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Publication Detail

Title: SHP-1 regulates hematopoietic stem cell quiescence by coordinating TGF-β signaling.

Authors: Jiang, Linjia; Han, Xue; Wang, Jin; Wang, Chen; Sun, Xiaoqiang; Xie, Jiayi; Wu, Guojin; Phan, Hiep; Liu, Zhenguo; Yeh, Edward T H; Zhang, ChengCheng; Zhao, Meng; Kang, Xunlei

Published In J Exp Med, (2018 05 07)

Abstract: Cell cycle quiescence is critical for hematopoietic stem cell (HSC) maintenance. TGF-β signaling in bone marrow niche has been identified in regulating HSC quiescence; however, the intrinsic regulatory mechanisms remain unclear. This study reports that Shp-1 knockout HSCs have attenuated quiescence and impaired long-term self-renewal. SHP-1-activated HSCs are surrounded by megakaryocytes, which regulate HSC quiescence by producing TGF-β1. Mechanistically, SHP-1 interacts with the immunoreceptor tyrosine-based inhibition motif on TGF-β receptor 1 and is critical for TGF-β signaling activation in HSCs. Functionally, Shp-1 knockout HSCs do not respond to TGF-β-enforced HSC quiescence regulation, both in vitro and in vivo. Therefore, we identify TGF-β-SHP-1 as a novel intrinsic regulatory mechanism for HSC quiescence maintenance.

PubMed ID: 29669741 Exiting the NIEHS site

MeSH Terms: Amino Acid Sequence; Animals; Cell Self Renewal; Hematopoietic Stem Cells/cytology*; Hematopoietic Stem Cells/metabolism*; Mice, Inbred C57BL; Protein Binding; Protein Tyrosine Phosphatase, Non-Receptor Type 6/chemistry; Protein Tyrosine Phosphatase, Non-Receptor Type 6/metabolism*; Receptors, Transforming Growth Factor beta/metabolism; Signal Transduction*; Stem Cell Niche; Time Factors; Transforming Growth Factor beta/metabolism*

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