Description
A20 was originally identified as a zinc finger protein, containing multiple Cys2/Cys2 finger motifs, induced by tumor necrosis factor alpha (TNFα). Further research has shown that A20 can negatively regulate NF-κB gene expression. NF-κB is an ubiquitously expressed transcription factor that regulates many genes involved in activation of inflammatory and cytokine responses. TNFα induces the activation of NF-κB by first recruiting a number of proteins to the TNF receptor. RIP and TRADD are two effector proteins which bind to the intracellular portion of the TNF receptor and form a multiprotein complex. Additional proteins, such as TRAF2 can interact with members of this complex. Although the exact mechanism of A20 regulation is unknown, it is believed that A20 interferes with either a TNF-induced RIP or TRAF2 mediated signaling pathway to block NF-κB expression.A20 mRNA is highly expressed in lymphoid tissues. A20 migrates in SDS/PAGE at ~80 kDa, which is equivalent to the predicted molecular weight. The antibody recognizes human A20. A fusion protein corresponding to the full length of human A20 was used as the immunogen.
Format
- FormatPurified
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Preparation and Storage
The monoclonal antibody was purified from tissue culture supernatant or ascites by affinity chromatography.Store undiluted at 4°C.
Product Notices
- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- Please refer to www.bdbiosciences.com/pharmingen/protocols for technical protocols.
- Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
Western blot: Please refer to http://www.bdbiosciences.com/pharmingen/protocols/Western_Blotting.shtml .
