IndraLab

Statements


TP53 is active.
6 139 | 4
TP53 phosphorylated on S15 is active. 10 / 29
1 28 |

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability. We have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"Ampk activation induces phosphorylation of p53 on serine 15, and this phosphorylation is required to initiate ampk-dependent cell-cycle arrest"

"Mutant p53 is constitutively phosphorylated at serine 15 in uv-induced mouse skin tumors: involvement of erk1/2 map kinase."

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"Dyrk1a phosphorylates p53 and inhibits proliferation of embryonic neuronal cells. we found that dyrk1a phosphorylates p53 at ser-15 in vitro and in immortalized rat embryonic hippocampal progenitor h19-7 cells. In addition, dyrk1a-induced p53 phosphorylation at ser-15 led to a robust induction of p53 target genes"

"Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway."

"Nhibition of atr kinase activity substantially reduces hypoxia-induced phosphorylation of p53 protein on serine 15 as well as p53 protein accumulation."

"Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway."

"PPM1D binds Chk1 and dephosphorylates the ATR-targeted phospho-Ser 345, leading to decreased Chk1 kinase activity. PPM1D also dephosphorylates p53 at phospho-Ser 15. PPM1D dephosphorylations are correlated with reduced cellular intra-S and G2/M checkpoint activity in response to DNA damage induced by ultraviolet and ionizing radiation. Thus, a primary function of PPM1D may be to reverse the p53 and Chk1-induced DNA damage and cell cycle checkpoint responses and return the cell to a homeostatic state following completion of DNA repair."
TP53 phosphorylated on S20 is active. 10 / 17
17 |

"Here we show that the direct association between a p53 n-terminal peptide and mdm2 is disrupted by phosphorylation of the peptide on thr(18) but not by phosphorylation at other n-terminal sites, including ser(15) and ser(37). Thr(18) was phosphorylated in vitro by casein kinase (ck1)."

"CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37"

"A cell-free ser(20) phosphorylation site assay was used to identify a broad range of calcium calmodulin kinase superfamily members, including chk2, chk1, dapk-1, dapk-3, drak-1, and ampk, as ser(20) kinases.Evaluation of these calcium calmodulin kinase superfamily members as candidate ser(20) kinases in vivo has shown that only chk1 or dapk-1 can stimulate p53 transactivation and induce ser(20) phosphorylation of p53."

"Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma|Inhibiting DUSP26 expression in the IMR-32 neuroblastoma cell line enhanced doxorubicin-induced p53 phosphorylation at Ser20 and Ser37, p21, Puma, Bax expression as well as apoptosis"

"The tumour suppressor protein p53 is stabilised and activated in response to ionising radiation. This is known to depend on the kinase atm;recent results suggest atm acts via the downstream kinase chk2/hcds1, which stabilises p53 at least in part by direct phosphorylation of residue serine 20"

"These findings strongly suggest that jnks are the major direct signaling mediators of uvb-induced p53 phosphorylation at serine 20. furthermore, phosphorylation of p53 at serine 20 by uvb-activated jnks and uvb-induced p53-dependent transcriptional activity were suppressed in jnk1 or jnk2 knockout (jnk1(-/-) or jnk2(-/-)) cells."

"These findings strongly suggest that jnks are the major direct signaling mediators of uvb-induced p53 phosphorylation at serine 20. furthermore, phosphorylation of p53 at serine 20 by uvb-activated jnks and uvb-induced p53-dependent transcriptional activity were suppressed in jnk1 or jnk2 knockout (jnk1(-/-) or jnk2(-/-)) cells."

"A cell-free ser(20) phosphorylation site assay was used to identify a broad range of calcium calmodulin kinase superfamily members, including chk2, chk1, dapk-1, dapk-3, drak-1, and ampk, as ser(20) kinases.Evaluation of these calcium calmodulin kinase superfamily members as candidate ser(20) kinases in vivo has shown that only chk1 or dapk-1 can stimulate p53 transactivation and induce ser(20) phosphorylation of p53."

"Although the stabilization of p53 was apparently concordant with its phosphorylation on N-terminal serine residues in HFFF-2 cells, it did not require the phosphorylation of Ser15 or Ser20 by ATM, a cellular kinase known to phosphorylate and promote the stabilization of p53 in response to DNA damage."

"Here, we demonstrate for the first time that cdk5 interacts with p53 and increases its stability through posttranslational regulation, leading to accumulation of p53, particularly in the nucleus. We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 in vitro,"
TP53 phosphorylated on S37 is active. 10 / 13
13 |

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"Furthermore, we show that prak activates p53 by direct phosphorylation. prak phosphorylates p53 at ser37"

"Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway."

"Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway."

"Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway."

"We found that dusp26 promotes the resistance of human neuroblastoma to doxorubicin-induced apoptosis by acting as a p53 phosphatase to downregulate p53 tumor suppressor function in neuroblastoma cells. / we found that dusp26 binds to p53 and dephosphorylates p53 at ser20 and ser37."

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. On activation, both of these kinases also phosphorylate multiple sites in the p53 N-terminal domain. These include Ser15, Thr18, Ser20, and Ser37, which are all DNA-damageinducible sites"

"Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma|Inhibiting DUSP26 expression in the IMR-32 neuroblastoma cell line enhanced doxorubicin-induced p53 phosphorylation at Ser20 and Ser37, p21, Puma, Bax expression as well as apoptosis"

"Phosphorylation of p53 at serine 37 is important for transcriptional activity and regulation in response to DNA damage| Furthermore, in vitro phosphatase assays show that PP2A dephosphorylates p53 at S37."
TP53 phosphorylated on S392 is active. 9 / 9
2 7 |

No evidence text available

"We recently demonstrated that through their physical interaction, cdk9 phosphorylates p53 on ser-392, leading to p53 stability and accumulation"

"Furthermore, we demonstrate that anisomycin- and tumor necrosis factor-alpha-induced phosphorylation of p53 at Ser-392, which is important for the transcriptional activity of this growth suppressor protein, requires p38 MAP kinase and CK2 activities."

