ArticleEMBO reports2019
Inherent DNA-binding specificities of the HIF-1α and HIF-2α transcription factors in chromatin.
Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
133 citing papers in PubMed, 196 citations in OpenAlex.
- The lariat RNA debranching enzyme DBR1 enhances HIF-1 signaling and chemoresistance at the expense of lariat RNA processing.The Journal of biological chemistry · 2026Article
- Article
- The clinical landscape of HIF2α inhibitors in oncology.Nature reviews. Clinical oncology · 2026Review
- Kidney-specific HIF-1α-dependent ARL10/miR-1271-5p overexpression in clear cell renal cell carcinoma.British journal of cancer · 2026Article
- HIF inhibition: Current strategies and clinical challenges.Redox biology · 2026Review
- The cistrome response to hypoxia in human umbilical vein endothelial cells.bioRxiv : the preprint server for biology · 2026Article
- Reduced Circulating HIF-1α, HIF-2α, HIF-3α, and VHL Levels in Patients With Pulmonary Arterial Hypertension.Pulmonary circulation · 2026Article
- Hypoxia-responsive interaction between P-TEFb, BHLHE40, and Tim8-Tim13 regulates hypoxic gene transcription.Science advances · 2026Article
- Association of Obstructive Sleep Apnea Risk with Hypoxia-Inducible Factor Expression in Chronic Rhinosinusitis by Inflammatory Endotype.Journal of clinical medicine · 2026Article
- Hypoxia inducible factors regulate pneumovirus replication by enhancing innate immune sensing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Prolyl hydroxylase-dependent proteolysis enables the orthogonal hypoxia responses in plants.Nature communications · 2026Article
- HIF sustain a transcriptional regulatory circuit of EPAS1 expression in renal clear cell carcinoma.Nature communications · 2026Article
- Hypoxia Signaling and Non-Coding RNAs: Regulatory Networks and Therapeutic Implications in Breast Cancer.Current issues in molecular biology · 2026Review
- Multimodal bHLH-PAS DNA binding controls specificity and drives obesity.Nucleic acids research · 2026Article
- Article
- Hypoxia-inducible factors link inflammation and lipid metabolism in atherosclerotic macrophages.Frontiers in cardiovascular medicine · 2026Review
- HIF-2-Dependent Regulation of PTHrP and Paraneoplastic Hypercalcemia in Aggressive Clear-Cell Renal Cell Carcinoma.Cancer discovery · 2025Article
- Ferroptosis-associated transcriptional factors in neurological diseases: molecular mechanisms and therapeutic prospects.Experimental & molecular medicine · 2025Review
- Hypoxia-inducible factors drive miRNA-mediated downregulation ofbioRxiv : the preprint server for biology · 2025Article
- Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Hypoxia-inducible factor (HIF) is the major transcriptional regulator of cellular responses to hypoxia. The two principal HIF-α isoforms, HIF-1α and HIF-2α, are progressively stabilized in response to hypoxia and form heterodimers with HIF-1β to activate a broad range of transcriptional responses. Here, we report on the pan-genomic distribution of isoform-specific HIF binding in response to hypoxia of varying severity and duration, and in response to genetic ablation of each HIF-α isoform. Our findings reveal that, despite an identical consensus recognition sequence in DNA, each HIF heterodimer loads progressively at a distinct repertoire of cell-type-specific sites across the genome, with little evidence of redistribution under any of the conditions examined. Marked biases towards promoter-proximal binding of HIF-1 and promoter-distant binding of HIF-2 were observed under all conditions and were consistent in multiple cell type. The findings imply that each HIF isoform has an inherent property that determines its binding distribution across the genome, which might be exploited to therapeutically target the specific transcriptional output of each isoform independently.
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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.