ArticleBlood2010
Loss-of-function Additional sex combs like 1 mutations disrupt hematopoiesis but do not cause severe myelodysplasia or leukemia.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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
80 citing papers in PubMed, 150 citations in OpenAlex.
- ASXL1 mutation-related clonal hematopoiesis and age-related diseases: clinical evidence and molecular insights.International journal of hematology · 2025Review
- Additional Sex Combs-like Family Associated with Epigenetic Regulation.International journal of molecular sciences · 2024Review
- Prognostic significance of ASXL1 mutations in acute myeloid leukemia: A systematic review and meta-analysis.Caspian journal of internal medicine · 2024Review
- Epigenetic regulation by ASXL1 in myeloid malignancies.International journal of hematology · 2023Review
- Molecular Pathogenesis of Myeloproliferative Neoplasms: From Molecular Landscape to Therapeutic Implications.International journal of molecular sciences · 2022Review
- Genetic Background of Polycythemia Vera.Genes · 2022Review
- Article
- Epigenetic disorders: Lessons from the animals-animal models in chromatinopathies.Frontiers in cell and developmental biology · 2022Review
- Exploring the Associations Between Clonal Hematopoiesis of Indeterminate Potential, Myeloid Malignancy, and Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Tumor-derived neomorphic mutations in ASXL1 impairs the BAP1-ASXL1-FOXK1/K2 transcription network.Protein & cell · 2021Article
- Therapeutic effects of quinine in a mouse model of atopic dermatitis.Molecular medicine reports · 2021Article
- The ASXL1-G643W variant accelerates the development of CEBPA mutant acute myeloid leukemia.Haematologica · 2021Article
- Roles and mechanisms of BAP1 deubiquitinase in tumor suppression.Cell death and differentiation · 2021Review
- AFrontiers in pediatrics · 2021Article
- Landscape of Tumor Suppressor Mutations in Acute Myeloid Leukemia.Journal of clinical medicine · 2020Review
- Invariant patterns of clonal succession determine specific clinical features of myelodysplastic syndromes.Nature communications · 2019Article
- Article
- The role of ASXL1 in hematopoiesis and myeloid malignancies.Cellular and molecular life sciences : CMLS · 2019Review
- Disruption ofDisease models & mechanisms · 2019Article
- Jumping translocations of chromosome 1q occurring by a multi-stage process in an acute myeloid leukemia progressed from myelodysplastic syndrome with aMolecular cytogenetics · 2019Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
The Additional sex combs like 1 (Asxl1) gene is 1 of 3 mammalian homologs of the Additional sex combs (Asx) gene of Drosophila. Asx is unusual because it is required to maintain both activation and silencing of Hox genes in flies and mice. Asxl proteins are characterized by an amino terminal homology domain, by interaction domains for nuclear receptors, and by a C-terminal plant homeodomain protein-protein interaction domain. A recent study of patients with myelodysplastic syndrome (MDS) and chronic myelomonocytic leukemia (CMML) revealed a high incidence of truncation mutations that would delete the PHD domain of ASXL1. Here, we show that Asxl1 is expressed in all hematopoietic cell fractions analyzed. Asxl1 knockout mice exhibit defects in frequency of differentiation of lymphoid and myeloid progenitors, but not in multipotent progenitors. We do not detect effects on hematopoietic stem cells, or in peripheral blood. Notably, we do not detect severe myelodysplastic phenotypes or leukemia in this loss-of-function model. We conclude that Asxl1 is needed for normal hematopoiesis. The mild phenotypes observed may be because other Asxl genes have redundant function with Asxl1, or alternatively, MDS or oncogenic phenotypes may result from gain-of-function Asxl mutations caused by genomic amplification, gene fusion, or truncation of Asxl1.
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What OpenQuestion holds
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.