protein

TWEAK/TNFSF12 Protein, Mouse (HEK293, rFc)

HY-P77265

5 μg;10 μg;50 μg

53;89;250 USD

TWEAK/TNFSF12 Protein, Mouse (HEK293, rFc)

proteins

HEK293

5 μg;10 μg;50 μg

53;89;250 USD

TWEAK Protein refers to the cytokine tumor necrosis factor-like weak inducer of apoptosis, belongs to tumor necrosis factor (TNF) superfamily. TWEAK protein binds to FN14 and TNRFSF12/APO3, is a weak inducer of apoptosis [1] . TWEAK does have pro-apoptotic activity for tumor cell, mediates NF-kappa-B activation, promotes angiogenesis and the proliferation of endothelial cells (ECs) [2] . TWEAK also increases IL-6 and IL-8 secretion, and could potentiate the pro-inflammatory activities of TNF and IL-1 [3] . Mouse TWEAK protein is a type II transmembrane protein (M1-H249) with a transmembrane domain (25-45 a.a.). TWEAK/TNFSF12 Protein, Mouse (HEK293, rFc) is the extracellular part (R105-H249) of TWEAK protein, produced by HEK293 cells (R105-H249) with N-terminal rFc-tag.

Mouse

TWEAK Protein refers to the cytokine tumor necrosis factor-like weak inducer of apoptosis. It is a multifunctional cytokine belonging to tumor necrosis factor (TNF) superfamily, acts function by binding TweakR/Fn14 receptor. TWEAK is a cell surface-associated type II transmembrane protein with 2 types protein chain: the membrane form and the secreted or soluble form. The soluble form derives from the membrane form by proteolytic processing. The protein sequences in human and mouse is very different with similarity of 24.79% [1] . TWEAK binds to FN14 and possibly also to TNRFSF12/APO3, is a weak inducer of apoptosis in some cell types. TWEAK mediates NF-kappa-B activation, promotes angiogenesis and the proliferation of endothelial cells [2] . TWEAK has multiple biological activities, many of which are associated with immune system development and function [1] . TWEAK does have pro-apoptotic activity on a select group of human tumor cell lines and on monocytes, while it promotes cell proliferation in human vascular EC and SMC. Furthermore, FGF-2 co-treatment can potentiate TWEAK-stimulated HUVEC proliferation, an effect that may be due to the ability of FGF-2 to up-regulate TweakR/Fn14 gene expression. At the meanwhile TWEAK-TweakR/Fn14 autocrine signaling promotes human microvascular renal EC (HMREC) migration [1] . TWEAK also plays key role in inflammatory response. TWEAK, stimulates interleukin (IL)-8 secretion in human tumor cell lines, WI-38 fibroblasts and astrocytes. TWEAK also increases IL-6 secretion and ICAM-1 expression in astrocyte cell. Moreover, TWEAK co-incubation could potentiate the pro-inflammatory activities of TNF and IL-1, and concluded that TWEAK could be involved in the pathogenesis of chronic inflammatory diseases [3] . Above all, TWEAK involves in stimulation of cell growth and angiogenesis, induction of inflammatory cytokines, and under some experimental conditions, stimulation of apoptosis [1] .

Tumor necrosis factor ligand superfamily member 12; TWEAK; APO3L; DR3LG

Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized from a 0.2 μm filtered solution of PB, 150 mM NaCl, pH 7.4.

Room temperature in continental US; may vary elsewhere.