<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhou J</submitter><funding>American Heart Association</funding><funding>Natural Science Foundation of China</funding><funding>NHLBI NIH HHS</funding><funding>Priority Academic Program Development of Jiangsu Higher Education Institutions</funding><funding>Temple University School of Medicine</funding><funding>NIH</funding><pagination>1890-7</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4229395</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(11)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>ERp57 is required for platelet function; however, whether ERp57 contributes to fibrin generation is unknown.&lt;h4>Methods and results&lt;/h4>Using an inhibitory anti-ERp57 antibody (mAb1), Pf4-Cre/ERp57(fl/fl) mice, Tie2-Cre/ERp57(fl/fl) mice, and mutants of ERp57, we analyzed the function of ERp57 in laser-induced thrombosis. Fibrin deposition was decreased in Pf4-Cre/ERp57(fl/fl) mice, consistent with a role for platelet ERp57 in fibrin generation. Fibrin deposition was further decreased with infusion of mAb1 and in Tie2-Cre/ERp57(fl/fl) mice, consistent with endothelial cells also contributing to fibrin deposition. Infusion of eptibifatide inhibited platelet and fibrin deposition, confirming a role for platelets in fibrin deposition. Infusion of recombinant ERp57 corrected</pubmed_abstract><journal>Journal of thrombosis and haemostasis : JTH</journal><pubmed_title>The disulfide isomerase ERp57 is required for fibrin deposition in vivo.</pubmed_title><pmcid>PMC4229395</pmcid><funding_grant_id>P01 HL110860</funding_grant_id><funding_grant_id>P01 HL064190</funding_grant_id><funding_grant_id>31201058</funding_grant_id><funding_grant_id>U01 HL099656</funding_grant_id><funding_grant_id>1R01HL118526</funding_grant_id><funding_grant_id>U01 HL099993</funding_grant_id><funding_grant_id>81270592</funding_grant_id><funding_grant_id>R01 HL118526</funding_grant_id><pubmed_authors>Hayes VM</pubmed_authors><pubmed_authors>Rauova L</pubmed_authors><pubmed_authors>Poncz M</pubmed_authors><pubmed_authors>Essex DW</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors><pubmed_authors>Zhou J</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>The disulfide isomerase ERp57 is required for fibrin deposition in vivo.</name><description>&lt;h4>Background&lt;/h4>ERp57 is required for platelet function; however, whether ERp57 contributes to fibrin generation is unknown.&lt;h4>Methods and results&lt;/h4>Using an inhibitory anti-ERp57 antibody (mAb1), Pf4-Cre/ERp57(fl/fl) mice, Tie2-Cre/ERp57(fl/fl) mice, and mutants of ERp57, we analyzed the function of ERp57 in laser-induced thrombosis. Fibrin deposition was decreased in Pf4-Cre/ERp57(fl/fl) mice, consistent with a role for platelet ERp57 in fibrin generation. Fibrin deposition was further decreased with infusion of mAb1 and in Tie2-Cre/ERp57(fl/fl) mice, consistent with endothelial cells also contributing to fibrin deposition. Infusion of eptibifatide inhibited platelet and fibrin deposition, confirming a role for platelets in fibrin deposition. Infusion of recombinant ERp57 corrected</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Nov</publication><modification>2025-07-02T03:04:29.758Z</modification><creation>2025-07-02T03:04:29.758Z</creation></dates><accession>S-EPMC4229395</accession><cross_references><pubmed>25156521</pubmed><doi>10.1111/jth.12709</doi></cross_references></HashMap>