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anti-Human CDKN2B Anticorps:
anti-Mouse (Murine) CDKN2B Anticorps:
anti-Rat (Rattus) CDKN2B Anticorps:
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Human Polyclonal CDKN2B Primary Antibody pour ICC, IF - ABIN407770
Siddiqi, Terry, Matushansky: Hiwi mediated tumorigenesis is associated with DNA hypermethylation. dans PLoS ONE 2012
Human Polyclonal CDKN2B Primary Antibody pour 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. dans FEBS letters 2013
Human Polyclonal CDKN2B Primary Antibody pour ELISA, WB - ABIN4342269
Geyer: Strategies to re-express epigenetically silenced p15(INK4b) and p21(WAF1) genes in acute myeloid leukemia. dans Epigenetics 2010
Polymorphisms rs1800796 in IL6 (Montrer IL6 Anticorps) 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 (Montrer FASL Anticorps) patients. Thus, p15 promoter hypermethylation is a prospective prognostic indicator and a reliable clinical aid in assessment of patients with APL (Montrer FASL Anticorps).
Patients with higher levels of DNA methylation of CDKN2B may bear increased risk for aortic arch calcification
E2F1 (Montrer E2F1 Anticorps) induces TINCR transcriptional activity and accelerates gastric cancer progression via activation of TINCR/STAU1 (Montrer STAU1 Anticorps)/CDKN2B signaling axis.
ANRIL may reduce p15INK4B expression through inhibiting TGF-beta (Montrer TGFB1 Anticorps)/Smad (Montrer SMAD1 Anticorps) signaling pathway, promoting invasion and metastasis of TC cells, and the silencing of ANRIL inhibits the invasion and metastasis of TPC-1 (Montrer TPCN1 Anticorps) cells
single nucleotide polymorphisms within the CDKN2A/2B region affect pancreatic cancer risk
The results of this study suggest an association between CDKN2A/2B gene rs10811661 polymorphism and gestational diabetes mellitus.
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 (Montrer PTGDR Anticorps), rs33912345 for SIX6 (Montrer SIX6 Anticorps), and rs9913911 for GAS7 (Montrer GAS7 Anticorps)) 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.
miR (Montrer MLXIP Anticorps)-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 (Montrer ube3a Anticorps)(-/-) 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 (Montrer NF2 Anticorps) and Cdkn2a/b have synergistic effects with PDGF-B (Montrer PDGFB Anticorps) overexpression promoting meningioma malignant transformation.
Loss of CDKN2B may not only promote cardiovascular disease through the development of atherosclerosis but may also impair TGFbeta (Montrer TGFB1 Anticorps) signaling and hypoxic neovessel maturation.
Control of CD8 (Montrer CD8A Anticorps) T cell proliferation and terminal differentiation by active STAT5 (Montrer STAT5A Anticorps) 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 (Montrer CDK4 Anticorps) and Cdk6 (Montrer CDK6 Anticorps) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (Montrer CDK6 Anticorps) in sequestering INK4 proteins away from Cdk4 (Montrer CDK4 Anticorps).
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene (Montrer RAB1A Anticorps) fusion protein Nup98 (Montrer NUP98 Anticorps)-HoxD13 (Montrer HOXD13 Anticorps) 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