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          Institute: MPI für biophysikalische Chemie     Collection: Abteilungsunabhängige Arbeitsgruppen     Display Documents



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ID: 270922.0, MPI für biophysikalische Chemie / Abteilungsunabhängige Arbeitsgruppen
Crosstalk between PKCzeta and the IL4/Stat6 pathway during T-cell-mediated hepatitis
Authors:Duran, A.; Rodriguez, A.; Martin, P.; Serrano, M.; Flores, J. M.; Leitges, M.; Diaz-Meco, M. T.; Moscat, J.
Date of Publication (YYYY-MM-DD):2004-11-24
Title of Journal:EMBO Journal
Volume:23
Issue / Number:23
Start Page:4595
End Page:4605
Review Status:Peer-review
Audience:Experts Only
Abstract / Description:PKCzeta is required for nuclear factor kappa-B (NF-kappaB) activation in several cell systems. NF-kappaB is a suppressor of liver apoptosis during development and in concanavalin A (ConA)-induced T-cell-mediated hepatitis. Here we show that PKCzeta-/- mice display inhibited ConA-induced NF-kappaB activation and reduced damage in liver. As the IL-4/Stat6 pathway is necessary for ConA-induced hepatitis, we addressed here the potential role of PKCzeta in this cascade. Interestingly, the loss of PKCzeta severely attenuated serum IL-5 and liver eotaxin-1 levels, two critical mediators of liver damage. Stat6 tyrosine phosphorylation and Jak1 activation were ablated in the liver of ConA-injected PKCzeta-/- mice and in IL-4-stimulated PKCzeta-/- fibroblasts. PKCzeta interacts with and phosphorylates Jak1 and PKCzeta activity is required for Jak1 function. In contrast, Par-4-/- mice have increased sensitivity to ConA-induced liver damage and IL-4 signaling. This unveils a novel and critical involvement of PKCzeta in the IL-4/Stat6 signaling pathway in vitro and in vivo.
External Publication Status:published
Document Type:Article
Communicated by:N. N.
Affiliations:MPI für biophysikalische Chemie/AG Leitges
MPI für biophysikalische Chemie/Abt. Eichele
Identifiers:URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=... [ID No:1]
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