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抗Human CDKN2B 抗体:
抗Mouse (Murine) CDKN2B 抗体:
抗Rat (Rattus) CDKN2B 抗体:
Human Polyclonal CDKN2B Primary Antibody for ICC, IF - ABIN407770
Siddiqi, Terry, Matushansky: Hiwi mediated tumorigenesis is associated with DNA hypermethylation. in PLoS ONE 2012
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
E2F1 (显示 E2F1 抗体) induces TINCR transcriptional activity and accelerates gastric cancer progression via activation of TINCR/STAU1 (显示 STAU1 抗体)/CDKN2B signaling axis.
ANRIL may reduce p15INK4B expression through inhibiting TGF-beta (显示 TGFB1 抗体)/Smad (显示 SMAD1 抗体) signaling pathway, promoting invasion and metastasis of TC cells, and the silencing of ANRIL inhibits the invasion and metastasis of TPC-1 (显示 TPCN1 抗体) 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 (显示 PTGDR 抗体), rs33912345 for SIX6 (显示 SIX6 抗体), and rs9913911 for GAS7 (显示 GAS7 抗体)) 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 (显示 CALR 抗体)) and its promotor is targeted by miR (显示 MLXIP 抗体)-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 抗体), thus contributing to the regulation of CRC (显示 CALR 抗体) 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 抗体)
The current study supports a relevant role for p15, p16, and DAPK (显示 DAPK1 抗体) hypermethylation in the genesis of the plasma cell neoplasm. DAPK (显示 DAPK1 抗体) hypermethylation also might be an important step in the progression from MGUS to MM.
miR (显示 MLXIP 抗体)-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 抗体)(-/-) 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 抗体) and Cdkn2a/b have synergistic effects with PDGF-B (显示 PDGFB 抗体) 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 抗体) signaling and hypoxic neovessel maturation.
Control of CD8 (显示 CD8A 抗体) T cell proliferation and terminal differentiation by active STAT5 (显示 STAT5A 抗体) 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 抗体) and Cdk6 (显示 CDK6 抗体) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (显示 CDK6 抗体) in sequestering INK4 proteins away from Cdk4 (显示 CDK4 抗体).
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene (显示 RAB1A 抗体) fusion protein Nup98 (显示 NUP98 抗体)-HoxD13 (显示 HOXD13 抗体) 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