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FAS (Fc-Fusion)

FAS (Fc-Fusion)

$ 415.00

Fas is a cell surface receptor that transduces apoptotic signals critical for the immune homeostasis and tolerance. The full length membrane anchored form of Fas contains a three CRD (cysteine-rich-domain) repeats that is characteristics of TNF receptor superfamily.

Interacting protein(s): FASL
Related products: TNF-Receptor Superfamily

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Quick Specs

Species: Human
Catalog no.: P7061F
Synonym: TNFRSF6, CD95, APT1, FAS1, Apo-1
Tag: mouse IgG2a-Fc
GenBank accession: NM_000034.1
SwissPro accession: P25445
Construction: h.Fas (A25-G169)-m-IgG-Fc
Expression host: 293T
MW (calculated): 43,386 daltons
MW (SDS-PAGE): 45 Kd
Abs 0.1% (= 1 mg/ml): 0.816
Purity: 95 %

Description

Fas is a cell surface receptor that transduces apoptotic signals critical for the immune homeostasis and tolerance. The full length membrane anchored form of Fas contains a three CRD (cysteine-rich-domain) repeats that is characteristics of TNF receptor superfamily.

The intracellular domain of Fas contains a death domain that interacts with FADD which, in turn, recruits caspase-8 to form death-inducing signaling complex (DISC) and initiate the cascade leading to apoptosis. Patients with heterozygous germ line mutations of Fas make both the wildtype and mutant proteins.

The mutated Fas is capable of associating with its wildtype counterpart via the N-terminal PLAD (pre-ligand-assembly domain) that renders the latter unable to transduce signals triggered by Fas ligand. This dominant decoy effect of the mutant Fas leads to a severe immune disorder, called autoimmune lymphoproliferative syndrome (ALPS) in human.

Amino Acid Sequence.

References

1. The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis. Itoh N., Yonehara S., Ishii A., Yonehara M., Mizushima S., Sameshima M., Hase A., Seto Y., Nagata S. Cell 66:233-243 (1991)

2. Fas/Apo-1 (CD95) receptor lacking the intracytoplasmic signaling domain protects tumor cells from Fas-mediated apoptosis. Cascino I., Papoff G., De Maria R., Testi R., Ruberti G. J. Immunol. 156:13-17 (1996)

3. The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations. Vaishnaw A.K., Orlinick J.R., Chu J.-L., Krammer P.H., Chao M.V., Elkon K.B. J. Clin. Invest. 103:355-363 (1999)

4. Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations. Siegel RM, Frederiksen JK, Zacharias DA, Chan FK, Johnson M, Lynch D, Tsien RY, Lenardo MJ. Science 288:2354-7 (2000)


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