NDLI: Lack of the ubiquitin-editing enzyme A20 results in loss of hematopoietic stem cell quiescence

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Lack of the ubiquitin-editing enzyme A20 results in loss of hematopoietic stem cell quiescence

Content Provider	Scilit
Author	Nakagawa, Masahiro Thummar, Keyur Mandelbaum, Jonathan Pasqualucci, Laura Rathinam, Chozha Vendan
Copyright Year	2015
Description	A balance between quiescence and proliferation is critical for proper maintenance of the hematopoietic stem cell (HSC) pool. Although a lot is known about hematopoiesis, molecular mechanisms that control HSC quiescence remain largely unknown. The ubiquitin-editing enzyme A20 functions as a central regulator of inflammation and adaptive immunity. Here, we show that a deficiency of A20 in the hematopoietic system causes anemia, lymphopenia, and postnatal lethality. Lack of A20 in HSCs results in diminished pool size, impaired radioprotection, defective repopulation, and loss of quiescence. A20-deficient HSCs display increased IFN-γ signaling, caused by augmented NF-κB activation. Strikingly, deletion of both IFN-γ and A20 in hematopoietic cells results in partial rescue of the HSC phenotype. We anticipate that our experiments will facilitate the understanding of mechanisms through which A20-mediated inflammatory signals control HSC quiescence and functions.
Related Links	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322050/pdf
Ending Page	216
Page Count	14
Starting Page	203
DOI	10.1084/jem.20132544
Journal	The Journal of experimental medicine
Issue Number	2
Volume Number	212
Language	English
Publisher	Rockefeller University Press
Publisher Date	2015-02-09
Access Restriction	Open
Subject Keyword	Research and Experimental Medicine Radioprotection Hematopoietic Stem Ifn Editing Functions Adaptive Quiescence A20 Journal: The Journal of experimental medicine (Vol- 212, Issue- 2)
Content Type	Text

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