The following FAS reagents supplied by CUSABIO are manufactured under a strict quality control system. Multiple applications have been validated and solid technical support is offered.

FAS Antibodies

FAS Antibodies for Homo sapiens (Human)

FAS Proteins

FAS Proteins for Homo sapiens (Human)

FAS Proteins for Rattus norvegicus (Rat)

FAS Proteins for Macaca nemestrina (Pig-tailed macaque)

FAS Proteins for Macaca mulatta (Rhesus macaque)

FAS Proteins for Cercocebus atys (Sooty mangabey) (Cercocebus torquatus atys)

FAS Proteins for Macaca fascicularis (Crab-eating macaque) (Cynomolgus monkey)

FAS Proteins for Bos taurus (Bovine)

FAS Proteins for Mus musculus (Mouse)

FAS Proteins for Sus scrofa (Pig)


FAS ELISA Kit for Homo sapiens (Human)

FAS ELISA Kit for Rattus norvegicus (Rat)

FAS ELISA Kit for Mus musculus (Mouse)

FAS Background

FAS, also known as CD95/Apo-1/TNFRSF6, is a type I transmembrane (TM) protein on the cell surface, and a death receptor that belongs to the TNF-receptor superfamily [1]. Fas contains an N-terminal ligand-binding extracellular domain (ECD), a TM domain, and a C-terminal cytoplasmic death domain (DD) [1]. Expressed at the cell surface as a homotrimer, the FAS receptor implements both apoptotic and non-apoptotic signaling pathways. The ligation of FAS with FAS ligand (FASL) leads to the activation of a caspase cascade that initiates apoptosis [2][3][4]. FAS triggers apoptosis through FADD-mediated recruitment and activation of caspase-8 [5]. Fas–FasL-induced apoptosis is an important mechanism for the maintenance of immune homeostasis &peripheral tolerance, and the surveillance of tumor [6]. Its non-apoptotic cues seem to promote oncogenesis [7]. FAS/CD95 engagement also induces non-apoptotic signaling pathways promoting cell motility, invasiveness [8], inflammation, and organ regeneration. A large fraction of human ALPS (autoimmune lymphoproliferative syndrome) patients have heterozygous inherited mutations in the FAS gene [9]. ALPS is an inherited disorder in which the body cannot properly regulate the number of immune system cells (lymphocytes). In consideration of the multiple roles of Fas–FasL in immune responses and diseases, therapeutic targets of the Fas/FasL pathway might not protect against a specific disease rather than influencing the patient's prognosis.

[1] Wu H, Hymowitz SG. Structure and function of tumor necrosis factor (TNF) at the cell surface. In: Bradshaw RA, Dennis EA, editors. Handbook of cell signaling [J]. Oxford: Academic Press; 2009. pp. 265–275.
[2] Nagata S, Golstein P. The Fas death factor [J]. Science (1995) 267(5203):1449–56.
[3] Chinnaiyan AM, O’Rourke K, et al. FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis [J]. Cell (1995) 81:505–12.
[4] Kischkel FC, Hellbardt S, et al. Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signaling complex (DISC) with the receptor [J]. EMBO J (1995) 14:5579–88.
[5] Nagata S. Apoptosis by death factor [J]. Cell (1997) 88(3):355–65.
[6] Strasser A, Jost PJ, et al. The many roles of FAS receptor signaling in the immune system [J]. Immunity. 2009 Feb 20;30(2):180-92.
[7] Le Gallo M, Poissonnier A, et al. CD95/Fas, Non-Apoptotic Signaling Pathways, and Kinases [J]. Front Immunol. 2017 Sep 27; 8:1216.
[8] Nijkamp MW, Hoogwater FJ, et al. CD95 is a key mediator of invasion and accelerated outgrowth of mouse colorectal liver metastases following radiofrequency ablation [J]. J Hepatol. 2010 Dec;53(6):1069-77.
[9] Dowdell KC, Niemela JE, et al. Somatic FAS mutations are common in patients with genetically undefined autoimmune lymphoproliferative syndrome [J]. Blood. 2010 Jun 24;115(25):5164-9.

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