<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Al-Ahmadi W</submitter><funding>Austrian Science Fund FWF</funding><funding>British Heart Foundation</funding><funding>Saudi Arabia Cultural Bureau in London</funding><pagination>e21892</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9549671</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>35(10)</volume><pubmed_abstract>Atherosclerosis is a chronic inflammatory disorder of the vasculature regulated by cytokines. We have previously shown that extracellular signal-regulated kinase-1/2 (ERK1/2) plays an important role in serine 727 phosphorylation of signal transducer and activator of transcription-1 (STAT1) transactivation domain, which is required for maximal interferon-γ signaling, and the regulation of modified LDL uptake by macrophages in vitro. Unfortunately, the roles of ERK1/2 and STAT1 serine 727 phosphorylation in atherosclerosis are poorly understood and were investigated using ERK1 deficient mice (ERK2 knockout mice die in utero) and STAT1 knock-in mice (serine 727 replaced by alanine; STAT1 S727A). Mouse Atherosclerosis RT² Profiler PCR Array analysis showed that ERK1 deficiency and STAT1 S727A </pubmed_abstract><journal>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</journal><pubmed_title>Pro-atherogenic actions of signal transducer and activator of transcription 1 serine 727 phosphorylation in LDL receptor deficient mice via modulation of plaque inflammation.</pubmed_title><pmcid>PMC9549671</pmcid><funding_grant_id>PG/12/50/29691</funding_grant_id><funding_grant_id>PG/16/25/32097</funding_grant_id><funding_grant_id>FS/17/75/33257</funding_grant_id><funding_grant_id>W 1261</funding_grant_id><pubmed_authors>Webberley TS</pubmed_authors><pubmed_authors>Decker T</pubmed_authors><pubmed_authors>Hughes TR</pubmed_authors><pubmed_authors>Al-Ahmadi W</pubmed_authors><pubmed_authors>Harris F</pubmed_authors><pubmed_authors>Alotibi R</pubmed_authors><pubmed_authors>Alahmadi A</pubmed_authors><pubmed_authors>Williams JO</pubmed_authors><pubmed_authors>Joseph A</pubmed_authors><pubmed_authors>Ramji DP</pubmed_authors><pubmed_authors>Chan YH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pro-atherogenic actions of signal transducer and activator of transcription 1 serine 727 phosphorylation in LDL receptor deficient mice via modulation of plaque inflammation.</name><description>Atherosclerosis is a chronic inflammatory disorder of the vasculature regulated by cytokines. We have previously shown that extracellular signal-regulated kinase-1/2 (ERK1/2) plays an important role in serine 727 phosphorylation of signal transducer and activator of transcription-1 (STAT1) transactivation domain, which is required for maximal interferon-γ signaling, and the regulation of modified LDL uptake by macrophages in vitro. Unfortunately, the roles of ERK1/2 and STAT1 serine 727 phosphorylation in atherosclerosis are poorly understood and were investigated using ERK1 deficient mice (ERK2 knockout mice die in utero) and STAT1 knock-in mice (serine 727 replaced by alanine; STAT1 S727A). Mouse Atherosclerosis RT² Profiler PCR Array analysis showed that ERK1 deficiency and STAT1 S727A </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2026-06-03T10:28:02.724Z</modification><creation>2025-04-04T09:29:39.106Z</creation></dates><accession>S-EPMC9549671</accession><cross_references><pubmed>34569651</pubmed><doi>10.1096/fj.202100571RR</doi></cross_references></HashMap>