"The double-stranded rna activated protein kinase pkr physically associates with the tumor suppressor p53 protein and phosphorylates human p53 on serine 392 in vitro."

"The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase."

"Here we showed that in the presence of wild-type lkb1, nuak1 directly interacts with and phosphorylates p53 in vitro and in vivo."

No evidence text available

"We demonstrate that anisomycin- and tumor necrosis factor--induced phosphorylation of p53 at Ser-392, which is important for the transcriptional activity of this growth suppressor protein, requires p38 MAP kinase"

"We show that lkb1 physically associates with p53 in the nucleus and directly or indirectly phosphorylates p53 ser15 (previously shown to be phosphorylated by amp-dependent kinase) and p53 ser392"
TP53 phosphorylated on S315 is active. 9 / 9
9 |

"The mitochondrial kinase activity of cyclin b1/cdk1 was found to specifically phosphorylate p53 at ser-315 residue, leading to enhanced mitochondrial atp production and reduced mitochondrial apoptosis."

"the present study it is shown that in apoptotic PC12 cells the levels of p53 and Cdk5 increase concomitantly. Further, Cdk5/p25 effectively phosphorylates recombinant p53 in vitro. Transient transfection of Cdk5/p25 into cells results in an increase in p53 levels, as well as the expression of the p53-responsive genes p21 and Bax. Furthermore, evidence is provided that increased Cdk5 activity increases p53 transcriptional activity significantly, suggesting that p53 is modulated in situ by Cdk5."

"We used non-radioactive electrophoretic mobility shift assays to show that c-terminal phosphorylation of p53 protein by cdk2/cyclin a on ser315 or by pkc on ser378 can efficiently stimulate p53 binding to dna in vitro."

"Cdk9 phosphorylates p53 on serine residues 33, 315 and 392."

"Stoichiometric phosphorylation of human p53 at ser315 stimulates p53-dependent transcription."

"We used non-radioactive electrophoretic mobility shift assays to show that c-terminal phosphorylation of p53 protein by cdk2/cyclin a on ser315 or by pkc on ser378 can efficiently stimulate p53 binding to dna in vitro."

"The human Cdc14 phosphatases interact with and dephosphorylate the tumor suppressor protein p53|. Furthermore, the hCdc14 phosphatases were found to dephosphorylate p53 specifically at the p34Cdc2/clb phosphorylation site (p53-phosphor-Ser315)|Earlier studies showed that Ser315 phosphorylation increases the sequence-specific DNA binding capacity of p53, suggesting that Ser315 phosphorylation is an activating modification"

"The human Cdc14 phosphatases interact with and dephosphorylate the tumor suppressor protein p53|. Furthermore, the hCdc14 phosphatases were found to dephosphorylate p53 specifically at the p34Cdc2/clb phosphorylation site (p53-phosphor-Ser315)|Earlier studies showed that Ser315 phosphorylation increases the sequence-specific DNA binding capacity of p53, suggesting that Ser315 phosphorylation is an activating modification"

"We recently demonstrated that through their physical interaction, cdk9 phosphorylates p53 on ser-392, leading to p53 stability and accumulation"
TP53 phosphorylated on T18 is active. 9 / 9
9 |

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"Vrk1 phosphorylates murine p53 in threonine 18. This threonine is within the p53 hydrophobic loop (residues 13-23) required for the interaction of p53 with the cleft of its inhibitor mdm-2."

"Protein kinase ck1 is a p53-threonine 18 kinase which requires prior phosphorylation of serine 15."

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"Dna damage-activated protein kinases like chk1/2 modify the box-i domain of p53 at thr18 and ser20 (46) by an allosteric mechanism (10)."

"Ttk/hmps1 mediates the p53-dependent postmitotic checkpoint by phosphorylating p53 at thr18. phosphorylation at thr18 enhances p53-dependent activation of not only p21 but also lats2, two mediators of the postmitotic checkpoint."

"CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37"
TP53 phosphorylated on S46 is active. 9 / 9
9 |

"Based on all these observations, it is legitimate to suggest that axin and daxx seem to adopt both parallel routes and a convergent means to activate p53. In either case, hipk2 seems to be the protein kinase that catalyzes the ser46 phosphorylation."

"In mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"Here, we show that the pro-apoptotic kinase, protein kinase c delta (pkcdelta), is involved in phosphorylation of p53 on ser(46). pkcdelta potentiates p53-dependent apoptosis by ser(46) phosphorylation in response to genotoxic stress."

"P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"Here, we demonstrate that the dual-specificity tyrosine-phosphorylation-regulated kinase 2 (dyrk2) directly phosphorylates p53 at ser46. these findings indicate that dyrk2 regulates p53 to induce apoptosis in response to dna damage."

"We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 cdk5-stabilized p53 protein is transcriptionally active"

"In response to ionizing radiation (ir), atm, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of ser15 and (indirectly) ser20. Here we show that phosphorylation of p53 on ser46, a residue important for p53 apoptotic activity, as well as on ser9, in response to ir also is dependent on the atm protein kinase. one pathway involves the phosphorylation of p53 and its negative regulator mdm2 by ataxia telangiectasia mutated (atm) and chk2 causing p53 activation and stabilization."

