ArticleBlood2016
Functional and molecular characterization of mouse Gata2-independent hematopoietic progenitors.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 38 citations in OpenAlex.
- GATA2 deficiency exacerbates chronic liver injuryWorld journal of stem cells · 2026Article
- ViableFrontiers in immunology · 2026Article
- The E3 ubiquitin ligase Cul5 regulates hematopoietic stem cell function for steady-state hematopoiesis in mice.The Journal of clinical investigation · 2025Article
- Hematological phenotypes in GATA2 deficiency syndrome arise from aging, maladaptation to proliferation, and somatic events.Blood advances · 2025Article
- Autophagy regulates the maturation of hematopoietic precursors in the embryo.Nature communications · 2024Article
- Linking GATA2 to myeloid dysplasia and complex cytogenetics in adult myelodysplastic neoplasm and acute myeloid leukemia.Blood advances · 2024Article
- The role of GATA2 in adult hematopoiesis and cell fate determination.Frontiers in cell and developmental biology · 2023Review
- GATA2 deficiency and MDS/AML: Experimental strategies for disease modelling and future therapeutic prospects.British journal of haematology · 2022Review
- TheiScience · 2022Article
- Redundant mechanisms driven independently by RUNX1 and GATA2 for hematopoietic development.Blood advances · 2021Article
- Regulation of Hemogenic Endothelial Cell Development and Function.Annual review of physiology · 2021Review
- Unexpected redundancy of Gpr56 and Gpr97 during hematopoietic cell development and differentiation.Blood advances · 2021Article
- E-cadherin is regulated by GATA-2 and marks the early commitment of mouse hematopoietic progenitors to the basophil and mast cell fates.Science immunology · 2021Article
- A Novel GATA2 Protein Reporter Mouse Reveals Hematopoietic Progenitor Cell Types.Stem cell reports · 2020Article
- Iterative Single-Cell Analyses Define the Transcriptome of the First Functional Hematopoietic Stem Cells.Cell reports · 2020Article
- Dynamic regulation of GATA2 in fate determination in hematopoiesis: possible approach to hPSC-derived hematopoietic stem/progenitor cells.Blood science (Baltimore, Md.) · 2020Review
- Mutations in the zebrafishBlood advances · 2019Article
- Rapid Mast Cell Generation from Gata2 Reporter Pluripotent Stem Cells.Stem cell reports · 2018Article
- GATA2 Is Dispensable for Specification of Hemogenic Endothelium but Promotes Endothelial-to-Hematopoietic Transition.Stem cell reports · 2018Article
- Cells with hematopoietic potential reside within mouse proepicardium.Histochemistry and cell biology · 2018Article
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 2 institutions in 3 countries.
Funding
Abstract
The Gata2 transcription factor is a pivotal regulator of hematopoietic cell development and maintenance, highlighted by the fact that Gata2 haploinsufficiency has been identified as the cause of some familial cases of acute myelogenous leukemia/myelodysplastic syndrome and in MonoMac syndrome. Genetic deletion in mice has shown that Gata2 is pivotal to the embryonic generation of hematopoietic stem cells (HSCs) and hematopoietic progenitor cells (HPCs). It functions in the embryo during endothelial cell to hematopoietic cell transition to affect hematopoietic cluster, HPC, and HSC formation. Gata2 conditional deletion and overexpression studies show the importance of Gata2 levels in hematopoiesis, during all developmental stages. Although previous studies of cell populations phenotypically enriched in HPCs and HSCs show expression of Gata2, there has been no direct study of Gata2 expressing cells during normal hematopoiesis. In this study, we generate a Gata2Venus reporter mouse model with unperturbed Gata2 expression to examine the hematopoietic function and transcriptome of Gata2 expressing and nonexpressing cells. We show that all the HSCs are Gata2 expressing. However, not all HPCs in the aorta, vitelline and umbilical arteries, and fetal liver require or express Gata2. These Gata2-independent HPCs exhibit a different functional output and genetic program, including Ras and cyclic AMP response element-binding protein pathways and other Gata factors, compared with Gata2-dependent HPCs. Our results, indicating that Gata2 is of major importance in programming toward HSC fate but not in all cells with HPC fate, have implications for current reprogramming strategies.
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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.