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Merck
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Key Documents

RAB0849

Sigma-Aldrich

Mouse Tnfsf10 / Tumor Necrosis Factor Ligand Superfamily Member 10 ELISA Kit

for serum, plasma and cell culture supernatants

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About This Item

UNSPSC Code:
41116158
NACRES:
NA.32

species reactivity

mouse

packaging

kit of 96 wells (12 strips x 8 wells)

technique(s)

ELISA: suitable

input

sample type plasma
sample type serum
sample type cell culture supernatant(s)

assay range

inter-assay cv: <12%
intra-assay cv: <10%
sensitivity: 2 pg/mL
standard curve range: 2.46-600 pg/mL

detection method

colorimetric

shipped in

wet ice

storage temp.

−20°C

Gene Information

mouse ... Tnfsf10(22035)

General description

The antibody pair provided in this kit recognizes mouse TRAIL/TNFSF10.

Application

For research use only. Not for use in diagnostic procedures.
Please refer to the attached General ELISA KIT Procedure (sandwich, competitive & Indirect ELISA)

Biochem/physiol Actions

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) activates the extrinsic apoptotic pathway by binding death receptors (DR)-4 and 5. In addition to DR 4 and 5, TRAIL activates several other receptors such as decoy receptor (DcR)1, DcR2 and a soluble receptor called osteoprotegerin. TRAIL plays a vital role in the inhibition of autoimmune inflammation and cell cycle progression. TRAIL selectively kills tumor cells without damaging normal tissues and therefore, it might act as a tumor-selective anticancer agent. TRAIL-induced apoptosis is involved in various cellular processes including activation-induced cell death, homeostasis, intrathymic negative selection, autoimmunity suppression, and immune surveillance. Repeated dosage of recombinant soluble TRAIL triggers apoptosis, inhibits tumor progression, and increases viability of mice suffering from cancer.

Other Notes

A sample Certificate of Analysis is available for this product.
Please type the word sample in the text box provided for lot number.

Los componentes del kit también están disponibles por separado

Referencia del producto
Descripción
SDS
  • RABTMB3ELISA Colorimetric TMB Reagent (HRP Substrate, Item H)SDS
  • RABSTOP3ELISA Stop Solution (Item I)SDS
  • RABELADAELISA 1X Assay/Sample Diluent Buffer A (Item D1)SDS
  • RABELADBELISA 5X Assay/Sample Diluent Buffer B (Item E1)SDS
  • RABWASH420X Wash Buffer (Item B)SDS

pictograms

Corrosion
GHS05

signalword

Warning

hcodes

H290

Hazard Classifications

Met. Corr. 1

Storage Class

8A - Combustible corrosive hazardous materials

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Overexpression of soluble TRAIL induces apoptosis in human lung adenocarcinoma and inhibits growth of tumor xenografts in nude mice
Shi J
Cancer Research, 65 (2005)
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induced mitochondrial pathway to apoptosis and caspase activation is potentiated by phospholipid scramblase-3
Ndebele K
Apoptosis, 13(7) (2008)
Exosomes secreted by human placenta carry functional Fas ligand and TRAIL molecules and convey apoptosis in activated immune cells, suggesting exosome-mediated immune privilege of the fetus
Stenqvist AC
Journal of Immunology, 191, 5515-5523 (2013)
Lin Li et al.
Acta biochimica et biophysica Sinica, 46(6), 471-476 (2014-04-18)
The apoptotic ligand TNF-related apoptosis-inducing ligand (TRAIL) is believed to be a promising candidate for cancer gene therapy, yet gene therapy strategies to tackle this disease systemically are often impaired by inefficient delivery of the vector to the tumor tissue.
A Ray et al.
Leukemia, 28(8), 1716-1724 (2014-01-31)
Our prior study in multiple myeloma (MM) patients showed increased numbers of plasmacytoid dendritic cells (pDCs) in the bone marrow (BM), which both contribute to immune dysfunction as well as promote tumor cell growth, survival and drug resistance. Here we

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