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Porphyromonas gingivalis-related cardiac cell apoptosis was majorly co-activated by p38 and extracellular signal-regulated kinase pathways.

Lee, Shin-Da

Porphyromonas gingivalis-related cardiac cell apoptosis was majorly co-activated by p38 and extracellular signal-regulated kinase pathways. [electronic resource] - Journal of periodontal research Feb 2006 - 39-46 p. digital

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

ISSN: 0022-3484

Standard No.: 10.1111/j.1600-0765.2005.00842.x doi

Subjects--Topical Terms:
Animals
Anthracenes--pharmacology
Apoptosis--physiology
Butadienes--pharmacology
Calcineurin Inhibitors
Caspases--physiology
Cell Nucleus--ultrastructure
Chromones--pharmacology
Cyclosporine--pharmacology
DNA Fragmentation
Enzyme Inhibitors--pharmacology
Fluorescent Dyes
Imidazoles--pharmacology
Indoles
MAP Kinase Kinase 4--antagonists & inhibitors
Mitogen-Activated Protein Kinase 1--antagonists & inhibitors
Mitogen-Activated Protein Kinase 3--antagonists & inhibitors
Mitogen-Activated Protein Kinase Kinases--antagonists & inhibitors
Morpholines--pharmacology
Myocardium--cytology
Nitriles--pharmacology
Phosphoinositide-3 Kinase Inhibitors
Porphyromonas gingivalis--physiology
Pyridines--pharmacology
Rats
p38 Mitogen-Activated Protein Kinases--antagonists & inhibitors