ArticleProceedings of the National Academy of Sciences of the United States of America2014
B-myb is an essential regulator of hematopoietic stem cell and myeloid progenitor cell development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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.
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Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
- Ancestral chromatin state constrains the functional landscape of bivalent domains in mammalian spermatogenesis.bioRxiv : the preprint server for biology · 2026Article
- Nonlinear transcriptional responses to gradual modulation of transcription factor dosage.eLife · 2026Article
- Fetal context conveys heritable protection against MLL-rearranged AML that depends on MLL3.Blood · 2026Article
- Cell cycle regulator MYBL2 is a distinct vulnerability in acute myeloid leukemia.Cell death discovery · 2025Article
- Nonlinear transcriptional responses to gradual modulation of transcription factor dosage.bioRxiv : the preprint server for biology · 2025Article
- Dysregulation of MYBL2 impairs extravillous trophoblast lineage development and function, contributing to recurrent spontaneous abortion.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer.Cancer research communications · 2024Article
- Fatecode enables cell fate regulator prediction using classification-supervised autoencoder perturbation.Cell reports methods · 2024Article
- Article
- Enhanced fetal hematopoiesis in response to symptomatic SARS-CoV-2 infection during pregnancy.Communications medicine · 2023Article
- APEX1 Nuclease and Redox Functions are Both Essential for Adult Mouse Hematopoietic Stem and Progenitor Cells.Stem cell reviews and reports · 2023Article
- TGFβ reprograms TNF stimulation of macrophages towards a non-canonical pathway driving inflammatory osteoclastogenesis.Nature communications · 2022Article
- Hoxb5 reprogrammes murine multipotent blood progenitors into haematopoietic stem cell-like cells.Cell proliferation · 2022Article
- MYB interacts with androgen receptor, sustains its ligand-independent activation and promotes castration resistance in prostate cancer.British journal of cancer · 2022Article
- Hematopoietic Stem Cell Factors: Their Functional Role in Self-Renewal and Clinical Aspects.Frontiers in cell and developmental biology · 2022Review
- Intricate crosstalk between MYB and noncoding RNAs in cancer.Cancer cell international · 2021Review
- Multi-omic profiling of primary mouse neutrophils predicts a pattern of sex and age-related functional regulation.Nature aging · 2021Article
- WNT inhibition creates a BRCA-like state in Wnt-addicted cancer.EMBO molecular medicine · 2021Article
- Deep learning-based enhancement of epigenomics data with AtacWorks.Nature communications · 2021Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The B-myb (MYBL2) gene is a member of the MYB family of transcription factors and is involved in cell cycle regulation, DNA replication, and maintenance of genomic integrity. However, its function during adult development and hematopoiesis is unknown. We show here that conditional inactivation of B-myb in vivo results in depletion of the hematopoietic stem cell (HSC) pool, leading to profound reductions in mature lymphoid, erythroid, and myeloid cells. This defect is autonomous to the bone marrow and is first evident in stem cells, which accumulate in the S and G2/M phases. B-myb inactivation also causes defects in the myeloid progenitor compartment, consisting of depletion of common myeloid progenitors but relative sparing of granulocyte-macrophage progenitors. Microarray studies indicate that B-myb-null LSK(+) cells differentially express genes that direct myeloid lineage development and commitment, suggesting that B-myb is a key player in controlling cell fate. Collectively, these studies demonstrate that B-myb is essential for HSC and progenitor maintenance and survival during hematopoiesis.
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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.