I-TRAF is a novel TRAF-interacting protein that regulates TRAF-mediated signal transduction.

Rothe, Mike; Xiong, Jessie; Shu, Hong‐Bing; Williamson, Keith; Goddard, Audrey D.; Goeddel, David V.

doi:10.1073/pnas.93.16.8241

Cited by 200 publications

(162 citation statements)

References 21 publications

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“…ORF-K13-induced NF-kB activation was effectively blocked by a dominant-negative mutant of TRAF2 (amino acids 87 ± 501) (Takeuchi et al, 1996) which has been previously shown to block NF-kB induction by several members of the TNFR family ( Figure 3a). Similarly, I-TRAF/Tank, a protein previously shown to bind to the TRAFs (Cheng and Baltimore, 1996;Rothe et al, 1996), could block NFkB induction by ORF-K13 (Figure 3a). Both the above proteins could also block NF-kB induction by Caspase 8 and MRIT (Figure 3a).…”

Section: Mechanism Of Orf-k13-induced Nf-kb Activationmentioning

confidence: 63%

Modulation of the NF-κB pathway by virally encoded Death Effector Domains-containing proteins

et al. 1999

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Death E ector Domains (DEDs) have been known to mediate the recruitment of Caspase 8 and its homologs to the aggregated death-inducing signaling complex (DISC), consisting of the death domain (DD)-containing receptors and various signaling proteins. In addition, several viruses were recently shown to encode proteins with DEDs (also called FLICE inhibitory proteins or vFLIPs) which have the ability of blocking cell death induced by DD-containing receptors. We provide evidence that vFLIPs can also modulate the NF-kB pathway and physically interact with several signaling proteins, such as the TRAFs, RIP, NIK and the IKKs. Modulation of the NF-kB pathway may play a role in the natural history of infection by these viruses.

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Section: Mechanism Of Orf-k13-induced Nf-kb Activationmentioning

confidence: 63%

Modulation of the NF-κB pathway by virally encoded Death Effector Domains-containing proteins

et al. 1999

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“…After reaching a maximum ϳ2 h, transcript levels of genes in these clusters dropped dramatically, to a minimum well below the initial expression level. Our data suggest one possible mechanism for this effect; the TRAF inhibitor TANK (Rothe et al, 1996), which was induced by ER stress (see below, Figure 5), could provide negative feedback to TRAF and result in a decreased AP-1 activity.…”

Section: Transcripts Encoding Many Signal Transduction Proteins Incrementioning

confidence: 99%

Diverse and Specific Gene Expression Responses to Stresses in Cultured Human Cells

Murray

Whitfield

Trinklein

et al. 2004

MBoC

276

236

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We used cDNA microarrays in a systematic study of the gene expression responses of HeLa cells and primary human lung fibroblasts to heat shock, endoplasmic reticulum stress, oxidative stress, and crowding. Hierarchical clustering of the data revealed groups of genes with coherent biological themes, including genes that responded to specific stresses and others that responded to multiple types of stress. Fewer genes increased in expression after multiple stresses than in free-living yeasts, which have a large general stress response program. Most of the genes induced by multiple diverse stresses are involved in cell-cell communication and other processes specific to higher organisms. We found substantial differences between the stress responses of HeLa cells and primary fibroblasts. For example, many genes were induced by oxidative stress and dithiothreitol in fibroblasts but not HeLa cells; conversely, a group of transcription factors, including c-fos and c-jun, were induced by heat shock in HeLa cells but not in fibroblasts. The dataset is freely available for search and download at http://microarray-pubs.stanford.edu/human_stress/Home.shtml.

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“…Overexpression of I-TRAF inhibits TRAF2-mediated NF-kB activation as signaled by CD40 and both TNF receptors. Thus, I-TRAF appears to act as a natural inhibitor of TRAF function (Rothe et al, 1996).…”

Section: Tumor Necrosis Factor Receptor-associated Factors (Trafs)mentioning

confidence: 99%

Diverse agents act at multiple levels to inhibit the Rel/NF-κB signal transduction pathway

1999

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I-TRAF is a novel TRAF-interacting protein that regulates TRAF-mediated signal transduction.

Cited by 200 publications

References 21 publications

Modulation of the NF-κB pathway by virally encoded Death Effector Domains-containing proteins

Modulation of the NF-κB pathway by virally encoded Death Effector Domains-containing proteins

Diverse and Specific Gene Expression Responses to Stresses in Cultured Human Cells

Diverse agents act at multiple levels to inhibit the Rel/NF-κB signal transduction pathway

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