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TNF receptor-associated factor 5

TRAF5, TNF Receptor-Associated Factor 5
The scaffold protein encoded by this gene is a member of the tumor necrosis factor receptor-associated factor (TRAF) protein family and contains a meprin and TRAF homology (MATH) domain, a RING-type zinc finger, and two TRAF-type zinc fingers. TRAF proteins are associated with, and mediate signal transduction from members of the TNF receptor superfamily. This protein is one of the components of a multiple protein complex which binds to tumor necrosis factor (TNF) receptor cytoplasmic domains and mediates TNF-induced activation. Alternate transcriptional splice variants have been characterized. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: TRAF2, NF-kappaB, TRAF6, IgM, CAN
Papers on TRAF5
Comparison of the peptide binding preferences of three closely related TRAF paralogs: TRAF2, TRAF3, and TRAF5.
Keating et al., Cambridge, United States. In Protein Sci, Feb 2016
We displayed single- and double-mutant peptide libraries based on the TRAF binding sites of CD40 or TANK on the surface of Escherichia coli and screened them for binding to TRAF2, TRAF3, and TRAF5.
TRAF5-mediated Lys-63-linked Polyubiquitination Plays an Essential Role in Positive Regulation of RORγt in Promoting IL-17A Expression.
Li et al., Shanghai, China. In J Biol Chem, Dec 2015
In this study, we show that tumor necrosis factor receptor-associated factor 5 (TRAF5), known as an E3 ubiquitin protein ligase and signal transducer, interacts with and ubiquitinates RORγt via Lys-63-linked polyubiquitination.
Retinoic acid-inducible gene-I-like receptor (RLR)-mediated antiviral innate immune responses in the lower respiratory tract: Roles of TRAF3 and TRAF5.
Ito et al., Hirosaki, Japan. In Biochem Biophys Res Commun, Dec 2015
The expression levels of TRAF3 and TRAF5, which have conserved domains that are nearly identical, in the LRT were examined.
The Anti-Inflammatory Effect of Algae-Derived Lipid Extracts on Lipopolysaccharide (LPS)-Stimulated Human THP-1 Macrophages.
Stanton et al., Cork, Ireland. In Mar Drugs, Aug 2015
Quantitative gene expression analysis of a panel of 92 genes linked to inflammatory signaling pathway revealed down-regulation of the expression of 14 pro-inflammatory genes (TLR1, TLR2, TLR4, TLR8, TRAF5, TRAF6, TNFSF18, IL6R, IL23, CCR1, CCR4, CCL17, STAT3, MAP3K1) by the lipid extracts.
The adaptor TRAF5 limits the differentiation of inflammatory CD4(+) T cells by antagonizing signaling via the receptor for IL-6.
So et al., Sendai, Japan. In Nat Immunol, 2014
We found that in the presence of interleukin 6 (IL-6), naive TRAF5-deficient CD4(+) T cells showed an enhanced ability to differentiate into the TH17 subset of helper T cells.
Skeletal muscle atrophy in R6/2 mice - altered circulating skeletal muscle markers and gene expression profile changes.
Björkqvist et al., Lund, Sweden. In J Huntingtons Dis, 2013
Alongside, we found increased expression of caspases (3 and 8) and key elements of the NFκB signaling pathway, p65/RelA, Tradd, and TRAF5.
Negative regulation of IL-17-mediated signaling and inflammation by the ubiquitin-specific protease USP25.
Dong et al., Houston, United States. In Nat Immunol, 2012
Mechanistically, stimulation with IL-17 induced the association of USP25 with the adaptors TRAF5 and TRAF6, and USP25 induced removal of Lys63-linked ubiquitination in TRAF5 and TRAF6 mediated by the adaptor Act1.
New insight into the functions of the interleukin-17 receptor adaptor protein Act1 in psoriatic arthritis.
Pennington et al., In Arthritis Res Ther, 2011
This key mutation in Act1 could lead to a greater association of the IL-17 receptor with TRAF2/TRAF5 and this in turn suggests an alternative function for IL-17 in PsA.
