Tumor Necrosis Factor Ligand Superfamily Member 6 (FASLG) Antibody (FITC)

Este producto es parte de FASLG - Fas ligand
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169€ (20 µg)

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935106861
info@markelab.com
name
Tumor Necrosis Factor Ligand Superfamily Member 6 (FASLG) Antibody (FITC)
category
Primary Antibodies
provider
Abbexa
reference
abx107440

Description

Tumor necrosis factor ligand superfamily member 6 Antibody (FITC) is a Rabbit Polyclonal antibody against Tumor necrosis factor ligand superfamily member 6 conjugated to FITC.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
Tumor Necrosis Factor Ligand Superfamily Member 6 (FASLG)
Host
Rabbit
Reactivity
Human
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
FITC
Isotype
IgG
Purity
> 95%
Purification
Purified by Protein G.
Size 1
20 µg
Size 2
50 µg
Size 3
100 µg
Size 4
200 µg
Size 5
1 mg
Form
Liquid
Buffer
0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% Glycerol.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid exposure to light. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
P48023
Gene ID
356
NCBI Accession
NP_000630.1, NM_000639.2
OMIM
134638
Alias
Tumor necrosis factor ligand superfamily member 6,APTL,FASL,CD178,CD95L,ALPS1B,CD95-L,TNFSF6,TNLG1A,APT1LG1,Apoptosis antigen ligand,Fas antigen ligand
Background
Antibody anti-FASLG
Status
RUO

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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