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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...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
2011
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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. |
format | Text |
id | pubmed-3105337 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
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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