Open Access. Powered by Scholars. Published by Universities.®

Biochemistry, Biophysics, and Structural Biology Commons

Open Access. Powered by Scholars. Published by Universities.®

Articles 1 - 2 of 2

Full-Text Articles in Biochemistry, Biophysics, and Structural Biology

C-Jun N-Terminal Kinase 1 Is Required For Toll-Like Receptor 1 Gene Expression In Macrophages, Hooman Izadi, Amirreza T. Motameni, Tonya C. Bates, Elias R. Olivera, Vega Villar-Suarez, Ila Joshi, Renu Garg, Barbara A. Osborne, Roger J. Davis, Mercedes Rincon, Juan Anguita Oct 2007

C-Jun N-Terminal Kinase 1 Is Required For Toll-Like Receptor 1 Gene Expression In Macrophages, Hooman Izadi, Amirreza T. Motameni, Tonya C. Bates, Elias R. Olivera, Vega Villar-Suarez, Ila Joshi, Renu Garg, Barbara A. Osborne, Roger J. Davis, Mercedes Rincon, Juan Anguita

Davis Lab Publications

The regulation of innate immune responses to pathogens occurs through the interaction of Toll-like receptors (TLRs) with pathogen-associated molecular patterns and the activation of several signaling pathways whose contribution to the overall innate immune response to pathogens is poorly understood. We demonstrate a mechanism of control of murine macrophage responses mediated by TLR1/2 heterodimers through c-Jun N-terminal kinase 1 (JNK1) activity. JNK controls tumor necrosis factor alpha production and TLR-mediated macrophage responses to Borrelia burgdorferi, the causative agent of Lyme disease, and the TLR1/TLR2-specific agonist PAM(3)CSK(4). JNK1, but not JNK2, activity regulates the expression of ...


Requirement Of Jip Scaffold Proteins For Nmda-Mediated Signal Transduction, Norman J. Kennedy, Gilles Martin, Anka G. Ehrhardt, Julie Cavanagh-Kyros, Chia-Yi Kuan, Pasko Rakic, Richard A. Flavell, Steven N. Treistman, Roger J. Davis Sep 2007

Requirement Of Jip Scaffold Proteins For Nmda-Mediated Signal Transduction, Norman J. Kennedy, Gilles Martin, Anka G. Ehrhardt, Julie Cavanagh-Kyros, Chia-Yi Kuan, Pasko Rakic, Richard A. Flavell, Steven N. Treistman, Roger J. Davis

Davis Lab Publications

JIP scaffold proteins are implicated in the regulation of protein kinase signal transduction pathways. To test the physiological role of these scaffold proteins, we examined the phenotype of compound mutant mice that lack expression of JIP proteins. These mice were found to exhibit severe defects in N-methyl-D-aspartic acid (NMDA) receptor function, including decreased NMDA-evoked current amplitude, cytoplasmic Ca(++), and gene expression. The decreased NMDA receptor activity in JIP-deficient neurons is associated with reduced tyrosine phosphorylation of NR2 subunits of the NMDA receptor. JIP complexes interact with the SH2 domain of cFyn and may therefore promote tyrosine phosphorylation and activity of ...