"Recombinant p38 phosphorylated recombinant p53 on serine 46 in vitro. Inhibition of p38 MAPK by pharmacological inhibitors, dominant-negative p38, or small interfering RNA, suppressed p53S46P"
TP53 acetylated on K382 is active. 7 / 7
3 4 |

"We show here that moz is an acetyltransferase of p53 at k120 and k382 and colocalizes with p53 in promyelocytic leukemia (pml) nuclear bodies following cellular stress. The moz-pml-p53 interaction enhances moz-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression"

"Sirt1 has been shown to regulate cell fate in part by deacetylating the p53 protein at lysine 382 and inhibiting p53-mediated transcriptional activation and apoptosis."

"P300 acetylates and activates the tumor suppressor p53 after dna damage."

"We show here that moz is an acetyltransferase of p53 at k120 and k382 and colocalizes with p53 in promyelocytic leukemia (pml) nuclear bodies following cellular stress. The moz-pml-p53 interaction enhances moz-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression"

No evidence text available

No evidence text available

No evidence text available
TP53 phosphorylated on S33 is active. 7 / 7
7 |

"P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 cdk5-stabilized p53 protein is transcriptionally active"

"In mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site."

"Glycogen synthase kinase3 beta phosphorylates serine 33 of p53 and activates p53's transcriptional activity."
Phosphorylated TP53 is active. 6 / 6
5 | 1

"Atm/atr are generally sensors of dna damage, but, together with the checkpoint kinases chk1 and chk2, they also function as response effectors by phosphorylation of key substrates, such as p53, brca1, and nbs1. In particular, p53 phosphorylation leads to protein accumulation and activation, which in turn promotes cell-cycle arrest or apoptosis."

"Furthermore, we show that prak activates p53 by direct phosphorylation. We propose that phosphorylation of p53 by prak following activation of p38 mapk by ras plays an important role in ras-induced senescence and tumor suppression."

trips
"active phospho-p53"

"Activated jnk phosphorylates p53"

"We show that prak activates p53 by direct phosphorylation."

"The targets of jnk include the transcription factors p53. P75ntr-mediated apoptosis was shown to be dependent of p53"
TP53 phosphorylated on S378 is active. 5 / 5
5 |

"Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage."

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage."

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."

"The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase."
TP53 phosphorylated on S366 is active. 3 / 3
3 |

"Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage."

"The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage."

"Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53."
TP53 phosphorylated on T81 is active. 2 / 2
2 |

"Jnk phosphorylated p53 at t81 in response to dna damage and stress-inducing agents, as determined by phospho-specific antibodies to t81 . Jun NH2-terminal kinase phosphorylation of p53 on Thr-81 is important for p53 stabilization and transcriptional activities in response to stress."

"Wr1065 activates the jnk (c-jun n-terminal kinase), decreases complex formation between p53 and inactive jnk, and phosphorylates p53 at thr-81, a known site of phosphorylation by jnk."
Acetylated TP53 is active. 2 / 2
2 |

"We found that sirt7 interacts with p53 and efficiently deacetylates p53 in vitro, which corresponds to hyperacetylation of p53 in vivo."

"HDAC8 mediates CM-induced deacetylation of p53.Collectively, these results indicate that although binding to p53 and HDAC8 occurs through distinct regions of the CM protein, simultaneous interaction with HDAC8 and p53 is required for aberrant deacetylation and inactivation of p53."
TP53 acetylated on K120 is active. 2 / 2
2 |

"We show here that moz is an acetyltransferase of p53 at k120 and k382 and colocalizes with p53 in promyelocytic leukemia (pml) nuclear bodies following cellular stress. The moz-pml-p53 interaction enhances moz-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression"

"We show here that moz is an acetyltransferase of p53 at k120 and k382 and colocalizes with p53 in promyelocytic leukemia (pml) nuclear bodies following cellular stress. The moz-pml-p53 interaction enhances moz-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression"
TP53 phosphorylated on S371 is active. 2 / 2
2 |

"The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase."

"Here, we demonstrate that cotransfection of p53 with either PKC alpha or PKC zeta increases p53's transcriptional activity. Mutagenesis of p53 indicates that serine 371 is the major site for phosphorylation by PKC alpha in vitro."
TP53 acetylated on K373 is active. 1 / 1
1 |

"P300 acetylates and activates the tumor suppressor p53 after dna damage."
TP53 bound to SMARCA4 is active. 1 / 1
1 |

"Using genetic and biochemical approaches, we show that several subunits of the human SWI/SNF complex bind to the tumor suppressor protein p53 in vivo and in vitro.Molecular connection between p53 and the SWI/SNF complex implicates that (i) the SWI/SNF complex is necessary for p53-driven transcriptional activation, and (ii) the SWI/SNF complex plays an important role in p53-mediated cell cycle control."
TP53-S15E is active. 1 / 1
| 1

trips
"active p53S15E expression construct"
TP53 phosphorylated on S6 is active. 1 / 1
1 |

"Our studies revealed a novel mechanism in which phosphorylation of jnk2 is mediated by jnk1 before phosphorylation of p53, and then p53 is directly phosphorylated by jnk2 at ser6. |Role of map kinases in uvb-induced phosphorylation of p53 at serine 20."
TP53 phosphorylated on S106 is active. 1 / 1
1 |

"Ser-106 phosphorylation of p53 decreases its interaction with mdm2 and prolongs the half-life of p53"
TP53 bound to TP53BP2 is active. 1 / 1
1 |

"53bp2 interacts with the tumour suppressor p53 and enhances p53-mediated activation of transcription, possibly by facilitating the dephosphorylation of one or more sites on p53"
TP53 phosphorylated on S376 is active. 1 / 1
1 |

"The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase."
TP53 bound to CDKN2AIP is active. 1 / 1
1 |

"In the nucleoplasm, carf interacts with p53 and enhances its function."
TP53 bound to NUMB is active. 1 / 1
1 |

