Anti-Mouse CD178 (FasL) - Purified In vivo GOLD Functional Grade

Antibody Details

Product Details

Reactivity Species

Mouse

Host Species

Armenian Hamster

Immunogen

B6 mouse FasL cDNA-transfected baby hamster kidney (B6 FasL/BHK) cells

Product Concentration

≥ 5.0 mg/ml

Endotoxin Level

≤ 1.0 EU/mg as determined by the LAL method

Purity

≥95% monomer by analytical SEC

⋅

> 95% by SDS Page

Formulation

This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added.

Product Preparation

Functional grade preclinical antibodies are manufactured in an animal free facility using only In vitro protein free cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.

Storage and Handling

Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at -80°C. Avoid Repeated Freeze Thaw Cycles.

Country of Origin

USA

Shipping

2-8°C

RRID

AB_2894121

Applications and Recommended Usage?
Quality Tested by Leinco

FC The suggested concentration for this CD178 antibody, clone MFL3, for staining cells in flow cytometry is ≤ 0.25 μg per 10⁶ cells in a volume of 100 μl. Titration of the reagent is recommended for optimal performance for each application.

Other Applications Reported In Literature ?

B
IF

Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Specificity

Clone MFL3 recognizes an epitope on mouse FasL.

Antigen Distribution

FasL is expressed on activated T cells, NK cells, the eye, and testis.

Background

FasL antibody, clone AFS98, recognizes Fas ligand (FasL), also known as CD178, Apo-1 ligand, and CD95 ligand. FasL is a 40 kDa type II integral membrane protein that belongs to the tumor necrosis factor (TNF) superfamily. FasL is expressed by activated T cells and natural killer (NK cells)^1-3. Binding of FasL to its receptor Fas (CD95, APO-1) induces apoptotic cell death in Fas-expressing target cells, contributing to anti-viral immunity. FasL also contributes to peripheral tolerance and the downregulation of immune responses through activation-induced autocrine and paracrine T cell death⁴. FasL is also found in the anterior chamber of the eye and on Sertoli cells in the testis, and is implicated in immune-privilege at these sites^{5, 6}. FasL also contributes to CD8 proliferation and neutrophil recruitment^{7, 8}. Soluble FasL (26 kDa) can be released following cleavage by metalloproteinases and block FasL-mediated signaling⁹. Fas/FasL-signaling is involved in the development of many human diseases, including autoimmunity and cancer10. Many human tumors over-express FasL, resulting in tumor infiltrating lymphocyte (TIL) apoptosis and immune evasion, which is associated with poor prognosis^11-14.

Antigen Details

Protein

CD178

Ligand/Receptor

Fas (CD95)

PubMed

CD178

NCBI Gene Bank ID

14103

Research Area

Apoptosis

.

Cell Biology

.

Cell Death

.

Immunology

.

Neuroscience

.

Tumor Suppressors

References & Citations

1. Okumura K., et al. (1994) Proc Natl Acad Sci USA. 91:4930–4934
2. Nagata S., et al. (1995) J Immunol. 154:3806–3813
3. Saito T., et al. (1995) J Exp Med. 181:1235–1238
4. Ferguson T A., et al. (1995) Science. 270:1189–1192
5. Duke R C., et al. (1995) Nature (London). 377:630–632
6. Fink PJ. (2000) J Immunol. 165(10):5537-43
7. Matsuzawa A., et al. (1998) J Immunol. 161: 4484–4488
8. Nagata S., et al. (1998) Nat Med. 4(1):31-6
9. Hueber AO., et al (2019) Cancers (Basel). 11(5):639
10. Kabelitz D., et al. (2000) Cancer Res. 60: 822–828
11. Giannarelli D., et al. (2000) Int J Cancer. 89: 127–132
12. Kanno H., et al. (2000) Br J Cancer. 82: 1446–1452.
13. Nagano H., et al. (Cancer) Br J Cancer. 82: 1211–1217

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