ArticleCell death & disease2025
Setd2 ensures the establishment of a precise basal inflammatory state within murine hematopoietic stem/progenitor cells.
Hong Tao, Xinyue Luo, Jiachun Song, Fuhui Wang, Yinyin Xie, Rong Fan, Xiaojian Sun, Qiuhua Huang, Yuanliang Zhang
Abstract read
In one paragraphArticle in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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1 · What the graph read from itWhat it found
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
9 authors.
Hong Tao *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID http://orcid.org/0000-0002-1474-7186 Xinyue Luo *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jiachun Song *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fuhui Wang *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yinyin XieShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Rong FanShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaojian SunShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID http://orcid.org/0000-0001-8826-4614 Qiuhua HuangShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. hqh10632@rjh.com.cn.ORCID http://orcid.org/0000-0002-5701-0117 Yuanliang ZhangShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. zyl11740@rjh.com.cn.ORCID http://orcid.org/0009-0004-3729-7976 Funding
National Natural Science Foundation of China (National Science Foundation of China) 82070150National Natural Science Foundation of China (National Science Foundation of China) 82370102
6 · The paper itselfAbstract
The maintenance of a basal immunoinflammatory signature in hematopoietic stem/progenitor cells (HSPCs) constitutes a fundamental regulatory axis governing hematopoietic competence and immune effector generation. While epigenetic repressors constrain this inflammatory phenotype, the molecular amplifiers that preserve this critical state remain undefined. Through integrated single-cell transcriptomic/epigenomic profiling and functional interrogation, we identify Setd2-mediated H3K36me3 as an indispensable epigenetic amplifier sustaining baseline inflammation in murine HSPCs. Setd2 ablation specifically eliminated interferon (IFN)-enriched HSPC subpopulations and attenuated inflammatory signaling cascades. Functionally, Setd2-deficient HSPCs exhibited impaired IFNγ responsiveness, compromised B-lymphopoiesis, and diminished reconstitution capacity due to Lin
Indexed as
Hematopoietic Stem CellsHistone-Lysine N-MethyltransferaseInflammationAnimalsChromatinEpigenesis, GeneticHistonesInterferon-gammaMiceMice, Inbred C57BLMyelodysplastic SyndromesChromatinHistone-Lysine N-MethyltransferaseHistonesInterferon-gammaSETD2 protein, mouse
Identifiers
PMID41198622
PMCPMC12592349
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LicenceCC BY
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