anti-Zinc Finger Protein 148 (ZNF148) Antibodies

Human Zinc Finger Protein 148 (ZNF148) interaction partners

1. Our findings suggested that ZBP-89 and Sp1 overexpression induced Bak expression in a genetic manner. Increased Bak level was associated with poor patient survival, whereas high level of Sp1 is a beneficial factor for patient survival.

2. The results indicate that the association with chr5p15.33-Region 2 may be explained by rs36115365, a variant influencing TERT expression via ZNF148 in a manner consistent with elevated TERT in carriers of the C allele.

3. 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.

4. A larger role ZBP-89 plays in gene regulation during inflammation.ZBP-89 regulates of MMP-1 expression.ZBP-89 and NF-kappaB appear to bind cooperatively on both promoters.

5. ZBP-89 attenuates HDAC3 by increasing IkappaB degradation, dependent on Pin1 but independent of NF-Kappab

6. zinc-binding protein-89 upregulates the expression of Bak by targeting multiple components of the epigenetic pathway in hepatocellular carcinoma.

7. 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

8. this study provides vigorous evidence that ZBP-89 was significantly downregulated in clear cell renal cell carcinoma(CCRCC) and could be served as a promising biomarker for prediction of distal metastasis and prognosis of patient with CCRCC.

9. 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.

10. We found that the TP53-G245D variant but not TP53-R249S abrogated HDAC inhibitor p21 induction by binding to ZBP-89 and retaining it in the cytoplasm.

11. ZBP-89 is a regulator of Pdcd4 gene, binding to the basal promoter either alone or by interacting with Sp family members.

12. An activating role for ZBP-89 in human globin gene regulation and erythroid differentiation.

13. Alternative binding of ZBP89 or SP1 to the described region in the IRS2 promoter regulates neuronal IRS2 expression in a PI3K-dependent manner.

14. ZBP-89 is a repressor of the human beta 2-integrin CD11b gene during differentiation of monocytes into macrophages

15. ZBP-89 co-localized with p53 in the nucleus in about 67% (12 of 18) of all cases positive for the nuclear p53 protein, suggesting that ZBP-89 may play a role in the nuclear accumulation of the p53 protein in a subset recurrent hepatocellular carcinoma.

16. interaction of Stat3 and ZBP-89 may be crucial for overcoming the effects of the repressor ZBP-89, which suggests a novel mode for Stat3 gene activation.

17. ZBP-89-mediated apoptosis occurs via a p53-independent mechanism that requires JNK activation.

18. No association with psoriasis susceptibility

19. We conclude that ZBP-89 is a direct transcriptional activator of the enterocyte differentiation marker IAP.

20. Ectopic expression of ZBP-89 amplified the inhibitory effect of Fatty Acids on L2 -GH promoter activity.

Mouse (Murine) Zinc Finger Protein 148 (ZNF148) interaction partners

1. 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.

2. The results suggest that Zfp148 controls the fate of newly transformed intestinal tumor cells by repressing p53 and that targeting Zfp148 might be useful in the treatment of colorectal cancer.

3. Study demonstrated that miR-20b suppressed ZFP-148 expression by directly binding to the 3'-UTR of target mRNA and repressed translation at posttranscriptional level during virus myocarditis.

4. Zfp148 deficiency increases p53 activity and protects against atherosclerosis by causing proliferation arrest of lesional macrophages.

5. These data identify an important role for ZBP-89 in regulating stress hematopoiesis in adult mouse bone marrow.

6. Results indicate that Zfp148-deficient mice generate normal mature hematopoietic populations.

7. Zfp148 deficiency causes lung maturation defects and lethality.

8. ZBP-89 is required for expression of the Tph1 gene and subsequent production of 5HT in response to bacterial infection in mice. Reductions in epithelial ZBP-89 increase susceptibility to colitis and sepsis after infection with S. typhimurium.

9. MiR-203 expression downregulated ZFP-148 mRNA translation by specifically targeting its 3' UTR, which resulted in differential expression of its downstream target genes, which in turn promote cell survival to foster Coxsackievirus B3 replication

10. ataxia telangiectasia mutated protein phosphorylation of ZBP-89 contributes to Histone deacetylase inhibitors induction of p21(waf1) gene expression

11. 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 and/or FOG-1 in a developmental stage-specific manner

12. The transcriptional repressor ZBP-89 and the lack of Sp1/Sp3, c-jun and Stat3 are important for the down-regulation of the vimentin gene during C2C12 myogenesis.

13. the G(5) string is necessary for Gata1 gene expression in vivo and ZBP-89 is the functional trans-acting factor for this cis-acting region.

Zebrafish Zinc Finger Protein 148 (ZNF148) interaction partners

1. 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 and/or FOG-1 in a developmental stage-specific manner