p53 Homo sapiens 106-109 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 tumor protein p53 Homo sapiens 22-25 17098746-6 2007 This is consistent with recent studies showing that a lysine to arginine mutation at Lys-320 significantly enhances p53 function, although Lys-320 was originally identified as an acetylation site involving PCAF-mediated activation of p53. Lysine 54-60 tumor protein p53 Homo sapiens 116-119 17098746-6 2007 This is consistent with recent studies showing that a lysine to arginine mutation at Lys-320 significantly enhances p53 function, although Lys-320 was originally identified as an acetylation site involving PCAF-mediated activation of p53. Lysine 54-60 tumor protein p53 Homo sapiens 234-237 17098746-6 2007 This is consistent with recent studies showing that a lysine to arginine mutation at Lys-320 significantly enhances p53 function, although Lys-320 was originally identified as an acetylation site involving PCAF-mediated activation of p53. Lysine 85-88 tumor protein p53 Homo sapiens 116-119 17098746-6 2007 This is consistent with recent studies showing that a lysine to arginine mutation at Lys-320 significantly enhances p53 function, although Lys-320 was originally identified as an acetylation site involving PCAF-mediated activation of p53. Lysine 85-88 tumor protein p53 Homo sapiens 234-237 17805299-8 2007 These observations show that p53 is dynamically regulated by lysine methylation and demethylation and that the methylation status at a single lysine residue confers distinct regulatory output. Lysine 61-67 tumor protein p53 Homo sapiens 29-32 17805299-8 2007 These observations show that p53 is dynamically regulated by lysine methylation and demethylation and that the methylation status at a single lysine residue confers distinct regulatory output. Lysine 142-148 tumor protein p53 Homo sapiens 29-32 17307730-7 2007 Nampt overexpression also reduced the fraction of p53 that was acetylated on lysine 382, a target of SIRT1, suppressed an age-related increase in p53 expression, and increased the rate of p53 degradation. Lysine 77-83 tumor protein p53 Homo sapiens 50-53 17307730-7 2007 Nampt overexpression also reduced the fraction of p53 that was acetylated on lysine 382, a target of SIRT1, suppressed an age-related increase in p53 expression, and increased the rate of p53 degradation. Lysine 77-83 tumor protein p53 Homo sapiens 146-149 17307730-7 2007 Nampt overexpression also reduced the fraction of p53 that was acetylated on lysine 382, a target of SIRT1, suppressed an age-related increase in p53 expression, and increased the rate of p53 degradation. Lysine 77-83 tumor protein p53 Homo sapiens 146-149 16924240-4 2007 Expression of ubiquitin derivatives with all lysines mutated except K48 or K63 demonstrated that K48-linked p53-ubiquitin conjugates were specifically induced after DNA damage. Lysine 45-52 tumor protein p53 Homo sapiens 108-111 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 tumor protein p53 Homo sapiens 199-202 17110336-3 2006 E4F1 stimulates oligo-ubiquitylation in the hinge region of p53 on lysine residues distinct from those targeted by Hdm2 and previously described to be acetylated by the acetyltransferase PCAF. Lysine 67-73 tumor protein p53 Homo sapiens 60-63 17108971-2 2006 The tumour suppressor p53 (refs 4-7) is one of only a few non-histone proteins known to be regulated by lysine methylation. Lysine 104-110 tumor protein p53 Homo sapiens 22-25 17108971-3 2006 Here we report a lysine methyltransferase, Smyd2, that methylates a previously unidentified site, Lys 370, in p53. Lysine 98-101 tumor protein p53 Homo sapiens 110-113 17108971-4 2006 This methylation site, in contrast to the known site Lys 372, is repressing to p53-mediated transcriptional regulation. Lysine 53-56 tumor protein p53 Homo sapiens 79-82 17108971-8 2006 In addition, we show that the inhibitory effect of Lys 372 methylation on Lys 370 methylation is caused, in part, by blocking the interaction between p53 and Smyd2. Lysine 51-54 tumor protein p53 Homo sapiens 150-153 17108971-8 2006 In addition, we