TRAIL/TNFSF10 Protein, Human

TRAIL Protein (TNFSF10), a member of the TNF superfamily, is a type II transmembrane protein. TRAIL Protein mainly interacts with TRAIL-R1 and TRAIL-R2, and induces apoptosis in tumor or infected cells. TRAIL Protein also binds with DR4, DR5, and OPG. TRAIL Protein can recruit FADD and further recruit and activates caspase-8 after binding to DR4 or DR5. Besides, TRAIL may also trigger nonapoptotic signaling through activating pro-inflammatory pathways^[1][2]. TRAIL protein is mainly expressed on surface of immune cells, such as cytotoxic T cells and natural killer (NK) cell^[1]. TRAIL/TNFSF10 Protein, Human is a recombinant human TRAIL (V114-G281) without any tag, which is expressed in E. coli.

TRAIL Protein (TNFSF10), a member of the TNF superfamily, is a type II transmembrane protein. TRAIL Protein is expressed in various tissues, especially in the spleen, lung, and prostate. TRAIL protein is mainly expressed on surface of immune cells, such as cytotoxic T cells and natural killer (NK) cell. TRAIL proteins on NK and T cells is critical for controlling virus infections and tumor immune surveillance^[1][2].
Human TRAIL consists of cytoplasmic domain (M1-V17), helical domain (L18-F38), and extracellular domain (T39-G281). Human TRAIL Protein shares < 70% common aa identity with mouse and rat. Mouse TRAIL Protein shares 86.94% common aa identity with rat.
TRAIL Protein mainly interacts with two agonistic TRAIL receptors (TRAIL-R1 and TRAIL-R2) and induces apoptosis in tumor or infected cells. TRAIL Protein also binds with DR4, DR5, and OPG. When binding to DR4 or DR5, TRAIL Protein can recruit FADD and further recruit and activates caspase-8. Besides, TRAIL may also trigger nonapoptotic signaling through activating pro-inflammatory pathways, such as NF-κB, PI3K/Akt, and MAPK pathway^[1][2].
TRAIL induces apoptosis of tumor cells in a p53 independent manner. TRAIL-based therapies has high anti-tumor potential^[3].

TRAIL (human, 10 ng/mL-10 μg/mL, 24 h) reduces cell viability of HepG2 cells^[4].
TRAIL (human, 1-10 ng, 24 h) induces pathognomic features of asthma and stimulates the production of CCL20 in primary human bronchial epithelium cells^[5].

1.The ED₅₀ is <40 ng/mL as measured by RPMI-8226 cells, corresponding to a specific activity of >2.5 × 10⁴ units/mg.
2.Measured in a cytotoxicity assay using L929 mouse fibroblast cells in the presence of the metabolic inhibitor actinomycin D. The ED₅₀ for this effect is 0.5-3 ng/mL.

• 
  Measured in a cytotoxicity assay using L929 mouse fibroblast cells in the presence of the metabolic inhibitor actinomycin D. The ED₅₀ for this effect is 1.484 ng/mL, corresponding to a specific activity is 6.738×10⁵ units/mg.

Human

E. coli

Tag Free

P50591 (V114-G281)

8743  [NCBI]

Partial

VRERGPQRVAAHITGTRGRSNTLSSPNSKNEKALGRKINSWESSRSGHSFLSNLHLRNGELVIHEKGFYYIYSQTYFRFQEEIKENTKNDKQMVQYIYKYTSYPDPILLMKSARNSCWSKDAEYGLYSIYQGGIFELKENDRIFVSVTNEHLIDMDHEASFFGAFLVG

Approximately 20 kDa, based on SDS-PAGE under reducing conditions.

• 
  ≥ 95%, as determined by reducing SDS-PAGE.

Lyophilized powder

1.Lyophilized from a 0.22 μm filtered solution of PBS.
2.Lyophilized from a 0.22 μm filtered solution of 50 mM Tris-HCl, 300 mM NaCl, pH 8.0.
Please refer to the lot-specific COA for specific buffer information.
Note: For SPR assay, please replace the buffer. Primary amine components (e.g., Tris, imidazole) can affect protein-coupled chips.

<0.2 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. /biology-dictionary/hek293-cell.html  [Content Brief]

  [2]. Cardoso Alves L, et al. The multifaceted role of TRAIL signaling in cancer and immunity. FEBS J. 2021 Oct;288(19):5530-5554.  [Content Brief]

  [3]. Almasan A, et al. Apo2L/TRAIL: apoptosis signaling, biology, and potential for cancer therapy. Cytokine Growth Factor Rev. 2003 Jun-Aug;14(3-4):337-48.  [Content Brief]

  [4]. Zhong HH, et al. TRAIL-based gene delivery and therapeutic strategies. Acta Pharmacol Sin. 2019 Nov;40(11):1373-1385.  [Content Brief]

  [5]. Braithwaite, Adam T, et al. "Divergent Roles for TRAIL in Lung Diseases". Frontiers in Medicine. Allan (2018)

  [6]. Snajdauf M, et al. The TRAIL in the Treatment of Human Cancer: An Update on Clinical Trials. Front Mol Biosci. 2021 Mar 10;8:628332.  [Content Brief]

  [7]. Ganten TM, et al. Preclinical differentiation between apparently safe and potentially hepatotoxic applications of TRAIL either alone or in combination with chemotherapeutic drugs. Clin Cancer Res. 2006 Apr 15;12(8):2640-6.  [Content Brief]

  [8]. Weckmann M, et al. Critical link between TRAIL and CCL20 for the activation of TH2 cells and the expression of allergic airway disease. Nat Med. 2007 Nov;13(11):1308-15.  [Content Brief]