{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T10:46:16Z","timestamp":1761216376828},"reference-count":22,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[1999,11,30]],"date-time":"1999-11-30T00:00:00Z","timestamp":943920000000},"content-version":"vor","delay-in-days":1240,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["FEBS Letters"],"published-print":{"date-parts":[[1996,7,8]]},"abstract":"<jats:p>The majority of cases of early\u2010onset familial Alzheimer disease are caused by mutations in the recently identified presenilin 1 (PS1) gene, located on chromosome 14. PS1, a 467 amino acid protein, is predicted to be an integral membrane protein containing seven putative transmembrane domains and a large hydrophilic loop between the sixth and seventh membrane\u2010spanning domain. We produced 7 monoclonal antibodies that react with 3 non\u2010overlapping epitopes on the N\u2010terminal hydrophilic tail of PS1. The monoclonal antibodies can detect the full\u2010size PS1 at <jats:italic>M<\/jats:italic>\n<jats:sub>r<\/jats:sub> 47 000 and a more abundant <jats:italic>M<\/jats:italic>\n<jats:sub>r<\/jats:sub> 28 000 product in membrane extracts from human brain and human cell lines. PC12 cells transiently transfected with PS1 constructs containing two different Alzheimer mutations fail to generate the 28 kDa degradation product in contrast to PC12 cells transfected with wild\u2010type PS1. Our results indicate that missense mutations in this form of familial Alzheimer disease may act via a mechanism of impaired proteolytic processing of PS1.<\/jats:p>","DOI":"10.1016\/0014-5793(96)00608-4","type":"journal-article","created":{"date-parts":[[2002,7,25]],"date-time":"2002-07-25T17:55:22Z","timestamp":1027619722000},"page":"297-303","source":"Crossref","is-referenced-by-count":102,"title":["Characterization of human presenilin 1 using N\u2010terminal specific monoclonal antibodies: Evidence that Alzheimer mutations affect proteolytic processing"],"prefix":"10.1002","volume":"389","author":[{"given":"Marc","family":"Mercken","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Takahashi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshiyuki","family":"Honda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuki","family":"Sato","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miyuki","family":"Murayama","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuko","family":"Nakazato","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kaori","family":"Noguchi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kasutomo","family":"Imahori","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akihiko","family":"Takashima","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1999,11,30]]},"reference":[{"key":"e_1_2_1_2_1","unstructured":"1995 Wiley Chichester D.M.A. Mann K. 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