Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human CDKN2B Antibodies:
anti-Mouse (Murine) CDKN2B Antibodies:
anti-Rat (Rattus) CDKN2B Antibodies:
Go to our pre-filtered search.
Human Polyclonal CDKN2B Primary Antibody for ELISA, WB - ABIN4342269
Geyer: Strategies to re-express epigenetically silenced p15(INK4b) and p21(WAF1) genes in acute myeloid leukemia. in Epigenetics 2010
Human Polyclonal CDKN2B Primary Antibody for ELISA, WB - ABIN560313
Ratovitski: Phospho-?Np63?-dependent microRNAs modulate chemoresistance of squamous cell carcinoma cells to cisplatin: at the crossroads of cell life and death. in FEBS letters 2013
Human Polyclonal CDKN2B Primary Antibody for ICC, IF - ABIN407770
Siddiqi, Terry, Matushansky: Hiwi mediated tumorigenesis is associated with DNA hypermethylation. in PLoS ONE 2012
Results show that expression of CDKN2B was reduced significantly in colorectal cancer (CRC (show CALR Antibodies)) and its promotor is targeted by miR (show MLXIP Antibodies)-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 Antibodies), thus contributing to the regulation of CRC (show CALR Antibodies) cell cycle and proliferation. Our results suggest that BLACAT1, as a cell cycle regulator (show CDKN2A Antibodies), may serve as a potential target for colon cancer prevention and treatment in human CRC (show CALR Antibodies)
The current study supports a relevant role for p15, p16 (show CDKN2A Antibodies), 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.
DNA methylation (show HELLS Antibodies) 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 Antibodies) and chromosomal losses in cyclin dependent kinase inhibitor 2A (CDKN2A (show CDKN2A Antibodies)) and cyclin dependent kinase inhibitor 2B (CDKN2B).
results provide evidence for the influence of genetic variants at CDKN2A (show CDKN2A Antibodies)/B locus with the risk of developing B-AL
Case Report: knee joint malignant tenosynovial giant cell tumor with CDKN2A (show CDKN2A Antibodies)/B genomic alteration.
Total 1208 differentially expressed genes were screened, and 5 coronary artery disease (CAD (show CAD Antibodies))-associated miRNAs (including miR (show MLXIP Antibodies)-92a) were predicted associated with CAD (show CAD Antibodies). 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 Antibodies)-92a was obtained.
In a suspicious INK4b-ARF-INK4a (show CDKN2A Antibodies) gene cluster at chromosome 9p21 in uveal melanoma cells, aberrant INK4a (show CDKN2A Antibodies) and INK4b defects were simultaneously endogenously auto-corrected after targeting the suppression of abnormal ANRIL lncRNA.
miR (show MLXIP Antibodies)-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 (show CDKN2A Antibodies) locus (p15(INK4b), p16(INK4a (show CDKN2A Antibodies)), and p19(ARF (show CDKN2A Antibodies))) was decreased in E6AP (show ube3a Antibodies)(-/-) embryo fibroblasts.
Data show that the Wnt (show WNT2 Antibodies)-effector hepatocyte nuclear factor 1-alpha (Tcf1 (show HNF1A Antibodies)) is recruited to and triggers transcription of the Ink4/Arf (show CDKN2A Antibodies) tumor suppressor locus, such as as p15Ink4b, p16Ink4a (show CDKN2A Antibodies) and p19Arf (show CDKN2A Antibodies).
Loss of Nf2 (show NF2 Antibodies) and Cdkn2a (show CDKN2A Antibodies)/b have synergistic effects with PDGF-B (show PDGFB Antibodies) 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 Antibodies) signaling and hypoxic neovessel maturation.
Control of CD8 (show CD8A Antibodies) T cell proliferation and terminal differentiation by active STAT5 (show STAT5A Antibodies) and CDKN2A/CDKN2B.
Radiation-induced double strand breaks cooperate with loss of Ink4 (show CDKN2A Antibodies) and Arf (show CDKN2A Antibodies) 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 (show CDKN2A Antibodies)/b) has stronger ability to induce cell-cycle arrest than either p15(INK4b) or p16(INK4a (show CDKN2A Antibodies)).
Cdk4 (show CDK4 Antibodies) and Cdk6 (show CDK6 Antibodies) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (show CDK6 Antibodies) in sequestering INK4 (show CDKN2A Antibodies) proteins away from Cdk4 (show CDK4 Antibodies).
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene (show RAB1A Antibodies) fusion protein Nup98 (show NUP98 Antibodies)-HoxD13 (show HOXD13 Antibodies) 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