Tumor Necrosis Factor Ligand Superfamily Member 6 (CD178) Antibody

Este producto es parte de FASLG - Fas ligand
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299€ (0.1 mg)

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935106861
info@markelab.com
name
Tumor Necrosis Factor Ligand Superfamily Member 6 (CD178) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx139054
tested applications
IHC, IF/ICC, FCM, IP, FUNC

Description

CD178 Antibody is a Mouse Monoclonal against CD178.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
Tumor Necrosis Factor Ligand Superfamily Member 6 (CD178)
Host
Mouse
Reactivity
Human
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Clonality
Monoclonal
Conjugation
Unconjugated
Isotype
IgG1
Clone ID
U373
Purity
> 95% (SDS-PAGE)
Purification
Purified by Protein A affinity chromatography.
Size 1
0.1 mg
Tested Applications
IHC, IF/ICC, FCM, IP, FUNC
Buffer
LE/AF PBS solution, 0.2 µm filter sterilized.
Availability
Shipped within 5-12 working days.
Storage
Store at 2-8°C. Do not freeze.
Dry Ice
No
UniProt ID
P48023
Gene ID
356
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
Note
Concentration: 1 mg/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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