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DNA methylation (show HELLS Proteins) of CDKN2B may play a potential role in artery calcification.
These data support the hypothesis that decreased p15 expression is a robust biomarker for distinguishing nevus from melanoma.
Here we present, as far as we are aware, the first case of metastatic microcystic adnexal carcinoma with DNA sequencing results indicating a mutation in TP53 (show TP53 Proteins) and chromosomal losses in cyclin dependent kinase inhibitor 2A (CDKN2A) and cyclin dependent kinase inhibitor 2B (CDKN2B).
results provide evidence for the influence of genetic variants at CDKN2A/B locus with the risk of developing B-AL
Case Report: knee joint malignant tenosynovial giant cell tumor with CDKN2A/B genomic alteration.
Total 1208 differentially expressed genes were screened, and 5 coronary artery disease (CAD)-associated miRNAs (including miR (show MLXIP Proteins)-92a) were predicted associated with CAD. The SVM classifier was constructed based on the 41 featured genes and had high recognition efficiency. Only one lncRNA CDKN2B-antisense targeting miR (show MLXIP Proteins)-92a was obtained.
In a suspicious INK4b-ARF-INK4a gene cluster at chromosome 9p21 in uveal melanoma cells, aberrant INK4a and INK4b defects were simultaneously endogenously auto-corrected after targeting the suppression of abnormal ANRIL lncRNA.
Upregulation of ZEB1-AS1 colorectal cancer promotes cell proliferation and inhibits cell apoptosis. In addition, cell cycle inhibitory protein p15 participates in the oncogenic function of ZEB1-AS1. Collectively, ZEB1-AS1 has asignificant effect on colorectal cancer pathological process and serves as a valuable prognostic biomarker for colorectal cancer.
Genetic association analyses using the cpRNFLT with 768 points suggest that the CDKN2B gene was associated with paracentral/lower hemifield scotomas.
We found that CDKN2B was a virtual target of miR (show MLXIP Proteins)-15a-5p with potential binding sites in the 3'UTR of CDKN2B (77-83 bp). We also showed that miR (show MLXIP Proteins)-15a-5p could bind to the CDKN2B 3'UTR. The data revealed a negative regulatory role of miR (show MLXIP Proteins)-15a-5p in the apoptosis of smooth muscle cells via targeting CDKN2B, and showed that miR (show MLXIP Proteins)-15a-5p could be a novel therapeutic target of AAA (show APP Proteins).
Data show that the Wnt-effector hepatocyte nuclear factor 1-alpha (Tcf1) is recruited to and triggers transcription of the Ink4/Arf tumor suppressor locus, such as as p15Ink4b, p16Ink4a and p19Arf.
Loss of Nf2 (show NF2 Proteins) and Cdkn2a/b have synergistic effects with PDGF-B (show PDGFB Proteins) overexpression promoting meningioma malignant transformation.
Loss of CDKN2B may not only promote cardiovascular disease through the development of atherosclerosis but may also impair TGFbeta (show TGFB1 Proteins) signaling and hypoxic neovessel maturation.
Control of CD8 (show CD8A Proteins) T cell proliferation and terminal differentiation by active STAT5 (show STAT5A Proteins) and CDKN2A/CDKN2B.
Radiation-induced double strand breaks cooperate with loss of Ink4 and Arf tumor suppressors to generate high-grade gliomas that are commonly driven by Met amplification and activation.
When overexpressed in naked mole rat or human cells, pALT(INK4a/b) has stronger ability to induce cell-cycle arrest than either p15(INK4b) or p16(INK4a).
Cdk4 (show CDK4 Proteins) and Cdk6 (show CDK6 Proteins) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (show CDK6 Proteins) in sequestering INK4 proteins away from Cdk4 (show CDK4 Proteins).
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene (show RAB1A Proteins) fusion protein Nup98 (show NUP98 Proteins)-HoxD13 (show HOXD13 Proteins) transgene in the development of predominantly myeloid neoplasms.
Loss of CDKN2B promotes atherosclerosis by increasing the size and complexity of the lipid-laden necrotic core through impaired efferocytosis.
Meningioma progression in mice triggered by Nf2 (show NF2 Proteins) and Cdkn2ab inactivation.
This gene lies adjacent to the tumor suppressor gene CDKN2A in a region that is frequently mutated and deleted in a wide variety of tumors. This gene encodes a cyclin-dependent kinase inhibitor, which forms a complex with CDK4 or CDK6, and prevents the activation of the CDK kinases, thus the encoded protein functions as a cell growth regulator that controls cell cycle G1 progression. The expression of this gene was found to be dramatically induced by TGF beta, which suggested its role in the TGF beta induced growth inhibition. Two alternatively spliced transcript variants of this gene, which encode distinct proteins, have been reported.
Cyclin-dependent kinase 4 inhibitor B
, CDK inhibitory protein
, CDK4B inhibitor
, cyclin-dependent kinase 4 inhibitor B
, cyclin-dependent kinases 4 and 6 binding protein
, multiple tumor suppressor 2
, p14_CDK inhibitor
, p15 CDK inhibitor
, cyclin-dependent kinase inhibitor p15
, cyclin-dependent kinase inhibitor p15INK4b
, cyclin-dependent kinase inhibitor protein
, Cyclin dependent kinase inhibitor 2B (p15, inhibits CDK4)
, cyclin dependant kinase inhibitor
, cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)
, cyclin-dependent kinase inhibitor 2B
, cyclin-dependent kinase inhibitor 2B (melanoma, p16, inhibits CDK4)
, p15INK4b tumor suppressor