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 - 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 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, ICC - ABIN6263936
Chen, Zhang, Mao, Zhou, Yu, Yin, Wu, Mou, Zhu: ANRIL inhibits p15(INK4b) through the TGFβ1 signaling pathway in human esophageal squamous cell carcinoma. in Cellular immunology 2014
Polymorphisms of the CDKN2B-AS1 gene are associated with the incidence of premature triple-vessel coronary disease in the Chinese population.
This study reveals an association of methylation status in the CDKN2B promoter with normal-tension glaucoma (NTG), particularly in females. This suggests that the observed genetic association with the disease at this locus could be in part due to epigenetic mechanisms, and is likely to be independent of the association of nonsynonymous coding variation within the gene.
Results show that epithelioid glioblastoma (E-GBM) frequently exhibit BRAF V600E, TERT promoter mutations and CDKN2A/B homozygous deletions, these alterations tend to coexist in E-GBM, and that diffuse glioma-like components as well as pleomorphic xanthoastrocytoma-like components are commonly observed in E-GBM.
HOTAIR inhibited p15 expression through zeste homolog 2 (EZH2)-enrolled tri-methylation of Lys 27 of histone H3 (H3K27me3) in p15 promoter. In addition, p15 partially reversed the decrease of colony and proliferation induced by HOTAIR knockdown, suggesting that p15 plays an important role in the leukemogenesis by HOTAIR.
Suggest that CDKN2A/B deletion and/or simultaneous mutations of MAP2K1 and NRAS may underlie the aggressive behavior of Langerhans cell tumors.
Study found reduced expression of CDKN2B with significant hypermethylation of its promoter region and its inactivation through epigenetic regulation may be important factor in tumorigenesis in substantial proportion of parathyroid adenomas.
Data indicate a cell regulatory mechanism through which lysine-specific demethylase 2B (KDM2B) promotes triple negative breast cancer (TNBC) cell proliferation by binding to the promoters of cell cycle inhibitors p15INK4B, p16INK4A, and p57KIP2.
Concurrent mutations, in genes such as CDKN2B or RB1, were associated with worse clinical outcome in lung adenocarcinoma patients with EGFR active mutations.
CDKN2B expression in HPDE6-C7 human pancreatic ductal cells is induced by oncogenic KRAS via TGF-beta signaling.
findings suggest that the GG genotype of the CDKN2B-AS1 gene variant rs4977574, which has been previously associated with an increased CAD risk, is also associated with a decreased susceptibility to the development of hypertension
Non-significant association was seen in the two single nucleotide polymorphisms (SNPs) of CDKAL1 (rs7754840) and CDKN2A/2B (rs10811661) with gestational diabetes mellitus (GDM).
CDKN2B gene locus is a cardiovascular risk in ethnic Saudi Arabs
It plays a role for small intestine-specific gene regulation and alterations of the CDKN2A/CDKN2B locus could affect the pathophysiology of inflammatory bowel disease.
ANRIL plays an important role in the formation of atherosclerosis, and the artificial modification of ANRIL transcripts should be considered following the development of this disease. (Review)
CDKN2A/B locus SNPs may impact T2D risk by modulating islet gene expression and beta-cell proliferation.
Studied CDKN2A/B gene variants and association with increased risk of breast cancer; results show a correlation between the genetic polymorphism, rs10811661, in CDKN2A/B gene and breast cancer.
Polymorphisms rs1800796 in IL6 gene and rs2383207 in CDKN2A/CDKN2B gene have significant associations with ischemic stroke in indigenous West African men. CDKN2A/CDKN2B SNP rs2383207 is independently associated with ischemic stroke in indigenous West African men.
Complete methylation and loss of p15 gene expression causes susceptibility to relapse and decreased survival in APL patients. Thus, p15 promoter hypermethylation is a prospective prognostic indicator and a reliable clinical aid in assessment of patients with APL.
Patients with higher levels of DNA methylation of CDKN2B may bear increased risk for aortic arch calcification
E2F1 induces TINCR transcriptional activity and accelerates gastric cancer progression via activation of TINCR/STAU1/CDKN2B signaling axis.
Pancreatic cancer was induced in adult mice by the combination of KRASG12D overexpression and loss of Tp53 and Cdkn2a only if Cdkn2b was concomitantly inactivated. inactivation of both Cdkn2b and Cdkn2a was necessary for Rb phosphorylation and to encompass oncogene-induced cellular senescence.
miR-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(-/-) 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 and Cdkn2a/b have synergistic effects with PDGF-B overexpression promoting meningioma malignant transformation.
Loss of CDKN2B may not only promote cardiovascular disease through the development of atherosclerosis but may also impair TGFbeta signaling and hypoxic neovessel maturation.
Control of CD8 T cell proliferation and terminal differentiation by active STAT5 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 and Cdk6 cooperate in hematopoietic tumor development and suggest a role for Cdk6 in sequestering INK4 proteins away from Cdk4.
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene fusion protein Nup98-HoxD13 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 and Cdkn2ab inactivation.
data demonstrate in vivo that Mule suppresses Ras-mediated tumorigenesis by preventing an accumulation of c-Myc/Miz1 complexes that mediates p21 and p15 down-regulation
Reduced CDKN2B expression and increased p53-dependent smooth muscle cell apoptosis may be one mechanism underlying the 9p21.3 association with aneurysmal disease.
mRNA expression of p15 gene in mouse bone marrow cells decreases after exposure to 1,4-benzoquinone, but the CpG islands methylation status in promoter is not affected.
p15Ink4b is an important modulator of cDC development and has a novel function for this tumor suppressor in the regulation of adaptive immune responses.
Increased gene dosage of the Ink4/Arf locus does not attenuate atherosclerosis development in hypercholesterolaemic mice.
findings indicate that in lymphoid tissue the inactivation of both p15 alleles is unlikely to be the first event in tumor development
new animal model demonstrates experimentally that p15Ink4b is a tumor suppressor for myeloid leukemia, and its loss may play an active role in the establishment of preleukemic conditions
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