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anti-Human TRAF5 Antikörper:
anti-Mouse (Murine) TRAF5 Antikörper:
anti-Rat (Rattus) TRAF5 Antikörper:
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Gerbil Polyclonal TRAF5 Primary Antibody für IHC (p), IP - ABIN537431
Zapata, Krajewska, Krajewski, Kitada, Welsh, Monks, McCloskey, Gordon, Kipps, Gascoyne, Shabaik, Reed: TNFR-associated factor family protein expression in normal tissues and lymphoid malignancies. in Journal of immunology (Baltimore, Md. : 1950) 2000
These findings suggest that upregulation of miR-29b-3p could protect cardiomyocytes against hypoxia-induced injury through downregulation of TRAF5.
High TRAF5 expression is associated with colorectal cancer.
Study presents the characterization of the peptide binding preferences of TRAFs 2, 3, and 5 using deep mutational scanning. The three TRAF proteins demonstrated different preferences for binding to members of the CD40 library, and three peptides from that library individually showed striking differences in affinity for the three TRAFs.
These findings indicate that miR-26b might influence TRAF5-MAPK signaling pathways to facilitate the malignant progression of melanoma cells.
findings reveal a direct link between TRAF5-mediated ubiquitination and RORgammat protein regulation
RIG-I-like receptor mediated antiviral innate immune responses in the lower respiratory tract involves TRAF3 and TRAF5 signaling.
This study provides evidence that TRAF5 and TRAF3IP2 genes are involved in the development of Behcet's disease (BD) and Vogt-Koyanagi-Harada (VKH) syndrome.
Data indicate that TNF receptor-associated factor 5 (TRAF5) gene is involved in the development of acute anterior uveitis (AAU) and pediatric uveitis.
Data indicate that in monocyte- derived macrophages (MDMs) acutely infected with HIV-1 and treated with HCV rCore and HIV-1 rNef, the HIV-1 replication depends on an upstream signal mediated through TRAF2, TRAF5 and TRAF6.
TRAF3 and TRAF5 are overexpressed in inflammatory bowel disease
Numbl interacted with tumor necrosis factor receptor-associated factor 5, which signals upstream and is required for the activation of NF-kappaB, and committed it to proteasomal degradation by promoting K48-linked polyubiquitination of TRAF5
Resutls indicate that TRAF5 may be a key molecule in the innate response against viral infection.
TRAF5 has a role in TNF-alpha induced IKK phosphorylation of NF-kappaB p65
TRAF3 specifically blocked the NF-kappaB activation via TRAF2/5.
These findings provide evidence for the association of an SNP upstream of a strong candidate RA susceptibility gene, TRAF5.
The results demonstrate that gp130-associated TRAF2 and TRAF5 inhibit the interaction between two JAK proteins in the IL-6R complex that is essential for initiating the JAK-STAT signaling pathway.
TRAF5 is crucially involved in OSM-mediated lung inflammation probably by inducing lung stromal/fibroblast cell activation.
our data indicate that Berberine exerts protective effects against chronic renal failurepartly through the TRAF5-mediated activation of the NF-kappaB signaling pathway in mouse podocytes
this study shows that TRAF2 and TRAF5 work as important regulators of the IL-6R signaling needed for Th17 development
The results indicated that TRAF5 deficiency significantly aggravated DSS-induced colitis, most likely by regulating Th cell-mediated inflammation.
In conclusion, our results suggest that as an intrinsic cardioprotective factor, TRAF5 plays a crucial role in the development of cardiac hypertrophy through the negative regulation of the MEK-ERK1/2 pathway
knock-out mice develop exaggerated experimental autoimmune encephalomyelitis due to enhanced Th17 cell differentiation
TRAF5 negatively regulates TLR signaling in B lymphocytes.
These results provide the first demonstration that TRAF5 is a critical mediator of brain ischemia/reperfusion in an experimental stroke model.
In vitro and cellular experiments showed that forms of TRAF5 with mutation of the corresponding residues to those of TRAF3 had TRAF3-like antiviral activity.
Treatment with IL-17 prolongs the half-life of chemokine CXCL1 mRNA via the adaptor TRAF5 and the splicing-regulatory factor SF2 (ASF).
TNF receptor-associated factor 5 (TRAF5) deficiency accelerates atherogenesis in mice by increasing inflammatory cell recruitment and foam cell formation.
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.
role in both RANKL- and TNFalpha-induced osteoclastogenesis
TRAF5 plays a limiting role during the differentiation of type 2 helper (Th2) cells by limiting certain responses driven by costimulatory molecules such as OX40/CD134.
Traf5 is a critical intermediate of costimulatory signaling pathways triggered by glucocorticoid-induced TNFR in T-lymphocytes.
Results implicate endothelial TRAF-1, -2, -3, -5, and -6 in CD40 signaling in atherogenesis, identifying these molecules as potential targets for selective therapeutic intervention.
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.
Both TRAF2 and TRAF5 are involved in TNF-induced NF-kappaB activation and protection from cell death.
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.
TNF receptor-associated factor 5
, RING finger protein 84