Tumor necrosis factor receptor-associated factors (TRAFs)

Bradley, John R.; Pober, Jordan S.

doi:10.1038/sj.onc.1204788

Cited by 586 publications

(503 citation statements)

References 105 publications

(102 reference statements)

Supporting

Mentioning

484

Contrasting

Unclassified

Order By: Relevance

“…Thus, TNF-induced NF-kB activation can be inhibited by using anti-TNF antibodies or agents that block the TNF-R, and this type of upstream anti-NF-kB therapy can have benefits in diseases such as inflammatory bowel disease, arthritis and Crohn's disease (Song et al, 2002). At the next step in cytokine signaling, members of the tumor necrosis factor receptor-associated factors (TRAF) protein family act as adaptor molecules for the activation of NF-kB by the TNF and IL-1 receptor superfamilies (Bradley and Pober, 2001). TRAF2 is recruited to the TNF-R1 and TNF-R2 receptors following TNF stimulation, and it is required for CD40-and TNFa-mediated activation of NF-kB.…”

Section: Inhibitors That Act Upstream Of the Ikk Complexmentioning

confidence: 99%

Inhibitors of NF-κB signaling: 785 and counting

2006

View full text Add to dashboard Cite

Section: Inhibitors That Act Upstream Of the Ikk Complexmentioning

confidence: 99%

Inhibitors of NF-κB signaling: 785 and counting

2006

View full text Add to dashboard Cite

“…Trafs are known mediators of TNF signaling, acting as intracellular adaptor molecules that bind to TNF receptors. It has been shown that Trafs mediate activation of NF-B (reviewed in Bradley and Pober, 2001;Wajant et al, 2001;Chung et al, 2002). For example Troy is believed to recruit Traf2, 5, 6 for NF-B activation (Kojima et al, 2000).…”

Section: Tooth Phenotype In Traf6 Mutant Micementioning

confidence: 99%

“…TNF receptor-associated factors (TRAFs) are a family of cytoplasmic adaptor proteins that interact with a wide variety of cell surface receptors such as the TNF receptor (TNFR) family and the interleukin-1 (IL-1) receptor/Toll-like receptors (reviewed in Bradley and Pober, 2001;Wajant et al, 2001;Chung et al, 2002). Traf6-deficient mice suggest that TRAF6 is essential molecule for osteoclast function, B-cell differentiation, IL-1 signalling, lipopolysaccharide signaling, lymph node organogenesis, and neural tube closure (Lomaga et al, 1999(Lomaga et al, , 2000Naito et al, 1999;Kobayashi et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Traf6 is essential for murine tooth cusp morphogenesis

Ohazama

Courtney

Tucker

et al. 2003

Developmental Dynamics

View full text Add to dashboard Cite

Ectodermal appendages such as skin, hair, teeth, and sweat glands are affected in patients with hypohidrotic (anhydrotic) ectodermal dysplasia (HED). It has been established that mutations in the tumor necrosis factor (TNF) superfamily of molecules, i.e., ectodysplasin (EDA), EDA receptor (EDAR), and EDAR-associated death domain (EDARADD; the intracellular adaptor for EDAR), are responsible for several forms of HED in humans and mice. We show here by in situ hybridisation that another TNF family (orphan) receptor, TROY (also known TAJ, TAJ-␣, TRADE, and TNFRSF19), is strongly coexpressed with Edar in the epithelial enamel knot signalling centres that are believe to regulate cuspal morphogenesis during murine tooth development. Traf6 is known to function as an intracellular adaptor protein for Troy and examination of Traf6 mutant mice revealed abnormalities in molar teeth that are similar but more severe than those produced by mutations in Eda signalling molecules. This finding suggests that, in additional to ectodysplasin, another TNF pathway involving Troy/Traf6 is involved in molar tooth cusp formation and identifies an essential role for a Traf in tooth development. Developmental Dynamics 229:131-135, 2004.

show abstract

“…In this regard, TNFR-associated factors are known to couple the proinflammatory cytokine receptors, such as IL-1 and TNF-␣, to downstream events (41)(42)(43)), yet they do not participate in IL-2R signaling (6). The missing link from the IL-2R to NF-B activation could entail activation of mitogen-activated protein kinases, which have been linked to IL-2R signaling (6).…”

Section: Control Of Perforin Transcription By Nf-bmentioning

confidence: 99%

A Role for NF-κB Activation in Perforin Expression of NK Cells Upon IL-2 Receptor Signaling

Zhou

Zhang

Lichtenheld

et al. 2002

The Journal of Immunology

View full text Add to dashboard Cite

Optimal NK cell development and activation as well as cytolytic activity involves IL-2Rβ signals that also up-regulate expression of the pore-forming effector molecule perforin. Although the Jak/Stat pathway and specifically Stat5 transcription factors are required to promote many of the respective downstream events, the role of additional signaling pathways and transcription factors remains to be clarified. This report investigates the role of NF-κB activation for perforin expression by NK cells. It is demonstrated that IL-2-induced up-regulation of perforin in primary NK cells and in a model cell line is blocked by two pharmacological agents known to inhibit NF-κB activation. Direct evidence for the activation of the NF-κB pathway by IL-2R signals in NK cells involves activation of the IKKα kinase, inhibitory protein κBα degradation, nuclear translocation of p50/p65 complexes, and ultimately, transcriptional activation of the perforin gene via an NF-κB binding element in its upstream enhancer. Taken together, these observations strongly suggest that IL-2R signals can activate a pathway leading to NF-κB activation in NK cells and that this pathway is involved in the control of perforin expression.

show abstract

Tumor necrosis factor receptor-associated factors (TRAFs)

Cited by 586 publications

References 105 publications

Inhibitors of NF-κB signaling: 785 and counting

Inhibitors of NF-κB signaling: 785 and counting

Traf6 is essential for murine tooth cusp morphogenesis

A Role for NF-κB Activation in Perforin Expression of NK Cells Upon IL-2 Receptor Signaling

Contact Info

Product

Resources

About