"Numb can actually interact in vivo with endogenous mdm2 and p53, resulting in a trimeric complex between the three proteins [10]. This interaction appears to regulate the stability of p53, as reduction of numb levels by rna interference (rnai) causes a decrease in the half-life of p53 and consequently a reduction in steady-state levels of the protein. Consistent with this observation, overexpression of numb increases the level of p53 in both unstressed and stressed cells."
TP53 in the nucleus is active. 1 / 1
| 1

trips
"active p53 in the nucleus"
TP53 bound to MAML1 is active. 1 / 1
1 |

"Unexpectedly, however, emerging evidence implicate maml proteins as exciting key transcriptional co-activators in other signal transduction pathways including: muscle differentiation and myopathies (mef2c), tumor suppressor pathway (p53) and colon carcinoma survival (beta-catenin)."
Sumoylated TP53 is active. 1 / 1
1 |

"Plk1-mediated phosphorylation of topors regulates p53 stability. Herein, we have identified topoisomerase i-binding protein (topors), a p53-binding protein, as a plk1 target. We show that plk1 phosphorylates topors on ser(718) in vivo. Significantly, expression of a plk1-unphosphorylatable topors mutant (s718a) leads to a dramatic accumulation of p53 through inhibition of p53 degradation. Topors is an ubiquitin and small ubiquitin-like modifier ubiquitin-protein isopeptide ligase (sumo e3) ligase. Plk1-mediated phosphorylation of topors inhibits topors-mediated sumoylation of p53, whereas p53 ubiquitination is enhanced, leading to p53 degradation."
TP53 bound to BAD is active. 1 / 1
1 |

"We also demonstrate that bad physically interacts with cytoplasmic p53. bad is able to direct p53 to the mitochondria and forms a p53/bad complex at the mitochondria. the mitochondrial p53/bad complex promotes apoptosis"
TP53 bound to GMPS is active. 1 / 1
1 |

"In response to genotoxic stress or nucleotide deprivation, gmps becomes nuclear and facilitates p53 stabilization by promoting its transfer from mdm2 to a gmps-usp7 deubiquitylation complex."
TP53 bound to DDX5 is active. 1 / 1
1 |

"The dead box protein p68: a novel transcriptional coactivator of the p53 tumour suppressor"
TP53 phosphorylated on T387 is active. 1 / 1
1 |

"Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage."
Ubiquitinated TP53 is active. 1 / 1
| 1

trips
"active non-ubiquitylated p53"
TP53 phosphorylated on S9 is active. 1 / 1
1 |

"In response to ionizing radiation (ir), atm, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of ser15 and (indirectly) ser20. Here we show that phosphorylation of p53 on ser46, a residue important for p53 apoptotic activity, as well as on ser9, in response to ir also is dependent on the atm protein kinase. one pathway involves the phosphorylation of p53 and its negative regulator mdm2 by ataxia telangiectasia mutated (atm) and chk2 causing p53 activation and stabilization."
TP53 is transcriptionally inactive.
2 80 |
TP53-R273H is transcriptionally inactive. 8 / 8
8 |

"From mutations file"

"From mutations file"

"We present evidence that ellipticine can restore the transactivation function of several transfected p53 mutants (175 H, 248W, 249S, 273 H, 281G), resulting in the induction of p53-responsive genes (p21(WAF1),MDM2) and activation of a p53-responsive luciferase reporter. Ellipticine also activates mutant p53 function in tumor cells expressing endogenous 194F, 233L, 241F, and 273C mutants. "

"From mutations file"

"Figure 3 showing mutations with loss of Transactivation activity"

"From mutations file"

"From mutations file"

"From mutations file"
TP53-R248Q is transcriptionally inactive. 5 / 5
5 |

"Figure 3 showing mutations with loss of Transactivation activity"

"From mutations file"

"From mutations file"

"From mutations file"

"From mutations file"
TP53-R248W is transcriptionally inactive. 4 / 4
4 |

"We present evidence that ellipticine can restore the transactivation function of several transfected p53 mutants (175 H, 248W, 249S, 273 H, 281G), resulting in the induction of p53-responsive genes (p21(WAF1),MDM2) and activation of a p53-responsive luciferase reporter. Ellipticine also activates mutant p53 function in tumor cells expressing endogenous 194F, 233L, 241F, and 273C mutants. "

"From mutations file"

"From mutations file"

"Figure 3 showing mutations with loss of Transactivation activity"
TP53-V274F is transcriptionally inactive. 4 / 4
4 |

"From mutations file"

"From mutations file"

"In these experiments p53â??223Leu was as active as wild-type p53 in transactivation of the reporter construct, whereas p53â??274Phe had no detectable activity (Fig. 4b). Coexpression of p53â??274Phe inhibited transactivation by p53â??223Leu, thus correlating with the above-described effects of this mutant on growth-inhibitory activity of p53â??223Leu. The lack of detectable transactivation activity of p53â??274Phe suggests that the toxicity of this protein to 10(1) cells is mediated not through p21."