T-cell intrinsic effects of GITR and 4-1BB during viral infection and cancer immunotherapy.
Watts et al., Toronto, Canada. In Immunol Rev, 2011
GITR uses TNFR-associated factor (TRAF) 2 and TRAF5, whereas 4-1BB recruits TRAF1 and TRAF2 to mediate survival signaling in T cells.
Roles of tumor necrosis factor receptor associated factor 3 (TRAF3) and TRAF5 in immune cell functions.
Bishop et al., Iowa City, United States. In Immunol Rev, 2011
In recent years, there has been a resurgence of interest and exploration of the roles played by TRAF3 and TRAF5 in cellular regulation, particularly in cells of the immune system, the cell types of focus in this review.
Treatment with IL-17 prolongs the half-life of chemokine CXCL1 mRNA via the adaptor TRAF5 and the splicing-regulatory factor SF2 (ASF).
Hamilton et al., Cleveland, United States. In Nat Immunol, 2011
Treatment with IL-17 prolongs the half-life of chemokine CXCL1 mRNA via the adaptor TRAF5 and the splicing-regulatory factor SF2 (ASF).
The inducible kinase IKKi is required for IL-17-dependent signaling associated with neutrophilia and pulmonary inflammation.
Li et al., Cleveland, United States. In Nat Immunol, 2011
IKKi deficiency abolished IL-17-induced formation of the complex of Act1 and the adaptors TRAF2 and TRAF5, activation of mitogen-activated protein kinases (MAPKs) and mRNA stability, whereas the Act1-TRAF6-transcription factor NF-κB axis was retained.
TRAF5 deficiency accelerates atherogenesis in mice by increasing inflammatory cell recruitment and foam cell formation.
Zirlik et al., Freiburg, Germany. In Circ Res, 2010
TNF receptor-associated factor 5 (TRAF5) deficiency accelerates atherogenesis in mice by increasing inflammatory cell recruitment and foam cell formation.
TRAF5 is a downstream target of MAVS in antiviral innate immune signaling.
Wang et al., Los Angeles, United States. In Plos One, 2009
Resutls indicate that TRAF5 may be a key molecule in the innate response against viral infection.
TRAF5 is a critical mediator of in vitro signals and in vivo functions of LMP1, the viral oncogenic mimic of CD40.
Bishop et al., Iowa City, United States. In Proc Natl Acad Sci U S A, 2009
Study is the first report showing a major requirement for TRAF5 in signaling by a specific receptor both in vitro and in vivo, as well as playing an important role in biological function in B lymphocytes.
Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphoma.
Pasqualucci et al., New York City, United States. In Nature, 2009
Here we show that >50% of ABC-DLBCL and a smaller fraction of GCB-DLBCL carry somatic mutations in multiple genes, including negative (TNFAIP3, also called A20) and positive (CARD11, TRAF2, TRAF5, MAP3K7 (TAK1) and TNFRSF11A (RANK)) regulators of NF-kappaB.
TNF receptor-associated factor 5 is required for optimal T cell expansion and survival in response to infection.
Bishop et al., Iowa City, United States. In J Immunol, 2009
TRAF5 as an important positive signaling element that enhances T cell expansion and pathogen containment by providing a survival advantage to responding Ag-specific CD8(+) T cells during infection.
Protein-protein interactions in TRAF3.
Wu et al., Los Angeles, United States. In Adv Exp Med Biol, 2006
In contrast, binding of lymphotoxin-beta receptor (LTbetaR) to TRAF2 and TRAF5 propagates signals leading to activation of NF-kappaB, while binding to TRAF3 induces negative regulation of this pathway and leads to apoptosis in tumor cells.
Physiological roles and mechanisms of signaling by TRAF2 and TRAF5.
Yeh et al., Toronto, Canada. In Adv Exp Med Biol, 2006
RAF2 and TRAF5 are closely related members of the TRAF family of proteins.
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