CDKN1B


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CDKN1B

A gene on chromosome 12p13.1-p12 that encodes a cyclin-dependent kinase inhibitor, which binds to and prevents activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, thus controlling cell cycle progression at G1. Degradation of cyclin-dependent kinase inhibitor 1B is triggered by its CDK-dependent phosphorylation and subsequent ubiquitination by SCF complexes, and is a necessary step for cell transition from quiescence to the proliferative state.
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TargetScans algorithm-based prediction demonstrated that CDKN1B (p27, Kip1), a cell cycle regulator, was a putative target of miR-24, and was confirmed by luciferase assay.
The fourteen DEGs identified by our analysis (SKIV2L2: Hs00299011_ml, SRPRB: Hs00253639_ml, JUNB: Hs00357891_sl, BNIP3: Hs00969291_ml, RAB22A: Hs00221082_ml, TMED2: Hs00607277_ml, ACAT1: Hs00608002_ ml, NDUFV2: Hs00221478_ml, LBR: Hs01032700_ml, NCL: Hs01066668_ml, AAAS: Hs00210351_ml, ATXN2: Hs00268077_ml, LGMN: Hs00271599_ml, and CDKN1B: Hs00153277_ml) were also analyzed and validated by realtime quantitative PCR.
Interestingly, NANOG upregulates histone deacetylases 1 (HDAC1) via binding to the promoter region and decreasing K14 and K27 histone H3 acetylation; as a result, it induces not only the stem-like features through epigenetic repression of cell cycle inhibitor CDKN2D and CDKN1B but also the immune resistance and chemoresistance through MCL-1 upregulation by epigenetic silencing of E3 ubiquitin-ligase TRIM17 and NOXA [148].
The vast majority of MEN-1 syndrome patients harbour a heterozygous germline mutation in the MEN1 gene, but a few cases have been identified with a CDKN1B mutation and a few have no recognized genetic background.
A total of 4 genes (PIK3CA, CDKN1B, KRAS, and E2F3) existed in All Sources and Lymphocyte Source sets, simultaneously.
As an important cell cycle regulatory gene, the p27 (also known as CDKN1B) controls the cell cycle check from G1 to S transition [13].
Boikos et al., "The role of germline AIP, MEN1, PRKAR1A, CDKN1B and CDKN2C mutations in causing pituitary adenomas in a large cohort of children, adolescents, and patients with genetic syndromes," Clinical Genetics, vol.
The mechanism underlying 1,25[(OH).sub.2][D.sub.3] induced G0/G1 phase growth arrest involves up-regulation of molecules like cyclin dependent kinase inhibitors such as [p21.sup.WAF1/CIP1] (CDKN1A) and [p27.sup.KIP1] (CDKN1B) (Verlinden et al., 1998; Katayama et al., 2003), as well as transforming growth factor [beta], TGF[beta] (which can inhibit the proliferation of epithelial cells), TGF[beta] receptors and insulin-like growth factor binding protein-3 (IGFBP-3), which regulates the availability of insulin-like growth factor (IGF), an important mitogen for normal mammary epithelial and breast cancer cells (Swami et al., 2003).
Hashimoto et al., "Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice," Nature Medicine, vol.
CDKN1A and CDKN1B are targeted by FOXO3A [30] and are downregulated in a variety of tumors.
(2012) reported an 82-year-old male patient had normal karyotype on bone marrow specimen by conventional cytogenetic analysis; losses of chromosome 6, 12 (CDKN1B and ETV6), and 13 on skin biopsy specimen and additional losses of chromosome 2 and 5 on bone marrow specimen by CGH; loss of 2p, 5q, 12p (ETV6), and 13q but not 17 (TP53) on bone marrow specimen; and loss of ETV6 on snap-frozen skin sections by FISH analysis, suggesting that the difference in CGH results between skin and bone marrow specimens may reflect genomic alterations associating with progression of the disease.