miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling

Myelodysplastic syndrome (MDS) is characterized by altered hematopoietic stem cell (HSC) and hematopoietic progenitor cell (HPC) regulation and reduction of miR-143 and miR-145 in some subtypes. Here the authors show that miR-143/145 loss leads to HSC depletion, HPC expansion and malignancy through...

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Autores principales:	Jeffrey Lam, Marion van den Bosch, Joanna Wegrzyn, Jeremy Parker, Rawa Ibrahim, Kate Slowski, Linda Chang, Sergio Martinez-Høyer, Gianluigi Condorelli, Mark Boldin, Yu Deng, Patricia Umlandt, Megan Fuller, Aly Karsan
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/790c5842cee2493c94acd0bef130e50e
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spelling	oai:doaj.org-article:790c5842cee2493c94acd0bef130e50e2021-12-02T14:39:45ZmiR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling10.1038/s41467-018-04831-32041-1723https://doaj.org/article/790c5842cee2493c94acd0bef130e50e2018-06-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-04831-3https://doaj.org/toc/2041-1723Myelodysplastic syndrome (MDS) is characterized by altered hematopoietic stem cell (HSC) and hematopoietic progenitor cell (HPC) regulation and reduction of miR-143 and miR-145 in some subtypes. Here the authors show that miR-143/145 loss leads to HSC depletion, HPC expansion and malignancy through Dab2 -mediated TGFβ pathway activation.Jeffrey LamMarion van den BoschJoanna WegrzynJeremy ParkerRawa IbrahimKate SlowskiLinda ChangSergio Martinez-HøyerGianluigi CondorelliMark BoldinYu DengPatricia UmlandtMegan FullerAly KarsanNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-14 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Jeffrey Lam Marion van den Bosch Joanna Wegrzyn Jeremy Parker Rawa Ibrahim Kate Slowski Linda Chang Sergio Martinez-Høyer Gianluigi Condorelli Mark Boldin Yu Deng Patricia Umlandt Megan Fuller Aly Karsan miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling
description	Myelodysplastic syndrome (MDS) is characterized by altered hematopoietic stem cell (HSC) and hematopoietic progenitor cell (HPC) regulation and reduction of miR-143 and miR-145 in some subtypes. Here the authors show that miR-143/145 loss leads to HSC depletion, HPC expansion and malignancy through Dab2 -mediated TGFβ pathway activation.
format	article
author	Jeffrey Lam Marion van den Bosch Joanna Wegrzyn Jeremy Parker Rawa Ibrahim Kate Slowski Linda Chang Sergio Martinez-Høyer Gianluigi Condorelli Mark Boldin Yu Deng Patricia Umlandt Megan Fuller Aly Karsan
author_facet	Jeffrey Lam Marion van den Bosch Joanna Wegrzyn Jeremy Parker Rawa Ibrahim Kate Slowski Linda Chang Sergio Martinez-Høyer Gianluigi Condorelli Mark Boldin Yu Deng Patricia Umlandt Megan Fuller Aly Karsan
author_sort	Jeffrey Lam
title	miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling
title_short	miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling
title_full	miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling
title_fullStr	miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling
title_full_unstemmed	miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling
title_sort	mir-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical tgfβ signaling
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/790c5842cee2493c94acd0bef130e50e
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miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling

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