| http://purl.uniprot.org/citations/15006698 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15006698 | http://www.w3.org/2000/01/rdf-schema#comment | "Complement-receptor-3 (CR3/MAC-1), scavenger-receptor-AI/II (SRAI/II) and Fcgamma-receptor (FcgammaR) can mediate phagocytosis of degenerated myelin in macrophages and microglia. However, CR3/MAC-1 and SRAI/II, but not FcgammaR, mediate phagocytosis after axonal injury. We tested for phosphatidylinositol 3-kinase (PI3K), phosphoinositide-specific phospholipase-Cgamma (PLCgamma) and protein kinase-C (PKC) signaling in myelin phagocytosis mediated by CR3/MAC-1 alone and by CR3/MAC-1 combined with SRAI/II. Phagocytosis was inhibited by PI3K inhibitors wortmannin and LY-294002, PLCgamma inhibitor U-73122, classical PKC (cPKC) inhibitor Go-6976, general PKC inhibitors Ro-318220 and calphostin-C, and BAPTA/AM which chelates intracellular Ca(2+) required for cPKC activation. PKC activator PMA augmented phagocytosis and further alleviated inhibitions induced by PI3K and PLCgamma inhibitors. Overall, altering PKC activity modulated phagocytosis 4-to 6-fold between inhibition and augmentation. PLCgamma activation did not require tyrosine phosphorylation. Thus, signaling of myelin phagocytosis mediated by CR3/MAC-1 alone and by CR3/MAC-1 combined with SRAI/II involves PI3K, PLCgamma and cPKC, the cascade PI3K-->PLCgamma-->cPKC, and wide-range modulation by PKC. This pathway may thus be targeted for in vivo modulation, which may explain differences in the efficiency of CR3/MAC-1-mediated myelin phagocytosis in different pathological conditions."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.nbd.2003.11.007"xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/author | "Kodama T."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/author | "Reichert F."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/author | "Baron A."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/author | "Cohen G."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/author | "Rotshenker S."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/author | "Levidor L."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/author | "Makranz C."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/name | "Neurobiol Dis"xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/pages | "279-286"xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/title | "Phosphatidylinositol 3-kinase, phosphoinositide-specific phospholipase-Cgamma and protein kinase-C signal myelin phagocytosis mediated by complement receptor-3 alone and combined with scavenger receptor-AI/II in macrophages."xsd:string |
| http://purl.uniprot.org/citations/15006698 | http://purl.uniprot.org/core/volume | "15"xsd:string |
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