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Hamster Anti-FASLG Recombinant Antibody (MFL3) (CBMAB-C11553-LY)

The product is antibody recognizes FASLG. The antibody MFL3 immunoassay techniques such as: FC.
See all FASLG antibodies
Published Data
Fig.1 Proportion of lymphocyte subset and percentage of FasL+ cells in liver MNCs.
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Fig.2 Expression of FasL was analyzed on electronically gated NK1.1.
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Fig.3 The effect of T-lineage cell HIF-2α inactivation on renal IRI.
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Summary

Host Animal
Hamster
Specificity
Mouse
Clone
MFL3
Antibody Isotype
IgG
Application
FC

Basic Information

Specificity
Mouse
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
0.1% gelatin
Preservative
0.09% sodium azide
Concentration
0.5 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Fas Ligand
Introduction
This gene is a member of the tumor necrosis factor superfamily. The primary function of the encoded transmembrane protein is the induction of apoptosis triggered by binding to FAS. The FAS/FASLG signaling pathway is essential for immune system regulation, including activation-induced cell death (AICD) of T cells and cytotoxic T lymphocyte induced cell death. It has also been implicated in the progression of several cancers. Defects in this gene may be related to some cases of systemic lupus erythematosus (SLE). Alternatively spliced transcript variants have been described. [provided by RefSeq, Nov 2014]
Entrez Gene ID
14103
UniProt ID
P41047
Research Area
Cytokine that binds to TNFRSF6/FAS, a receptor that transduces the apoptotic signal into cells (PubMed:26334989, PubMed:9228058).

Involved in cytotoxic T-cell-mediated apoptosis, natural killer cell-mediated apoptosis and in T-cell development (PubMed:9228058, PubMed:7528780, PubMed:9427603).

Initiates fratricidal/suicidal activation-induced cell death (AICD) in antigen-activated T-cells contributing to the termination of immune responses (By similarity).

TNFRSF6/FAS-mediated apoptosis has also a role in the induction of peripheral tolerance (By similarity).

Binds to TNFRSF6B/DcR3, a decoy receptor that blocks apoptosis (PubMed:27806260).

Tumor necrosis factor ligand superfamily member 6, soluble form:
Induces FAS-mediated activation of NF-kappa-B, initiating non-apoptotic signaling pathways (By similarity).

Can induce apoptosis but does not appear to be essential for this process (PubMed:27806260).

FasL intracellular domain:
Cytoplasmic form induces gene transcription inhibition.
Biological Process
Activation of cysteine-type endopeptidase activity involved in apoptotic process Source: BHF-UCL
Apoptotic process Source: ProtInc
Apoptotic signaling pathway Source: BHF-UCL
Cell-cell signaling Source: ProtInc
Cellular chloride ion homeostasis Source: Ensembl
Cellular response to interferon-gamma Source: Ensembl
Endosomal lumen acidification Source: Ensembl
Extrinsic apoptotic signaling pathway Source: UniProtKB
Extrinsic apoptotic signaling pathway via death domain receptors Source: BHF-UCL
Inflammatory cell apoptotic process Source: Ensembl
Necroptotic process Source: BHF-UCL
Necroptotic signaling pathway Source: BHF-UCL
Negative regulation of angiogenesis Source: BHF-UCL
Negative regulation of transcription by RNA polymerase II Source: UniProtKB
Positive regulation of apoptotic process Source: UniProtKB
Positive regulation of cell population proliferation Source: Ensembl
Positive regulation of endothelial cell apoptotic process Source: BHF-UCL
Positive regulation of epidermal growth factor receptor signaling pathway Source: Ensembl
Positive regulation of I-kappaB kinase/NF-kappaB signaling Source: UniProtKB
Positive regulation of neuron apoptotic process Source: Ensembl
Positive regulation of phosphatidylserine exposure on apoptotic cell surface Source: UniProtKB
Release of sequestered calcium ion into cytosol by endoplasmic reticulum Source: MGI
Response to growth factor Source: Ensembl
Response to lipopolysaccharide Source: Ensembl
Retinal cell programmed cell death Source: Ensembl
Signal transduction Source: ProtInc
T cell apoptotic process Source: UniProtKB
Cellular Location
Lysosome lumen; Cell membrane; Cytoplasmic vesicle lumen. Is internalized into multivesicular bodies of secretory lysosomes after phosphorylation by FGR and monoubiquitination (PubMed:17164290). Colocalizes with the SPPL2A protease at the cell membrane (PubMed:17557115).
Tumor necrosis factor ligand superfamily member 6, soluble form: Secreted. May be released into the extracellular fluid by cleavage from the cell surface.
FasL intracellular domain: Nucleus. The FasL ICD cytoplasmic form is translocated into the nucleus.
Involvement in disease
Autoimmune lymphoproliferative syndrome 1B (ALPS1B):
A disorder of apoptosis that manifests in early childhood and results in the accumulation of autoreactive lymphocytes. It is characterized by non-malignant lymphadenopathy with hepatosplenomegaly, and autoimmune hemolytic anemia, thrombocytopenia and neutropenia.
Topology
Cytoplasmic: 1-80
Helical: 81-102
Extracellular: 103-281
PTM
The soluble form derives from the membrane form by proteolytic processing. The membrane-bound form undergoes two successive intramembrane proteolytic cleavages. The first one is processed by ADAM10 producing an N-terminal fragment, which lacks the receptor-binding extracellular domain. This ADAM10-processed FasL (FasL APL) remnant form is still membrane anchored and further processed by SPPL2A that liberates the FasL intracellular domain (FasL ICD). FasL shedding by ADAM10 is a prerequisite for subsequent intramembrane cleavage by SPPL2A in T-cells.
N-glycosylated (PubMed:9228058). Glycosylation enhances apoptotic activity (PubMed:27806260).
Phosphorylated by FGR on tyrosine residues; this is required for ubiquitination and subsequent internalization.
Monoubiquitinated.

