Human Tumor Necrosis Factor Ligand Superfamily Member 6 (FASLG) Protein

Product specifications

Proteins and Peptides

Tumor Necrosis Factor Ligand Superfamily Member 6 (FASLG)

E. coli

Activity: Not tested
Sequence Fragment: Gln103-Leu281
Tag: N-terminal His tag and GST tag

Human

Unconjugated

Calculated MW: 52.4 kDa

Recombinant

> 95%

10 µg

50 µg

100 µg

200 µg

500 µg

Lyophilized

WB, SDS-PAGE

Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 1 mM DTT, 5% Trehalose and Proclin-300.

Shipped within 5-7 working days.

Store lyophilized form at 2-8°C for up to 1 month. For longer periods, store lyophilized or liquid at -80°C. Avoid repeated freeze–thaw cycles.

No

P48023

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

Protein FASLG

RUO

THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION.
To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex.
Concentration: Prior to lyophilization: 200 µg/ml

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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