TP53

Level: Level 1A

Description:

tumor protein p53 [Source:HGNC Symbol;Acc:11998]

Other Names: p53, LFS1, TP53
Overview
Ensembl ID | ENSG00000141510
Transcript ID | ENST00000269305
CDS length | 1182
NCBI | 7157
HGNC Id | 11998
Refseq ID | NM_000546
Related Link
Uniprot ID | P04637
UCSC ID | uc060aur.1
OMIM ID | 191170
CIViC ID | 45
OncoKB |
Pharos |
Gene info
Gene position | 17:7565097-7590856
Cytoband | 17p13.1
Gene Type | protein-coding gene
Protein family | P53 family
Pathway(Rectome) | Activation of BH3-only proteins, Activation of NOXA and translocation to mitochondria, Activation of PUMA and translocation to mitochondria, Antiviral mechanism by IFN-stimulated genes, Apoptosis, Association of TriC/CCT with target proteins during biosynthesis, Autodegradation of the E3 ubiquitin ligase COP1, Cell Cycle, Cell Cycle Checkpoints, Cell Cycle, Mitotic, Cellular Senescence, Cellular responses to stimuli, Cellular responses to stress, Chaperonin-mediated protein folding, Cytokine Signaling in Immune system, DNA Damage/Telomere Stress Induced Senescence, DNA Double Strand Break Response, DNA Double-Strand Break Repair, DNA Repair, Defective Intrinsic Pathway for Apoptosis, Deubiquitination, Developmental Biology, Disease, Diseases of programmed cell death, Diseases of signal transduction by growth factor receptors and second messengers, Factors involved in megakaryocyte development and platelet production, Formation of Senescence-Associated Heterochromatin Foci (SAHF), G1/S DNA Damage Checkpoints, G2/M Checkpoints, G2/M DNA damage checkpoint, G2/M Transition, Gene expression (Transcription), Generic Transcription Pathway, Hemostasis, Immune System, Innate Immune System, Interferon Signaling, Interleukin-1 family signaling, Interleukin-1 signaling, Interleukin-4 and Interleukin-13 signaling, Intracellular signaling by second messengers, Intrinsic Pathway for Apoptosis, Loss of Function of TP53 in Cancer, Loss of function of TP53 in cancer due to loss of tetramerization ability, Maternal to zygotic transition (MZT), Metabolism of proteins, Mitotic G2-G2/M phases, MyD88 cascade initiated on plasma membrane, MyD88 dependent cascade initiated on endosome, MyD88-independent TLR4 cascade, MyD88:MAL(TIRAP) cascade initiated on plasma membrane, Oncogene Induced Senescence, Ovarian tumor domain proteases, Oxidative Stress Induced Senescence, PI5P Regulates TP53 Acetylation, PIP3 activates AKT signaling, PKR-mediated signaling, PTEN Regulation, Post-translational protein modification, Pre-NOTCH Expression and Processing, Pre-NOTCH Transcription and Translation, Programmed Cell Death, Protein folding, Pyroptosis, RNA Polymerase II Transcription, RUNX3 regulates CDKN1A transcription, Recruitment and ATM-mediated phosphorylation of repair and signaling proteins at DNA double strand breaks, Regulated Necrosis, Regulation of NF-kappa B signaling, Regulation of PTEN gene transcription, Regulation of TP53 Activity, Regulation of TP53 Activity through Acetylation, Regulation of TP53 Activity through Association with Co-factors, Regulation of TP53 Activity through Methylation, Regulation of TP53 Activity through Phosphorylation, Regulation of TP53 Degradation, Regulation of TP53 Expression, Regulation of TP53 Expression and Degradation, SUMO E3 ligases SUMOylate target proteins, SUMOylation, SUMOylation of transcription factors, Signal Transduction, Signaling by ALK fusions and activated point mutants, Signaling by ALK in cancer, Signaling by Interleukins, Signaling by NOTCH, Stabilization of p53, TAK1-dependent IKK and NF-kappa-B activation, TP53 Regulates Metabolic Genes, TP53 Regulates Transcription of Caspase Activators and Caspases, TP53 Regulates Transcription of Cell Cycle Genes, TP53 Regulates Transcription of Cell Death Genes, TP53 Regulates Transcription of DNA Repair Genes, TP53 Regulates Transcription of Death Receptors and Ligands, TP53 Regulates Transcription of Genes Involved in Cytochrome C Release, TP53 Regulates Transcription of Genes Involved in G1 Cell Cycle Arrest, TP53 Regulates Transcription of Genes Involved in G2 Cell Cycle Arrest, TP53 regulates transcription of additional cell cycle genes whose exact role in the p53 pathway remain uncertain, TP53 regulates transcription of several additional cell death genes whose specific roles in p53-dependent apoptosis remain uncertain, TRAF6 mediated induction of NFkB and MAP kinases upon TLR7/8 or 9 activation, TRIF (TICAM1)-mediated TLR4 signaling, The role of GTSE1 in G2/M progression after G2 checkpoint, Toll Like Receptor 10 (TLR10) Cascade, Toll Like Receptor 2 (TLR2) Cascade, Toll Like Receptor 3 (TLR3) Cascade, Toll Like Receptor 4 (TLR4) Cascade, Toll Like Receptor 5 (TLR5) Cascade, Toll Like Receptor 7/8 (TLR7/8) Cascade, Toll Like Receptor 9 (TLR9) Cascade, Toll Like Receptor TLR1:TLR2 Cascade, Toll Like Receptor TLR6:TLR2 Cascade, Toll-like Receptor Cascades, Transcriptional activation of cell cycle inhibitor p21, Transcriptional Regulation by TP53, Transcriptional Regulation by VENTX, Transcriptional activation of p53 responsive genes, Transcriptional regulation by RUNX3, Ub-specific processing proteases, Zygotic genome activation (ZGA), p53-Dependent G1 DNA Damage Response, p53-Dependent G1/S DNA damage checkpoint,
Pathway(Uniprot) | /
Description

