ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
FIH-1 engages novel binding partners to positively influence epithelial proliferation via p63.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Factor-inhibiting HIF (FIH) promotes lung cancer progression.JCI insight · 2023Article
- FAM193A is a positive regulator of p53 activity.Cell reports · 2023Article
- Eph signaling is regulated by miRNA-210: Implications for corneal epithelial repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Ciliogenesis and autophagy are coordinately regulated by EphA2 in the cornea to maintain proper epithelial architecture.The ocular surface · 2021Article
- Corneal epithelial biology: Lessons stemming from old to new.Experimental eye research · 2020Review
- Autophagy plays a positive role in induction of epidermal proliferation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The ACE2-deficient mouse: A model for a cytokine storm-driven inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Whereas much is known about the genes regulated by ΔNp63α in keratinocytes, how ΔNp63α is regulated is less clear. During studies with the hydroxylase, factor inhibiting hypoxia-inducible factor 1 (FIH-1), we observed increases in epidermal ΔNp63α expression along with proliferative capacity in a conditional FIH-1 transgenic mouse. Conversely, loss of FIH-1 in vivo and in vitro attenuated ΔNp63α expression. To elucidate the FIH-1/p63 relationship, BioID proteomics assays identified FIH-1 binding partners that had the potential to regulate p63 expression. FIH-1 interacts with two previously unknown partners, Plectin1 and signal transducer and activator of transcription 1 (STAT1) leading to the regulation of ΔNp63α expression. Two known interactors of FIH-1, apoptosis-stimulating of P53 protein 2 (ASPP2) and histone deacetylase 1 (HDAC1), were also identified. Knockdown of ASPP2 upregulated ΔNp63α and reversed the decrease in ΔNp63α by FIH-1 depletion. Additionally, FIH-1 regulates growth arrest and DNA damage-45 alpha (GADD45α), a negative regulator of ΔNp63α by interacting with HDAC1. GADD45α knockdown rescued reduction in ΔNp63α by FIH-1 depletion. Collectively, our data reveal that FIH-1 positively regulates ΔNp63α in keratinocytes via variety of signaling partners: (a) Plectin1/STAT1, (b) ASPP2, and (c) HDAC1/GADD45α signaling pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.