TRAF6, a molecular bridge spanning adaptive immunity, innate immunity and osteoimmunology

@article{Wu2003TRAF6AM,
  title={TRAF6, a molecular bridge spanning adaptive immunity, innate immunity and osteoimmunology},
  author={Hao Wu and Joseph R. Arron},
  journal={BioEssays},
  year={2003},
  volume={25}
}
Tumor necrosis factor (TNF) receptor associated factor 6 (TRAF6) is a crucial signaling molecule regulating a diverse array of physiological processes, including adaptive immunity, innate immunity, bone metabolism and the development of several tissues including lymph nodes, mammary glands, skin and the central nervous system. It is a member of a group of six closely related TRAF proteins, which serve as adapter molecules, coupling the TNF receptor (TNFR) superfamily to intracellular signaling… 
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The role of TRAf6 in certain immune cells, as well as the function and potential effect of TRAF6 in autoimmune diseases and cancer, are reviewed and indicates that TRAF 6 may be a novel target for autoimmune Diseases and cancer.
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TLDR
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  • 2004
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Roles of TRAF6 in Central Nervous System
TLDR
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TRAFs in RANK signaling.
TLDR
Evidence from various research laboratories indicates TRAFs, but more importantly TRAF6, is the key to understanding how RANKL links cytoplasmic signaling to the nuclear transcriptional program.
Keratin 8 limits TLR-triggered inflammatory responses through inhibiting TRAF6 polyubiquitination
TLDR
It is reported that down-regulation of CK8 in mice enhanced TLR-mediated responses, rendering mice more susceptible to lipopolysaccharide (LPS)-induced endotoxin shock and Escherichia coli–caused septic peritonitis with reduced survival, elevated levels of inflammation cytokines and more severe tissue damage.
Increased A20-E3 ubiquitin ligase interactions in bid-deficient glia attenuate TLR3- and TLR4-induced inflammation
TLDR
This study demonstrates that Bid promotes E3 ubiquitin ligase-mediated signaling downstream of TLR3 and TLR4 and provides further evidence for the potential of Bid inhibition as a therapeutic for the attenuation of the robust pro-inflammatory response culminating in TLR activation.
TRAF6 deficiency promotes TNF-induced cell death through inactivation of GSK3β
TLDR
A role for TRAF6 is suggested in the maintenance of cell survival by regulating GSK3β activity in TNF signaling by regulating TNF-induced p65/RelA phosphorylation and inactivation of glycogen synthase kinase 3β.
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TLDR
Crystal structures of TRAF6 are reported to identify a universal mechanism by which TRAF 6 regulates several signalling cascades in adaptive immunity, innate immunity and bone homeostasis.
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TLDR
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TLDR
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The tumor necrosis factor receptor (TNFR) superfamily can induce diverse biological effects, including cell survival, proliferation, differentiation, and apoptosis. The major signal transducers for
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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