High impact information on Zfp148

• Recent studies have shown that Zfp148 activates p53, which has an important role in cell-cycle regulation [1].
• Zfp148 is expressed in fetal germ cells in 13.5-d-old (E13.5) mouse embryos [1].
• Zfp148 belongs to a large family of C2H2-type zinc-finger transcription factors [1].
• Phosphorylation of p53 is impaired in Zfp148(+/-) embryonic stem cells and in fetal germ cells from chimeric Zfp148(+/-) embryos [1].
• Germ-line transmission of mutations were not observed in chimeric Zfp148(+/-) mice, and some of these mice completely lacked spermatogonia [1].

Biological context of Zfp148

• Heterozygosity with respect to Zfp148 causes complete loss of fetal germ cells during mouse embryogenesis [1].
• Furthermore, we show that the complex transcription pattern of the Zfp148 gene might be due to a combination of alternative splicing and differential polyadenylation sites utilization [2].
• The cloned Zfp148 gene spans 110 kb of genomic DNA encompassing the 5'-end region, 9 exons, 8 introns, and the 3'-untranslated region [2].
• Three cDNA clones were isolated that encoded portions of the mouse SPR2 transcription factor, whereas a fourth cDNA contained a potential open reading frame for a polypeptide of 775 amino acids and was designated BFCOL1 [3].
• Here, we report the identification and characterization of a Kruppel-like zinc finger protein, termed beta enolase repressor factor 1, that binds in a sequence-specific manner to the G-rich box and functions as a repressor of the beta enolase gene transcription in transient transfection assays [4].

Anatomical context of Zfp148

• In undifferentiated muscle cells, GTG motif-bound ZBP-89 physically and functionally interacted with CATR motif-bound YY-1 to mediate transcription repression [5].
• In the present study, we demonstrate that elevated levels of ZBP-89 induce growth arrest and apoptosis in human gastrointestinal cell lines [6].
• Our data establish a novel experimental model for thymocyte-specific gene expression and suggest an important role for ZBP-89 in T cell development [7].
• These findings establish a unique regulatory role for ZBP-89, positioned at the interface between early blood and blood vessel development [8].
• Injection of mRNA for Stem Cell Leukemia (SCL), a transcription factor that directs hemangioblast development into blood cell precursors, rescues the bloodless phenotype in ZBP-89 zebrafish morphants [8].

Associations of Zfp148 with chemical compounds

• ATM(Ser1981) phosphorylation in the colons of mutant mice expressing an N-terminally truncated form of ZBP-89 was not observed after ingestion of dextran sodium sulfate and correlated with exacerbation of the mucosal injury [9].

Analytical, diagnostic and therapeutic context of Zfp148

• Co-immunoprecipitation revealed that ATM associates with ZBP-89 in an HDACi-dependent manner [9].
• Chromatin immunoprecipitation and DNA affinity precipitation assays showed that both ZBP-89 and ATM are recruited to the GC-rich DNA elements of the p21(waf1) promoter with HDACi treatment [9].

References