show that the inhibitory effect of Lys 372 methylation on Lys 370 methylation is caused, in part, by blocking the interaction between p53 and Smyd2. Lysine 74-77 tumor protein p53 Homo sapiens 150-153 17108971-9 2006 Thus, similar to histones, p53 is subject to both activating and repressing lysine methylation. Lysine 76-82 tumor protein p53 Homo sapiens 27-30 17012228-9 2006 Site-directed mutagenesis studies showed that Lys-386 of p53, the SUMO-1 modification site, is also the modification site for SUMO-2/3. Lysine 46-49 tumor protein p53 Homo sapiens 57-60 16918599-10 2006 Similar to the primary tumour, the cell line showed p53 overexpression and had p53 mutation at codon 132: AAG (lys)-->AAT (asp). Lysine 111-114 tumor protein p53 Homo sapiens 79-82 16579792-6 2006 The p53(F270A:6KR) chimaeric mutant (where 6KR refers to the simultaneous mutation of lysine residues at positions 370, 372, 373, 381, 382 and 386 to arginine) maintains the high-molecular-mass covalent adducts and is modified in an MDM2-dependent manner. Lysine 86-92 tumor protein p53 Homo sapiens 4-7 16314399-6 2006 Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction). Lysine 80-83 tumor protein p53 Homo sapiens 222-225 16314399-6 2006 Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction). Lysine 206-209 tumor protein p53 Homo sapiens 88-91 16314399-6 2006 Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction). Lysine 206-209 tumor protein p53 Homo sapiens 222-225 16314399-6 2006 Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction). Lysine 206-209 tumor protein p53 Homo sapiens 88-91 16314399-6 2006 Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction). Lysine 206-209 tumor protein p53 Homo sapiens 222-225 16436515-4 2006 First, it induced the acetylation of p53 at lysine 320 and its dephosphorylation at serine 392 but not p53 activity. Lysine 44-50 tumor protein p53 Homo sapiens 37-40 16537920-0 2006 Acetylation of p53 at lysine 373/382 by the histone deacetylase inhibitor depsipeptide induces expression of p21(Waf1/Cip1). Lysine 22-28 tumor protein p53 Homo sapiens 15-18 16537920-4 2006 That p53 was acetylated after depsipeptide treatment was tested by sequential immunoprecipitation/Western immunoblot analysis with anti-acetylated lysines and anti-p53 antibodies. Lysine 147-154 tumor protein p53 Homo sapiens 5-8 15302922-10 2004 A DNA-free p53 structure model predicts that Arg-174 is important for dimerization, whereas Spalax Lys-174 prevents such interactions. Lysine 99-102 tumor protein p53 Homo sapiens 11-14 16291740-0 2006 Charge modification at multiple C-terminal lysine residues regulates p53 oligomerization and its nucleus-cytoplasm trafficking. Lysine 43-49 tumor protein p53 Homo sapiens 69-72 16291740-1 2006 The basal level of the tumor suppressor p53 is regulated by MDM2-mediated ubiquitination at specific lysines, which leads to p53 nuclear export and degradation. Lysine 101-108 tumor protein p53 Homo sapiens 40-43 16291740-1 2006 The basal level of the tumor suppressor p53 is regulated by MDM2-mediated ubiquitination at specific lysines, which leads to p53 nuclear export and degradation. Lysine 101-108 tumor protein p53 Homo sapiens 125-128 16291740-2 2006 Upon p53 activation, however, these lysines become acetylated by p300/CREB-binding protein. Lysine 36-43 tumor protein p53 Homo sapiens 5-8 15846102-1 2005 We have previously shown that the HDAC inhibitors (HDACI) activate the p53 molecule through acetylation of 320 and 373 lysine residues, upregulate PIG3 and NOXA and induce apoptosis in cancer cells expressing wild and pseudo-wild type p53 genes (Terui T, et al. Lysine 119-125 tumor protein p53 Homo sapiens 71-74 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. Lysine 149-152 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. Lysine 149-152 tumor protein p53 Homo sapiens 235-238 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. Lysine 185-188 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. Lysine 185-188 tumor protein p53 Homo sapiens 235-238 16293626-0 2006 DNA damage promotes histone