Fas/TNFRSF6/CD95 Antibody - BSA Free

Tumor Necrosis Family Receptor (TNFR) superfamily member Fas, also known as CD95, APO-1, and TNFRSF6, is a 40-50 kDa type I transmembrane glycoprotein that is traditionally considered a death receptor but also functions in non-apoptotic signaling (1-4). The human Fas/TNFRSF6/CD95 protein is encoded by the FAS gene which contains 9 exons and is located on chromosome 10 (10q23.3-4) (1,2). The mature canonical Fas/TNFRSF6 protein isoform is 335 aa in length, which includes the signal sequence, and has a theoretical molecular weight of 37.7 kDa (1,5). The protein contains an extracellular domain (ECD) consisting of three calcium rich domains (CRDs), a transmembrane domain (TM), and an intracellular domain (ICD) comprised of a calcium-inducing domain (CID) and characteristic dead domain (DD) (1,2,5,6). The Fas protein is expressed on the plasma membrane of activated lymphocytes as a homotrimer formed via CRD1 interactions (1,2,3,6). The DD is crucial for apoptotic signaling which is triggered by the Fas receptor binding its ligand, Fas ligand (FasL) (1,2,6,7). Upon Fas-FasL interaction, the DD recruits an adapter protein Fas-associated DD (FADD) and procaspase-8, generating the death-inducing signaling complex (DISC) (1-4,6-8). Formation of DISC activates caspase-8 and leads to cleavage of caspase-3, initiating a caspase-signaling cascade and cell death (1-4,6-8).

Fas-FasL-mediated apoptosis is important in immune homeostasis and removal of autoreactive T cells, autoreactive B cells, cytotoxic natural killer (NK) cells, and more (1,2,7). Dysfunction and mutations in the Fas receptor and the Fas-FasL signaling axis is associated a loss of apoptotic signaling and removal of autoreactive cells, which correlates with several autoimmune diseases including systemic lupus erythematosus (SLE), autoimmune lymphoproliferative syndrome (ALPS), and multiple sclerosis (MS) (1-4,6,7). In addition to apoptosis and cell death signaling, FasL/TNFRSF6/CD95 mediates other pathways involved in proliferation, survival, and differentiation (3,4,6,8). More specifically, Fas has been shown to activate the NF-kappaB pathway, driving innate immunity which includes IL-1beta production and functioning in host defense (3,4,6,8). Fas is also involved in adaptive immunity playing a role in co-stimulation of CD4+ and CD8+ T cell activation as well as precocious differentiation of naive cells to effector memory T cells (3,4,6). Differentiation into effector memory T cells shows protection against autoimmunity but also limits antitumor response to a form of cancer immunotherapy called adoptive cell transfer (ACT) (3,4). The non-apoptotic roles of the Fas/TNFRSF6/CD95 receptor highlight its potential as a target for both treating autoimmune diseases and in cancer immunotherapy (3,4).

References

1. Singh R, Pradhan V, Patwardhan M, Ghosh K. APO-1/Fas gene: Structural and functional characteristics in systemic lupus erythematosus and other autoimmune diseases. Indian J Hum Genet. 2009;15(3):98-102. https://doi.org/10.4103/0971-6866.60184

2. Magerus A, Bercher-Brayer C, Rieux-Laucat F. The genetic landscape of the FAS pathway deficiencies. Biomed J. 2021;44(4):388-399. https://doi.org/1010.1016/j.bj.2021.06.005

3. Guegan JP, Legembre P. Nonapoptotic functions of Fas/CD95 in the immune response. FEBS J. 2018;285(5):809-827. https://doi.org/10.1111/febs.14292

4. Yi F, Frazzette N, Cruz AC, Klebanoff CA, Siegel RM. Beyond Cell Death: New Functions for TNF Family Cytokines in Autoimmunity and Tumor Immunotherapy. Trends Mol Med. 2018;24(7):642-653. https://doi.org/10.1016/j.molmed.2018.05.004

5. Uniprot (P25445)

6. Guegan JP, Ginestier C, Charafe-Jauffret E, et al. CD95/Fas and metastatic disease: What does not kill you makes you stronger. Semin Cancer Biol. 2020;60:121-131. https://doi.org/10.1016/j.semcancer.2019.06.004

7. Volpe E, Sambucci M, Battistini L, Borsellino G. Fas-Fas Ligand: Checkpoint of T Cell Functions in Multiple Sclerosis. Front Immunol. 2016;7:382. Published 2016 Sep 27. https://doi.org/10.3389/fimmu.2016.00382

8. Cullen SP, Martin SJ. Fas and TRAIL 'death receptors' as initiators of inflammation: Implications for cancer. Semin Cell Dev Biol. 2015;39:26-34. https://doi.org/10.1016/j.semcdb.2015.01.012

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

We have publications tested in 3 confirmed species: Human, Mouse, Rat.

We have publications tested in 3 applications: ICC/IF, IF/IHC, WB.

Showing Publications 1 - 4 of 4.

Publications using NB120-13550	Applications	Species
Yang Y, Wang Y, Zhang J et al. Dietary methionine restriction reduces hepatic steatosis and oxidative stress in high-fat-fed mice by promoting H2S production. Food Funct. 2018-11-17 [PMID: 30534793] (WB, Mouse)	WB	Mouse
Vodret S, Bortolussi G, Jasprova J et al. Inflammatory signature of cerebellar neurodegeneration during neonatal hyperbilirubinemia in Ugt1 (-/-) mouse model. J Neuroinflammation. 2017-03-24 [PMID: 28340583] (ICC/IF, Mouse)	ICC/IF	Mouse
Topcu-Tarladacalisir Y, Sapmaz-Metin M, Karaca T. Curcumin counteracts cisplatin-induced nephrotoxicity by preventing renal tubular cell apoptosis. Ren Fail 2016-10-19 [PMID: 27758164] (IF/IHC, Rat)	IF/IHC	Rat
Chen YL, Yan MY, Chien SY et al. Sann-Joong-Kuey-Jian-Tang inhibits hepatocellular carcinoma Hep-G2 cell proliferation by increasing TNF-alpha, Caspase-8, Caspase- 3 and Bax but by decreasing TCTP and Mcl-1 expression in vitro. Mol Med Rep 2013-05-01 [PMID: 23525225] (Human)		Human

Images	Ratings	Applications	Species	Date	Details
Enlarge	5 reviewed by: Ranveer Singh	WB	Mouse	07/24/2014	View Summary Application Western Blot Sample Tested Lysate from testis of six week old mouse Species Mouse

Array NB120-13550

• Fas/TNFRSF6/CD95 Antibodies
• Fas/TNFRSF6/CD95 Antibody Pair
• Fas/TNFRSF6/CD95 ELISA Kits
• Fas/TNFRSF6/CD95 Lysates
• Fas/TNFRSF6/CD95 Proteins
• Fas/TNFRSF6/CD95 Proteins and Enzymes
• Fas/TNFRSF6/CD95 ELISA