A-to-I RNA editing and hematopoiesis.

Autor: Liang Z; St Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia; Department of Medicine, Eastern Hill Precinct, Melbourne Medical School, University of Melbourne, Fitzroy, Victoria, Australia., Walkley CR; St Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia; Department of Medicine, Eastern Hill Precinct, Melbourne Medical School, University of Melbourne, Fitzroy, Victoria, Australia. Electronic address: Carl.Walkley@hudson.org.au., Heraud-Farlow JE; St Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia; Department of Medicine, Eastern Hill Precinct, Melbourne Medical School, University of Melbourne, Fitzroy, Victoria, Australia. Electronic address: Jacki.Heraud-Farlow@hudson.org.au.
Jazyk: angličtina
Zdroj: Experimental hematology [Exp Hematol] 2024 Nov; Vol. 139, pp. 104621. Date of Electronic Publication: 2024 Aug 24.
DOI: 10.1016/j.exphem.2024.104621
Abstrakt: Adenosine-to-inosine (A-to-I) RNA editing plays essential roles in modulating normal development and homeostasis. This process is catalyzed by adenosine deaminase acting on RNA (ADAR) family proteins. The most well-understood biological processes modulated by A-to-I editing are innate immunity and neurological development, attributed to ADAR1 and ADAR2, respectively. A-to-I editing by ADAR1 is also critical in regulating hematopoiesis. This review will focus on the role of A-to-I RNA editing and ADAR enzymes, particularly ADAR1, during normal hematopoiesis in humans and mice. Furthermore, we will discuss Adar1 mouse models that have been developed to understand the contribution of ADAR1 to hematopoiesis and its role in innate immune pathways.
Competing Interests: Conflict of Interest Disclosure The authors do not have any conflicts of interest to declare in relation to this work.
(Copyright © 2024 International Society for Experimental Hematology. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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