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SUMOylation 不会影响肌钙蛋白 I 的稳定性，但会间接改变对 Ca 的力响应的发展。

SUMOylation does not affect cardiac troponin I stability but alters indirectly the development of force in response to Ca.

机构信息

Institute of Cardiovascular and Medical Sciences, College of Veterinary, Medical and Life Sciences, Glasgow University, UK.

Department of Physiology, Amsterdam UMC, Amsterdam Cardiovascular Sciences, Vrije Universiteit Amsterdam, The Netherlands.

出版信息

FEBS J. 2022 Oct;289(20):6267-6285. doi: 10.1111/febs.16537. Epub 2022 Jun 8.

DOI:10.1111/febs.16537
PMID:35633070
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9588612/
Abstract

Post-translational modification of the myofilament protein troponin I by phosphorylation is known to trigger functional changes that support enhanced contraction and relaxation of the heart. We report for the first time that human troponin I can also be modified by SUMOylation at lysine 177. Functionally, TnI SUMOylation is not a factor in the development of passive and maximal force generation in response to calcium, however this modification seems to act indirectly by preventing SUMOylation of other myofilament proteins to alter calcium sensitivity and cooperativity of myofilaments. Utilising a novel, custom SUMO site-specific antibody that recognises only the SUMOylated form of troponin I, we verify that this modification occurs in human heart and that it is upregulated during disease.

摘要

肌钙蛋白 I 的翻译后修饰，如磷酸化，已知可引发功能变化，从而支持心脏的收缩和舒张增强。我们首次报告称，人肌钙蛋白 I 还可以通过赖氨酸 177 的 SUMO 化修饰进行修饰。从功能上讲，TnI SUMO 化不是钙反应中被动和最大力产生发展的因素，但这种修饰似乎通过防止其他肌丝蛋白的 SUMO 化而间接起作用，从而改变肌丝的钙敏感性和协同性。我们利用一种新颖的、定制的 SUMO 特异性抗体，该抗体仅识别肌钙蛋白 I 的 SUMO 化形式，验证了这种修饰发生在人心肌中，并且在疾病期间上调。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0139/9796357/6cb5476ed1c1/FEBS-289-6267-g011.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0139/9796357/168a5e71a10f/FEBS-289-6267-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0139/9796357/5152697f144a/FEBS-289-6267-g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0139/9796357/6aea7016ba7c/FEBS-289-6267-g002.jpg
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