• PN: B115609

COMPONENTS

1x Ab-conjugated beads (S4P6 - Human TWEAK Ab-bead). PN: B115609A. One vial containing 100 µL of anti-human TWEAK conjugated to AimPlex Bead S4P6.

2x Biotin-detection Ab (Human TWEAK Biotin-dAb). PN: B115609B. One vial containing    100 µL of biotinylated anti-Human TWEAK.

Lyophilized Standard Mix - Human TWEAK. PN: B115609S. One vial containing lyophilized TWEAK.

STORAGE:  2-8 C in the dark.

IMPORTANT: Sodium azide forms explosive compounds with heavy metals. These products contain <0.05% (w/w) azide which with repeated contact with lead and copper commonly found in plumbing drains may result in the buildup of shock sensitive compounds. Dispose in accordance with regulations from your institute.

APPLICATION: Optimal antibody pair and antigen standard for assaying human TWEAK/TNFSF12/Apo3 Ligand. To be used in conjunction with the AimPlex NR Basic Kit (PN: P100001) and a diluent kit. Refer to the AimPlex Multiplex Immunoassay User Manual and kit inserts for the assay procedure.

For Research Use Only.  Not for use in diagnostic procedures.

Assay Specifications:

Sample types: Cell culture supernatant, serum, plasma, bodily fluid and tissue/cell lysate

Sensitivity (LOD): < 20 pg/mL

Quantitation range:

LLOQ: <40 pg/mL

ULOQ: > 5,000 pg/mL

Standard dose recovery: 70-130%

Intra-assay CV: < 10%

Inter-assay CV: < 20%

Sample volume: 15 µL/test

Description:

Tumor necrosis factor ligand superfamily member 12 also known as TNF-related weak inducer of apoptosis (TWEAK) can induce apoptosis via multiple pathways of cell death in a cell type-specific manner. Leukocytes are the main source of TWEAK including human resting and activated monocytes, dendritic cells and natural killer cells. This cytokine is also found to promote proliferation and migration of endothelial cells, and thus acts as a regulator of angiogenesis. Excessive activation of the TWEAK pathway in chronic injury has been described to promote pathological tissue changes including chronic inflammation, fibrosis and angiogenesis. In chronic liver disease for example TWEAK expression is enhanced and causes hepatic stellate cells, which are key regulators of liver fibrosis, to proliferate. Diseases associated with TWEAK include Common Variable Immunodeficiency.

References:

1.       Chicheportiche Y, Bourdon PR, Xu H, Hsu YM, Scott H, Hession C, Garcia I, Browning JL (December 1997). "TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis". The Journal of Biological Chemistry. 272 (51): 32401–10. doi:10.1074/jbc.272.51.32401. PMID 9405449.

2.       Marsters SA, Sheridan JP, Pitti RM, Brush J, Goddard A, Ashkenazi A (April 1998). "Identification of a ligand for the death-domain-containing receptor Apo3". Current Biology. 8 (9): 525–8. doi:10.1016/S0960-9822(98)70204-0. PMID 9560343.

3.       Maecker H, Varfolomeev E, Kischkel F, Lawrence D, LeBlanc H, Lee W, Hurst S, Danilenko D, Li J, Filvaroff E, Yang B, Daniel D, Ashkenazi A (December 2005). "TWEAK attenuates the transition from innate to adaptive immunity". Cell. 123 (5): 931–44. doi:10.1016/j.cell.2005.09.022. PMID 16325585.

4.       Burkly LC (June 2014). "TWEAK/Fn14 axis: the current paradigm of tissue injury-inducible function in the midst of complexities". Seminars in Immunology. The TNF family - challenges ahead. 26 (3): 229–36. doi:10.1016/j.smim.2014.02.006. PMID 24636536.