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"
TP53-R175H is transcriptionally inactive. 4 / 4
4 |

"From mutations file"

"From mutations file"

"We present evidence that ellipticine can restore the transactivation function of several transfected p53 mutants (175 H, 248W, 249S, 273 H, 281G), resulting in the induction of p53-responsive genes (p21(WAF1),MDM2) and activation of a p53-responsive luciferase reporter. Ellipticine also activates mutant p53 function in tumor cells expressing endogenous 194F, 233L, 241F, and 273C mutants. "

"Figure 3 showing mutations with loss of Transactivation activity"
TP53-G245S is transcriptionally inactive. 3 / 3
3 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"

"From mutations file"

"Figure 3 showing mutations with loss of Transactivation activity"
TP53-R249S is transcriptionally inactive. 3 / 3
3 |

"From mutations file"

"We present evidence that ellipticine can restore the transactivation function of several transfected p53 mutants (175 H, 248W, 249S, 273 H, 281G), resulting in the induction of p53-responsive genes (p21(WAF1),MDM2) and activation of a p53-responsive luciferase reporter. Ellipticine also activates mutant p53 function in tumor cells expressing endogenous 194F, 233L, 241F, and 273C mutants. "

"Figure 3 showing mutations with loss of Transactivation activity"
TP53-Y220C is transcriptionally inactive. 3 / 3
3 |

"From mutations file"

"Figure 3 showing mutations with loss of Transactivation activity"

"From mutations file"
TP53-Y234H is transcriptionally inactive. 2 / 2
2 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"

"Table 3 EÂ?ect of temperature on the ability of p53 mutants to discriminate between diÂ?erent p53 responsive elements"
TP53-S241F is transcriptionally inactive. 2 / 2
2 |

"We present evidence that ellipticine can restore the transactivation function of several transfected p53 mutants (175 H, 248W, 249S, 273 H, 281G), resulting in the induction of p53-responsive genes (p21(WAF1),MDM2) and activation of a p53-responsive luciferase reporter. Ellipticine also activates mutant p53 function in tumor cells expressing endogenous 194F, 233L, 241F, and 273C mutants. "

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-Y126S is transcriptionally inactive. 2 / 2
2 |

"Table 2 p53 mutants unable to discriminate between diÂ?erent p53 responsive elements"

"Table 3 EÂ?ect of temperature on the ability of p53 mutants to discriminate between diÂ?erent p53 responsive elements"
TP53-L194F is transcriptionally inactive. 2 / 2
2 |

"From mutations file"

"We present evidence that ellipticine can restore the transactivation function of several transfected p53 mutants (175 H, 248W, 249S, 273 H, 281G), resulting in the induction of p53-responsive genes (p21(WAF1),MDM2) and activation of a p53-responsive luciferase reporter. Ellipticine also activates mutant p53 function in tumor cells expressing endogenous 194F, 233L, 241F, and 273C mutants. "
TP53-A276G is transcriptionally inactive. 2 / 2
2 |

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"

"Table 3 EÂ?ect of temperature on the ability of p53 mutants to discriminate between diÂ?erent p53 responsive elements"
TP53-R181G is transcriptionally inactive. 2 / 2
2 |

"Table 2 p53 mutants unable to discriminate between diÂ?erent p53 responsive elements"

"Table 3 EÂ?ect of temperature on the ability of p53 mutants to discriminate between diÂ?erent p53 responsive elements"
TP53-E286K is transcriptionally inactive. 2 / 2
2 |

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"

"Table 3 EÂ?ect of temperature on the ability of p53 mutants to discriminate between diÂ?erent p53 responsive elements"
TP53-P309S is transcriptionally inactive. 2 / 2
2 |

"From mutations file"

"From mutations file"
TP53-Y205N is transcriptionally inactive. 2 / 2
2 |

"Table 2 p53 mutants unable to discriminate between diÂ?erent p53 responsive elements"

"Table 3 EÂ?ect of temperature on the ability of p53 mutants to discriminate between diÂ?erent p53 responsive elements"
TP53-G266E is transcriptionally inactive. 2 / 2
2 |

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"

"Table 3 EÂ?ect of temperature on the ability of p53 mutants to discriminate between diÂ?erent p53 responsive elements"
TP53-R181H is transcriptionally inactive. 2 / 2
2 |

"Table 3 EÂ?ect of temperature on the ability of p53 mutants to discriminate between diÂ?erent p53 responsive elements"

"Table 2 p53 mutants unable to discriminate between diÂ?erent p53 responsive elements"
TP53-L145R is transcriptionally inactive. 1 / 1
1 |

"From mutations file"
TP53-G245D is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-G279E is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"
TP53-D281N is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"
TP53-Y163H is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÂ?erent p53 responsive elements"
TP53-C242Y is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-M246L is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-T230S is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-H233L is transcriptionally inactive. 1 / 1
1 |

"We present evidence that ellipticine can restore the transactivation function of several transfected p53 mutants (175 H, 248W, 249S, 273 H, 281G), resulting in the induction of p53-responsive genes (p21(WAF1),MDM2) and activation of a p53-responsive luciferase reporter. Ellipticine also activates mutant p53 function in tumor cells expressing endogenous 194F, 233L, 241F, and 273C mutants. "
TP53-P151H is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÂ?erent p53 responsive elements"
TP53-S241T is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-C238W is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-L308M is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ????erent p53 responsive elements"
TP53-F134I is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÂ?erent p53 responsive elements"
TP53-L323P is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ????erent p53 responsive elements"
TP53 acetylated on K382 is transcriptionally inactive. 1 / 1
1 |

"deacetylates the p53 protein with a specificity for its C-terminal Lys382 residue, modification of which has been implicated in the activation of p53 as a transcription factor."
TP53-P278S is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"
TP53-G244S is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-R337G is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ????erent p53 responsive elements"
TP53-R156P is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÂ?erent p53 responsive elements"
TP53 phosphorylated on S215 is transcriptionally inactive. 1 / 1
1 |

"Here we show that p53 is phosphorylated by the mitotic kinase Aurora-A at serine 215. Unlike most identified phosphorylation sites of p53 that positively associate with p53 function (Brooks, C. L., and Gu, W. (2003) Curr. Opin. Cell Biol. 15, 164-171), the phosphorylation of p53 by Aurora-A at Ser-215 abrogates p53 DNA binding and transactivation activity."
TP53 phosphorylated on S15 is transcriptionally inactive. 1 / 1
1 |

"<p17> Ser392 phosphorylation of P53 increases 10-fold the association constant for tetramerization, but this effect is reversed by Ser315 phosphorylation. The tetramerization activates P53 for specific DNA binding and transcription"
TP53-E258K is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"
TP53-N239S is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ??erent p53 responsive elements"
TP53-D281E is transcriptionally inactive. 1 / 1
1 |

"Table 2 p53 mutants unable to discriminate between diÃ???erent p53 responsive elements"
TP53-R282W is transcriptionally inactive. 1 / 1
1 |

"Figure 3 showing mutations with loss of Transactivation activity"
TP53 is transcriptionally active.
20 29 |
TP53 phosphorylated on S15 is transcriptionally active. 10 / 15
7 8 |

"PRPK phosphorylates serine-15 residue of p53 and enhances transcriptional activity."

