ArticleScientific reports2020
Genomic profiling of the transcription factor Zfp148 and its impact on the p53 pathway.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- ZFP148 is a transcriptional repressor of cytolytic effector CD8Nature immunology · 2026Article
- A Large-Scale Method to Measure the Stoichiometries of Protein Poly-ADP-Ribosylation.ACS chemical biology · 2026Article
- BRAF inhibition increases TGFβ2 production and stimulates metastasis in mice with endogenous BRAFProceedings of the National Academy of Sciences of the United States of America · 2025Article
- p63 and ZNF148 cooperate to regulate head and neck squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The transcription activity ofTranslational cancer research · 2023Article
- Upregulation of the ZNF148/PTX3 axis promotes malignant transformation of dendritic cells in glioma stem-like cells microenvironment.CNS neuroscience & therapeutics · 2023Article
- Loss of ZNF148 enhances insulin secretion in human pancreatic β cells.JCI insight · 2023Article
- β Cell-specific deletion of Zfp148 improves nutrient-stimulated β cell Ca2+ responses.JCI insight · 2022Article
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent data suggest that the transcription factor Zfp148 represses activation of the tumor suppressor p53 in mice and that therapeutic targeting of the human orthologue ZNF148 could activate the p53 pathway without causing detrimental side effects. We have previously shown that Zfp148 deficiency promotes p53-dependent proliferation arrest of mouse embryonic fibroblasts (MEFs), but the underlying mechanism is not clear. Here, we showed that Zfp148 deficiency downregulated cell cycle genes in MEFs in a p53-dependent manner. Proliferation arrest of Zfp148-deficient cells required increased expression of ARF, a potent activator of the p53 pathway. Chromatin immunoprecipitation showed that Zfp148 bound to the ARF promoter, suggesting that Zfp148 represses ARF transcription. However, Zfp148 preferentially bound to promoters of other transcription factors, indicating that deletion of Zfp148 may have pleiotropic effects that activate ARF and p53 indirectly. In line with this, we found no evidence of genetic interaction between TP53 and ZNF148 in CRISPR and siRNA screen data from hundreds of human cancer cell lines. We conclude that Zfp148 deficiency, by increasing ARF transcription, downregulates cell cycle genes and cell proliferation in a p53-dependent manner. However, the lack of genetic interaction between ZNF148 and TP53 in human cancer cells suggests that therapeutic targeting of ZNF148 may not increase p53 activity in humans.
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