ArticleBlood2010
Depletion of L3MBTL1 promotes the erythroid differentiation of human hematopoietic progenitor cells: possible role in 20q- polycythemia vera.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Prognostic impact of somatic mutations and additional chromosomal abnormalities in patients with myelodysplastic syndromes and chromosome 20q deletion.Clinical and experimental medicine · 2025Article
- Sticky, Adaptable, and Many-sided: SAM protein versatility in normal and pathological hematopoietic states.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Review
- Myelodysplastic Syndromes with Isolated 20q Deletion: A New Clinical-Biological Entity?Journal of clinical medicine · 2022Article
- Case Report: Refractory Cytopenia With a Switch From a Transient Monosomy 7 to a Disease-Ameliorating del(20q) in aFrontiers in immunology · 2022Article
- Reticulocytosis As a Whistleblower: A Rare Case of Acquired Elliptocytosis in a Myelodysplastic Syndrome Patient With Trisomy 8.HemaSphere · 2021Article
- Hippo kinase loss contributes to del(20q) hematologic malignancies through chronic innate immune activation.Blood · 2019Article
- Targeting epigenetic modifications in cancer therapy: erasing the roadmap to cancer.Nature medicine · 2019Review
- Atypical erythroblastosis in a patient with Diamond-Blackfan anemia who developed del(20q) myelodysplasia.International journal of hematology · 2018Article
- Activity-Induced Regulation of Synaptic Strength through the Chromatin Reader L3mbtl1.Cell reports · 2018Article
- Acquired Elliptocytosis as a Manifestation of Myelodysplastic Syndrome Associated with Deletion of Chromosome 20q.Case reports in hematology · 2018Article
- High-altitude adaptation in humans: from genomics to integrative physiology.Journal of molecular medicine (Berlin, Germany) · 2017Review
- Dpy30 is critical for maintaining the identity and function of adult hematopoietic stem cells.The Journal of experimental medicine · 2016Article
- Review
- The polycomb group protein L3MBTL1 represses a SMAD5-mediated hematopoietic transcriptional program in human pluripotent stem cells.Stem cell reports · 2015Article
- Bmi1 promotes erythroid development through regulating ribosome biogenesis.Stem cells (Dayton, Ohio) · 2015Article
- Complete remission of paraneoplastic vanishing bile duct syndrome after the successful treatment of Hodgkin's lymphoma: a case report and review of the literature.BMC research notes · 2014Review
- The AML1/ETO target gene LAT2 interferes with differentiation of normal hematopoietic precursor cells.Leukemia research · 2014Article
- Cooperativity of imprinted genes inactivated by acquired chromosome 20q deletions.The Journal of clinical investigation · 2013Article
- Discovery of a chemical probe for the L3MBTL3 methyllysine reader domain.Nature chemical biology · 2013Article
- Methylome profiling reveals distinct alterations in phenotypic and mutational subgroups of myeloproliferative neoplasms.Cancer research · 2013Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
L3MBTL1, the human homolog of the Drosophila L(3)MBT polycomb group tumor suppressor gene, is located on chromosome 20q12, within the common deleted region identified in patients with 20q deletion-associated polycythemia vera, myelodysplastic syndrome, and acute myeloid leukemia. L3MBTL1 is expressed within hematopoietic CD34(+) cells; thus, it may contribute to the pathogenesis of these disorders. To define its role in hematopoiesis, we knocked down L3MBTL1 expression in primary hematopoietic stem/progenitor (ie, CD34(+)) cells isolated from human cord blood (using short hairpin RNAs) and observed an enhanced commitment to and acceleration of erythroid differentiation. Consistent with this effect, overexpression of L3MBTL1 in primary hematopoietic CD34(+) cells as well as in 20q- cell lines restricted erythroid differentiation. Furthermore, L3MBTL1 levels decrease during hemin-induced erythroid differentiation or erythropoietin exposure, suggesting a specific role for L3MBTL1 down-regulation in enforcing cell fate decisions toward the erythroid lineage. Indeed, L3MBTL1 knockdown enhanced the sensitivity of hematopoietic stem/progenitor cells to erythropoietin (Epo), with increased Epo-induced phosphorylation of STAT5, AKT, and MAPK as well as detectable phosphorylation in the absence of Epo. Our data suggest that haploinsufficiency of L3MBTL1 contributes to some (20q-) myeloproliferative neoplasms, especially polycythemia vera, by promoting erythroid differentiation.
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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.