ArticlePloS one2013
Zfp148 deficiency causes lung maturation defects and lethality in newborn mice that are rescued by deletion of p53 or antioxidant treatment.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- β Cell-specific deletion of Zfp148 improves nutrient-stimulated β cell Ca2+ responses.JCI insight · 2022Article
- Cellular Redox Homeostasis.Antioxidants (Basel, Switzerland) · 2021Article
- Antioxidants Promote Intestinal Tumor Progression in Mice.Antioxidants (Basel, Switzerland) · 2021Article
- Genomic profiling of the transcription factor Zfp148 and its impact on the p53 pathway.Scientific reports · 2020Article
- Zfp281 (ZBP-99) plays a functionally redundant role with Zfp148 (ZBP-89) during erythroid development.Blood advances · 2019Article
- Chronic prostatitis alters the prostatic microenvironment and accelerates preneoplastic lesions in C57BL/6 mice.Biological research · 2019Article
- Progression of pathology in PINK1-deficient mouse brain from splicing via ubiquitination, ER stress, and mitophagy changes to neuroinflammation.Journal of neuroinflammation · 2017Article
- MicroRNA-20b suppresses the expression of ZFP-148 in viral myocarditis.Molecular and cellular biochemistry · 2017Article
- Article
- Oncogene-induced senescence underlies the mutual exclusive nature of oncogenic KRAS and BRAF.Oncogene · 2016Article
- ZNF281/ZBP-99: a new player in epithelial-mesenchymal transition, stemness, and cancer.Journal of molecular medicine (Berlin, Germany) · 2014Review
- Zinc finger protein 148 is dispensable for primitive and definitive hematopoiesis in mice.PloS one · 2013Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor Zfp148 (Zbp-89, BFCOL, BERF1, htβ) interacts physically with the tumor suppressor p53 and is implicated in cell cycle control, but the physiological role of Zfp148 remains unknown. Here we show that Zfp148 deficiency leads to respiratory distress and lethality in newborn mice. Zfp148 deficiency prevented structural maturation of the prenatal lung without affecting type II cell differentiation or surfactant production. BrdU analyses revealed that Zfp148 deficiency caused proliferation arrest of pulmonary cells at E18.5-19.5. Similarly, Zfp148-deficient fibroblasts exhibited proliferative arrest that was dependent on p53, raising the possibility that cell stress is part of the underlying mechanism. Indeed, Zfp148 deficiency lowered the threshold for activation of p53 under oxidative conditions. Moreover, both in vivo and cellular phenotypes were rescued on Trp53(+/-) or Trp53(-/-) backgrounds and by antioxidant treatment. Thus, Zfp148 prevents respiratory distress and lethality in newborn mice by attenuating oxidative stress-dependent p53-activity during the saccular stage of lung development. Our results establish Zfp148 as a novel player in mammalian lung maturation and demonstrate that Zfp148 is critical for cell cycle progression in vivo.
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