TNF Receptor-Associated Factor 3 (TRAF3) Antibody (Biotin)

Este producto es parte de TRAF - TNF receptor associated factor
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169€ (20 µg)

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935106861
info@markelab.com
name
TNF Receptor-Associated Factor 3 (TRAF3) Antibody (Biotin)
category
Primary Antibodies
provider
Abbexa
reference
abx300023
tested applications
ELISA

Description

TRAF3 Antibody (Biotin) is a Rabbit Polyclonal against TRAF3 conjugated to Biotin.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
TNF Receptor-Associated Factor 3 (TRAF3)
Host
Rabbit
Reactivity
Human
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Biotin
Isotype
IgG
Purity
> 95%
Purification
Purified by Protein G.
Size 1
20 µg
Size 2
50 µg
Size 3
100 µg
Size 4
200 µg
Size 5
1 mg
Form
Liquid
Tested Applications
ELISA
Buffer
0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% Glycerol.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid exposure to light. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
Q13114
Gene ID
7187
NCBI Accession
NP_001186356.1, NM_001199427.1, NP_003291.2, NM_003300.3
OMIM
601896
Alias
TRAF-3,TRAF3, CAP-1, CAP1, CD40bp, CRAF1, IIAE5, LAP1, TNF receptor associated factor 3, RNF118
Background
Antibody anti-TRAF3
Status
RUO

Descripción

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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