{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T11:04:03Z","timestamp":1773140643657,"version":"3.50.1"},"reference-count":31,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2023,3,22]],"date-time":"2023-03-22T00:00:00Z","timestamp":1679443200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["FEBS Letters"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:p>Autoimmune coagulation factor XIII (FXIII) deficiency (AiF13D) is a bleeding disorder caused by anti\u2010FXIII autoantibodies. Recently, we generated human monoclonal antibodies (mAbs) from the peripheral blood of an AiF13D patient and classified them into three groups: FXIII\u2010dissociation inhibitor, FXIII\u2010assembly inhibitor, and non\u2010neutralizing\/inhibitory mAbs. However, the epitope region and molecular inhibitory mechanism of each mAb remain unknown. Here, we localized the epitope regions of the representative inhibitory mAbs A69K (dissociation inhibitor) and A78L (assembly inhibitor) to the \u03b2\u2010barrel\u20102 domain and boundary of \u03b2\u2010barrel\u20101&amp;2 domains, respectively, of the FXIII\u2010A subunit, by combining a binding assay using its synthesized peptides and a protease\u2010protection assay. Our findings suggest that A69K inhibits the activation\u2010related conformational changes and dissociation of FXIII and that A78L competitively inhibits FXIII\u2010assembly.<\/jats:p>","DOI":"10.1002\/1873-3468.14606","type":"journal-article","created":{"date-parts":[[2023,3,6]],"date-time":"2023-03-06T08:38:28Z","timestamp":1678091908000},"page":"1275-1289","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Epitope analysis of human monoclonal antibodies from a patient with autoimmune factor\n                    <scp>XIII<\/scp>\n                    deficiency reveals their inhibitory mechanisms"],"prefix":"10.1002","volume":"597","author":[{"given":"Tsukasa","family":"Osaki","sequence":"first","affiliation":[{"name":"Department of Molecular Patho\u2010Biochemistry and Patho\u2010Biology Yamagata University School of Medicine  Japan"},{"name":"The Japanese Collaborative Research Group (JCRG) on Autoimmune Acquired Coagulation Factor Deficiencies supported by the Japanese Ministry of Health, Labor and Welfare (MHLW)  Yamagata Japan"},{"name":"Department of Public Health and Hygiene Yamagata University Graduate School of Medical Science  Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masayoshi","family":"Souri","sequence":"additional","affiliation":[{"name":"Department of Molecular Patho\u2010Biochemistry and Patho\u2010Biology Yamagata University School of Medicine  Japan"},{"name":"The Japanese Collaborative Research Group (JCRG) on Autoimmune Acquired Coagulation Factor Deficiencies supported by the Japanese Ministry of Health, Labor and Welfare (MHLW)  Yamagata Japan"},{"name":"Department of Public Health and Hygiene Yamagata University Graduate School of Medical Science  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