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cancer cell in dish icon p53 Pathway


p53 is a transcription factor and tumor suppressor activated by cellular stresses like DNA damage, oxidative stress, and nutrient deprivation. p53 is activated through both phosphorylation and acetylation, which disrupt its interaction with negative regulators, increase its stability and DNA binding activity, and allow it to bind transcriptional co-activators and modulate transcription. The list of p53 transcriptional targets is ever-expanding; the best-characterized effects of p53 are in promoting cell cycle arrest, apoptosis, or senescence in damaged cells. The p53 name arose from its observed molecular weight (53 kDa) when run on an SDS-PAGE gel.

Cancer Impact

p53 is the most frequently mutated gene (>50%) in human cancer; most of these mutations are missense mutations in the DNA-binding domain, often at one of six hotspot residues. These mutations can be inherited or arise through exposure to mutagens like radiation or viruses (e.g., HPV, the human papillomavirus). These mutations interfere with p53’s ability to activate transcription, and they also have a dominant negative effect on functional p53 through oligomerization. In particular, the loss of p53’s pro-apoptotic effects is especially important to tumorigenesis. Inheriting only one functional copy of the p53 gene causes a large reduction in tumor suppression activity, leading to the development of tumors in early adulthood, a disorder known as Li-Fraumeni syndrome. Recently some impacts of p53 mutations have been characterized as gain-of-function, expanding the mechanisms by which mutant p53 is known to function in cancer.

p53 Pathway Plasmids

Click on a name to find available plasmids for the gene, or browse the gene list below. For multiple isoforms or subunits, individual links to each gene page are provided below. Color is used for clarity and does not indicate a specific relationship.

p53 Pathway

Color is used for clarity and does not indicate a specific relationship.

The content for this page was generated with the help of .

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p53 Pathway - Gene List

Click on a name to find available plasmids for the gene. For components with multiple isoforms or subunits, individual links to each gene page are provided below.

Symbol Name
14-3-3-σ Stratifin
Apaf-1 Apoptotic peptidase activating factor 1
ATM ATM serine/threonine kinase
ATR ATR serine/threonine kinase
B99 G-2 and S-phase expressed 1; also known as GTSE1
BAI-1 Brain-specific angiogenesis inhibitor 1
Bax BCL2-associated X protein
Bid BH3 interacting domain death agonist
CASP3 Caspase 3, apoptosis-related cysteine peptidase
CASP8 Caspase 8, apoptosis-related cysteine peptidase
CASP9 Caspase 9, apoptosis-related cysteine peptidase
Cyclin B Cyclin B1, 2, or 3
Cyclin D Cyclin D1, 2, or 3
Cyclin E Cyclin E1 or E2
Cyclin G Cyclin G1 or G2
CDC25 Cell division cycle 25C
Cdk4/6 Cyclin-dependent kinase 4 or 6
CHK1 Checkpoint kinase 1
CHK2 Checkpoint kinase 2
Cop-1 Ring finger and WD repeat domain 2 (RFWD2); E3 ubiquitin protein ligase
cytoC Cytochrome c
DR5 Tumor necrosis factor receptor superfamily, member 10b
E2F-1 E2F transcription factor 1
Fas Fas cell surface death receptor
Gadd45 Growth arrest and DNA-damage-inducible; alpha, beta, or gamma
IGF-BP3 Insulin-like growth factor binding protein 3
KAI CD82 molecule
Maspin Serpin family B member 5
MDM2 MDM2 proto-oncogene, E3 ubiquitin protein ligase
MDMX p53 regulator; also known as MDM4
Noxa Phorbol-12-myristate-13-acetate-induced protein 1; also known as PMAIP1
p14ARF Cyclin-dependent kinase inhibitor 2A
p21 Cyclin-dependent kinase inhibitor 1A
p48 Damage-specific DNA binding protein 2, 48kDa
p53 Tumor protein p53
p53AIP1 Tumor protein p53 regulated apoptosis inducing protein 1
p53R2 p53 inducible, ribonucleotide reductase M2 B (RRM2B)
PAG608 Zinc finger, matrin-type 3
PAI Serpin peptidase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1), member 1
PERP TP53 apoptosis effector
PIDD p53-induced death domain protein 1
PIGs Etoposide induced 2.4
PIRH-2 Ring finger and CHY zinc finger domain containing 1 (RCHY1); E3 ubiquitin protein ligase
PTEN Phosphatase and tensin homolog
PUMA BCL2 binding component 3
Reprimo TP53 dependent G2 arrest mediator candidate
Scotin Shisa family member 5
Sestrins Sestrins 1, 2, or 3
Siah Siah E3 ubiquitin protein ligase 1
TSC2 Tuberous sclerosis 2
TSP1 Thrombospondin 1

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Unravelling mechanisms of p53-mediated tumour suppression. Bieging KT, Mello SS, Attardi LD. Nat Rev Cancer. 2014 May;14(5):359-70. PubMed PMID: 24739573.

Uncovering the role of p53 splice variants in human malignancy: a clinical perspective. Surget S, Khoury MP, Bourdon JC. Onco Targets Ther. 2013 Dec 19;7:57-68. doi: 10.2147/OTT.S53876. PubMed PMID: 24379683.

When mutants gain new powers: news from the mutant p53 field. Brosh R, Rotter V. Nat Rev Cancer. 2009 Oct;9(10):701-13. PubMed PMID: 19693097 .

The expanding universe of p53 targets. Menendez D, Inga A, Resnick MA. Nat Rev Cancer. 2009 Oct;9(10):724-37. PubMed PMID: 19776742.

Germline TP53 mutations and Li-Fraumeni syndrome. Varley JM. Hum Mutat. 2003 Mar;21(3):313-20. PubMed PMID: 12619118.

p53 mutant mice that display early ageing-associated phenotypes. Tyner SD, Venkatachalam S, Choi J, Jones S, Ghebranious N, Igelmann H, Lu X, Soron G, Cooper B, Brayton C, Park SH, Thompson T, Karsenty G, Bradley A, Donehower LA. Nature. 2002 Jan 3;415(6867):45-53. PubMed PMID: 11780111.

p53 mutations in human cancers. Hollstein M, Sidransky D, Vogelstein B, Harris CC. Science. 1991 Jul 5;253(5015):49-53. PubMed PMID: 1905840.

Recruitment of p300/CBP in p53-dependent signal pathways. Avantaggiati ML, Ogryzko V, Gardner K, Giordano A, Levine AS, Kelly K. Nature. 1997 Jun 27;89(7):1175-84. PubMed PMID: 9215639.

Mutant p53 gain-of-function in cancer. Oren, M. and V. Rotter. Cold Spring Harbor Perspectives in Biology. 2010 Feb;2(2):a001107. PMC PMID: 20182618.

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