deacetylase 4 nuclear localization and repression of G2/M promoters, via p53 C-terminal lysines. Lysine 116-123 tumor protein p53 Homo sapiens 101-104 16293626-5 2006 The C-terminal lysines of p53, which are acetylated and methylated, are required for HDAC4 recruitment and transcriptional repression. Lysine 15-22 tumor protein p53 Homo sapiens 26-29 16291740-4 2006 This activity is independent of MDM2 but requires a p53 nuclear export signal and acetylation of multiple lysines by p300. Lysine 106-113 tumor protein p53 Homo sapiens 52-55 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. Lysine 70-77 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. Lysine 70-77 tumor protein p53 Homo sapiens 209-212 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. Lysine 70-76 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. Lysine 70-76 tumor protein p53 Homo sapiens 209-212 16291740-6 2006 Our study suggested a threshold mechanism whereby the degree of acetylation regulates p53 nucleus-cytoplasm trafficking by neutralizing a lysine-dependent charge patch, which in turn, controls oligomerization-dependent p53 nuclear export. Lysine 138-144 tumor protein p53 Homo sapiens 86-89 16291740-6 2006 Our study suggested a threshold mechanism whereby the degree of acetylation regulates p53 nucleus-cytoplasm trafficking by neutralizing a lysine-dependent charge patch, which in turn, controls oligomerization-dependent p53 nuclear export. Lysine 138-144 tumor protein p53 Homo sapiens 219-222 16426974-1 2006 Lysine acetylation of human tumor suppressor p53 in response to cellular stress signals is required for its function as a transcription factor that regulates cell cycle arrest, senescence, or apoptosis. Lysine 0-6 tumor protein p53 Homo sapiens 45-48 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 tumor protein p53 Homo sapiens 65-68 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 tumor protein p53 Homo sapiens 155-158 16354677-3 2006 Treatment with EX-527 dramatically increased acetylation at lysine 382 of p53 after different types of DNA damage in primary human mammary epithelial cells and several cell lines. Lysine 60-66 tumor protein p53 Homo sapiens 74-77 16446403-3 2006 Lysine residues at the COOH-terminal region of p53 are implicated as sites for ubiquitination and other post-translational modifications. Lysine 0-6 tumor protein p53 Homo sapiens 47-50 16446403-8 2006 In contrast, several conserved lysine residues in the DNA-binding domain are critical for p53 ubiquitination. Lysine 31-37 tumor protein p53 Homo sapiens 90-93 15525938-0 2004 Regulation of p53 activity through lysine methylation. Lysine 35-41 tumor protein p53 Homo sapiens 14-17 15525938-3 2004 Here we report a novel mechanism of p53 regulation through lysine methylation by Set9 methyltransferase. Lysine 59-65 tumor protein p53 Homo sapiens 36-39 14584049-5 2004 Exposure of proliferating KCs to UV-light induces post-translational modifications of p53 including acetylation of lysine-382 residues. Lysine 115-121 tumor protein p53 Homo sapiens 86-89 14968111-5 2004 In both cases, however, HCV core protein increased the p53 DNA-binding affinity in gel retardation analyses, likely due to the hyperacetylation of p53 Lys(373) and Lys(382) residues. Lysine 151-154 tumor protein p53 Homo sapiens 55-58 14968111-5 2004 In both cases, however, HCV core protein increased the p53 DNA-binding affinity in gel retardation analyses, likely due to the hyperacetylation of p53 Lys(373) and Lys(382) residues. Lysine 151-154 tumor protein p53 Homo sapiens 147-150 14968111-5 2004 In both cases, however, HCV core protein increased the p53 DNA-binding affinity in gel retardation analyses, likely due to the hyperacetylation of p53 Lys(373) and Lys(382) residues. Lysine 164-167 tumor protein p53 Homo sapiens 55-58 14759370-1 2004 Lysine acetylation of the tumor suppressor protein p53 in response to a wide variety of cellular stress signals is required for its activation as a transcription factor that regulates cell cycle arrest, senescence, or apoptosis. Lysine 0-6 tumor protein p53 