{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hou S"],"funding":["HHS | NIH | National Institute of General Medical Sciences","NHLBI NIH HHS","HHS | NIH | National Heart, Lung, and Blood Institute","NIGMS NIH HHS"],"pagination":["13798-13803"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5748199"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["114(52)"],"pubmed_abstract":["Phosphatidylethanolamine (PE) is a major phospholipid species with important roles in membrane trafficking and reorganization. Accumulating clinical data indicate that the presence of circulating antibodies against PE is positively correlated with the symptoms of antiphospholipid syndromes (APS), including thrombosis and repeated pregnancy loss. However, PE is generally sequestered inside a normal resting cell, and the mechanism by which circulating anti-PE antibodies access cellular PE remains unknown. The studies presented here were conducted with synthetic PE-binding agents, plasma samples from patients with anti-PE autoimmunity, and purified anti-PE antibodies. The results suggest that the cellular vulnerability to anti-PE antibodies may be mediated by the binding of PE molecules in th"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Early endosome as a pathogenic target for antiphosphatidylethanolamine antibodies."],"pmcid":["PMC5748199"],"funding_grant_id":["5R01HL102085","R01 HL102085","R01 GM070736","GM070736"],"pubmed_authors":["Zhao M","Ke K","Ramsey-Goldman R","Cook Mills J","Folsch H","Hou S"],"additional_accession":[]},"is_claimable":false,"name":"Early endosome as a pathogenic target for antiphosphatidylethanolamine antibodies.","description":"Phosphatidylethanolamine (PE) is a major phospholipid species with important roles in membrane trafficking and reorganization. Accumulating clinical data indicate that the presence of circulating antibodies against PE is positively correlated with the symptoms of antiphospholipid syndromes (APS), including thrombosis and repeated pregnancy loss. However, PE is generally sequestered inside a normal resting cell, and the mechanism by which circulating anti-PE antibodies access cellular PE remains unknown. The studies presented here were conducted with synthetic PE-binding agents, plasma samples from patients with anti-PE autoimmunity, and purified anti-PE antibodies. The results suggest that the cellular vulnerability to anti-PE antibodies may be mediated by the binding of PE molecules in th","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Dec","modification":"2025-04-26T18:36:13.553Z","creation":"2019-03-26T23:42:38Z"},"accession":"S-EPMC5748199","cross_references":{"pubmed":["29229837"],"doi":["10.1073/pnas.1714027115"]}}