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Among 8 SNPs in 3 loci that showed at least nominal association (P < 5.00E-02) in the primary cohort, a representative SNP for each loci (rs2157719 for CDKN2B-AS1 (show PTGDR ELISA Kits), rs33912345 for SIX6 (show SIX6 ELISA Kits), and rs9913911 for GAS7 (show GAS7 ELISA Kits)) were selected
The role of CDKN2A/B deletions in pediatric acute lymphoblastic leukemia
The summary of evidences suggesting that RD(INK4/ARF) enhancer deletion represents a novel mutation in the INK4-ARF locus independent of well-known p15, p16, p14ARF alterations.
Results show that expression of CDKN2B was reduced significantly in colorectal cancer (CRC (show CALR ELISA Kits)) and its promotor is targeted by miR (show MLXIP ELISA Kits)-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 (show EZH2 ELISA Kits), thus contributing to the regulation of CRC (show CALR ELISA Kits) 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 (show CALR ELISA Kits)
The current study supports a relevant role for p15, p16, and DAPK (show DAPK1 ELISA Kits) hypermethylation in the genesis of the plasma cell neoplasm. DAPK (show DAPK1 ELISA Kits) hypermethylation also might be an important step in the progression from MGUS to MM.
DNA methylation (show HELLS ELISA Kits) 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 ELISA Kits) 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
miR (show MLXIP ELISA Kits)-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 (show ube3a ELISA Kits)(-/-) 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 (show NF2 ELISA Kits) and Cdkn2a/b have synergistic effects with PDGF-B (show PDGFB ELISA Kits) 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 ELISA Kits) signaling and hypoxic neovessel maturation.
Control of CD8 (show CD8A ELISA Kits) T cell proliferation and terminal differentiation by active STAT5 (show STAT5A ELISA Kits) 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 ELISA Kits) and Cdk6 (show CDK6 ELISA Kits) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (show CDK6 ELISA Kits) in sequestering INK4 proteins away from Cdk4 (show CDK4 ELISA Kits).
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene (show RAB1A ELISA Kits) fusion protein Nup98 (show NUP98 ELISA Kits)-HoxD13 (show HOXD13 ELISA Kits) 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