Anti- Human BAFF
Description:
Background: Members in the TNF superfamily regulate immune responses and induce apoptosis. A novel member in the TNF family was recently identified by several groups and designated BAFF (for B cell Activating Factor belonging to the TNF Family), BLyS (for B Lymphocyte Stimulator), TALL-1 (for TNF- and ApoL-related Leukocyte-expressed Ligand), and THANK (for TNF Homologue that Activate Apoptosis, NF-kB and c-jun N-terminal Kinase).1-4 BAFF/BLyS was characterized as a B cell stimulator since it induced B cell proliferation and immunoglobulin secretion.1,2 Two receptors for BAFF were recently identified and designated TACI and BCMA.5 BAFF and its receptors are involved in the development of systemic lupus erythaematosus and other B cell associated autoimmune diseases.5,6 Like TNFa and TRAIL, THANK was shown to activate NF-kB and c-jun N-terminal kinase (JNK) and to induce apoptosis.4
Application:
ELISA 5-6 micrograms/ml
Sensitivity: 0.5 nonagrams/well with peroxidase- goat anti-mouse.
Immunogen:
Recombinant human BAFF
Species Reactivity:
Human others-not-tested.
Recommended Positive Control:
Human BAFF
Epitope:
Not determined.
Presentation:
0.25 mg in 0.5 mls of PBS containing 0.05% azide.
Antibody Form:
Purified
Specificity:
Reacts with human BAFF.
Storage:
2-8 C
Notes:
Background: Members in the TNF superfamily regulate immune responses and induce apoptosis. A novel member in the TNF family was recently identified by several groups and designated BAFF (for B cell Activating Factor belonging to the TNF Family), BLyS (for B Lymphocyte Stimulator), TALL-1 (for TNF- and ApoL-related Leukocyte-expressed Ligand), and THANK (for TNF Homologue that Activate Apoptosis, NF-kB and c-jun N-terminal Kinase).
1-4 BAFF/BLyS was characterized as a B cell stimulator since it induced B cell proliferation and immunoglobulin secretion.
1,2 Two receptors for BAFF were recently identified and designated TACI and BCMA.5 BAFF and its receptors are involved in the development of systemic lupus erythaematosus and other B cell associated autoimmune diseases.5,6 Like TNFa and TRAIL, THANK was shown to activate NF-kB and c-jun N-terminal kinase (JNK) and to induce apoptosis.4
References:
1. Moore, P. A. et al. (1999) Science 285:260
2. Schneider, P. et al. (1999) J. Exp. Med. 189:1747
3. Shu, H. B. et al. (1999) J. Leukoc. Biol. 65:680
4. Mukhopadhyay, A. et al. (1999) J. Biol. Chem. 274:15978
5. Gross, J. A. et al. (2000) Nature 404:995
6. Khare, S. D. et al. (2000) Proc. Natl. Acad. Sci. USA 97:3370