Abstract
Several tumor necrosis factor receptor (TNFR) family members activate both the classical and the alternative NF-κB pathways. However, how a single receptor engages these two distinct pathways is still poorly understood. Using lymphotoxin β receptor (LTβR) as a prototype, we showed that activation of the alternative, but not the classical, NF-κB pathway relied on internalization of the receptor. Further molecular analyses revealed a specific cytosolic region of LTβR essential for its internalization, TRAF3 recruitment, and p100 processing. Interestingly, we found that dynamin-dependent, but clathrin-independent, internalization of LTβR appeared to be required for the activation of the alternative, but not the classical, NF-κB pathway. In vivo, ligand-induced internalization of LTβR in mesenteric lymph node stromal cells correlated with induction of alternative NF-κB target genes. Thus, our data shed light on LTβR cellular trafficking as a process required for specific biological functions of NF-κB.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Base Sequence
-
Biological Transport, Active
-
Clathrin Heavy Chains / antagonists & inhibitors
-
Clathrin Heavy Chains / genetics
-
Clathrin Heavy Chains / metabolism
-
Cytosol / metabolism
-
Dynamin II / antagonists & inhibitors
-
Dynamin II / genetics
-
Dynamin II / metabolism
-
HEK293 Cells
-
HeLa Cells
-
Humans
-
Lymphotoxin alpha1, beta2 Heterotrimer / metabolism*
-
Lymphotoxin beta Receptor / chemistry
-
Lymphotoxin beta Receptor / deficiency
-
Lymphotoxin beta Receptor / genetics
-
Lymphotoxin beta Receptor / metabolism*
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Models, Biological
-
NF-kappa B / metabolism*
-
NF-kappa B p52 Subunit / metabolism
-
NF-kappaB-Inducing Kinase
-
Protein Processing, Post-Translational
-
Protein Serine-Threonine Kinases / metabolism
-
RNA, Small Interfering / genetics
-
Signal Transduction
-
TNF Receptor-Associated Factor 3 / metabolism
-
Transcription Factor RelB / deficiency
-
Transcription Factor RelB / genetics
-
Transcription Factor RelB / metabolism
Substances
-
Lymphotoxin alpha1, beta2 Heterotrimer
-
Lymphotoxin beta Receptor
-
NF-kappa B
-
NF-kappa B p52 Subunit
-
RNA, Small Interfering
-
Relb protein, mouse
-
TNF Receptor-Associated Factor 3
-
Clathrin Heavy Chains
-
Transcription Factor RelB
-
Protein Serine-Threonine Kinases
-
Dynamin II