Oppermann, Martin

[["dc.bibliographiccitation.artnumber","e0157502"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Liebick, Marcel"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Oppermann, Martin"],["dc.date.accessioned","2018-11-07T10:12:44Z"],["dc.date.available","2018-11-07T10:12:44Z"],["dc.date.issued","2016"],["dc.description.abstract","Chemokine receptors undergo internalization and desensitization in response to ligand activation. Internalized receptors are either preferentially directed towards recycling pathways (e.g. CCR5) or sorted for proteasomal degradation (e.g. CXCR4). Here we describe a method for the analysis of receptor internalization and recycling based on specific Bir A-mediated biotinylation of an acceptor peptide coupled to the receptor, which allows a more detailed analysis of receptor trafficking compared to classical antibody-based detection methods. Studies on constitutive internalization of the chemokine receptors CXCR4 (12.1% +/- 0.99% receptor internalization/h) and CCR5 (13.7% +/- 0.68%/h) reveals modulation of these processes by inverse (TAK779; 10.9% +/- 0.95%/h) or partial agonists (Met-CCL5; 15.6% +/- 0.5%/h). These results suggest an actively driven internalization process. We also demonstrate the advantages of specific biotinylation compared to classical antibody detection during agonist-induced receptor internalization, which may be used for immunofluorescence analysis as well. Site-specific biotinylation may be applicable to studies on trafficking of transmembrane proteins, in general."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [DFG Op42-10]"],["dc.identifier.doi","10.1371/journal.pone.0157502"],["dc.identifier.isi","000378029800087"],["dc.identifier.pmid","27310579"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13389"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40296"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Analysis of Chemokine Receptor Trafficking by Site-Specific Biotinylation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2593"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Scholl, Hendrik P. N."],["dc.contributor.author","Issa, Peter Charbel"],["dc.contributor.author","Walier, Maja"],["dc.contributor.author","Janzer, Stefanie"],["dc.contributor.author","Pollok-Kopp, Beatrix"],["dc.contributor.author","Boerncke, Florian"],["dc.contributor.author","Fritsche, Lars G."],["dc.contributor.author","Chong, Ngaihang V."],["dc.contributor.author","Fimmers, Rolf"],["dc.contributor.author","Wienker, Thomas F."],["dc.contributor.author","Holz, Frank G."],["dc.contributor.author","Weber, Bernhard H. F."],["dc.contributor.author","Oppermann, Martin"],["dc.date.accessioned","2018-11-07T11:13:05Z"],["dc.date.available","2018-11-07T11:13:05Z"],["dc.date.issued","2008"],["dc.description.abstract","Dysregulation of the alternative pathway (AP) of complement cascade has been implicated in the pathogenesis of age-related macular degeneration (AMD), the leading cause of blindness in the elderly. To further test the hypothesis that defective control of complement activation underlies AMD, parameters of complement activation in blood plasma were determined together with disease-associated genetic markers in AMD patients. Plasma concentrations of activation products C3d, Ba, C3a, C5a, SC5b-9, substrate proteins C3, C4, factor B and regulators factor H and factor D were quantified in patients (n = 112) and controls (n = 67). Subjects were analyzed for single nucleotide polymorphisms in factor H (CFH), factor B-C2 (BF-C2) and complement C3 (C3) genes which were previously found to be associated with AMD. All activation products, especially markers of chronic complement activation Ba and C3d (p<0.001), were significantly elevated in AMD patients compared to controls. Similar alterations were observed in factor D, but not in C3, C4 or factor H. Logistic regression analysis revealed better discriminative accuracy of a model that is based only on complement activation markers Ba, C3d and factor D compared to a model based on genetic markers of the complement system within our study population. In both the controls' and AMD patients' group, the protein markers of complement activation were correlated with CFH haplotypes. This study is the first to show systemic complement activation in AMD patients. This suggests that AMD is a systemic disease with local disease manifestation at the ageing macula. Furthermore, the data provide evidence for an association of systemic activation of the alternative complement pathway with genetic variants of CFH that were previously linked to AMD susceptibility."],["dc.identifier.doi","10.1371/journal.pone.0002593"],["dc.identifier.isi","000263288200052"],["dc.identifier.pmid","18596911"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8260"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53812"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Systemic Complement Activation in Age-Related Macular Degeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]