Human Fas Ligand / TNFSF6 Protein, His Tag, active trimer (MALS verified)
Proteins and Peptides
- 貨號 Cat. No.
- FAL-H5241
- 規格 Size
- 50ug
- 品牌 Brand
- ACROBiosystems
- Species
- Human
- Conjugate
- Unconjugated
- Expression System
- HEK293
- Tag
- His Tag
Description
Source :
Human Fas Ligand, His Tag, active trimer (FAL-H5241) is expressed from human 293 cells (HEK293). It contains AA Pro 134 - Leu 281 (Accession # AAH17502.1).
Molecule : Fas Ligand
Synonyms : FASLG,ALPS1B,APT1LG1,CD178,CD95L,FASL,TNFSF6
Format : Powder
Category : Bio-Markers & CD Antigens
Accession : AAH17502.1
Storage : -20℃
Shipping condition : Powder,RT
Molecular Weight : 17.7 kDa
Characteristics :
This protein carries a polyhistidine tag at the N-terminus. The protein has a calculated MW of 17.7 kDa. The protein migrates as 25-30 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Endotoxin Level : Less than 1.0 EU per μg by the LAL method.
Buffer : PBS, pH7.4
Description :
Fas ligand is also known as FasL, CD178, CD95L, or TNFSF6, is a homotrimeric type-II transmembrane protein that belongs to the tumor necrosis factor (TNF) family. Its binding with its receptor induces apoptosis. Fas ligand/receptor interactions play an important role in the regulation of the immune system and the progression of cancer. Mature human Fas Ligand consists of a 179 amino acid (aa) extracellular domain (ECD), a 22 aa transmembrane segment, and a 80 aa cytoplasmic domain. Within the ECD, human Fas Ligand shares 81% and 78% aa sequence identity with mouse and rat Fas Ligand, respectively. Apoptosis triggered by Fas-Fas ligand binding plays a fundamental role in the regulation of the immune system. Its functions include:T-cell homeostasis, cytotoxic T-cell activity, immune privilege, maternal tolerance, tumor counterattack. Defective Fas-mediated apoptosis may lead to oncogenesis as well as drug resistance in existing tumors. Germline mutation of Fas is associated with autoimmune lymphoproliferative syndrome (ALPS), a childhood disorder of apoptosis.
References :
(1) Sheikh MS, Fornace AJ., 2000, Leukemia 14 (8): 1509–1513.
(2) Andersen MH, et al., 2006, J. Invest. Dermatol. 126 (1): 32–41.
(3) Igney FH, Krammer PH., 2005, Cancer Immunol. Immunother. 54 (11): 1127–1136.

