<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yao Q</submitter><funding>National Natural Science Foundation of China</funding><funding>Ministry of Science and Technology of the People&amp;amp;apos;s Republic of China</funding><pagination>102765</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9808002</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>299(1)</volume><pubmed_abstract>Hyperlipidemia characterized by high blood levels of free fatty acids (FFAs) is important for the progression of inflammatory cardiovascular diseases. Integrin β&lt;sub>1&lt;/sub> is a transmembrane receptor that drives various cellular functions, including differentiation, migration, and phagocytosis. However, the underlying mechanisms modifying integrin β&lt;sub>1&lt;/sub> protein and activity in mediating monocyte/macrophage adhesion to endothelium remain poorly understood. In this study, we demonstrated that integrin β&lt;sub>1&lt;/sub> protein underwent S-nitrosylation in response to nitrosative stress in macrophages. To examine the effect of elevated levels of FFA on the modulation of integrin β&lt;sub>1&lt;/sub> expression, we treated the macrophages with a combination of oleic acid and palmitic acid (2:1)</pubmed_abstract><journal>The Journal of biological chemistry</journal><pubmed_title>Free fatty acids stabilize integrin β&lt;sub>1&lt;/sub>via S-nitrosylation to promote monocyte-endothelial adhesion.</pubmed_title><pmcid>PMC9808002</pmcid><funding_grant_id>81770497</funding_grant_id><funding_grant_id>91939108</funding_grant_id><funding_grant_id>81600389</funding_grant_id><funding_grant_id>2018YFA0800600</funding_grant_id><funding_grant_id>82070829</funding_grant_id><funding_grant_id>81830015</funding_grant_id><pubmed_authors>Wang N</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Xiao L</pubmed_authors><pubmed_authors>Xie X</pubmed_authors><pubmed_authors>Zhao W</pubmed_authors><pubmed_authors>Du X</pubmed_authors><pubmed_authors>Lai B</pubmed_authors><pubmed_authors>Yao Q</pubmed_authors><pubmed_authors>Jiang T</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors><pubmed_authors>Cui Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>Free fatty acids stabilize integrin β&lt;sub>1&lt;/sub>via S-nitrosylation to promote monocyte-endothelial adhesion.</name><description>Hyperlipidemia characterized by high blood levels of free fatty acids (FFAs) is important for the progression of inflammatory cardiovascular diseases. Integrin β&lt;sub>1&lt;/sub> is a transmembrane receptor that drives various cellular functions, including differentiation, migration, and phagocytosis. However, the underlying mechanisms modifying integrin β&lt;sub>1&lt;/sub> protein and activity in mediating monocyte/macrophage adhesion to endothelium remain poorly understood. In this study, we demonstrated that integrin β&lt;sub>1&lt;/sub> protein underwent S-nitrosylation in response to nitrosative stress in macrophages. To examine the effect of elevated levels of FFA on the modulation of integrin β&lt;sub>1&lt;/sub> expression, we treated the macrophages with a combination of oleic acid and palmitic acid (2:1)</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-04T21:04:41.119Z</modification><creation>2025-04-04T21:04:41.119Z</creation></dates><accession>S-EPMC9808002</accession><cross_references><pubmed>36470423</pubmed><doi>10.1016/j.jbc.2022.102765</doi></cross_references></HashMap>