CDKN2B

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.
References in periodicals archive ?
The effect of maternal choline deficient diet has been studied on three candidate genes cdkn3, cdkn2b and calb2.
The top 5 down-regulated genes were glutathione peroxidase 3, CDKN2B (p15), phospholipase A2 receptor 1, plasminogen activator, and diacylglycerol lipase.
The analysis of this list reveals that associated mutations of cellular cycle, such as CDKN2A and CDKN2B, with mutations of genes located on chromosome 9, have been rarely detected in atypical type and more constantly in malignant types of meningiomas [15].
Liu et al., "CDKN2B polymorphism is associated with primary open-angle glaucoma (POAG) in the Afro-Caribbean population of Barbados, West Indies," PLoS ONE, vol.
ANRIL, the antisense lncRNA of the cyclin-dependent kinase inhibitor 2b (CDKN2B) gene, is involved in the development of the melanoma and neural system tumor syndrome, familial melanoma syndrome, and various tumor types; however, its association with PD has not yet been investigated [22].
Among them, we found the principal components of major regulatory clusters, involving inflammatory responses (IFNy, IL6, several members of the interleukin 1 pathway, including ILIA, IL1B, IL1RN, and the TNF pathway members TNF, TNFAIP6, TNFSF15, TNFRSF9), angiogenesis (CXCL10, PTGS2), immune regulation (CD80, CD274, CSF3, IL23R), leukocyte chemotaxis (CCL2, CCL3, CCL4, CCL20, CCL23, CCL3L3, CXCL1, CXCL2, CXCL5, CXCL9), transcriptional regulation (EGR1, GATA6, HEY1), proliferation (CDKN2B, FGFR1), adhesion (ITGB8), extracellular matrix remodeling (ADAMTS4), cell-cell communication (GJB2), cell signaling (EDNRB, IRS1, RIN2), ion transmembrane transport (KCNJ2, CLIC4), and response to oxidative stress (SOD2).
MYCN knockdown in human neural crest stem cells leads to cell cycle arrest in the G0/G1 phase and a significant increase in the expression of Cdknla, Cdkn2a, and Cdkn2b, and at the same time a significant decrease in Cyclin D1 expression occurs, which facilitates the G1/S transition [49].
displayed the most common abnormality was the deletion of 9p21.3 which contained CDKN2A and CDKN2B genes, and they found that deletion of 6q21 ( PRDM1 ) was associated with shorter OS.[sup][51] The deletion involving 6q21-6q23 also happens regularly whereas it contains candidate genes such as PRDM1 and TNFAIP3 , the former as a tumor suppressor regulates B-cell differentiation and the latter as a key negative regulator of NF-?B pathway.
Frequent loss of chromosome 9, homozygous involving CDKN2A/p14ARF/ CDKN2B deletion and low TSC1 mRNA expression in pleomorphic xanthoastrocytomas.
Como ejemplo de esto estan los estudios en Chile, de los genes APAF1, ASSP1, p73 y FHIT,p15, p16, ESR1, IGSF4, SOCS1(9); en Colombia, de los genes RARB y DAPK;CDKN2B y DBC1(10);en Brasil, del gen CDKN2B (p15) (11) y en Espana de CDH1, p73, p16, p15, p57, NES-1, DKK-3, CDH13, p14, TMS-1, Apaf-1, DAPK, Parkin, LATS-1(12).
Mutations in several genes implicated in human InvUC (EGFR [9, 50, 81], CDKN2B [82, 83], PIK3CA [9, 82], BRCA2 [84], and NFkB [85]) have been identified in dogs [72].
For example, Achille and collaborators investigated global DNA methylation and gene expression of CDKN2A (cyclin-dependent kinase inhibitor 2A), CDKN2B (cyclin-dependent kinase inhibitor 2B), both regulators of the cell cycle at the G1 checkpoint; HIC1 (transcriptional repressor 1), a growth regulatory molecule that acts as a tumor repressor; RARB (retinoic acid receptor beta), a retinoic acid nuclear receptor which also mediates cellular signalling, growth, and differentiation; CDH1; and APAF1 (apoptotic peptidase activating factor 1), an apoptosis initiator by cleavage of caspase 9, before and during hypomethylating therapy, with the purpose of observing whether early changes could predict clinical response.