ArticleThe Journal of biological chemistry2016
Oxygen-dependent Regulation of Erythropoietin Receptor Turnover and Signaling.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Beyond hypoxia and ccRCC: the expanding universe of VHL novel targets and next-generation therapeutics.Biomarker research · 2026Review
- P4HA2 hydroxylates SUFU to regulate the paracrine Hedgehog signaling and promote B-cell lymphoma progression.Leukemia · 2024Article
- Expression of erythropoietin receptor protein in the mouse hippocampus in response to normobaric hypoxia.Heliyon · 2024Article
- Oxygen-regulated post-translation modifications as master signalling pathway in cells.EMBO reports · 2023Review
- PHD3 inhibits colon cancer cell metastasis through the occludin-p38 pathway.Acta biochimica et biophysica Sinica · 2023Article
- HypDB: A functionally annotated web-based database of the proline hydroxylation proteome.PLoS biology · 2022Article
- PHD3 inhibits cell proliferation through hydroxylation of PAX2 at proline 9.Acta biochimica et biophysica Sinica · 2022Article
- Von Hippel-Lindau tumor suppressor pathways & corresponding therapeutics in kidney cancer.Journal of genetics and genomics = Yi chuan xue bao · 2021Review
- Hypoxia and Oxygen-Sensing Signaling in Gene Regulation and Cancer Progression.International journal of molecular sciences · 2020Review
- Understanding the Oxygen-Sensing Pathway and Its Therapeutic Implications in Diseases.The American journal of pathology · 2020Review
- The long form of pVHL is artifactually modified by serine protease inhibitor AEBSF.Protein science : a publication of the Protein Society · 2020Article
- The pVHL neglected functions, a tale of hypoxia-dependent and -independent regulations in cancer.Open biology · 2020Review
- Assessing predictors for new post translational modification sites: A case study on hydroxylation.PLoS computational biology · 2020Article
- Erythropoietin regulation of red blood cell production: from bench to bedside and back.F1000Research · 2020Review
- Effect of high altitude on human placental amino acid transport.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Prolyl hydroxylase substrate adenylosuccinate lyase is an oncogenic driver in triple negative breast cancer.Nature communications · 2019Article
- Lack of activity of recombinant HIF prolyl hydroxylases (PHDs) on reported non-HIF substrates.eLife · 2019Article
- Evolution of metazoan oxygen-sensing involved a conserved divergence of VHL affinity for HIF1α and HIF2α.Nature communications · 2019Article
- Genotype-phenotype relations of the von Hippel-Lindau tumor suppressor inferred from a large-scale analysis of disease mutations and interactors.PLoS computational biology · 2019Article
- Translational and HIF-1α-Dependent Metabolic Reprogramming Underpin Metabolic Plasticity and Responses to Kinase Inhibitors and Biguanides.Cell metabolism · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
von Hippel-Lindau (VHL) disease is a rare familial cancer predisposition syndrome caused by a loss or mutation in a single gene,VHL, but it exhibits a wide phenotypic variability that can be categorized into distinct subtypes. The phenotypic variability has been largely argued to be attributable to the extent of deregulation of the α subunit of hypoxia-inducible factor α, a well established target of VHL E3 ubiquitin ligase, ECV (Elongins/Cul2/VHL). Here, we show that erythropoietin receptor (EPOR) is hydroxylated on proline 419 and 426 via prolyl hydroxylase 3. EPOR hydroxylation is required for binding to the β domain of VHL and polyubiquitylation via ECV, leading to increased EPOR turnover. In addition, several type-specific VHL disease-causing mutants, including those that have retained proper binding and regulation of hypoxia-inducible factor α, showed a severe defect in binding prolyl hydroxylated EPOR peptides. These results identify EPOR as the secondbona fidehydroxylation-dependent substrate of VHL that potentially influences oxygen homeostasis and contributes to the complex genotype-phenotype correlation in VHL disease.
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Registered trials
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.