ArticleExperimental hematology2013
A germline point mutation in Runx1 uncouples its role in definitive hematopoiesis from differentiation.
Article in Experimental hematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Upregulation of Runt related transcription factor 1 (RUNX1) contributes to tendon-bone healing after anterior cruciate ligament reconstruction using bone mesenchymal stem cells.Journal of orthopaedic surgery and research · 2022Article
- Hematopoietic Stem Cell Factors: Their Functional Role in Self-Renewal and Clinical Aspects.Frontiers in cell and developmental biology · 2022Review
- Biomechanical Regulation of Hematopoietic Stem Cells in the Developing Embryo.Current tissue microenvironment reports · 2021Article
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- RUNX1 mutations enhance self-renewal and block granulocytic differentiation in human in vitro models and primary AMLs.Blood advances · 2019Article
- An AML1-ETO/miR-29b-1 regulatory circuit modulates phenotypic properties of acute myeloid leukemia cells.Oncotarget · 2017Article
- Intracellular Signaling Pathways Involved in Childhood Acute Lymphoblastic Leukemia; Molecular Targets.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2016Review
- Loss of RUNX1/AML1 arginine-methylation impairs peripheral T cell homeostasis.British journal of haematology · 2015Article
- Runx1 deficiency permits granulocyte lineage commitment but impairs subsequent maturation.Oncogenesis · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Definitive hematopoiesis requires the master hematopoietic transcription factor Runx1, which is a frequent target of leukemia-related chromosomal translocations. Several of the translocation-generated fusion proteins retain the DNA binding activity of Runx1, but lose subnuclear targeting and associated transactivation potential. Complete loss of these functions in vivo resembles Runx1 ablation, which causes embryonic lethality. We developed a knock-in mouse that expresses full-length Runx1 with a mutation in the subnuclear targeting cofactor interaction domain, Runx1(HTY350-352AAA). Mutant mice survive to adulthood, and hematopoietic stem cell emergence appears to be unaltered. However, defects are observed in multiple differentiated hematopoietic lineages at stages where Runx1 is known to play key roles. Thus, a germline mutation in Runx1 reveals uncoupling of its functions during developmental hematopoiesis from subsequent differentiation across multiple hematopoietic lineages in the adult. These findings indicate that subnuclear targeting and cofactor interactions with Runx1 are important in many compartments throughout hematopoietic differentiation.
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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.