ArticleMolecular and cellular biology2004
Cross talk between retinoic acid signaling and transcription factor GATA-2.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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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
16 citing papers in PubMed, 42 citations in OpenAlex.
- PML-driven sumoylation of PML::RARA-bound repressors drives hematopoietic progenitor immortalization.The Journal of experimental medicine · 2026Article
- Rat embryonic stem cell-basedFrontiers in toxicology · 2025Article
- PML::RARA and GATA2 proteins interact via DNA templates to induce aberrant self-renewal in mouse and human hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Role of the pioneer transcription factor GATA2 in health and disease.Journal of molecular medicine (Berlin, Germany) · 2023Review
- A feedback loop between GATA2-AS1 and GATA2 promotes colorectal cancer cell proliferation, invasion, epithelial-mesenchymal transition and stemness via recruiting DDX3X.Journal of translational medicine · 2022Article
- Deletion of theInternational journal of molecular sciences · 2020Article
- CHD8 dosage regulates transcription in pluripotency and early murine neural differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Hematopoietic Differentiation of Human Pluripotent Stem Cells: HOX and GATA Transcription Factors as Master Regulators.Current genomics · 2019Review
- Retinoic Acid-Signaling Regulates the Proliferative and Neurogenic Capacity of Müller Glia-Derived Progenitor Cells in the Avian Retina.Stem cells (Dayton, Ohio) · 2018Article
- GATA2 is required for lymphatic vessel valve development and maintenance.The Journal of clinical investigation · 2015Article
- Synergistic activation of steroidogenic acute regulatory protein expression and steroid biosynthesis by retinoids: involvement of cAMP/PKA signaling.Endocrinology · 2014Article
- Article
- Expression of a retinoic acid signature in circulating CD34 cells from coronary artery disease patients.BMC genomics · 2010Article
- Retinoic acid receptors and GATA transcription factors activate the transcription of the human lecithin:retinol acyltransferase gene.The international journal of biochemistry & cell biology · 2009Article
- Retinoic acid-stimulated sequential phosphorylation, PML recruitment, and SUMOylation of nuclear receptor TR2 to suppress Oct4 expression.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Mast cell transcriptional networks.Blood cells, molecules & diseasesReview
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All-trans-retinoic acid (RA) stimulates differentiation of normal hematopoietic progenitors and acute myeloid leukemia cells. GATA-2 is a transcription factor expressed in early progenitor cells and implicated in the control of the fate of hematopoietic stem cells and progenitor cells. We have investigated the possibility that the GATA and nuclear hormone receptor pathways are functionally linked through direct protein-protein interaction. Here we demonstrate that in human myeloid KG1 cells, RA receptor alpha (RARalpha), the major RAR expressed in hematopoietic cells, associates with GATA-2. This association is mediated by the zinc fingers of GATA-2 and the DNA-binding domain of RARalpha. As a consequence of this interaction, RARalpha is tethered to the DNA sites that are recognized and bound by GATA-2, and the transcriptional activity of GATA-2 becomes RA responsive. The RA responsiveness of GATA-dependent transcription is eliminated by expression of either a dominant negative form of RARalpha or a GATA-2 mutant that fails to interact with RARalpha. Overexpression of RXRalpha inhibits RARalpha binding to the GATA-2-DNA complex, thus resulting in attenuation of the effects of RARalpha on GATA-2 activity. In addition, inhibition by RA of GATA-2-dependent hematopoietic colony formation in an embryonic stem cell model of hematopoietic differentiation provided biological evidence for functional cross talk between RA and GATA-2-dependent pathways.
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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.