TRAF3 antibody

Este producto es parte de TRAF - TNF receptor associated factor
TRAF3 antibody
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Name
TRAF3 antibody
Category
Primary Antibodies
Provider
FineTest
Reference
FNab10240
Tested Applications
ELISA, WB, IHC, IF

Documentos del producto

Instrucciones
Descargar
Data sheet
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Especificaciones del producto

Category
Primary Antibodies
Immunogen Target
TNF receptor-associated factor 3 (TRAF3)
Host
Rabbit
Reactivity
Human, Mouse, Rat
Recommended Dilution
WB: 1:500-1:2000; IHC: 1:50-1:200; IF: 1:10-1:100
Clonality
polyclonal
Conjugation
Unconjugated
Isotype
IgG
Observed MW
64 kDa
Purity
≥95% as determined by SDS-PAGE
Purification
Immunogen affinity purified
Size 1
100µg
Form
liquid
Tested Applications
ELISA, WB, IHC, IF
Storage
PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.)
UniProt ID
Q13114
Gene ID
7187
Alias
TRAF-3,TRAF3, CAP-1, CAP1, CD40bp, CRAF1, IIAE5, LAP1, TNF receptor associated factor 3, RNF118
Background
Antibody anti-TRAF3
Status
RUO
Note
Mol. Weight 64 kDa

Background

TRAF3 is an adaptor protein that regulates signaling downstream of receptors like CD40, BAFF-R, and Toll-like receptors (TLRs), playing a crucial role in immune regulation, lymphocyte activation, and antiviral responses. Unlike TRAF1 and TRAF2, TRAF3 functions as a negative regulator of the non-canonical NF-κB pathway by targeting NIK (NF-κB-inducing kinase) for degradation, thereby preventing constitutive activation of NF-κB2 signaling. TRAF3 is widely expressed in immune cells, where it regulates B-cell survival, interferon production, and immune tolerance. Dysregulation of TRAF3 is associated with B-cell malignancies, autoimmune diseases, and viral infections due to uncontrolled NF-κB activation and impaired immune signaling. Functional studies in knockout models demonstrate defects in B-cell homeostasis, increased susceptibility to autoimmunity, and reduced antiviral immunity, underscoring its dual role in restraining excessive signaling and supporting immune regulation.

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