SUMO and cellular adaptive mechanisms
Stress response: how cells wrestle with SUMO disruption Cellular stress caused by disrupting attachment of the ubiquitous small ubiquitin-like modifier (SUMO) proteins, which are present in most organisms and regulate numerous DNA processes and stress responses by attaching to key proteins, results...
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2020-06-01
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Online Access: | https://doi.org/10.1038/s12276-020-0457-2 |
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doaj-e284bab50fa64d9ab5b52117e9c0a65e2021-06-27T11:44:52ZengNature Publishing GroupExperimental and Molecular Medicine1226-36132092-64132020-06-0152693193910.1038/s12276-020-0457-2SUMO and cellular adaptive mechanismsHong-Yeoul Ryu0Seong Hoon Ahn1Mark Hochstrasser2School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of National Sciences, Kyungpook National UniversityDepartment of Molecular and Life Science, College of Science and Convergence Technology, Hanyang UniversityDepartment of Molecular Biophysics and Biochemistry, Yale UniversityStress response: how cells wrestle with SUMO disruption Cellular stress caused by disrupting attachment of the ubiquitous small ubiquitin-like modifier (SUMO) proteins, which are present in most organisms and regulate numerous DNA processes and stress responses by attaching to key proteins, results in some remarkable adaptations. Mark Hochstrasser at Yale University, New Haven, USA, and co-workers review how this “sumoylation” is reversed by protease enzymes, and how imbalances between sumoylation and desumoylation may be linked to diseases including cancer. When certain SUMO proteases are deliberately disrupted, the cells quickly become aneuploid, i.e., carry an abnormal number of chromosomes. These cells show severe growth defects, but over many generations they regain the normal number of chromosomes. They also undergo genetic changes that promote alternative mechanisms that compensate for losing the SUMO protease and facilitate the same efficient stress responses as the original cells.https://doi.org/10.1038/s12276-020-0457-2 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Hong-Yeoul Ryu Seong Hoon Ahn Mark Hochstrasser |
spellingShingle |
Hong-Yeoul Ryu Seong Hoon Ahn Mark Hochstrasser SUMO and cellular adaptive mechanisms Experimental and Molecular Medicine |
author_facet |
Hong-Yeoul Ryu Seong Hoon Ahn Mark Hochstrasser |
author_sort |
Hong-Yeoul Ryu |
title |
SUMO and cellular adaptive mechanisms |
title_short |
SUMO and cellular adaptive mechanisms |
title_full |
SUMO and cellular adaptive mechanisms |
title_fullStr |
SUMO and cellular adaptive mechanisms |
title_full_unstemmed |
SUMO and cellular adaptive mechanisms |
title_sort |
sumo and cellular adaptive mechanisms |
publisher |
Nature Publishing Group |
series |
Experimental and Molecular Medicine |
issn |
1226-3613 2092-6413 |
publishDate |
2020-06-01 |
description |
Stress response: how cells wrestle with SUMO disruption Cellular stress caused by disrupting attachment of the ubiquitous small ubiquitin-like modifier (SUMO) proteins, which are present in most organisms and regulate numerous DNA processes and stress responses by attaching to key proteins, results in some remarkable adaptations. Mark Hochstrasser at Yale University, New Haven, USA, and co-workers review how this “sumoylation” is reversed by protease enzymes, and how imbalances between sumoylation and desumoylation may be linked to diseases including cancer. When certain SUMO proteases are deliberately disrupted, the cells quickly become aneuploid, i.e., carry an abnormal number of chromosomes. These cells show severe growth defects, but over many generations they regain the normal number of chromosomes. They also undergo genetic changes that promote alternative mechanisms that compensate for losing the SUMO protease and facilitate the same efficient stress responses as the original cells. |
url |
https://doi.org/10.1038/s12276-020-0457-2 |
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