TRAIL is a cytotoxic protein, which activates rapid apoptosis in tumor cells, but not in normal cells. TRAIL induced apoptosis is achieved through binding to two death-signaling receptors, DR4 and DR5. These receptors belong to the TNFR superfamily of transmembrane proteins and contain a cytoplasmic “death domain”, which activates the cell′s apoptotic machinery. Recombinant murine TRAIL is a 174 amino acid polypeptide (20.0 kDa), consisting of the TNF homologous portion of the extracellular domain of the full length TRAIL protein.
forma física
Sterile filtered through a 0.2 micron filter. Lyophilized from 10 mM Sodium Phosphate, pH 7.0.
Reconstituição
Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/mL. Do not vortex. This solution can be stored at 2-8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at -20°C to -80°C.
Código de classe de armazenamento
11 - Combustible Solids
Classe de risco de água (WGK)
WGK 1
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
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Influenza viruses (IV) cause pneumonia in humans with progression to lung failure and fatal outcome. Dysregulated release of cytokines including type I interferons (IFNs) has been attributed a crucial role in immune-mediated pulmonary injury during severe IV infection. Using ex
Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine, 29(1), 39-52 (2015-11-20)
Copper(II) complexes [Cu(H2O)2 (L1)(phen)](ClO4) (1) and [Cu(H2O)(L2)(phen)](ClO4) (2) (HL1 = naringenin; HL2 = hesperetin) were obtained, in which an anionic flavonoid ligand is attached to the metal center along with 1,10-phenanthroline (phen) as co-ligand. Complexes (1) and (2) were assayed
The Journal of experimental medicine, 209(11), 1937-1952 (2012-10-17)
Apoptotic death of alveolar macrophages observed during lung infection with Streptococcus pneumoniae is thought to limit overwhelming lung inflammation in response to bacterial challenge. However, the underlying apoptotic death mechanism has not been defined. Here, we examined the role of
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