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The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice

Post-translational protein modifications are systems designed to expand restricted genomic information through functional conversion of target molecules. Ubiquitin-like post-translational modifiers regulate numerous cellular events through their covalent linkages to target protein(s) by an enzymatic...

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Autores principales: Tatsumi, Kanako, Yamamoto-Mukai, Harumi, Shimizu, Ritsuko, Waguri, Satoshi, Sou, Yu-Shin, Sakamoto, Ayako, Taya, Choji, Shitara, Hiroshi, Hara, Takahiko, Chung, Chin Ha, Tanaka, Keiji, Yamamoto, Masayuki, Komatsu, Masaaki
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3105337/
https://www.ncbi.nlm.nih.gov/pubmed/21304510
http://dx.doi.org/10.1038/ncomms1182
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author Tatsumi, Kanako
Yamamoto-Mukai, Harumi
Shimizu, Ritsuko
Waguri, Satoshi
Sou, Yu-Shin
Sakamoto, Ayako
Taya, Choji
Shitara, Hiroshi
Hara, Takahiko
Chung, Chin Ha
Tanaka, Keiji
Yamamoto, Masayuki
Komatsu, Masaaki
author_facet Tatsumi, Kanako
Yamamoto-Mukai, Harumi
Shimizu, Ritsuko
Waguri, Satoshi
Sou, Yu-Shin
Sakamoto, Ayako
Taya, Choji
Shitara, Hiroshi
Hara, Takahiko
Chung, Chin Ha
Tanaka, Keiji
Yamamoto, Masayuki
Komatsu, Masaaki
author_sort Tatsumi, Kanako
collection PubMed
description Post-translational protein modifications are systems designed to expand restricted genomic information through functional conversion of target molecules. Ubiquitin-like post-translational modifiers regulate numerous cellular events through their covalent linkages to target protein(s) by an enzymatic cascade analogous to ubiquitylation consisting of E1 (activating), E2 (conjugating) and E3 (ligating) enzymes. In this study, we report the essential role of Uba5, a specific activating enzyme for the ubiquitin-like modifier, Ufm1, in erythroid development. Mice lacking Uba5 exhibited severe anaemia, followed by death in utero. Although Uba5 was dispensable for the production of erythropoietin, its genetic loss led to impaired development of megakaryocyte and erythroid progenitors from common myeloid progenitors. Intriguingly, transgenic expression of Uba5 in the erythroid lineage rescued the Uba5-deficient embryos from anaemia and prolonged their survival, demonstrating the importance of Uba5 in cell-autonomous erythroid differentiation. Our results suggest that one of the ubiquitin-like protein modification systems, the Ufm1 system, is involved in the regulation of haematopoiesis.
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spelling pubmed-31053372011-06-01 The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice Tatsumi, Kanako Yamamoto-Mukai, Harumi Shimizu, Ritsuko Waguri, Satoshi Sou, Yu-Shin Sakamoto, Ayako Taya, Choji Shitara, Hiroshi Hara, Takahiko Chung, Chin Ha Tanaka, Keiji Yamamoto, Masayuki Komatsu, Masaaki Nat Commun Article Post-translational protein modifications are systems designed to expand restricted genomic information through functional conversion of target molecules. Ubiquitin-like post-translational modifiers regulate numerous cellular events through their covalent linkages to target protein(s) by an enzymatic cascade analogous to ubiquitylation consisting of E1 (activating), E2 (conjugating) and E3 (ligating) enzymes. In this study, we report the essential role of Uba5, a specific activating enzyme for the ubiquitin-like modifier, Ufm1, in erythroid development. Mice lacking Uba5 exhibited severe anaemia, followed by death in utero. Although Uba5 was dispensable for the production of erythropoietin, its genetic loss led to impaired development of megakaryocyte and erythroid progenitors from common myeloid progenitors. Intriguingly, transgenic expression of Uba5 in the erythroid lineage rescued the Uba5-deficient embryos from anaemia and prolonged their survival, demonstrating the importance of Uba5 in cell-autonomous erythroid differentiation. Our results suggest that one of the ubiquitin-like protein modification systems, the Ufm1 system, is involved in the regulation of haematopoiesis. Nature Publishing Group 2011-02-08 /pmc/articles/PMC3105337/ /pubmed/21304510 http://dx.doi.org/10.1038/ncomms1182 Text en Copyright © 2011, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. http://creativecommons.org/licenses/by-nc-sa/3.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/
spellingShingle Article
Tatsumi, Kanako
Yamamoto-Mukai, Harumi
Shimizu, Ritsuko
Waguri, Satoshi
Sou, Yu-Shin
Sakamoto, Ayako
Taya, Choji
Shitara, Hiroshi
Hara, Takahiko
Chung, Chin Ha
Tanaka, Keiji
Yamamoto, Masayuki
Komatsu, Masaaki
The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice
title The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice
title_full The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice
title_fullStr The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice
title_full_unstemmed The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice
title_short The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice
title_sort ufm1-activating enzyme uba5 is indispensable for erythroid differentiation in mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3105337/
https://www.ncbi.nlm.nih.gov/pubmed/21304510
http://dx.doi.org/10.1038/ncomms1182
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