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p16(INK4a) modulates epicardial adipose tissue development, providing a potential mechanistic link between the genetic association of the CDKN2A/B locus and cardiovascular disease risk.
p16 FISH with an appropriately set cutoff value is useful for differentiating MPM from RMH in the FFPE tissue samples. p16 homo-d positive status, which is correlated with shorter OS, serves as a prognostic biomarker in MPM.
CDKN2A plays a role in nevogenesis. Pathogenic mutation carriers are significantly more likely to exhibit higher-than-median nevus counts in all three categories of nevus phenotype simultaneously compared with those without pathogenic CDKN2A mutations.
Results indicate complex rearrangements involving CDKN2A locus and frequent occurrence of fusion transcripts involving methylthioadenosine phosphorylase (MTAP (show MTAP Antibodies)) and ANRIL genes.
Biological differences, characterized by loss of p16 expression without gains of 1q in iEPN-PFs, as well as deregulated E2F (show E2F1 Antibodies) target gene transcription, are indicative of deregulated p16-CDK4/6 (show CDK4 Antibodies)-pRB (show RB1 Antibodies)-E2F (show E2F1 Antibodies) pathway activity
Promoter methylation was observed for the p16 gene, which was considered an early potential marker in gastric cancer.
Results show that non-promoter hypermethylation of the CDKN2A downstream locus correlates with increased ARF and INK4a mRNA expression, and that activation of these CDKN2A transcripts is associated with improved locoregional control in laryngeal squamous cell carcinomas.
E6AP (UBE3A) abundance is down-regulated in a proportion of NSCLC (non-small cell lung (show CDKN2B Antibodies)cancer) patients, and this correlates with low p16 (show ube3a Antibodies)INK4a in tumors and worse overall survival.
The current study supports a relevant role for p15 (show CDKN2B Antibodies), p16, and DAPK (show DAPK1 Antibodies) hypermethylation in the genesis of the plasma cell neoplasm. DAPK (show DAPK1 Antibodies) hypermethylation also might be an important step in the progression from MGUS to MM.
Transcriptome analysis revealed ARID1A (show ARID1A Antibodies) knockdown led to miR (show MLXIP Antibodies)-503 upregulation. CDKN2A was identified as a target of miR (show MLXIP Antibodies)-503, which contributes to cell senescence. Thus, the data suggests that ARID1A (show ARID1A Antibodies) deficiency promote KRAS(G12D)-driven pancreatic tumorigenesis through miR (show MLXIP Antibodies)-503/CDKN2A-mediated senescence.
Cdkn2a transcripts modulate platelet production and activity in the setting of hypercholesterolemic LDLR (show LDLR Antibodies) knockout mice.
The expression of three tumor suppressor genes encoded in the INK4/ARF locus (p15(INK4b (show CDKN2B Antibodies)), p16(INK4a), and p19(ARF)) was decreased in E6AP (show ube3a Antibodies)(-/-) embryo fibroblasts.
Consistent with this cellular infection spectrum, we show that intra-uterine injection of ecotropic MuLE viruses expressing oncogenic HrasG12V together with knockdown of Cdkn2a induce high-grade endometrial stromal sarcomas
ARF inhibits tumor growth by suppressing the ability of NRF2 (show NFE2L2 Antibodies) to transcriptionally activate its target genes, including SLC7A11 (show SLC7A11 Antibodies), a component of the cystine/glutamate (show GRIN1 Antibodies) antiporter that regulates reactive oxygen species (ROS (show ROS1 Antibodies))-induced ferroptosis.
These findings strongly suggest that the enhanced Arf expression in oxidative stress plays compensatory protective roles against aging-related dysregulation of gene expression in adipocytes.
Increased expression of Arf in tumor stromal cells, as in tumor keratinocytes themselves, contributes to suppression of BCC carcinogenesis.
Loss of p16(INK4a) expression is associated with tumorigenesis.
TBK1 (show TBK1 Antibodies) regulates p16 expression and retinal ganglion cell senescence.
median survival of KPIC mice was longer than that of LSL-KrasG12D; Ink4flox/flox; Ptf1/p48 (show PTF1A Antibodies)-Cre mice (KIC) (89 vs 62 days) and shorter than that of KRAS (KrasG12D), TP53 (show TP53 Antibodies) (Trp53R172H/+) and Ptf1/p48 (show PTF1A Antibodies)-Cre (KPC) mice
This gene generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene\; this transcript contains an alternate open reading frame (ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control. This gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene.
, Cyclin dependent kinase inhibitor 2A (p16, inhibits CDK4)
, cell cycle inhibitor
, cell cycle regulator
, cyclin-dependent kinase 4 inhibitor A
, cyclin-dependent kinase inhibitor 2a p16Ink4a
, cyclin-dependent kinase inhibitor 2a p19Arf
, CDK4 inhibitor p16-INK4
, cell cycle negative regulator beta
, cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)
, multiple tumor suppressor 1
, cyclin-dependent kinase inhibitor 2A (p16, inhibits CDK4)
, cyclin-dependent kinase inhibitor 2A, isoforms 1/2
, cyclin-dependent kinase inhibitor protein
, mitochondrial smARF