T3067
Monoclonal Anti-TRAIL antibody produced in mouse
clone 75411, purified immunoglobulin, lyophilized powder
Synonym(s):
Anti-Apo-2L, Anti-TNF-Related Apoptosis-Inducing Ligand, Anti-TNFSF10
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
75411, monoclonal
form
lyophilized powder
species reactivity
human
technique(s)
immunohistochemistry (formalin-fixed, paraffin-embedded sections): 8-25 μg/mL using human brain (occipital cortex) tissue sections
neutralization: 28 ng/mL using L929 mouse fibroblast cell line
isotype
IgG1
UniProt accession no.
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... TNFSF10(8743)
General description
Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor (TNF) cytokine family. This ligand is a type II transmembrane protein that contains a short cytoplasmic N-terminal domain and a long C-terminal extracellular receptor-binding domain. TRAIL is highly expressed in immune system cells. The TRAIL gene is located on the human chromosome at 3q26.31.
Immunogen
purified, NSO-derived, recombinant human TRAIL extracellular domain.
Application
Monoclonal Anti-TRAIL antibody produced in mouse has been used in fluorescence-activated cell sorting (FACS).
Biochem/physiol Actions
Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) binds to TRAIL 1 & 2 receptors and induces apoptosis. This ligand is involved in the homeostasis of T-cells and natural killer (NK) cells. TRAIL also aids in the T-cell-mediated killing of virus-infected cells and oncogenic transformed cells.
Physical form
Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline containing carbohydrates.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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ZhengQiang Yuan et al.
Journal of extracellular vesicles, 6(1), 1265291-1265291 (2017-03-23)
Extracellular vesicles (EVs) are lipid membrane-enclosed nanoparticles released by cells. They mediate intercellular communication by transferring biological molecules and therefore have potential as innovative drug delivery vehicles. TNF-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis of cancer cells. Unfortunately, the clinical
Devalingam Mahalingam et al.
Cancer treatment reviews, 35(3), 280-288 (2009-01-02)
Tumour necrosis factor-related apoptosis-inducing ligand or Apo2 ligand (TRAIL/Apo2L) is a member of the tumour necrosis factor (TNF) superfamily of cytokines that induces apoptosis upon binding to its death domain-containing transmembrane receptors, death receptors 4 and 5 (DR4, DR5). Importantly
Christina Falschlehner et al.
The international journal of biochemistry & cell biology, 39(7-8), 1462-1475 (2007-04-04)
The TNF-related apoptosis-inducing ligand, TRAIL, has been shown to selectively kill tumour cells. This property has made TRAIL and agonistic antibodies against its death inducing receptors (TRAIL-R1 and TRAIL-R2) to some of the most promising novel biotherapeutic agents for cancer
Shashank Tummala et al.
Artificial cells, nanomedicine, and biotechnology, 44(8), 1835-1850 (2015-12-25)
Conventional chemotherapy majorly lacks clinical application attributed to its inspecificity, adverse effects and inability to penetrate into tumor cells. Hence, the aim of the study was to prepare oxaliplatin solid lipid nanoparticles (OP-SLN) by microemulsion method optimizing it by Box-Behnken
Djamel Aggoune et al.
Oncoscience, 1(1), 57-68 (2015-01-17)
Tyrosine kinase inhibitors (TKIs) have profoundly changed the natural history of chronic myeloid leukemia (CML). However, acquired resistance to imatinib, dasatinib or nilotinib (1(st) and 2(nd) generation TKIs), due in part to BCR-ABL1 kinase mutations, has been largely described. These
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