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

Lymphotoxin Beta (LT-beta) also known as TNFSF3, is a type II transmembrane glycoprotein of the TNF family. Lymphotoxin Beta binds to LTα to form membrane-anchored heterotrimers that activate canonical/noncanonical nuclear factor-κB (NF-κB) signaling thus inducing chemokine, cytokine or adhesion molecule expression, cell proliferation and cell survival. Lymphotoxin Beta also shows anti-inflammatory, anti-cancer activity^[1]. Lymphotoxin Beta regulates hepatic stellate cell function and wound healing in a murine model of chronic liver injury^[2]. TNFSF3/Lymphotoxin Beta Protein, Cynomolgus (sf9, His) is a recombinant protein with a N-Terminal His label, It consists of 197 amino acids (Q49-G244) and is produced in Sf9 insect cells.

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].

Cynomolgus

Sf9 insect cells

N-His

XP_003897389 (Q49-G244)

101013049

Approximately 22.8 kDa.

Greater than 90% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.

• [1]. Wolf MJ, et al. The unexpected role of lymphotoxin beta receptor signaling in carcinogenesis: from lymphoid tissue formation to liver and prostate cancer development. Oncogene. 2010 Sep 9;29(36):5006-18.  [Content Brief]

  [2]. Ruddell RG, et al. Lymphotoxin-beta receptor signaling regulates hepatic stellate cell function and wound healing in a murine model of chronic liver injury. Hepatology. 2009 Jan;49(1):227-39.  [Content Brief]

  [3]. Shen M, et al. Lymphotoxin β receptor activation promotes mRNA expression of RelA and pro-inflammatory cytokines TNFα and IL-1β in bladder cancer cells. Mol Med Rep. 2017 Jul;16(1):937-942.  [Content Brief]