|Application ||WB, E|
|Other Accession||NP_060617, 8922536|
|Calculated MW||20215 Da|
|Application Notes||FAIM antibody can be used for detection of FAIM by Western blot at 5 - 10 µg/mL.|
|Other Names||FAIM Antibody: FAIM1, FAIM1, Fas apoptotic inhibitory molecule 1, Fas apoptotic inhibitory molecule|
|Reconstitution & Storage||FAIM antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||FAIM Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Plays a role as an inducible effector molecule that mediates Fas resistance produced by surface Ig engagement in B cells.|
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Provided below are standard protocols that you may find useful for product applications.
FAIM Antibody: The susceptibility of primary splenic B cells to Fas-mediated apoptosis is regulated in a receptor-specific fashion. Terminal effectors of B cell Fas-resistance include the known anti-apoptotic proteins Bcl-xL, FLIP, and a recently identified protein termed FAIM. This molecule is broadly expressed in various tissues and exists in at least three isoforms. It is thought that resistance to Fas killing via increased expression of FAIM protects foreign antigen-specific B cells during interactions with FasL-bearing T cells whereas autoreactive B cells are deleted via Fas-dependent cytotoxicity. More recent results have indicated that FAIM interacts with both Trk and p75 neurotrophin receptor and may play a role in promoting neurite outgrowth in different neuronal systems by a mechanism involving the activation of NF-κB and the Ras-ERK pathway.
Rothstein TL. Inducible resistance to Fas-mediated apoptosis in B cells. Cell Res. 2000; 10:245-66.
Schneider TJ, Fischer GM, Donohoe TJ, et al. A novel gene coding for a Fas apoptosis inhibitory molecule (FAIM) isolated from inducibly Fas-resistant B lymphocytes. J. Exp. Med. 1999; 189:949-55.
Sole C, Dolcet X, Segura MF, et al. The death receptor antagonist FAIM promotes neurite outgrowth by a mechanism that depends on ERK and NF-kappa B signaling. J. Cell Biol. 2004; 167:479-92.
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