Recombinant human TWEAK protein is a Human Full Length protein, in the 96 to 249 aa range, expressed in Escherichia coli, with >98% purity and suitable for SDS-PAGE, FuncS.
>98% SDS-PAGE
Escherichia coli
Tag free
SDS-PAGE, FuncS
Yes
M K G R K T R A R R A I A A H Y E V H P R P G Q D G A Q A G V D G T V S G W E E A R I N S S S P L R Y N R Q I G E F I V T R A G L Y Y L Y C Q V H F D E G K A V Y L K L D L L V D G V L A L R C L E E F S A T A A S S L G P Q L R L C Q V S G L L A L R P G S S L R I R T L P W A H L K A A P F L T Y F G L F Q V H
| Application | Reactivity | Dilution info | Notes |
|---|---|---|---|
Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application FuncS | Reactivity Reacts | Dilution info - | Notes - |
Select an associated product type
Binds to FN14 and possibly also to TNRFSF12/APO3. Weak inducer of apoptosis in some cell types. Mediates NF-kappa-B activation. Promotes angiogenesis and the proliferation of endothelial cells. Also involved in induction of inflammatory cytokines. Promotes IL8 secretion.
Tumor necrosis factor ligand superfamily member 12, APO3 ligand, TNF-related weak inducer of apoptosis, TWEAK, DR3LG, APO3L, TNFSF12, UNQ181/PRO207
Recombinant human TWEAK protein is a Human Full Length protein, in the 96 to 249 aa range, expressed in Escherichia coli, with >98% purity and suitable for SDS-PAGE, FuncS.
Tumor necrosis factor ligand superfamily member 12, APO3 ligand, TNF-related weak inducer of apoptosis, TWEAK, DR3LG, APO3L, TNFSF12, UNQ181/PRO207
>98% SDS-PAGE
Escherichia coli
Tag free
SDS-PAGE, FuncS
Yes
The ED50 as determined by the dose-dependent stimulation of IL-8 production by Human PBMC is less than 10 ng/ml.
TWEAK weakly induces the death of HT29 cells when cultured in the presence of IFN-γ. The ED50 for this effect is between 30-45 ng/ml.
No
Human
Reconstitute in 10 mM sodium phosphate, pH 7.5
M K G R K T R A R R A I A A H Y E V H P R P G Q D G A Q A G V D G T V S G W E E A R I N S S S P L R Y N R Q I G E F I V T R A G L Y Y L Y C Q V H F D E G K A V Y L K L D L L V D G V L A L R C L E E F S A T A A S S L G P Q L R L C Q V S G L L A L R P G S S L R I R T L P W A H L K A A P F L T Y F G L F Q V H
Full Length
17 kDa
96 to 249
Recombinant
Lyophilized
Sterile filtered Greater than 98% pure by HPLC analyses. Endotoxin level is less than 0.1 ng per g (1EU/g).
Binds to FN14 and possibly also to TNRFSF12/APO3. Weak inducer of apoptosis in some cell types. Mediates NF-kappa-B activation. Promotes angiogenesis and the proliferation of endothelial cells. Also involved in induction of inflammatory cytokines. Promotes IL8 secretion.
Belongs to the tumor necrosis factor family.
The soluble form derives from the membrane form by proteolytic processing.
Blue Ice
1-2 weeks
+4°C
-20°C
Upon delivery aliquot
Avoid freeze / thaw cycle
This product is an active protein and may elicit a biological response in vivo, handle with caution.
The ED50 as determined by the dose-dependent stimulation of IL-8 production by human PBMC is less than 10ng/ml.
The TNF-like weak inducer of apoptosis (TWEAK) also known as CD255 is a cytokine involved in a variety of cellular processes. This protein has an approximate mass of 24 kDa. TWEAK is expressed in many tissues including the heart brain and spleen. It functions by binding to the fibroblast growth factor-inducible 14 (Fn14) receptor leading to the activation of downstream signaling pathways. TWEAK's role as a ligand places it in the tumor necrosis factor (TNF) superfamily highlighting its involvement in cell death and inflammation signaling.
TWEAK modulates processes like cell proliferation differentiation and apoptosis. This cytokine affects the immune response and tissue regeneration becoming significant in processes that require tissue remodeling. While acting independently TWEAK does not form part of a larger protein complex. Instead it signals mainly through its exclusive receptor Fn14 on responsive cells triggering cellular responses that influence its biological activities.
TWEAK plays an important role in the NF-kB and MAPK signaling pathways. These pathways are important for immune response regulation and cell survival. In these pathways TWEAK closely interacts with TNF receptor-associated factors (TRAFs) which facilitate TWEAK signaling. The connections to pathways involving inflammatory response highlight its significance in maintaining homeostasis within the cellular environment.
TWEAK's activity links to conditions like cancer and rheumatoid arthritis. In cancer excessive TWEAK signaling can contribute to tumor growth and metastasis through its pro-inflammatory and pro-angiogenic effects. In rheumatoid arthritis TWEAK expression relates to joint inflammation and tissue damage where it interacts with proteins like IL-6 and TNF-alpha. These interactions suggest potential therapeutic targets by modulating TWEAK or its signaling partners to treat these diseases.
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