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ZNF148(FL) could increase proliferation, invasion, and migration of colorectal cancer cells, while ZNF148(DeltaN) showed opposite effect; the two splicing isoforms of ZNF148 may exert a mutual antagonistic effect to each other on the malignant biological activities.
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Downregulation of ZNF148 drives the formation of a muscle phenotype with rapid expression of myosin heavy chain, even in proliferative conditions. This phenotype was most likely mediated by the robust and swift upregulation of MYOD and MEF2C.
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ZBP-89 is a potential tumor suppressor in hepatocellular carcinoma (HCC) and it can inhibit the growth of HCC via multiple channels; higher expression of ZBP-89 may predict better survivals and lower recurrence of HCC patients
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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.
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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.
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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.
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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.
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ZBP-89 attenuates HDAC3 by increasing IkappaB degradation, dependent on Pin1 but independent of NF-Kappab
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zinc-binding protein-89 upregulates the expression of Bak by targeting multiple components of the epigenetic pathway in hepatocellular carcinoma.
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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
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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.
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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.
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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.
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ZBP-89 is a regulator of Pdcd4 gene, binding to the basal promoter either alone or by interacting with Sp family members.
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An activating role for ZBP-89 in human globin gene regulation and erythroid differentiation.
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Alternative binding of ZBP89 or SP1 to the described region in the IRS2 promoter regulates neuronal IRS2 expression in a PI3K-dependent manner.
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ZBP-89 is a repressor of the human beta 2-integrin CD11b gene during differentiation of monocytes into macrophages
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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.
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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.
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ZBP-89-mediated apoptosis occurs via a p53-independent mechanism that requires JNK activation.