"The intrinsic transcriptional activity of p53 was up-regulated by a transient transfection of PRPK to COS-7 cells. PRPK was shown to bind to p53 and to phosphorylate p53 at Ser-15."

"In addition, treatment of cells with the PKC activator phorbol ester stimulated the ubiquitination of p53 and reduced its ability to accumulate after stress. H7 did not induce the phosphorylation of human p53 on Ser-15 (Ser-18 in mouse protein), a modification that occurs in response to DNA damage and leads to the release of MDM2 and to transactivation by p53"

"In addition, treatment of cells with the PKC activator phorbol ester stimulated the ubiquitination of p53 and reduced its ability to accumulate after stress. H7 did not induce the phosphorylation of human p53 on Ser-15 (Ser-18 in mouse protein), a modification that occurs in response to DNA damage and leads to the release of MDM2 and to transactivation by p53"

"Phosphorylation of serine 15 increases the transcriptional activity of p53 (ref. 22)."

"Phosphorylation of serine 15 increases the transcriptional activity of p53 (ref. 22)."

"Fractionation of HeLa nuclear extracts and biochemical analyses indicate that this kinase is distinct from the DNA-dependent protein kinase (DNA-PK) and corresponds to the human cell cycle checkpoint protein ATR. Immunoprecipitation studies of recombinant ATR reveal that catalytic activity of this polypeptide is required for DNA-stimulated phosphorylation of p53 on serine-15. These data suggest that ATR may function upstream of p53 in a signal transduction cascade initiated upon DNA damage and provide a biochemical assay system for ATR activity."

"Fractionation of HeLa nuclear extracts and biochemical analyses indicate that this kinase is distinct from the DNA-dependent protein kinase (DNA-PK) and corresponds to the human cell cycle checkpoint protein ATR. Immunoprecipitation studies of recombinant ATR reveal that catalytic activity of this polypeptide is required for DNA-stimulated phosphorylation of p53 on serine-15. These data suggest that ATR may function upstream of p53 in a signal transduction cascade initiated upon DNA damage and provide a biochemical assay system for ATR activity."

"The most characteristic post-translational modification after NO· exposure is phosphorylation at Ser-15 (37) which interferes with p53 binding to MDM2 and its subsequent degradation."

"In the present study, we demonstrate that PP-1 can dephosphorylate p53 at Ser-15 and Ser-37 through co-immunoprecipitation, in vitro and in vivo dephosphorylation assays, overexpression and silence of the gene encoding the catalytic subunit for PP-1. We further show that mutations mimicking constitutive dephosphorylation or phosphorylation of p53 at these sites attenuate or enhance its transcriptional activity, respectively. "
TP53 phosphorylated on S46 is transcriptionally active. 10 / 14
7 7 |

"Recent studies revealed that phosphorylation of p53 on Ser(46) was associated with induction of p53AIP1 expression, resulting in the commitment of the cell fate into apoptotic cell death."

"Co-exposure to C75 and Taxol induced a remarkable nuclear accumulation of activated p38 mitogen-activated protein kinase (p38 MAPK), which was accompanied by a synergistic nuclear accumulation of the p53 tumor-suppressor protein that was phosphorylated at Ser46, a p38 MAPK-regulated pro-apoptotic modification of p53"

"HIPK2 is activated by ultraviolet (UV) radiation and selectively phosphorylates p53 at Ser 46 ... Accordingly, the kinase function of HIPK2 mediates the increased expression of p53 target genes"

"Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes"

"Through direct cloning of p53 binding sequences from human genomic DNA, we have isolated a novel gene, designated p53AIP1 (p53-regulated Apoptosis-Inducing Protein 1), whose expression is inducible by wild-type p53. Ectopically expressed p53AIP1, which is localized within mitochondria, leads to apoptotic cell death through dissipation of mitochondrial A(psi)m. We have found that upon severe DNA damage, Ser-46 on p53 is phosphorylated and apoptosis is induced. In addition, substitution of Ser-46 inhibits the ability of p53 to induce apoptosis and selectively blocks expression of p53AIP1. Our results suggest that p53AIP1 is likely to play an important role in mediating p53-dependent apoptosis, and phosphorylation of Ser-46 regulates the transcriptional activation of this apoptosis-inducing gene."

"Here we demonstrate that homeodomain-interacting protein kinase-2 (HIPK2), a member of a novel family of nuclear serine/threonine kinases, binds to and activates p53 by directly phosphorylating it at Ser 46"

"Here we demonstrate that homeodomain-interacting protein kinase-2 (HIPK2), a member of a novel family of nuclear serine/threonine kinases, binds to and activates p53 by directly phosphorylating it at Ser 46"

"Recent studies revealed that phosphorylation of p53 on Ser(46) was associated with induction of p53AIP1 expression, resulting in the commitment of the cell fate into apoptotic cell death."

