Implications of molecular contacts and signaling initiated by Neisseria gonorrhoeae.
Neisseria gonorrhoeae employs diverse strategies with which to adhere to and invade host cells during the course of infection. These primary encounters provide means by which biologically active molecules can be efficiently targeted to disrupt or exploit normal host cell metabolism and immune response elements, which in turn leads to the pathological responses characteristic of gonococcal disease. Current studies have begun to elucidate in detail the molecular interactions orchestrating these processes and the signaling events that they provoke.
Koomey
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The Biotechnology Centre of Oslo, University of Oslo, PO Box 1125 Blindern, N-0349, Oslo, Norway. johnk@biotek.uio.no
D000818:Animals; D000942:Antigens, Bacterial / Q000378:metabolism; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism; D017209:Apoptosis; D001425:Bacterial Outer Membrane Proteins / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D006801:Humans; D051916:Membrane Cofactor Protein; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism; D009344:Neisseria gonorrhoeae / Q000378:metabolism* / Q000472:pathogenicity; D018272:Porins / Q000378:metabolism; D011485:Protein Binding; D015398:Signal Transduction
D000942:Antigens, Bacterial; D015703:Antigens, CD; D001425:Bacterial Outer Membrane Proteins; C497857:CD46 protein, human; D051916:Membrane Cofactor Protein; D008562:Membrane Glycoproteins; D018272:Porins; C090348:Opa protein, Neisseria; D002118:Calcium