Rat LTBR / TNFRSF3 Protein (His Tag)

LTBR

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Catalog Number	P80178-R08H
Organism Species	Rat
Host	Human Cells
Synonyms	LTBR
Molecular Weight	The recombinant rat LTBR comprises 202 amino acids and predicts a molecular mass of 23 kDa. The apparent molecular mass of the ratLTBR is approximately 35 kDa in SDS-PAGE under reducing conditions due to glycosylation.
predicted N	Ser 28
SDS-PAGE
Purity	> 96 % as determined by SDS-PAGE
Protein Construction	A DNA sequence encoding the rat LTBR (NP_001008316.1) extracellular domain (Met 1-Ala 218) was expressed, fused with a polyhistidine tag at the C-terminus.
Bio-activity
Research Area	Immunology |Inflammation / Inflammatory Mediator |Inflammatory Cytokines & Chemoki and Receptors |TNF Superfamily |Processes Regulated by TNF Superfamily Members |Other Cell Type-specific Responses Regulated by TNF Superfamily Members |
Formulation	Lyophilized from sterile PBS, pH 7.4 1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background	LTBR (lymphotoxin beta receptor (TNFR superfamily, member 3)) is a member of the tumor necrosis factor (TNF) family of receptors. Tumor necrosis factor receptor is a trimeric cytokine receptor that binds tumor necrosis factors. The receptor cooperates with an adaptor protein (such as TRADD, TRAF, RIP), which is important in determining the outcome of the response. LTBR is expressed on the surface of most cell types, including cells of epithelial and myeloid lineages, but not on T and B lymphocytes. LTBR specifically binds the lymphotoxin membrane form (a complex of lymphotoxin-alpha and lymphtoxin-beta). LTBR and its ligand play a role in the development and organization of lymphoid tissue and tranformed cells. Activation of this protein can trigger apoptosis. Not only does the LTBR help trigger apoptosis, it can lead to the release of the cytokine interleukin 8. Overexpression of LTBR in HEK293 cells increases IL-8 promoter activity and leads to IL-8 release. It is also essential for development and organization of the secondary lymphoid organs and chemokine release.
Reference	Summers deLuca L, et al. (2011) A LTβR signaling in dendritic cells induces a type I IFN response that is required for optimal clonal expansion of CD8+ T cells. Proc Natl Acad Sci. 108(5):2046-51. Bista P, et al. (2010) TRAF3 controls activation of the canonical and alternative NFkappaB by the lymphotoxin beta receptor. J Biol Chem. 285(17):12971-8. Xu Y, et al. (2011) Adiponectin inhibits lymphotoxin-β receptor-mediated NF-κB signaling in human umbilical vein endothelial cells. Biochem Biophys Res Commun. 404(4):1060-4.