Genomic profiling of the transcription factor Zfp148 and its impact on the p53 pathway.
作者： Zhiyuan V. Zou , Nadia Gul , Markus Lindberg , Abdulmalik A. Bokhari , Ella M. Eklund
DOI: 10.1038/S41598-020-70824-2
关键词:
摘要: Recent data suggest that the transcription factor Zfp148 represses activation of tumor suppressor p53 in mice and therapeutic targeting human orthologue ZNF148 could activate pathway without causing detrimental side effects. We have previously shown deficiency promotes p53-dependent proliferation arrest mouse embryonic fibroblasts (MEFs), but underlying mechanism is not clear. Here, we showed downregulated cell cycle genes MEFs a manner. Proliferation Zfp148-deficient cells required increased expression ARF, potent activator pathway. Chromatin immunoprecipitation bound to ARF promoter, suggesting transcription. However, preferentially promoters other factors, indicating deletion may pleiotropic effects indirectly. In line with this, found no evidence genetic interaction between TP53 CRISPR siRNA screen from hundreds cancer lines. conclude deficiency, by increasing transcription, downregulates lack suggests increase activity humans.
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