ArticleCommunications biology2024
Deficiency in PHD2-mediated hydroxylation of HIF2α underlies Pacak-Zhuang syndrome.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Expanding the clinical tumor phenotype of the EPAS1-asssociated tumor syndrome.The Journal of clinical endocrinology and metabolism · 2026Article
- Divergent Roles of HIF-1α and HIF-2α in Embryonic Development and Early Pregnancy.International journal of molecular sciences · 2026Review
- Assessment of HIF2α mutational pathogenicity using microscale thermophoresis.Biology methods & protocols · 2026Review
- Article
- A schema for sporadic and heritable disease pathogenesis integrating spatiotemporal distribution with the character of genetic variants.Communications medicine · 2025Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Pacak-Zhuang syndrome is caused by mutations in the EPAS1 gene, which encodes for one of the three hypoxia-inducible factor alpha (HIFα) paralogs HIF2α and is associated with defined but varied phenotypic presentations including neuroendocrine tumors and polycythemia. However, the mechanisms underlying the complex genotype-phenotype correlations remain incompletely understood. Here, we devised a quantitative method for determining the dissociation constant (K
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Registered trials
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