CDKN2B

(redirected from p15INK4b)

CDKN2B

A gene on chromosome 9p21 that encodes a member of the INK4 family of cyclin-dependent kinase inhibitors, which form a complex with CDK4 or CDK6, preventing activation of CDK kinases and thus acting as cell growth regulators by controlling cell cycle progression through G1. CDKN2B expression is dramatically induced by TGF beta, suggesting a role in TGF-beta-induced growth inhibition.
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The main components of RB pathway involves five family proteins; retinoblastoma tumor suppressor RB- family of pocket proteins (p110, p107, p130), E2F-family of transcription factors (heterodimers of E2F1-8 with DP1-2), cyclins (D and E-type), cyclin-dependent protein kinases (cdk4, cdk6) and cyclin-dependent kinase inhibitor CDKIs (p16Ink4a, p15Ink4b, p18Ink4c and p19Ink4d).
Promoter hypermethylation of p15INK4B, HIC1, CDH1, and ER is frequent in myelodysplastic syndrome and predicts poor prognosis in early-stage patients.
Extensive intra- and interindividual heterogeneity of p15INK4B methylation in acute myeloid leukemia.
TGF--dependent active demethylation and expression of the p15ink4b tumor suppressor are impaired by the ZNF217/CoREST complex.
at genes called p16INK4a, p15INK4b, and RB), resulting in the silencing by is the most recognized epigenetic disruption in human tumors.
The inhibitors of CDK such as p16Ink4a, p15Ink4b, p27Kip1, and p21Cip1 negatively regulate CDK activities (D'Andrilli et al.
Aberrant methylation of p16INK4a and deletion of p15INK4b are frequent events in human esophageal cancer in Linxian, China.
p15INK4B is a potential effector of TGF-beta-induced cell cycle arrest.
The present study showed 61 per cent hypermethylation in P15INK4B which is in concordance with earlier studies.
TGFbeta influences Myc, Miz-1 and Smad to control the CDK inhibitor p15INK4b.