"TP53INP1 mediates phosphorylation of p53 on serine 46 (S46). ASPP-1 and ASPP-2 modulate the cellular apoptotic threshold by direct interaction with p53, thereby enhancing the DNA binding and trans-activation function of p53 on the promoters of pro-apoptotic genes in vivo"

"TP53INP1 mediates phosphorylation of p53 on serine 46 (S46). ASPP-1 and ASPP-2 modulate the cellular apoptotic threshold by direct interaction with p53, thereby enhancing the DNA binding and trans-activation function of p53 on the promoters of pro-apoptotic genes in vivo"
TP53 phosphorylated on T18 is transcriptionally active. 4 / 4
2 2 |

"Endogenous p53 is also phosphorylated in Thr18 by VRK2B, promoting its stabilization and transcriptional activation in A549 cells"

"Endogenous p53 is also phosphorylated in Thr18 by VRK2B, promoting its stabilization and transcriptional activation in A549 cells"

"Thr18 residue phosphorylation, in the transactivation domain of p53, has been implicated in both disruption of p53-Mdm2 interaction and p300 coactivator recruitment, which acetylates the p53 carboxy terminus. This leads to a decrease in p53 degradation and its subsequent stabilization and to an increase in p53-dependent transactivation activity."

"Thr18 residue phosphorylation, in the transactivation domain of p53, has been implicated in both disruption of p53-Mdm2 interaction and p300 coactivator recruitment, which acetylates the p53 carboxy terminus. This leads to a decrease in p53 degradation and its subsequent stabilization and to an increase in p53-dependent transactivation activity. "
Phosphorylated TP53 is transcriptionally active. 3 / 3
3 |

"We concluded that H7 inhibits constitutive C-terminal phosphorylation of p53, which regulates its turnover in unstressed cells."

"In the p53-dependent pathway, p53 accumulates following E2F1 expression [29] through activation of the cyclin-dependent kinase inhibitor 2A (CDKN2A) transcript p14ARF, which in turn interacts with mouse double minutes (MDM2), thereby preventing MDM2 from targeting p53 for ubiquitination and subsequent degradation"

"Furthermore, evidence is provided that increased Cdk5 activity increases p53 transcriptional activity significantly, suggesting that p53 is modulated in situ by Cdk5. This is the first demonstration that p53 is a substrate of Cdk5, and that Cdk5 can modulate p53 levels and activity."
Serine-phosphorylated TP53 is transcriptionally active. 3 / 3
3 |

"In the p53-dependent pathway, p53 accumulates following E2F1 expression [29] through activation of the cyclin-dependent kinase inhibitor 2A (CDKN2A) transcript p14ARF, which in turn interacts with mouse double minutes (MDM2), thereby preventing MDM2 from targeting p53 for ubiquitination and subsequent degradation"

"phosphorylation by the kinase complex enhances p53 activity."

"Co-exposure to C75 and Taxol induced a remarkable nuclear accumulation of activated p38 mitogen-activated protein kinase (p38 MAPK), which was accompanied by a synergistic nuclear accumulation of the p53 tumor-suppressor protein that was phosphorylated at Ser46, a p38 MAPK-regulated pro-apoptotic modification of p53"
TP53 phosphorylated on S20 is transcriptionally active. 2 / 2
2 |

"Pretreatment with an inhibitor of poly(ADP-ribose) polymerase 1 (PARP1), NU1025, nearly doubled the DNA damage produced by 5 microM 3MI, implying that PARP1, which among other activities, functions to repair single-strand breaks in DNA, repaired at least some of the 3MI-induced DNA fragmentation. A key cellular response to DNA damage, phosphorylation, and nuclear localization of p53 was seen at subtoxic levels of 3MI exposure ... from Fig 6, TP53 P@S20"

"Upon DNA damage, the amino terminus of p53 is phosphorylated at a number of serine residues including S20, a site that is particularly important in regulating stability and function of the protein."
TP53 phosphorylated on S37 is transcriptionally active. 2 / 2
2 |

"In the present study, we demonstrate that PP-1 can dephosphorylate p53 at Ser-15 and Ser-37 through co-immunoprecipitation, in vitro and in vivo dephosphorylation assays, overexpression and silence of the gene encoding the catalytic subunit for PP-1. We further show that mutations mimicking constitutive dephosphorylation or phosphorylation of p53 at these sites attenuate or enhance its transcriptional activity, respectively."

"Here we describe a role for PRAK in tumor suppression by demonstrating that PRAK mediates senescence upon activation by p38 in response to oncogenic ras ... Furthermore, we show that PRAK activates p53 by direct phosphorylation. We propose that phosphorylation of p53 by PRAK following activation of p38 MAPK by ras plays an important role in ras-induced senescence and tumor suppression ... from full text, oncogenic ras is HRAS G12V and TP53 is phosphorylated at S37 ... human primary BJ fibroblasts"
TP53 phosphorylated on T55 is transcriptionally active. 1 / 1
1 |

"\"Phosphorylation of p53 on Thr55 by ERK2 is necessary for doxorubicin-induced p53 activation and cell death.\""
TP53 phosphorylated on T81 is transcriptionally active. 1 / 1
1 |

"Forced expression of MKP5, a JNK phosphatase, in JNK kinase-expressing cells decreased T81 phosphorylation while reducing p53 transcriptional activity and p53-mediated apoptosis."
TP53 phosphorylated on S315 is transcriptionally active. 1 / 1
1 |

"Transfection of the p53 gene with an alanine mutation at the Ser(315) site into Saos-2 cells gave rise to a form of p53 protein with a substantially reduced specific activity as a transcription factor"
TP53 is transcriptionally active. 1 / 1
1 |

"However, treatment with ADR or cisplatin is accompanied by a significant increase and redistribution of RAD6 to DNA, and RAD6, RAD18, PCNA, phosphohistone H3, as well as p53 proteins are all found in the DNA fractions."
TP53 phosphorylated on S392 is transcriptionally active. 1 / 1
1 |

"<p17> Ser392 phosphorylation of P53 increases 10-fold the association constant for tetramerization, but this effect is reversed by Ser315 phosphorylation. The tetramerization activates P53 for specific DNA binding and transcription"
TP53 phosphorylated on S33 is transcriptionally active. 1 / 1
1 |

"In this paper, we present a comprehensive pathway map of EGFR signaling and other related pathways."
TP53 is inactive.
19 |
Ubiquitinated TP53 is inactive. 6 / 6
6 |

"The E3 ubiquitin ligase, MDM2, uses a dual-site mechanism to ubiquitinate and degrade the tumor suppressor protein p53, involving interactions with the N-terminal hydrophobic pocket and the acidic domain of MDM2."

