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Literature summary for 1.6.3.1 extracted from

  • Paul, R.; Obermaier, B.; Van Ziffle, J.; Angele, B.; Pfister, H.W.; Lowell, C.A.; Koedel, U.
    Myeloid Src kinases regulate phagocytosis and oxidative burst in pneumococcal meningitis by activating NADPH oxidase (2008), J. Leukoc. Biol., 84, 1141-1150.
    View publication on PubMedView publication on EuropePMC
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Application

Application Comment Organism
medicine pivotal role of myeloid Src family kinases and complement receptor 3 in mounting an effective defense against infection with Streptococcus pneumonia by regulating phagocytosis and NADPH oxidase-dependent superoxide production. Leukocyte recruitment into the cerebrospinal fluid space and bacterial clearance is hampered in mice deficient in all three myeloid Src family kinases during pneumococcal meningitis. The mice develop increased intracranial pressure and a worse clinical outcome with increased neurologic deficits and mortality, compared with wildtype mice. In neutrophils of mice deficient for myeloid Src family kinases p59/61hck, p58c-fgr, and p53/56lyn, phosphorylation of NAD(P)H oxidase subunit p40phox is absent, indicating a defect in enzyme activation Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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Posttranslational Modification

Posttranslational Modification Comment Organism
phosphoprotein in neutrophils of mice deficient for myeloid Src family kinases p59/61hck, p58c-fgr, and p53/56lyn, phosphorylation of NAD(P)H oxidase subunit p40phox is absent, indicating a defect in enzyme activation Mus musculus