TNF Receptor Associated Factor 2 (TRAF2) Antibody

Este producto es parte de TRAF - TNF receptor associated factor
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383.5€ (100 µl)

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935106861
info@markelab.com
name
TNF Receptor Associated Factor 2 (TRAF2) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx224420
tested applications
ELISA, WB, FCM

Description

TRAF2 Antibody is a Mouse Monoclonal against TRAF2.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
TNF Receptor Associated Factor 2 (TRAF2)
Host
Mouse
Reactivity
Human
Recommended Dilution
ELISA: 1/10000, WB: 1/500 - 1/2000, FCM: 1/200 - 1/400. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Monoclonal
Conjugation
Unconjugated
Isotype
IgG2b
Purification
Purified from ascites by Protein G chromatography.
Size 1
100 µl
Form
Liquid
Tested Applications
ELISA, WB, FCM
Buffer
PBS, containing 0.05% sodium azide.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
Q12933
Gene ID
7186
OMIM
601895
Alias
TRAF-2,TRAF2, MGC:45012, TRAP, TRAP3, TNF receptor associated factor 2, RNF117
Background
Antibody anti-TRAF2
Status
RUO
Note
Concentration: 1 mg/ml - 

Descripción

TRAF2 is a key adaptor protein that links TNF receptors and other immune receptors to downstream signaling pathways, particularly NF-κB and JNK activation, to regulate inflammation, cell survival, and apoptosis. TRAF2 interacts with TNFR1, TNFR2, and CD40 to recruit signaling intermediates like RIPK1 and IKK, facilitating the activation of NF-κB-dependent transcription of pro-survival and pro-inflammatory genes. It plays a critical role in immune homeostasis and inflammation, particularly in T cells, B cells, and macrophages. TRAF2 also regulates apoptosis by inhibiting caspase-8 activation through recruitment of cIAP proteins. Dysregulation of TRAF2 is implicated in autoimmune diseases, chronic inflammatory conditions, and cancers, where excessive or impaired NF-κB signaling contributes to disease pathogenesis. Knockout studies reveal embryonic lethality, defective TNF-induced NF-κB activation, and increased apoptosis, highlighting its essential role in maintaining cell survival and immune responses.

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