TRAF5 antibody

Este producto es parte de TRAF - TNF receptor associated factor
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935106861
info@markelab.com
name
TRAF5 antibody
category
Primary Antibodies
provider
FineTest
reference
FNab10075
tested applications
ELISA, WB, IHC

Description

Adapter protein and signal transducer that links members of the tumor necrosis factor receptor family to different signaling pathways by association with the receptor cytoplasmic domain and kinases. Mediates activation of NF-kappa-B and probably JNK. Seems to be involved in apoptosis. Plays a role in mediating activation of NF-kappa-B by EIF2AK2/PKR.

Documents del producto

Instrucciones
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Data sheet
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Product specifications

Category
Primary Antibodies
Immunogen Target
TNF receptor-associated factor 5 (TRAF5)
Host
Rabbit
Reactivity
Human, mouse, Rat
Recommended Dilution
WB: 1:500-1:2000; IHC: 1:50-1:500
Clonality
polyclonal
Conjugation
Unconjugated
Isotype
IgG
Observed MW
52-70 kDa
Purity
≥95% as determined by SDS-PAGE
Purification
Immunogen affinity purified
Size 1
100µg
Form
liquid
Tested Applications
ELISA, WB, IHC
Storage
PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.)
UniProt ID
O00463
Gene ID
7189
Alias
TRAF-5,TRAF5, MGC:39780, RNF84, TNF receptor associated factor 5
Background
Antibody anti-TRAF5
Status
RUO
Note
Mol. Weight 52-70 kDa

Descripción

TRAF5 is a signaling adaptor protein that mediates pathways downstream of TNF receptors (TNFR), CD40, and BAFF-R, activating NF-κB and JNK to regulate inflammation, immune cell activation, and survival. TRAF5 plays a critical role in adaptive immune responses, particularly in T and B cell activation, cytokine production, and lymphoid tissue development. It works redundantly with TRAF2 to promote canonical NF-κB activation, ensuring appropriate immune responses to inflammatory and survival signals. TRAF5 is widely expressed in immune cells and epithelial tissues, where it supports cellular signaling during infections and tissue repair. Dysregulation of TRAF5 contributes to autoimmune diseases and inflammatory conditions, where altered NF-κB signaling enhances cytokine production and immune cell proliferation. Knockout studies reveal defects in lymphocyte activation, impaired cytokine signaling, and altered immune responses, highlighting its importance in immune regulation and inflammatory signaling.

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