Wang, G., Duan, P., Liu, F., & Wei, Z. (2021). Long non-coding RNA CASC7 suppresses malignant behaviors of breast cancer by regulating miR-21-5p/FASLG axis. Bioengineered, 12(2), 11555-11566.

Ji, W., Xin, Y., Zhang, L., & Liu, X. (2020). ALG2 Influences T cell apoptosis by regulating FASLG intracellular transportation. Biochemical Journal, 477(16), 3105-3121.

Zou, L., Ma, X., Wu, B., Chen, Y., Xie, D., & Peng, C. (2020). Protective effect of bone marrow mesenchymal stem cell-derived exosomes on cardiomyoblast hypoxia-reperfusion injury through the miR-149/let-7c/Faslg axis. Free Radical Research, 54(10), 722-731.

Pang, T., Du, L., Li, F., Liu, Y., Ma, X., Cao, Q., ... & Yang, P. (2020). Association of apoptosis genes in PDCD1 but not PDCD1LG2, FAS, and FASLG with pediatric idiopathic uveitis in Han Chinese. Pediatric Research, 87(4), 634-638.

de Almeida Chuffa, L. G., dos Santos Souza, J., de Mello, M. C., de Oliveira Neto, M., & Carvalho, R. F. (2020). The aging whole blood transcriptome reveals a potential role of FASLG in COVID-19. bioRxiv.

Tang, M., Pan, H., Zheng, Z., Guo, Y., Peng, J., Yang, J., ... & Zhou, Y. (2019). Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis. Bioscience reports, 39(12).

Du, X., Hong, L., Sun, L., Sang, H., Qian, A., Li, W., ... & Li, X. (2019). miR-21 induces endothelial progenitor cells proliferation and angiogenesis via targeting FASLG and is a potential prognostic marker in deep venous thrombosis. Journal of translational medicine, 17(1), 1-13.

Chen, S., Yang, C., Sun, C., Sun, Y., Yang, Z., Cheng, S., & Zhuge, B. (2019). miR-21-5p suppressed the sensitivity of hepatocellular carcinoma cells to cisplatin by targeting FASLG. DNA and cell biology, 38(8), 865-873.

Li, Y., Sun, Y., Cai, M., Zhang, H., Gao, N., Huang, H., ... & Yao, D. (2018). Fas Ligand Gene (Faslg) plays an important role in nerve degeneration and regeneration after rat sciatic nerve injury. Frontiers in Molecular Neuroscience, 11, 210.

Blaes, J., Thomé, C. M., Pfenning, P. N., Rübmann, P., Sahm, F., Wick, A., ... & Lemke, D. (2018). Inhibition of CD95/CD95L (FAS/FASLG) Signaling with APG101 Prevents Invasion and Enhances Radiation Therapy for GlioblastomaInhibition of CD95/CD95L Signaling by APG101. Molecular Cancer Research, 16(5), 767-776.

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For research use only. Not intended for any clinical use.

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