Anti-TRAF3 (full length) polyclonal antibody

Name: Anti-TRAF3 (full length) polyclonal antibody
SKU: DPABH-09678
Rating: 5 (1 reviews)

Mouse anti-Human TRAF3 (full length) polyclonal antibody for WB

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human

Immunogen

Recombinant full length protein corresponding to Human TRAF3 aa 1-568.Sequence: MESSKKMDSPGALQTNPPLKLHTDRSAGTPVFVPEQGGYKEKFVKTVEDK YKCEKCHLVLCSPKQTECGHRFCESCMAALLSSSSPKCTACQESIVKDKV FKDNCCKREILALQIYCRNESRGCAEQLMLGHLLVHLKNDCHFEELPCVR PDCKEKVLRKDLRDHVEKACKY

Conjugate

Unconjugated

Applications

Application Notes

WB: 1 μg/ml.

Target

Alternative Names

TRAF3; TNF receptor-associated factor 3; CAP 1; CD40bp; CRAF1; LAP1; CD40 binding protein; CD40 associated protein 1; LMP1-associated protein 1; CD40 receptor associated factor 1; CAP-1;

Entrez Gene ID

7187

UniProt ID

Q13114

Product Background

Antigen Description

Regulates pathways leading to the activation of NF-kappa-B and MAP kinases, and plays a central role in the regulation of B cell survival. Part of signaling pathways leading to the production of cytokines and interferon. Required for normal antibody isotype switching from IgM to IgG. Plays a role T-cell dependent immune responses. Plays a role in the regulation of antiviral responses. Is an essential constituent of several E3 ubiquitin-protein ligase complexes. May have E3 ubiquitin-protein ligase activity and promote Lys-63-linked ubiquitination of target proteins. Inhibits activation of NF-kappa-B in response to LTBR stimulation. Inhibits TRAF2-mediated activation of NF-kappa-B. Down-regulates proteolytic processing of NFKB2, and thereby inhibits non-canonical activation of NF-kappa-B. Promotes ubiquitination and proteasomal degradation of MAP3K14.

Pathway

Apoptosis; CD40/CD40L signaling; Hepatitis C; Herpes simplex infection; Immune System;

Citations

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Documents

pdf COA

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pdf Datasheet

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References

The Autoimmunity-Associated Gene PTPN22 Potentiates Toll-like Receptor-Driven, Type 1 Interferon-Dependent Immunity

IMMUNITY

Authors: Wang, Yaya; Shaked, Iftach; Stanford, Stephanie M.; Zhou, Wenbo; Curtsinger, Julie M.; Mikulski, Zbigniew; Shaheen, Zachary R.; Cheng, Genhong; Sawatzke, Kristy; Campbell, Amanda M.; Auger, Jennifer L.; Bilgic, Hatice; Shoyama, Fernanda M.; Schmeling, David O.; Balfour, Henry H., Jr.; Hasegawa, Kiminori; Chan, Andrew C.; Corbett, John A.; Binstadt, Bryce A.; Mescher, Matthew F.; Ley, Klaus; Bottini, Nunzio; Peterson, Erik J.

Abstract

Immune cells sense microbial products through Toll-like receptors (TLR), which trigger host defense responses including type 1 interferons (IFNs) secretion. A coding polymorphism in the protein tyrosine phosphatase nonreceptor type 22 (PTPN22) gene is a susceptibility allele for human autoimmune and infectious disease. We report that Ptpn22 selectively regulated type 1 IFN production after TLR engagement in myeloid cells. Ptpn22 promoted host antiviral responses and was critical for TLR agonist-induced, type 1 IFN-dependent suppression of inflammation in colitis and arthritis. PTPN22 directly associated with TNF receptor-associated factor 3 (TRAF3) and promotes TRAF3 lysine 63-linked ubiquitination. The disease-associated PTPN22W variant failed to promote TRAF3 ubiquitination, type 1 IFN upregulation, and type 1 IFN-dependent suppression of arthritis. The findings establish a candidate innate immune mechanism of action for a human autoimmunity "risk" gene in the regulation of host defense and inflammation.

Development of an in vitro immunobiotic evaluation system against rotavirus infection in bovine intestinal epitheliocytes

BENEFICIAL MICROBES

Authors: Kobayashi, H.; Kanmani, P.; Ishizuka, T.; Miyazaki, A.; Soma, J.; Albarracin, L.; Suda, Y.; Nochi, T.; Aso, H.; Iwabuchi, N.; Xiao, J. -Z.; Saito, T.; Villena, J.; Kitazawa, H.

Abstract

The bovine intestinal epithelial cell line (BIE cells) expresses the Toll-like receptor (TLR)3 and is able to mount anantiviral immune response after the stimulation with poly(I:C). In the present study, we aimed to further characterise the antiviral defence mechanisms in BIE cells by evaluating the innate immune response triggered by rotavirus (RV) infection. In addition, we attempted to determine whether immunobiotic bifidobacteria are able to confer protection of BIE cells against RV infection by beneficially modulating the antiviral immune response. RV OSU (porcine) and UK (bovine) effectively infected BIE cells, while a significant lower capacity to infect BIE cells was observed for human (Wa) and murine (EW) RV. We observed that viral infection in BIE cells triggered TLR3/RIG-I-mediated immune responses with activation of IRF3 and TRAF3, induction of interferon beta (IFN-beta) and up-regulation of inflammatory cytokines. Our results also demonstrated that preventive treatments with Bifidobacterium infantis MCC12 or Bifidobacterium breve MCC1274 significantly reduced RV titres in infected BIE cells and differentially modulated the innate immune response. Of note, both strains significantly improved the production of the antiviral factor IFN-beta in RV-infected BIE cells. In conclusion, this work provides comprehensive information on the antiviral immune response of BIE cells against RV, that can be further studied for the development of strategies aimed to improve antiviral defences in bovine intestinal epithelial cells. Our results also demonstrate that BIE cells could be used as a newly immunobiotic evaluation system against RV infection for application in the bovine host.