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Mbd3/NuRD controls ...
Mbd3/NuRD controls lymphoid cell fate and inhibits tumorigenesis by repressing a B cell transcriptional program
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Loughran, SJ (författare)
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Comoglio, F (författare)
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Hamey, FK (författare)
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Giustacchini, A (författare)
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Errami, Y (författare)
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Earp, E (författare)
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Gottgens, B (författare)
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- Jacobsen, SEW (författare)
- Karolinska Institutet
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Mead, AJ (författare)
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Hendrich, B (författare)
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Green, AR (författare)
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(creator_code:org_t)
- 2017-09-12
- 2017
- Engelska.
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Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 214:10, s. 3085-3104
- Relaterad länk:
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https://rupress.org/...
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http://kipublication...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Differentiation of lineage-committed cells from multipotent progenitors requires the establishment of accessible chromatin at lineage-specific transcriptional enhancers and promoters, which is mediated by pioneer transcription factors that recruit activating chromatin remodeling complexes. Here we show that the Mbd3/nucleosome remodeling and deacetylation (NuRD) chromatin remodeling complex opposes this transcriptional pioneering during B cell programming of multipotent lymphoid progenitors by restricting chromatin accessibility at B cell enhancers and promoters. Mbd3/NuRD-deficient lymphoid progenitors therefore prematurely activate a B cell transcriptional program and are biased toward overproduction of pro–B cells at the expense of T cell progenitors. The striking reduction in early thymic T cell progenitors results in compensatory hyperproliferation of immature thymocytes and development of T cell lymphoma. Our results reveal that Mbd3/NuRD can regulate multilineage differentiation by constraining the activation of dormant lineage-specific enhancers and promoters. In this way, Mbd3/NuRD protects the multipotency of lymphoid progenitors, preventing B cell–programming transcription factors from prematurely enacting lineage commitment. Mbd3/NuRD therefore controls the fate of lymphoid progenitors, ensuring appropriate production of lineage-committed progeny and suppressing tumor formation.
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- art (ämneskategori)
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Till lärosätets databas
- Av författaren/redakt...
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Loughran, SJ
-
Comoglio, F
-
Hamey, FK
-
Giustacchini, A
-
Errami, Y
-
Earp, E
-
visa fler...
-
Gottgens, B
-
Jacobsen, SEW
-
Mead, AJ
-
Hendrich, B
-
Green, AR
-
visa färre...
- Artiklar i publikationen
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The Journal of e ...
- Av lärosätet
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Karolinska Institutet