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|Application ||IHC-P, WB, IF, E|
|Other Accession||NP_000380.1, NP_510867.1|
|Calculated MW||18119 Da|
|Antigen Region||117-146 aa|
|Other Names||Cyclin-dependent kinase inhibitor 1, CDK-interacting protein 1, Melanoma differentiation-associated protein 6, MDA-6, p21, CDKN1A, CAP20, CDKN1, CIP1, MDA6, PIC1, SDI1, WAF1|
|Target/Specificity||This CDKN1A antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 117-146 amino acids from the C-terminal region of human CDKN1A.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Synonyms||CAP20, CDKN1, CIP1, MDA6, PIC1, SDI1, WA|
|Function||May be the important intermediate by which p53/TP53 mediates its role as an inhibitor of cellular proliferation in response to DNA damage. Binds to and inhibits cyclin-dependent kinase activity, preventing phosphorylation of critical cyclin- dependent kinase substrates and blocking cell cycle progression. Functions in the nuclear localization and assembly of cyclin D- CDK4 complex and promotes its kinase activity towards RB1. At higher stoichiometric ratios, inhibits the kinase activity of the cyclin D-CDK4 complex.|
|Cellular Location||Cytoplasm. Nucleus.|
|Tissue Location||Expressed in all adult tissues, with 5-fold lower levels observed in the brain|
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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. Multiple alternatively spliced variants have been found for this gene.
Hu, F., et al. Oncogene 29(40):5464-5474(2010) Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010) Jiang, P., et al. Acta Biochim. Biophys. Sin. (Shanghai) 42(9):671-676(2010) Ho-Pun-Cheung, A., et al. Pharmacogenomics J. (2010) In press : Do Nascimento Borges, B., et al. In Vivo 24(4):579-582(2010)
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