ArticleHaematologica2021
MYB bi-allelic targeting abrogates primitive clonogenic progenitors while the emergence of primitive blood cells is not affected.
Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Variants ofLife science alliance · 2026Article
- Human pluripotent stem cell-derived innate and adaptive immune cells for cancer immunotherapy.Cell stem cell · 2026Review
- Generation of thymus-reconstituting T cell progenitors from human pluripotent stem cells.Cell reports methods · 2026Article
- Human anti-PSCA CAR macrophages possess potent antitumor activity against pancreatic cancer.Cell stem cell · 2024Article
- The genesis of human hematopoietic stem cells.Blood · 2023Article
- New insights into the characteristics of DRAK2 and its role in apoptosis: From molecular mechanisms to clinically applied potential.Frontiers in pharmacology · 2022Review
- Germline competent mesoderm: the substrate for vertebrate germline and somatic stem cells?Biology open · 2021Article
- Recapitulative haematopoietic development of human pluripotent stem cells in the absence of exogenous haematopoietic cytokines.Journal of cellular and molecular medicine · 2021Article
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9 authors.
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Abstract
MYB is a key regulator of definitive hematopoiesis and it is dispensable for the development of primitive hematopoietic cells in vertebrates. To delineate definitive versus primitive hematopoiesis during differentiation of human embryonic stem cells, we have introduced reporters into the MYB locus and inactivated the gene by bi-allelic targeting. To recapitulate the early developmental events more adequately, the mutant and wild type human embryonic stem cell lines were differentiated in defined culture conditions without the addition of hematopoietic cytokines. The differentiation of the reporter cell lines demonstrated that MYB is specifically expressed throughout emerging hematopoietic cell populations. Here we show that the disruption of the MYB gene leads to severe defects in the development and proliferation of primitive hematopoietic progenitors while the emergence of primitive blood cells is not affected. We also provide evidence that MYB is essential for neutrophil and T cell development and the upregulation of innate immunity genes during hematopoietic differentiation. Our results suggest that the endothelial origin of primitive blood cells is direct and does not include the intermediate step of primitive hematopoietic progenitors.
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