| http://purl.uniprot.org/citations/27279373 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27279373 | http://www.w3.org/2000/01/rdf-schema#comment | "The autoimmune renal disease deficient for complement factor H-related (CFHR) genes and autoantibody-positive form of hemolytic uremic syndrome is characterized by the presence of autoantibodies specific for the central complement regulator, factor H, combined with a homozygous deficiency, mostly in CFHR3 and CFHR1 Because FHR3 and FHR1 bind to C3d and inactivated C3b, which are ligands for complement receptor type 2 (CR2/CD21), the aim of the current study was to examine whether FHR3-C3d or FHR1-C3d complexes modulate B cell activation. Laser-scanning microscopy and automated image-based analysis showed that FHR3, but not FHR1 or factor H, blocked B cell activation by the BCR coreceptor complex (CD19/CD21/CD81). FHR3 bound to C3d, thereby inhibiting the interaction between C3d and CD21 and preventing colocalization of the coreceptor complex with the BCR. FHR3 neutralized the adjuvant effect of C3d on B cells, as shown by inhibited intracellular CD19 and Akt phosphorylation in Raji cells, as well as Ca(2+) release in peripheral B cells. In cases of CFHR3/CFHR1 deficiency, the FHR3 binding sites on C3d are occupied by factor H, which lacks B cell-inhibitory functions. These data provide evidence that FHR3, which is absent in patients with the autoimmune form of hemolytic uremic syndrome, is involved in B cell regulation."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1600053"xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/author | "Skerka C."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/author | "Zipfel P.F."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/author | "Figge M.T."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/author | "Prodinger W.M."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/author | "Eberhardt H.U."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/author | "Buhlmann D."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/author | "Medyukhina A."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/pages | "620-629"xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/title | "FHR3 Blocks C3d-Mediated Coactivation of Human B Cells."xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://purl.uniprot.org/core/volume | "197"xsd:string |
| http://purl.uniprot.org/citations/27279373 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/27279373 |
| http://purl.uniprot.org/citations/27279373 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/27279373 |
| http://purl.uniprot.org/uniprot/#_Q02985-mappedCitation-27279373 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/27279373 |
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| http://purl.uniprot.org/uniprot/#_Q8WW96-mappedCitation-27279373 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/27279373 |
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| http://purl.uniprot.org/uniprot/Q8WW96 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/27279373 |