Human Factor Related Apoptosis Ligand / TNFSF6 (FASLG) CLIA Kit

Product specifications

CLIA Kits

Factor Related Apoptosis Ligand / TNFSF6 (FASLG)

Human

Chemiluminescent

Quantitative

Sandwich

15.6 pg/ml - 1000 pg/ml

9.38 pg/ml

Optimal dilutions/concentrations should be determined by the end user.

96 tests

Lyophilized

CLIA

Serum, plasma and other biological fluids.

Shipped within 5-12 working days.

 Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual.

No

Tumor necrosis factor ligand superfamily member 6,APTL,FASL,CD178,CD95L,ALPS1B,CD95-L,TNFSF6,TNLG1A,APT1LG1,Apoptosis antigen ligand,Fas antigen ligand

CLIA Kits FASLG

RUO

The validity for this kit is 6 months.   This product is for research use only.   The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments.   Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein.

Descripción

Fas Ligand (FASLG), also referred to as CD95L, is a type-II transmembrane protein belonging to the tumor necrosis factor (TNF) family. FASLG plays a pivotal role in regulating apoptosis, particularly in immune system homeostasis and cytotoxic T-cell-mediated killing. It binds to its receptor, Fas (CD95), triggering the formation of the death-inducing signaling complex (DISC) and initiating the caspase cascade, ultimately leading to programmed cell death. This pathway is crucial for eliminating autoreactive lymphocytes, maintaining immune tolerance, and resolving immune responses after infections. Dysregulation of FASLG-Fas signaling has been implicated in various pathological conditions, including autoimmune disorders, cancer, and chronic inflammatory diseases. In cancer, tumor cells often evade apoptosis by downregulating Fas or mutating components of the pathway. Conversely, overexpression of FASLG in the tumor microenvironment can contribute to immune evasion by inducing apoptosis in Fas-expressing tumor-infiltrating lymphocytes. Therapeutic strategies targeting FASLG or its signaling pathway are being explored for their potential in cancer immunotherapy, autoimmune disease modulation, and transplantation tolerance. Additionally, genetic polymorphisms in the FASLG gene have been associated with altered susceptibility to diseases, further highlighting its importance in immune regulation and disease pathology.

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