Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.11.25 (
MEKK1
)
1,856
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Virus infection of susceptible cells activates multiple signaling pathways that orchestrate the activation of genes, such as cytokines, involved in the antiviral and innate immune response. Among the kinases induced are the mitogen-activated protein (MAP) kinases, Jun-amino terminal kinases (JNK) and p38, the IkappaB kinase (IKK) and DNA-PK. In addition, virus infection also activates an uncharacterized VAK responsible for the C-terminal phosphorylation and subsequent activation of
interferon regulatory factor 3
(
IRF-3
). Virus-mediated activation of
IRF-3
through VAK is dependent on viral entry and transcription, since replication deficient virus failed to induce
IRF-3
activity. The pathways leading to VAK activation are not well characterized, but
IRF-3
appears to represent a novel cellular detection pathway that recognizes viral nucleocapsid (N) structure. Recently, the range of inducers responsible for
IRF-3
activation has increased. In addition to virus infection, recognition of bacterial infection mediated through lipopolysaccharide by Toll-like receptor 4 has also been reported. Furthermore,
MAP kinase kinase kinase
(MAP KKK)-related pathways and DNA-PK induce N-terminal phosphorylation of
IRF-3
. This review summarizes recent observations in the identification of novel signaling pathways leading to
IRF-3
activation.
...
PMID:Multiple signaling pathways leading to the activation of interferon regulatory factor 3. 1221 96
