p21
Cyclin-dependent kinase inhibitor 1A (p21, Cip1), also known as CDKN1A, is a human gene.
Cyclin-dependent kinase inhibitor 1A (p21, Cip1) | |||||||||||
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Identifiers | |||||||||||
Symbols | CDKN1A ; CAP20; CDKN1; CIP1; MDA-6; P21; SDI1; WAF1; p21CIP1 | ||||||||||
External IDs | Template:OMIM5 Template:MGI HomoloGene: 333 | ||||||||||
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RNA expression pattern | |||||||||||
File:PBB GE CDKN1A 202284 s at.png | |||||||||||
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Orthologs | |||||||||||
Template:GNF Ortholog box | |||||||||||
Species | Human | Mouse | |||||||||
Entrez | n/a | n/a | |||||||||
Ensembl | n/a | n/a | |||||||||
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RefSeq (mRNA) | n/a | n/a | |||||||||
RefSeq (protein) | n/a | n/a | |||||||||
Location (UCSC) | n/a | n/a | |||||||||
PubMed search | n/a | n/a |
This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of this gene is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation. Two alternatively spliced variants, which encode an identical protein, have been reported.[1]
p21, also known as cyclin-dependent kinase inhibitor 1A or CDKN1A, is a human gene on chromosome 6 (location 6p21.2), that encodes a cyclin-dependent kinase inhibitor that directly inhibits the activity of cyclin-CDK2 and cyclin-CDK4 complexes. p21 functions as a regulator of cell cycle progression at G1 phase[2]. The expression of p21 is controlled by the tumor suppressor protein p53.
The function of this gene relates in part to stress response [3].
p21 is also mediating the resistance of hematopoietic cells to an infection with HIV [4] by complexing with the HIV integrase and thereby aborting chromosomal integration of the provirus.
External links
- Cyclin-Dependent+Kinase+Inhibitor+p21 at the US National Library of Medicine Medical Subject Headings (MeSH)
References
- ↑ "Entrez Gene: CDKN1A cyclin-dependent kinase inhibitor 1A (p21, Cip1)".
- ↑ A. L. Gartel and S. K. Radhakrishnan (2005) "Lost in transcription: p21 repression, mechanisms, and consequences" in Cancer Research Volume 65, pages 3980-3985. Template:Entrez Pubmed
- ↑ R. Rodriguez and M. Meuth. (2006) "Chk1 and p21 cooperate to prevent apoptosis during DNA replication fork stress" in Molecular Biology of the Cell Volume 17, pages 402-412. Template:Entrez Pubmed
- ↑ Zhang J, Scadden DT, Crumpacker CS.: Primitive hematopoietic cells resist HIV-1 infection via p21. J Clin Invest. 2007 Feb 1;117(2):473-481. PMID 17273559
Further reading
- Marone M, Bonanno G, Rutella S; et al. (2003). "Survival and cell cycle control in early hematopoiesis: role of bcl-2, and the cyclin dependent kinase inhibitors P27 and P21". Leuk. Lymphoma. 43 (1): 51–7. PMID 11908736.
- Fang JY, Lu YY (2002). "Effects of histone acetylation and DNA methylation on p21( WAF1) regulation". World J. Gastroenterol. 8 (3): 400–5. PMID 12046058.
- Tokumoto M, Tsuruya K, Fukuda K; et al. (2003). "Parathyroid cell growth in patients with advanced secondary hyperparathyroidism: vitamin D receptor and cyclin-dependent kinase inhibitors, p21 and p27". Nephrol. Dial. Transplant. 18 Suppl 3: iii9–12. PMID 12771291.
- Amini S, Khalili K, Sawaya BE (2004). "Effect of HIV-1 Vpr on cell cycle regulators". DNA Cell Biol. 23 (4): 249–60. doi:10.1089/104454904773819833. PMID 15142382.
- Zhang Z, Wang H, Li M; et al. (2006). "Novel MDM2 p53-independent functions identified through RNA silencing technologies". Ann. N. Y. Acad. Sci. 1058: 205–14. doi:10.1196/annals.1359.030. PMID 16394138.
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