{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T06:59:09Z","timestamp":1772953149891,"version":"3.50.1"},"reference-count":0,"publisher":"Portland Press Ltd.","issue":"3","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1996,3,15]]},"abstract":"<jats:p>We have investigated the mechanisms of defects in the glycosyl-phosphatidylinositol (GPI)-anchored complement regulatory proteins delay-accelerating factor (DAF) and\/or CD59 in a panel of human leukaemia cell lines that lack surface expression of these proteins: U937 (DAF+\/CD59-), CEM (DAF-\/CD59+), TALL (DAF-\/CD59-) and a substrain of Ramos [Ramos(-)] (DAF-\/CD59-). Northern blotting and reverse transcription-PCR revealed that the main cause of the DAF and\/or CD59 deficiency is the failure of mRNA expression in most of the cell lines, except in Ramos(-) in which sufficient mRNA for DAF and CD59 was produced. U937, CEM and TALL cells were not defective in GPI anchor formation as assessed by the detection of other GPI-anchored proteins. No gene abnormality corresponding to DAF or CD59 was detected by Southern blotting. Thus the cause of the defects of DAF and\/or CD59 in these leukaemia cell lines except for Ramos(-) is virtually undetectable steady-state levels of the relevant mRNA, most likely attributable to lack of transcription in these cell lines. On the other hand, Ramos(-) cells failed to generate a GPI anchor, whereas they normally expressed DAF and CD59 transcripts. The transfection of phosphatidylinositol-glycan class A (PIG-A) cDNA into Ramos(-) cells restored DAF and CD59 expression, indicating that the defective mechanism in GPI anchor formation is similar to that in paroxysmal nocturnal haemoglobinuria (PNH) cells, i.e. a deficiency of the PIG-A gene product. Thus the mechanisms of the defects of DAF and\/or CD59 in human leukaemia cell lines are not uniform, and in most cases are different from that proposed to cause PNH.<\/jats:p>","DOI":"10.1042\/bj3140969","type":"journal-article","created":{"date-parts":[[2015,8,10]],"date-time":"2015-08-10T21:47:57Z","timestamp":1439243277000},"page":"969-976","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Mechanisms by which the surface expression of the glycosyl-phosphatidylinositol-anchored complement regulatory proteins decay-accelerating factor (CD55) and CD59 is lost in human leukaemia cell lines"],"prefix":"10.1042","volume":"314","author":[{"given":"Michiyo","family":"HATANAKA","sequence":"first","affiliation":[{"name":"Department of Clinical Pathology, Osaka Medical College, Takatsuki 569, Japan"},{"name":"Department of Immunology, Center for Adult Diseases Osaka, Higashinari-ku, Osaka 537, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"SEYA","family":"SEYA","sequence":"additional","affiliation":[{"name":"Department of Immunology, Center for Adult Diseases Osaka, Higashinari-ku, Osaka 537, Japan"},{"name":"PRESTO, JRDC, Kyoto 619-02, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Misako","family":"MATSUMOTO","sequence":"additional","affiliation":[{"name":"Department of Immunology, Center for Adult Diseases Osaka, Higashinari-ku, Osaka 537, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomoko","family":"HARA","sequence":"additional","affiliation":[{"name":"Department of Immunology, Center for Adult Diseases Osaka, Higashinari-ku, Osaka 537, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaru","family":"NONAKA","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Nagoya City University Medical School, Mizuho-ku, Nagoya 467, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norimitsu","family":"INOUE","sequence":"additional","affiliation":[{"name":"Department of Immunoregulation, Research Institute for Microbial Diseases, Suita, Osaka 565, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Junji","family":"TAKEDA","sequence":"additional","affiliation":[{"name":"Department of Immunoregulation, Research Institute for Microbial Diseases, Suita, Osaka 565, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akira","family":"SHIMIZU","sequence":"additional","affiliation":[{"name":"Department of Clinical Pathology, Osaka Medical College, Takatsuki 569, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","container-title":["Biochemical Journal"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/portlandpress.com\/biochemj\/article-pdf\/314\/3\/969\/618630\/bj3140969.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/portlandpress.com\/biochemj\/article-pdf\/314\/3\/969\/618630\/bj3140969.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,24]],"date-time":"2021-11-24T01:02:06Z","timestamp":1637715726000},"score":1,"resource":{"primary":{"URL":"https:\/\/portlandpress.com\/biochemj\/article\/314\/3\/969\/37358\/Mechanisms-by-which-the-surface-expression-of-the"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,3,15]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,3,15]]}},"URL":"https:\/\/doi.org\/10.1042\/bj3140969","relation":{},"ISSN":["0264-6021","1470-8728"],"issn-type":[{"value":"0264-6021","type":"print"},{"value":"1470-8728","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,3,15]]}}}