FUNCTION: Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA- Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seems to have an effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis. Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1- mediated transcriptional activation of PER2 (PubMed:24051492). {ECO:0000269|PubMed:11025664, ECO:0000269|PubMed:12810724, ECO:0000269|PubMed:15186775, ECO:0000269|PubMed:15340061, ECO:0000269|PubMed:17317671, ECO:0000269|PubMed:17349958, ECO:0000269|PubMed:19556538, ECO:0000269|PubMed:20673990, ECO:0000269|PubMed:20959462, ECO:0000269|PubMed:22726440, ECO:0000269|PubMed:24051492, ECO:0000269|PubMed:9840937}.

Gene Class

  • Role in Cancer TSG
  • Essential Gene /
  • Cell Senescence Gene CSGene
  • Type of Senescence Replicative;Stress-induced;Oncogene-induced
  • Regeneration Gene REGene

Evidence Source

  • Clinical CIViC
  • Validate NCG;OncoKB;CGC T1
  • Literature CancerMine;TSGene;SEECancer
  • Experimental CCGD Rank A
  • Predict CnCs-calculator T1;NCG predicted

Gene Essential Source

  • Essential Gene E
  • CRISPR N
  • CRISPR2 S
  • Gene-Trap N
  • Gene Indispensability Score 1.0
  • Gene Indispensability E

Gene Damage Prediction

  • All Disease-causing Medium
  • All Mendelian Disease-causing Medium
  • All PID Disease-causing Medium
  • All Cancer Disease-causing Medium
  • Cancer Recessive Disease-causing Medium
  • Cancer Dominant Disease-causing Medium
GO annotation
Cancer Associated Splicing Events (CASE)
Method Classification
  • Evolutionary selective pressure(dN/dS) based: CN/CS-calculator dNdScv CBaSE
  • Mutation frequency based: MuSiC MuSig2CV OncodriveCLUST
  • Feature(e.g. functional impact) based: 20/20+ CompositeDriver OncodriveFML
  • Structural(Domain) based: e-Driver ActiveDriver
  • Omic/Network or pathway based: DriverNet
  • Machine learning based: DawnRank
  • Result in Pan-cancer
  • dNdSCNCS-calculator;CBaSE;dNdScv
  • FrequencyMuSiC;MutSig2CV
  • Feature 2020plus;OncodriveFML
  • DomainActiveDriver;e-Driver
  • Result in Cancer
Cohort:    Project: