Blood stem cells SELect quiescence.
Accepted version
Peer-reviewed
Repository URI
Repository DOI
Change log
Authors
Laurenti, Elisa https://orcid.org/0000-0002-9917-9092
Abstract
In this issue of Blood, Liu and colleagues demonstrate that active endoplasmic reticulum associated degradation (ERAD) of misfolded proteins is required to maintain hematopoietic stem cell (HSC) quiescence, and hence proper long-term blood formation 1. They identify a mechanism by which the Sel1L protein, a key member of the ERAD complex, maintains HSCs in a state of low mTORC1 activity, thereby preventing HSC proliferation. This data implicate that steady-state protein quality control directly contributes to keeping HSCs outside of the cell cycle.
Description
Keywords
Cell Division, Endoplasmic Reticulum-Associated Degradation, Hematopoietic Stem Cells, TOR Serine-Threonine Kinases
Journal Title
Blood
Conference Name
Journal ISSN
0006-4971
1528-0020
1528-0020
Volume Title
136
Publisher
American Society of Hematology
Publisher DOI
Rights
All rights reserved
Sponsorship
Medical Research Council (MC_PC_12009)
Medical Research Council (MR/M008975/1)
Medical Research Council (MC_PC_17230)
Medical Research Council (MR/M008975/1)
Medical Research Council (MC_PC_17230)
None