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Involved in transcriptional regulation. De plus, nous expédions Zinc Finger Protein 148 Protéines (4) et beaucoup plus de produits pour cette protéine.
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Human Polyclonal ZNF148 Primary Antibody pour WB - ABIN1882015
Udelhoven, Pasieka, Leeser, Krone, Schubert: Neuronal insulin receptor substrate 2 (IRS2) expression is regulated by ZBP89 and SP1 binding to the IRS2 promoter. dans The Journal of endocrinology 2010
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Human Polyclonal ZNF148 Primary Antibody pour ICC, IF - ABIN4367002
Sayin, Nilton, Ibrahim, Ågren, Larsson, Petit, Hultén, Ståhlman, Johansson, Bergo, Lindahl: Zfp148 deficiency causes lung maturation defects and lethality in newborn mice that are rescued by deletion of p53 or antioxidant treatment. dans PLoS ONE 2013
Cow (Bovine) Polyclonal ZNF148 Primary Antibody pour WB - ABIN2775856
Chupreta, Brevig, Bai, Merchant, Iñiguez-Lluhí: Sumoylation-dependent control of homotypic and heterotypic synergy by the Kruppel-type zinc finger protein ZBP-89. dans The Journal of biological chemistry 2007
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The results indicate that the association with chr5p15.33-Region 2 may be explained by rs36115365, a variant influencing TERT (Montrer TERT Anticorps) expression via ZNF148 in a manner consistent with elevated TERT (Montrer TERT Anticorps) in carriers of the C allele.
ZNF148 as a gene involved in a newly described intellectual disability syndrome with a recurrent phenotype and postulate that the ZNF148 is a hitherto unrecognized but crucial transcription factor in the development of the corpus callosum.
A larger role ZBP-89 plays in gene regulation during inflammation.ZBP-89 regulates of MMP-1 (Montrer MMP1 Anticorps) expression.ZBP-89 and NF-kappaB (Montrer NFKB1 Anticorps) appear to bind cooperatively on both promoters.
ZBP-89 attenuates HDAC3 (Montrer HDAC3 Anticorps) by increasing IkappaB degradation, dependent on Pin1 (Montrer PIN1 Anticorps) but independent of NF-Kappab (Montrer NFKB1 Anticorps)
zinc-binding protein (Montrer PTMS Anticorps)-89 upregulates the expression of Bak (Montrer BAK1 Anticorps) by targeting multiple components of the epigenetic pathway in hepatocellular carcinoma.
lower expression of ZNF148 in colorectal cancer was significantly associated with worse clinicopathologic variables, including lymph node metastases, poor differentiation, and a higher rate of disease recurrence
this study provides vigorous evidence that ZBP-89 was significantly downregulated in clear cell renal cell carcinoma (Montrer MOK Anticorps)(CCRCC) and could be served as a promising biomarker for prediction of distal metastasis and prognosis of patient with CCRCC.
Colony formation was reduced dramatically in those hepatocellular carcinoma cell lines in which ZBP-89 overexpression was demonstrated; this appeared to correlate with increased apoptosis.
We found that the TP53 (Montrer TP53 Anticorps)-G245D variant but not TP53 (Montrer TP53 Anticorps)-R249S abrogated HDAC (Montrer HDAC3 Anticorps) inhibitor p21 (Montrer CDKN1A Anticorps) induction by binding to ZBP-89 and retaining it in the cytoplasm.
ZBP-89 is a regulator of Pdcd4 (Montrer PDCD4 Anticorps) gene, binding to the basal promoter either alone or by interacting with Sp family members.
Data indicate zinc finger protein 148 (ZFP148) as a transcription factor that differentially binds to the zinc finger protein 30 protein (Zfp30) promoter region harboring rs51434084.
The results suggest that Zfp148 controls the fate of newly transformed intestinal tumor cells by repressing p53 (Montrer TP53 Anticorps) and that targeting Zfp148 might be useful in the treatment of colorectal cancer.
Study demonstrated that miR (Montrer MLXIP Anticorps)-20b suppressed ZFP-148 expression by directly binding to the 3'-UTR (Montrer UTS2R Anticorps) of target mRNA and repressed translation at posttranscriptional level during virus myocarditis.
Zfp148 deficiency increases p53 (Montrer TP53 Anticorps) activity and protects against atherosclerosis by causing proliferation arrest of lesional macrophages.
These data identify an important role for ZBP-89 in regulating stress hematopoiesis in adult mouse bone marrow.
Results indicate that Zfp148-deficient mice generate normal mature hematopoietic populations.
Zfp148 deficiency causes lung maturation defects and lethality.
ZBP-89 is required for expression of the Tph1 (Montrer TPH1 Anticorps) gene and subsequent production of 5HT (Montrer DDC Anticorps) in response to bacterial infection in mice. Reductions in epithelial ZBP-89 increase susceptibility to colitis and sepsis after infection with S. typhimurium.
MiR (Montrer MLXIP Anticorps)-203 expression downregulated ZFP-148 mRNA translation by specifically targeting its 3' UTR (Montrer UTS2R Anticorps), which resulted in differential expression of its downstream target genes, which in turn promote cell survival to foster Coxsackievirus B3 replication
ataxia telangiectasia mutated (Montrer ATM Anticorps) protein phosphorylation of ZBP-89 contributes to Histone deacetylase (Montrer HDAC1 Anticorps) inhibitors induction of p21(waf1 (Montrer CDKN1A Anticorps)) gene expression
identify ZBP-89 as being a novel transcription factor involved in erythroid and megakaryocytic development and suggest that it serves a cooperative function with GATA-1 (Montrer GATA1 Anticorps) and/or FOG-1 (Montrer ZFPM1 Anticorps) in a developmental stage-specific manner
Involved in transcriptional regulation. Represses the transcription of a number of genes including gastrin, stromelysin and enolase. Binds to the G-rich box in the enhancer region of these genes.
CACCC box-binding protein
, CLL-associated antigen KW-10
, transcription factor ZBP-89
, zinc finger DNA-binding protein 89
, G-rich box-binding protein
, beta enolase repressor factor 1
, transcription factor BFCOL1
, zinc finger binding protein 89
, zinc finger DNA binding protein 89
, solute carrier family 12 (potassium/chloride transporters), member 8
, zinc finger protein 148 (pHZ-52)