A Mammalian Homolog of Drosophila schnurri, KRC, Regulates TNF Receptor-Driven Responses and Interacts with TRAF2

The cytokine TNFα launches cascades of gene activation that control inflammation and apoptosis through NFκB and JNK/SAPK signal transduction pathways. Here we describe a function for the zinc finger transcription factor kappa recognition component (KRC) in regulating patterns of gene activation in r...

Full description

Saved in:
Bibliographic Details
Published in:Molecular cell 2002, Vol.9 (1), p.121-131
Main Authors: Oukka, Mohamed, Kim, Sean T., Lugo, Geancarlo, Sun, Jenny, Wu, Lai-Chu, Glimcher, Laurie H.
Format: Article
Language:English
Subjects:
3T3 Cells
Animals
Apoptosis - genetics
Cytokines - biosynthesis
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Drosophila
Drosophila Proteins
HeLa Cells
Humans
Immunology
Inflammation - genetics
Inflammation - metabolism
JNK protein
KRC protein
Life Sciences
Mammalia
Mice
NF-B protein
NF-kappa B - genetics
NF-kappa B - metabolism
Proteins - genetics
Proteins - metabolism
Receptors, Tumor Necrosis Factor - genetics
Receptors, Tumor Necrosis Factor - metabolism
Signal Transduction - genetics
TNF Receptor-Associated Factor 2
TRAF2 protein
Transcription Factors - genetics
Transcriptional Activation
tumor necrosis factor receptors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The cytokine TNFα launches cascades of gene activation that control inflammation and apoptosis through NFκB and JNK/SAPK signal transduction pathways. Here we describe a function for the zinc finger transcription factor kappa recognition component (KRC) in regulating patterns of gene activation in response to proinflammatory stimuli. We demonstrate that KRC overexpression inhibits while antisense or dominant-negative KRC enhances NFκB-dependent transactivation and JNK phosphorylation and consequently, apoptosis and cytokine gene expression. The effect of KRC is mediated through its interaction with the adaptor protein TRAF2, which intersects both pathways. KRC is a hitherto unrecognized participant in the signal transduction pathway leading from the TNF receptor to gene activation and may play a critical role in inflammatory and apoptotic responses.
ISSN:1097-2765
1097-4164
DOI:10.1016/S1097-2765(01)00434-8