ArticleStem cell reports2016
GATA Factor-G-Protein-Coupled Receptor Circuit Suppresses Hematopoiesis.
Article in Stem cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Gpr171 regulates embryonic hematopoietic stem cell emergence via ERK1/2 and Notch signaling.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Loss of G-protein coupled receptor 68 in hematopoietic tissues enhances long-term hematopoietic stem cell function upon aging.Stem cell research & therapy · 2025Article
- Engineered hematopoietic and immune cells derived from human pluripotent stem cells.Experimental hematology · 2023Review
- Overexpression of miR-17 predicts adverse prognosis and disease recurrence for acute myeloid leukemia.International journal of clinical oncology · 2022Article
- Whole body deletion of Gpr68 does not change hematopoietic stem cell function.Stem cell research · 2020Article
- Transcription factor mutations as a cause of familial myeloid neoplasms.The Journal of clinical investigation · 2019Review
- An optimised pipeline for parallel image-based quantification of gene expression and genotyping afterBiology open · 2018Article
- Dissecting Regulatory Mechanisms Using Mouse Fetal Liver-Derived Erythroid Cells.Methods in molecular biology (Clifton, N.J.) · 2018Article
- The GATA factor revolution in hematology.Blood · 2017Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Hematopoietic stem cells (HSCs) originate from hemogenic endothelium within the aorta-gonad-mesonephros (AGM) region of the mammalian embryo. The relationship between genetic circuits controlling stem cell genesis and multi-potency is not understood. A Gata2 cis element (+9.5) enhances Gata2 expression in the AGM and induces the endothelial to HSC transition. We demonstrated that GATA-2 rescued hematopoiesis in +9.5(-/-) AGMs. As G-protein-coupled receptors (GPCRs) are the most common targets for FDA-approved drugs, we analyzed the GPCR gene ensemble to identify GATA-2-regulated GPCRs. Of the 20 GATA-2-activated GPCR genes, four were GATA-1-activated, and only Gpr65 expression resembled Gata2. Contrasting with the paradigm in which GATA-2-activated genes promote hematopoietic stem and progenitor cell genesis/function, our mouse and zebrafish studies indicated that GPR65 suppressed hematopoiesis. GPR65 established repressive chromatin at the +9.5 site, restricted occupancy by the activator Scl/TAL1, and repressed Gata2 transcription. Thus, a Gata2 cis element creates a GATA-2-GPCR circuit that limits positive regulators that promote hematopoiesis.
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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.