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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.
ARF inhibits tumor growth by suppressing the ability of NRF2 (show GABPA 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.
The expression of the nuclear and cytoplasmic forms of p16 represent two independent mechanisms, and both seemed to control proliferation in response to oncogenic stimuli, protecting the cell from malignant transformation in BRAF (show BRAF Antibodies)-mutated gastrointestinal stromal tumors.
Report the accuracy of ambiguous p16 immunoreactivity in predicting oncogenic HPV and high-grade squamous intraepithelial lesion outcome.
p16 hypermethylation might be a predictive factor of poor prognosis in some surgically treated cancers, particularly in NSCLC.
P16 gene expression has prognostic significance in head and neck squamous cell carcinoma.
P16(ink4a)-overexpression was correlated with prolonged overall survival in vulvar squamous cell carcinoma.
Diffuse p16 expression may occur in follicular dendritic cell sarcoma.
The loss of heterozygosity methylation in the promoter region of the CDKN2A gene, occurred only in the rhabdomyosarcomatous cells with increases in both p16 and p14 (show S100A9 Antibodies) expression.
have shown that p16(INK4A) negatively controls leptin (show LEP Antibodies) at the mRNA level through microRNAs 141 and 146b-5p (miR (show MLXIP Antibodies)-141 and miR (show MLXIP Antibodies)-146b-5p), which bind the leptin (show LEP Antibodies) mRNA at a specific sequence in the 3' untranslated region
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
importance of p19(Arf) for the cellular response to the low-level DNA damage incurred in culture or upon oncogene (show RAB1A Antibodies) expression, providing new insight into how p19(Arf) serves as a tumor suppressor.
p19ARF prevents neoplastic transformation of Trp53 (show TP53 Antibodies)-deficient hepatocytes.
Cdkn2a gene deletion is associated with colorectal carcinomas.
p16 deficiency promotes nonalcoholic steatohepatitis via dysregulation of lipid metabolism and development of hepatic oxidative stress.
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