"New ring-domain e3-ubiquitin ligase trim24 that targets p53 for degradation"

"Many posttranslational modifications of p53, such as phosphorylation, dephosphorylation, acetylation and ribosylation, have been shown to occur following cellular stress. Some of these modifications may activate the p53 protein, interfere with MDM2 binding and/or dictate cellular localization of p53."

"Hausp counteracts the destabilizing effect of mdm2 by direct deubiquitination of p53."

"Dual Roles of MDM2 in the Regulation of p53: Ubiquitination Dependent and Ubiquitination Independent Mechanisms of MDM2 Repression of p53 Activity"

"Plk1-mediated phosphorylation of topors regulates p53 stabilityherein, we have identified topoisomerase i-binding protein (topors), a p53-binding protein, as a plk1 target. We show that plk1 phosphorylates topors on ser(718) in vivo. Significantly, expression of a plk1-unphosphorylatable topors mutant (s718a) leads to a dramatic accumulation of p53 through inhibition of p53 degradation. Topors is an ubiquitin and small ubiquitin-like modifier ubiquitin-protein isopeptide ligase (sumo e3) ligase. Plk1-mediated phosphorylation of topors inhibits topors-mediated sumoylation of p53, whereas p53 ubiquitination is enhanced, leading to p53 degradation."
TP53 phosphorylated on T55 is inactive. 4 / 4
4 |

"Grk5, but not grk2 or grk6, phosphorylates p53 at thr-55, which promotes the degradation of p53, leading to inhibition of p53-dependent apoptotic response to genotoxic damage."

"A specific PP2A regulatory subunit, B56gamma, mediates DNA damage-induced dephosphorylation of p53 at Thr55| In this study, we reported that the specific B regulatory subunits of PP2A B56gamma1 and B56gamma3 mediate dephosphorylation of p53 at Thr55. Ablation of the B56gamma protein by RNAi, which abolishes the Thr55 dephosphorylation in response to DNA damage, reduces p53 stabilization, Bax expression and cell apoptosis"

"Phosphorylation on thr-55 by taf1 mediates degradation of p53"

"A specific PP2A regulatory subunit, B56gamma, mediates DNA damage-induced dephosphorylation of p53 at Thr55| In this study, we reported that the specific B regulatory subunits of PP2A B56gamma1 and B56gamma3 mediate dephosphorylation of p53 at Thr55. Ablation of the B56gamma protein by RNAi, which abolishes the Thr55 dephosphorylation in response to DNA damage, reduces p53 stabilization, Bax expression and cell apoptosis"
TP53 phosphorylated on S215 is inactive. 2 / 2
2 |

"Here we show that p53 is phosphorylated by the mitotic kinase aurora-a at serine 215. Unlike most identified phosphorylation sites of p53 that positively associate with p53 function (brooks, c. L., and gu, w. (2003) curr. Opin. Cell biol. 15, 164-171), the phosphorylation of p53 by aurora-a at ser-215 abrogates p53 dna binding and transactivation activity."

"We show that aurora b phosphorylates p53 at s183, t211, and s215 to accelerate the degradation of p53 through the polyubiquitination-proteasome pathway, thus functionally suppressing the expression of p53 target genes involved in cell cycle inhibition and apoptosis (e.g., p21 and puma)."
TP53 phosphorylated on T284 is inactive. 1 / 1
1 |

"Importantly, the aurora b-mediated phosphorylation on ser(269) or thr(284) significantly compromises p53 transcriptional activity."
TP53 phosphorylated on S315 is inactive. 1 / 1
1 |

"Aurora kinase a phosphorylates p53 at ser315, leading to its ubiquitination by mdm2 and proteolysis"
TP53 phosphorylated on S269 is inactive. 1 / 1
1 |

"Importantly, the aurora b-mediated phosphorylation on ser(269) or thr(284) significantly compromises p53 transcriptional activity."
TP53 phosphorylated on T155 is inactive. 1 / 1
1 |

"CK2 phosphoryl ates Thr155, which targets p53 to degradation by the Ub system."
TP53 bound to CBFβ-MYH11 is inactive. 1 / 1
1 |

"Here, we show that p53 activity is inhibited in inv(16)+ AML LSCs via interactions with the CBFβ-SMMHC (CM) fusion protein and histone deacetylase 8 (HDAC8).Altogether, these results indicate that CM fusion protein binds to p53 and impairs acetylation and activation of p53."
TP53 phosphorylated on S183 is inactive. 1 / 1
1 |

"We show that aurora b phosphorylates p53 at s183, t211, and s215 to accelerate the degradation of p53 through the polyubiquitination-proteasome pathway, thus functionally suppressing the expression of p53 target genes involved in cell cycle inhibition and apoptosis (e.g., p21 and puma)."
TP53 phosphorylated on T211 is inactive. 1 / 1
1 |

"We show that aurora b phosphorylates p53 at s183, t211, and s215 to accelerate the degradation of p53 through the polyubiquitination-proteasome pathway, thus functionally suppressing the expression of p53 target genes involved in cell cycle inhibition and apoptosis (e.g., p21 and puma)."