Human Polyclonal TRAF1 Ab
- Known as:
- Human Polyclonal TRAF1 Antibody
- Catalog number:
- a0150
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal TRAF1
Ask about this productRelated genes to: Human Polyclonal TRAF1 Ab
- Gene:
- TRAF1 NIH gene
- Name:
- TNF receptor associated factor 1
- Previous symbol:
- -
- Synonyms:
- EBI6
- Chromosome:
- 9q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-12
- Date modifiied:
- 2016-10-05
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- The tumor necrosis factor receptor (TNFR)-associated factor (TRAF) family of molecules are intracellular adaptors that regulate cellular signaling through members of the TNFR and Toll-like receptor superfamily. Mammals have seven TRAF molecules numbered sequentially from TRAF1 to TRAF7. Although TRAF5 was identified as a potential regulator of TNFR superfamily members, the in vivo function of TRAF5 has not yet been fully elucidated. We identified an unconventional role of TRAF5 in interleukin-6 (IL-6) receptor signaling involving CD4 T cells. Moreover, TRAF5 binds to the signal-transducing glycoprotein 130 (gp130) receptor for IL-6 and inhibits the activity of the janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway. In addition, Traf5-deficient CD4 T cells exhibit significantly enhanced IL-6-driven differentiation of T helper 17 (Th17) cells, which exacerbates neuroinflammation in experimental autoimmune encephalomyelitis. Furthermore, TRAF5 demonstrates a similar activity to gp130 for IL-27, another cytokine of the IL-6 family. Additionally, Traf5-deficient CD4 T cells display significantly increased IL-27-mediated differentiation of Th1 cells, which increases footpad swelling in delayed-type hypersensitivity response. Thus, TRAF5 functions as a negative regulator of gp130 in CD4 T cells. This review aimed to explain how TRAF5 controls the differentiation of CD4 T cells and discuss how the expression of TRAF5 in T cells and other cell types can influence the development and progression of autoimmune and inflammatory diseases. - Source: PubMed
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