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Oppermann, Martin
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Oppermann, Martin
Official Name
Oppermann, Martin
Alternative Name
Oppermann, M.
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2007Journal Article [["dc.bibliographiccitation.firstpage","1516"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","1518"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Jozsi, Mihaly"],["dc.contributor.author","Strobel, Stefanie"],["dc.contributor.author","Dahse, Hans-Martin"],["dc.contributor.author","Liu, Wei-Shih"],["dc.contributor.author","Hoyer, Peter F."],["dc.contributor.author","Oppermann, Martin"],["dc.contributor.author","Skerka, Christine"],["dc.contributor.author","Zipfel, Peter F."],["dc.date.accessioned","2018-11-07T10:58:46Z"],["dc.date.available","2018-11-07T10:58:46Z"],["dc.date.issued","2007"],["dc.description.abstract","The atypical form of the kidney disease hemolytic uremic syndrome (aHUS) is associated with defective complement regulation. In addition to mutations in complement regulators, factor H (FH)specific autoantibodies have been reported for aHUS patients. The aim of the present study was to understand the role of these autoantibodies in aHUS. First, the binding sites of FH autoantibodies from 5 unrelated aHUS patients were mapped using recombinant FH fragments and competitor antibodies. For all 5 autoantibodies, the binding site was localized to the FH C-terminus. In a functional assay, isolated patient IgG inhibited FH binding to C3b. In addition, autoantibody positive patients' plasma caused enhanced hemolysis of sheep erythrocytes, which was reversed by adding FH in excess. These results suggest that aHUS associated FH autoantibodies mimic the effect of C-terminal FH mutations, as they inhibit the regulatory function of FH at cell surfaces by blocking its C-terminal recognition region."],["dc.identifier.doi","10.1182/blood-2007-02-071472"],["dc.identifier.isi","000249151800026"],["dc.identifier.pmid","17495132"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50540"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.relation.issn","0006-4971"],["dc.title","Anti-factor H autoantibodies block C-terminal recognition function of factor H in hemolytic uremic syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2010Conference Abstract [["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Molecular Immunology"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Lauer, Nadine"],["dc.contributor.author","Fritsche, Lars G."],["dc.contributor.author","Weber, Bernhard H. F."],["dc.contributor.author","Hartmann, Andrea"],["dc.contributor.author","Keilhauer, Claudia N."],["dc.contributor.author","Haelbich, Steffi"],["dc.contributor.author","Oppermann, Martin"],["dc.contributor.author","Pandey, Manoij"],["dc.contributor.author","Koehl, Joerg"],["dc.contributor.author","Zipfel, Peter F."],["dc.contributor.author","Skerka, Christine"],["dc.date.accessioned","2018-11-07T08:41:00Z"],["dc.date.available","2018-11-07T08:41:00Z"],["dc.date.issued","2010"],["dc.format.extent","2211"],["dc.identifier.doi","10.1016/j.molimm.2010.05.049"],["dc.identifier.isi","000280268400043"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19372"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","New York, NY"],["dc.relation.issn","0161-5890"],["dc.title","Imbalance of complement regulatory proteins CFHR1, CFHR3 and factor H influences risk for age related macular degeneration (AMD)"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2007Conference Abstract [["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Molecular Immunology"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Strobel, Stefanie"],["dc.contributor.author","Dahse, Hans-Martin"],["dc.contributor.author","Liu, Wei-shih"],["dc.contributor.author","Hoyer, Peter F."],["dc.contributor.author","Oppermann, Martin"],["dc.contributor.author","Terenyi, Nora"],["dc.contributor.author","Skerka, Christine"],["dc.contributor.author","Zipfel, Peter F."],["dc.contributor.author","Jozsi, Mihaly"],["dc.date.accessioned","2018-11-07T10:59:12Z"],["dc.date.available","2018-11-07T10:59:12Z"],["dc.date.issued","2007"],["dc.format.extent","3974"],["dc.identifier.doi","10.1016/j.molimm.2007.06.171"],["dc.identifier.isi","000249512100156"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50647"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","11th European Meeting on Complement in Human Disease"],["dc.relation.eventlocation","Cardiff, WALES"],["dc.relation.issn","0161-5890"],["dc.title","Factor H-autoantibodies in atypical hemolytic uremic syndrome"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2010Journal Article [["dc.bibliographiccitation.firstpage","4694"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","4704"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Fritsche, Lars G."],["dc.contributor.author","Lauer, Nadine"],["dc.contributor.author","Hartmann, Andrea"],["dc.contributor.author","Stippa, Selina"],["dc.contributor.author","Keilhauer, Claudia N."],["dc.contributor.author","Oppermann, Martin"],["dc.contributor.author","Pandey, Manoj K."],["dc.contributor.author","Koehl, Joerg"],["dc.contributor.author","Zipfel, Peter F."],["dc.contributor.author","Weber, Bernhard H. F."],["dc.contributor.author","Skerka, Christine"],["dc.date.accessioned","2018-11-07T08:36:15Z"],["dc.date.available","2018-11-07T08:36:15Z"],["dc.date.issued","2010"],["dc.description.abstract","A frequent deletion of complement factor H (CFH)-related genes CFHR3 and CFHR1 (Delta CFHR3/CFHR1) is considered to have a protective effect against age-related macular degeneration (AMD), although the underlying mechanism remains elusive. The deletion seems to be linked to one of the two protective CFH haplotypes which are both tagged by the protective allele of single nucleotide polymorphism rs2274700 (CFH:A473A). In a German cohort of 530 AMD patients, we now show that protection against AMD conferred by Delta CFHR3/CFHR1 is independent of the effects of rs2274700 and rs1061170 (CFH:Y402H). This suggests a functional role of CFHR1 and/or CFHR3 in disease pathogenesis. We therefore characterized the CFHR3 function and identified CFHR3 as a novel human complement regulator that inhibits C3 convertase activity. CFHR3 displays anti-inflammatory effects by blocking C5a generation and C5a-mediated chemoattraction of neutrophils. In addition, CFHR3 and CFHR1 compete with factor H for binding to the central complement component C3. Thus, deficiency of CFHR3 and CFHR1 results in a loss of complement control but enhances local regulation by factor H. Our findings allude to a critical balance between the complement regulators CFHR3, CFHR1 and factor H and further emphasize the central role of complement regulation in AMD pathology."],["dc.identifier.doi","10.1093/hmg/ddq399"],["dc.identifier.isi","000283930200013"],["dc.identifier.pmid","20843825"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18266"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0964-6906"],["dc.title","An imbalance of human complement regulatory proteins CFHR1, CFHR3 and factor H influences risk for age-related macular degeneration (AMD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS