anti-LTβR (mouse), mAb (3C8)
370 CHF CHF 370.00
AG-20B-0041-C100100 µgCHF 370.00
|Synonyms||Lymphotoxin-β Receptor; Tumor Necrosis Factor Receptor 2 Related Protein; Tumor Necrosis Factor C Receptor; Tumor Necrosis Factor Receptor Superfamily Member 3; TNFRSF3|
|Product Type||Monoclonal Antibody|
|Source/Host||Purified from concentrated hybridoma tissue culture supernatant.|
|Immunogen/Antigen||Recombinant mouse LTβR (cysteine-rich region/aa 31-221).|
|Application||Functional Application: Agonist inducing BAFF, chemokines and integrins in vitro and in vivo.|
|Specificity||Recognizes mouse LTβR.|
|Formulation||Liquid. In PBS containing 10% glycerol and 0.02% sodium azide.|
|Other Product Data||The monoclonal antibody to mouse LTβR is an agonist that can be used for the investigation of the regulation of BAFF (BlyS), chemokines and integrins using in vivo and tissue culture models, the development of NK cells and NK T cells, to study the regulation of NF-κB family of transcription factors in regulation of inflammation and homeostasis, particularly RelB NF-κB2 pathway. For use as an agonist the MAb to LTβR is added to cell cultures at 2μg/ml. For in vivo use, mice are injected intraperitoneally with 50μg of agonistic MAb to LTβR in sterile phosphate saline buffer.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
After opening, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
|Use/Stability||Stable for at least 1 year after receipt when stored at -20°C.|
|Product Specification Sheet|
The LTβR activates two different NF-κB pathways that lead to distinct patterns of gene induction, including selected chemokines and the cytokine BAFF, which is essential for the survival of mature B lymphocytes. LTβR activates the classical NF-κB (relA/p50) pathway, like the type 1 TNF receptor (TNFR1), that regulates proinflammatory genes, like the chemokine MIP1β. However, LTβR, unlike TNFR1, also activates the processing of p100 to form RelB/p52 complexes, which activate genes involved in lymphoid organ formation and lymphocyte survival.
- A lymphotoxin-IFN-beta axis essential for lymphocyte survival revealed during cytomegalovirus infection: T.A. Banks, et al.; J. Immunol. 174, 7217 (2005)
- Specific Remodeling of Splenic Architecture by Cytomegalovirus: C.A. Benedict et al.; PLoS Pathog. 2, e16 (2006)
- LTβR Signaling Induces Cytokine Expression and Up-Regulates Lymphangiogenic Factors in Lymph Node Anlagen: M.F. Vondenhoff, et al.; J. Immunol. 182, 5439 (2009)