ArticleAmerican journal of respiratory cell and molecular biology2025
Stub1 Acetylation by CBP/p300 Attenuates Chronic Hypoxic-Driven Pulmonary Hypertension by Suppressing HIF-2α.
Article in American journal of respiratory cell and molecular biology, 2025. 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.
- Elevated lactate production exacerbates PM2.5-induced pulmonary fibrosis by stabilizing TGF-β1.Journal of advanced research · 2026Article
- Emerging significance of E3 ubiquitin ligases and Deubiquitinases in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2026Review
- From nanotechnology to immunomodulation: emerging strategies targeting macrophages in high altitude pulmonary hypertension.Journal of nanobiotechnology · 2026Review
- Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026Review
- Hypoxic microenvironment and pulmonary hypertension.Respiratory research · 2025Review
- Epigenetic reprogramming drives endothelial dysfunction via neuropilin-1 in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2025Article
- Will Stub1 Be the Next Target for Pulmonary Hypertension Therapy Development?American journal of respiratory cell and molecular biology · 2025Article
- Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025Review
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12 authors.
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Abstract
HIF-1/2 (Hypoxia-Inducible Factors 1/2) are fundamental to the development of pulmonary hypertension (PH). Prolonged hypoxia can trigger the shift from HIF-1 to HIF-2 activity, which is critical in PH progression. Ubiquitin ligases regulate HIF activity through protein degradation. However, little is known about if or how these ligases control the HIF-1/2 switch associated with PH progression. We demonstrate that Stub1 (STIP1 homology and U-box containing protein1), an E3 ubiquitin ligase, influences HIF response to hypoxia by suppressing HIF-2 and enhancing HIF-1 mRNA, protein stability, and activity. Stub1 transgenic mice exposed to prolonged hypoxia exhibited significant decreases in pulmonary vessel and right ventricular remodeling, resulting from a failure of chronic hypoxia to trigger the transition from HIF-1α to HIF-2α and activate HIF-2α. Specifically, acute hypoxia induced the acetylation of Stub1 at lysine 287, promoting its translocation into the nucleus and selectively suppressing HIF-2 activity. Despite the decreased total Stub1 expression, the marginal increase in Stub1
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