Homo sapiens 51-54 14759370-2 2004 Here, we report that the conserved bromo-domain of the transcriptional coactivator CBP (CREB binding protein) binds specifically to p53 at the C-terminal acetylated lysine 382. Lysine 165-171 tumor protein p53 Homo sapiens 132-135 14759370-4 2004 We further present the three-dimensional nuclear magnetic resonance structure of the CBP bromodomain in complex with a lysine 382-acetylated p53 peptide. Lysine 119-125 tumor protein p53 Homo sapiens 141-144 14695212-0 2003 Induction of PIG3 and NOXA through acetylation of p53 at 320 and 373 lysine residues as a mechanism for apoptotic cell death by histone deacetylase inhibitors. Lysine 69-75 tumor protein p53 Homo sapiens 50-53 14661947-3 2003 Interestingly, the Gcn5/PCAF HAT family has a remarkable ability to acetylate lysine residues within diverse cognate sites such as those found around lysines 14, 8, and 320 of histones H3, H4, and p53, respectively. Lysine 78-84 tumor protein p53 Homo sapiens 197-200 14661947-3 2003 Interestingly, the Gcn5/PCAF HAT family has a remarkable ability to acetylate lysine residues within diverse cognate sites such as those found around lysines 14, 8, and 320 of histones H3, H4, and p53, respectively. Lysine 150-157 tumor protein p53 Homo sapiens 197-200 14695212-3 2003 By Western blotting, using specific antibodies, we then demonstrated that residues 320, 373, and 382 lysines of p53 were acetylated in KATO-III cells transfected with wild-type p53 (KATO-III/p53) treated with a HDAC inhibitor. Lysine 101-108 tumor protein p53 Homo sapiens 112-115 14695212-3 2003 By Western blotting, using specific antibodies, we then demonstrated that residues 320, 373, and 382 lysines of p53 were acetylated in KATO-III cells transfected with wild-type p53 (KATO-III/p53) treated with a HDAC inhibitor. Lysine 101-108 tumor protein p53 Homo sapiens 177-180 14695212-3 2003 By Western blotting, using specific antibodies, we then demonstrated that residues 320, 373, and 382 lysines of p53 were acetylated in KATO-III cells transfected with wild-type p53 (KATO-III/p53) treated with a HDAC inhibitor. Lysine 101-108 tumor protein p53 Homo sapiens 177-180 14583461-7 2003 We provide evidence that p53 influences histone H3 acetylation at lysine 9 (K9) and K14, whereas acetylation of K18 appears to be p53 independent. Lysine 66-72 tumor protein p53 Homo sapiens 25-28 14517211-5 2003 The p53 accumulating in these cells was nuclear but was not phosphorylated at serines 6, 15, and 20, nor was it acetylated at lysines 373 or 382. Lysine 126-133 tumor protein p53 Homo sapiens 4-7 12501250-5 2003 Further, p53 trans-activation of the 14-3-3varsigma promoter was markedly repressed by Tat-histone acetyltransferase interactions, and p53 acetylation by p300/CREB-binding protein-associated factor on residue Lys(320) was diminished as a result of Tat-histone acetyltransferase binding in vivo and in vitro. Lysine 209-212 tumor protein p53 Homo sapiens 9-12 12844488-8 2003 However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test). Lysine 136-139 tumor protein p53 Homo sapiens 13-16 12750254-5 2003 p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically interact with p300, a member of histone acetyl transferase complexes, and p53 in vivo. Lysine 47-50 tumor protein p53 Homo sapiens 28-31 12750254-5 2003 p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically interact with p300, a member of histone acetyl transferase complexes, and p53 in vivo. Lysine 47-50 tumor protein p53 Homo sapiens 154-157 14522900-11 2003 In addition, we found that p33(ING1b) physically interacts with hSIR2, reverses its ability to induce the AFP promoter, and induces acetylation of p53 residues at Lys(373) and/or Lys(382). Lysine 163-166 tumor protein p53 Homo sapiens 147-150 12724314-0 2003 Identification and characterization of a novel p300-mediated p53 acetylation site, lysine 305. Lysine 83-89 tumor protein p53 Homo sapiens 61-64 12724314-9 2003 Thus, p300 may further regulate the transcriptional activity of p53 through a novel acetylation site, Lys-305. Lysine 102-105 