CDKN1A

(redirected from p21CIP1)

CDKN1A

A gene on chromosome 6p21.2 that encodes a cyclin-dependent kinase inhibitor, which binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, thus acting as a regulator of cell cycle progression at G1. CDKN1A expression is controlled by p53, a tumour suppressor that mediates p53-dependent cell cycle G1-phase arrest in response to various stress stimuli. CDKN1A is specifically cleaved by CASP3-like caspases, activating CDK2 and possibly also the apoptosis pathway.
References in periodicals archive ?
Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21CIP1, but not p16INK4a.
Aspirin inhibits camptothecin-induced p21CIP1 levels and potentiates apoptosis in human breast cancer cells.
p57KIP2, a structurally distinct member of the p21CIP1 Cdk inhibitor family, is a candidate tumor suppressor gene.
From the other XJAR apply indirectly it's anti -apoptotic effect by stimulating P21CiP1 that cause stopping in the cell propagation cycle in the grade G1/S.
Tetrandrine induces early G1 arrest in human colon carcinoma cells by down-regulating the activity and inducing the degradation of G1-S-specific cyclin-dependent kinases and by inducing p53 and p21Cip1.
Induction of apoptosis in U937 human leukemia cells by suberoylanilide hydroxamic acid(SAHA) proceeds through pathways that are regulated by Bcl-2/Bcl-XL, c-Jun, and p21CIP1, but independent of p53.
Normally, Myc accelerates cell division by suppressing two proteins, called p27Kip1 and p21Cip1, which act as brakes on this process.
Cell cycle arrest in Metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and requires p27Kip1 or p21Cip1.
Contribution of p161NK4a and p21CIP1 pathways to induction of premature senescence of human endothelial cells: permissive role of p53.
Poster Session -- #3167 - Exposure of Human AML Cells to 5-Aza-2'-Deoxycytidine (decitabine) Alone or in Combination with Trichostatin A Induces p21CIP1 in the Absence of Dense Promoter Methylation.
2] induces a transient multi-phase cell cycle arrest in mouse fibroblasts through modulating cyclin D and p21Cip1 expression.
Combined treatment of leukemia cells with vitamin K2 and 1alpha,25-dihydroxy vitamin D3 enhances monocytic differentiation along with becoming resistant to apoptosis by induction of cytoplasmic p21CIP1.