ArticleBlood2017
The chromatin-associated Sin3B protein is required for hematopoietic stem cell functions in mice.
Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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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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
13 citing papers in PubMed, 18 citations in OpenAlex.
- Integrative analysis of transcriptome and single-cell sequencing combined with experimental validation identifies biomarkers associated with T cell and senescence in sepsis.Scientific reports · 2026Article
- Chromatin accessibility and cell cycle progression are controlled by the HDAC-associated Sin3B protein in murine hematopoietic stem cells.Epigenetics & chromatin · 2024Article
- An integrated workflow for quantitative analysis of the newly synthesized proteome.Nature communications · 2023Article
- Chromatin-Associated SIN3B Protects Cancer Cells from Genotoxic Stress-Induced Apoptosis and Dictates DNA Damage Repair Pathway Choice.Molecular cancer research : MCR · 2023Article
- Functions and regulatory mechanisms of resting hematopoietic stem cells: a promising targeted therapeutic strategy.Stem cell research & therapy · 2023Review
- Molecular and epigenetic alterations in normal and malignant myelopoiesis in human leukemia 60 (HL60) promyelocytic cell line model.Frontiers in cell and developmental biology · 2023Article
- Impaired Neurodevelopmental Genes in Slovenian Autistic Children Elucidate the Comorbidity of Autism With Other Developmental Disorders.Frontiers in molecular neuroscience · 2022Article
- Effect of bFGF on fibroblasts derived from the golden snub-nosed monkey.Primates; journal of primatology · 2021Article
- Stem cell quiescence and its clinical relevance.World journal of stem cells · 2020Review
- The HDAC-Associated Sin3B Protein Represses DREAM Complex Targets and Cooperates with APC/C to Promote Quiescence.Cell reports · 2018Article
- Same agent, different messages: insight into transcriptional regulation by SIN3 isoforms.Epigenetics & chromatin · 2018Review
- Zebrafish sin3b mutants are viable but have size, skeletal, and locomotor defects.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- The potential of targeting Sin3B and its associated complexes for cancer therapy.Expert opinion on therapeutic targets · 2017Review
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2 authors at 1 institution in 1 country.
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Abstract
Hematopoietic stem cells (HSCs) reside at the top of the hematopoietic hierarchy and are the origin of all blood cells produced throughout an individual's life. The balance between HSC self-renewal and differentiation is maintained by various intrinsic and extrinsic mechanisms. Among these, the molecular pathways that restrict cell cycle progression are critical to the maintenance of functional HSCs. Alterations in the regulation of cell cycle progression in HSCs invariably lead to the development of hematologic malignancies or bone marrow failure syndromes. Here we report that hematopoietic-specific genetic inactivation of Sin3B, an essential component of the mammalian Sin3-histone deacetylase corepressor complex, severely impairs the competitive repopulation capacity of HSCs. Sin3B-deleted HSCs accumulate and fail to properly differentiate following transplantation. Moreover, Sin3B inactivation impairs HSC quiescence and sensitizes mice to myelosuppressive therapy. Together, these results identify Sin3B as a novel and critical regulator of HSC functions.
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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.