tumor protein p53 Homo sapiens 64-67 12716906-3 2003 The application of a laminar flow (12 dyn/cm2) increased the deacetylation at Lys-320 and Lys-373 of p53 and the acetylation at Lys-382 in human umbilical vein endothelial cells. Lysine 78-81 tumor protein p53 Homo sapiens 101-104 12716906-3 2003 The application of a laminar flow (12 dyn/cm2) increased the deacetylation at Lys-320 and Lys-373 of p53 and the acetylation at Lys-382 in human umbilical vein endothelial cells. Lysine 90-93 tumor protein p53 Homo sapiens 101-104 12716906-3 2003 The application of a laminar flow (12 dyn/cm2) increased the deacetylation at Lys-320 and Lys-373 of p53 and the acetylation at Lys-382 in human umbilical vein endothelial cells. Lysine 90-93 tumor protein p53 Homo sapiens 101-104 12716906-5 2003 Treating human umbilical vein endothelial cells with trichostatin A (TSA), an HDAC inhibitor, abolished the flow-induced p53 deacetylation at Lys-320 and Lys-373. Lysine 142-145 tumor protein p53 Homo sapiens 121-124 12726776-5 2003 Another is its intrinsic and associated enzymatic activity, which transfers an acetyl-base to the epsilon ( epsilon ) portion of lysine-residues in histones and certain nuclear proteins (factor acetyltransferases; FATs), such as p53, lymphoid enhancer-binding factor (LEF), and transcription factor IIE (TFIIE), which often results in increased transcriptional activity. Lysine 129-135 tumor protein p53 Homo sapiens 229-232 12501250-7 2003 Finally, HIV-1-infected Molt-4 cells displayed reduced p53 acetylation on lysines 320 and 373 in response to UV irradiation. Lysine 74-81 tumor protein p53 Homo sapiens 55-58 11875057-5 2002 p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18). Lysine 43-46 tumor protein p53 Homo sapiens 0-3 12421820-2 2002 Interestingly, both acetylation and ubiquitination can modify the same lysine residues at the C terminus of p53, implicating a role of acetylation in the regulation of p53 stability. Lysine 71-77 tumor protein p53 Homo sapiens 108-111 12421820-2 2002 Interestingly, both acetylation and ubiquitination can modify the same lysine residues at the C terminus of p53, implicating a role of acetylation in the regulation of p53 stability. Lysine 71-77 tumor protein p53 Homo sapiens 168-171 12391296-1 2002 Histone acetyltransferases (HATs) use acetyl CoA to acetylate target lysine residues within histones and other transcription factors, such as the p53 tumor suppressor, to promote gene activation. Lysine 69-75 tumor protein p53 Homo sapiens 146-149 12586367-5 2003 Accordingly, we confirm that the effect of E6 and p53 is independent of the six C-terminal lysine residues in p53, which have previously been described to play an important role for effective ubiquitination and degradation of 53 mediated by Mdm2. Lysine 91-97 tumor protein p53 Homo sapiens 110-113 12426395-4 2002 The HDAC1 complex binds MDM2 in a p53-independent manner and deacetylates p53 at all known acetylated lysines in vivo. Lysine 102-109 tumor protein p53 Homo sapiens 74-77 12426395-8 2002 As the acetylated p53 lysine residues overlap with those that are ubiquitylated, our results suggest that one major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups. Lysine 22-28 tumor protein p53 Homo sapiens 18-21 12426395-8 2002 As the acetylated p53 lysine residues overlap with those that are ubiquitylated, our results suggest that one major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups. Lysine 22-28 tumor protein p53 Homo sapiens 128-131 12426395-8 2002 As the acetylated p53 lysine residues overlap with those that are ubiquitylated, our results suggest that one major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups. Lysine 22-28 tumor protein p53 Homo sapiens 128-131 12426395-8 2002 As the acetylated p53 lysine residues overlap with those that are ubiquitylated, our results suggest that one major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups. Lysine 22-28 tumor protein p53 Homo sapiens 128-131 12019170-10 2002 Modeling of p53 interaction with DNA suggests that R283H mutation may weaken the sequence-specific