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Results show that expression of CDKN2B was reduced significantly in colorectal cancer (CRC (显示 CALR ELISA试剂盒)) and its promotor is targeted by miR (显示 MLXIP ELISA试剂盒)-18b which controls its regulation.
Mechanistic investigations demonstrated that BLACAT1 had a key role in G1/G0 arrest, and showed that BLACAT1 can repress p15 expression by binding to EZH2 (显示 EZH2 ELISA试剂盒), thus contributing to the regulation of CRC (显示 CALR ELISA试剂盒) cell cycle and proliferation. Our results suggest that BLACAT1, as a cell cycle regulator, may serve as a potential target for colon cancer prevention and treatment in human CRC (显示 CALR ELISA试剂盒)
The current study supports a relevant role for p15, p16, and DAPK (显示 DAPK1 ELISA试剂盒) hypermethylation in the genesis of the plasma cell neoplasm. DAPK (显示 DAPK1 ELISA试剂盒) hypermethylation also might be an important step in the progression from MGUS to MM.
DNA methylation (显示 HELLS ELISA试剂盒) 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 (显示 TP53 ELISA试剂盒) 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 (显示 CAD ELISA试剂盒))-associated miRNAs (including miR (显示 MLXIP ELISA试剂盒)-92a) were predicted associated with CAD (显示 CAD ELISA试剂盒). The SVM classifier was constructed based on the 41 featured genes and had high recognition efficiency. Only one lncRNA CDKN2B-antisense targeting miR (显示 MLXIP ELISA试剂盒)-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.
miR (显示 MLXIP ELISA试剂盒)-541 contributes to microcystin-LR-induced testicular toxicity by regulating the expression of p15 and promoting apoptosis.
The expression of three tumor suppressor genes encoded in the INK4/ARF locus (p15(INK4b), p16(INK4a), and p19(ARF)) was decreased in E6AP (显示 ube3a ELISA试剂盒)(-/-) embryo fibroblasts.
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 (显示 NF2 ELISA试剂盒) and Cdkn2a/b have synergistic effects with PDGF-B (显示 PDGFB ELISA试剂盒) overexpression promoting meningioma malignant transformation.
Loss of CDKN2B may not only promote cardiovascular disease through the development of atherosclerosis but may also impair TGFbeta (显示 TGFB1 ELISA试剂盒) signaling and hypoxic neovessel maturation.
Control of CD8 (显示 CD8A ELISA试剂盒) T cell proliferation and terminal differentiation by active STAT5 (显示 STAT5A ELISA试剂盒) 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 (显示 CDK4 ELISA试剂盒) and Cdk6 (显示 CDK6 ELISA试剂盒) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (显示 CDK6 ELISA试剂盒) in sequestering INK4 proteins away from Cdk4 (显示 CDK4 ELISA试剂盒).
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene (显示 RAB1A ELISA试剂盒) fusion protein Nup98 (显示 NUP98 ELISA试剂盒)-HoxD13 (显示 HOXD13 ELISA试剂盒) transgene in the development of predominantly myeloid neoplasms.
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