TNFSF3/Lymphotoxin Beta Protein, Cynomolgus (sf9, His)

LT is expressed by T, B, natural killer (NK)- and lymphoid tissue-inducer cells. While, Lymphotoxin Beta is expressed on inflammatory cells, LPCs, and occasional small hepatocytes adjacent to fibrous septa^[1][2].
The amino acid sequence of human Lymphotoxin Beta protein has low homology to mouse Lymphotoxin Beta protein. While human Lymphotoxin Beta shares 96.72% aa sequence identity with Rhesus macaque Lymphotoxin Beta protein.
Lymphotoxin-β (LTβ) is exclusively anchored in the membrane as a type II transmembrane protein, binding LTα to form membrane-anchored heterotrimers (LTα1β2 and LTα2β1). LTα1β2 triggers LTβR, whereas LTα2β1 was reported to bind TNFR1 and TNFR2, LIGHT (TNFSF14) is an alternative ligand for the LTβR. Besides, LTαβ heterotrimers activate canonical/noncanonical nuclear factor-κB (NF-κB) signaling, a significant regulator of innate and adaptive immune responses, cell survival or apoptosis, cellular stress responses, development and maintenance of lymphoid organs^[1].
Lymphotoxin-β (LTβ) is a proinflammatory cytokine of the tumor necrosis factor (TNF) family. Lymphotoxin-β activates NF-κB signaling and shows anti-inflammatory, anti-cancer activity^[1]. Lymphotoxin-β increases the expression of IκBα mRNA and protein in hepatic stellate cells, and regulates hepatic stellate cell function and wound healing in a murine model of chronic liver injury^[2]. Lymphotoxin-β promotes the mRNA expression of pro-inflammatory cytokines TNFα and IL-1β, enhances the mRNA expression of RelA, and may be a potential therapeutic target for bladder cancer^[3].

Lymphotoxin-β (mouse) (-1 ng/mL; 12 h) increases the expression of IκBα mRNA, an NF-κB-responsive gene in a time and dose dependent manner, and increases the protein levels of IκBα in hepatic stellate cells (HSCs)^[2].