interaction of p53 lysine 120 with the BAX gene but not the CDKN1A p53-responsive elements. Lysine 118-124 tumor protein p53 Homo sapiens 12-15 12019170-10 2002 Modeling of p53 interaction with DNA suggests that R283H mutation may weaken the sequence-specific interaction of p53 lysine 120 with the BAX gene but not the CDKN1A p53-responsive elements. Lysine 118-124 tumor protein p53 Homo sapiens 114-117 12019170-10 2002 Modeling of p53 interaction with DNA suggests that R283H mutation may weaken the sequence-specific interaction of p53 lysine 120 with the BAX gene but not the CDKN1A p53-responsive elements. Lysine 118-124 tumor protein p53 Homo sapiens 114-117 11875057-5 2002 p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18). Lysine 43-46 tumor protein p53 Homo sapiens 73-76 11971195-0 2002 Multiple lysine mutations in the C-terminus of p53 make it resistant to degradation mediated by MDM2 but not by human papillomavirus E6 and induce growth inhibition in MDM2-overexpressing cells. Lysine 9-15 tumor protein p53 Homo sapiens 47-50 11971195-1 2002 We have recently shown that lysine mutations in p53"s putative C-terminal acetylation sites result in increased stability and cytoplasmic distribution of the p53 protein in a human lung cancer cell line. Lysine 28-34 tumor protein p53 Homo sapiens 48-51 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). Lysine 46-52 tumor protein p53 Homo sapiens 26-29 11971195-1 2002 We have recently shown that lysine mutations in p53"s putative C-terminal acetylation sites result in increased stability and cytoplasmic distribution of the p53 protein in a human lung cancer cell line. Lysine 28-34 tumor protein p53 Homo sapiens 158-161 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. Lysine 42-48 tumor protein p53 Homo sapiens 84-87 11960383-1 2002 Mutation of four lysine residues in the p53 C-terminal domain inhibits MDM2-dependent ubiquitination of p53 and alters its subcellular distribution. Lysine 17-23 tumor protein p53 Homo sapiens 40-43 11960383-1 2002 Mutation of four lysine residues in the p53 C-terminal domain inhibits MDM2-dependent ubiquitination of p53 and alters its subcellular distribution. Lysine 17-23 tumor protein p53 Homo sapiens 104-107 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. Lysine 45-51 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. Lysine 45-51 tumor protein p53 Homo sapiens 170-173 11740489-3 2002 HIPK2 is activated by ultraviolet (UV) radiation and selectively phosphorylates p53 at Ser 46, thus facilitating the CBP-mediated acetylation of p53 at Lys 382, and promoting p53-dependent gene expression. Lysine 152-155 tumor protein p53 Homo sapiens 80-83 11740489-3 2002 HIPK2 is activated by ultraviolet (UV) radiation and selectively phosphorylates p53 at Ser 46, thus facilitating the CBP-mediated acetylation of p53 at Lys 382, and promoting p53-dependent gene expression. Lysine 152-155 tumor protein p53 Homo sapiens 145-148 11740489-3 2002 HIPK2 is activated by ultraviolet (UV) radiation and selectively phosphorylates p53 at Ser 46, thus facilitating the CBP-mediated acetylation of p53 at Lys 382, and promoting p53-dependent gene expression. Lysine 152-155 tumor protein p53 Homo sapiens 145-148 11875057-5 2002 p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18). Lysine 30-33 tumor protein p53 Homo sapiens 0-3 11875057-5 2002 p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18). Lysine 30-33 tumor protein p53 Homo sapiens 73-76 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). Lysine 46-52 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). Lysine 46-52 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). Lysine 256-263 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). Lysine 256-263 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). Lysine 256-263 tumor protein p53 Homo sapiens 126-129 11713288-7 2001 Finally, the region between the DBD and the oligomerization domain of p53, specifically lysine 305, also plays a critical role in fully revealing p53NES. Lysine 88-94 tumor protein p53 Homo sapiens 70-73