T0938
Anti-Tumor Necrosis Factor-α antibody produced in goat
affinity isolated antibody, lyophilized powder
Synonym(s):
Anti-TNF-α
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About This Item
UNSPSC Code:
51111800
NACRES:
NA.41
Recommended Products
biological source
goat
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
mouse
technique(s)
capture ELISA: suitable
flow cytometry: 5-25 μg/mL
indirect immunofluorescence: 15 μg/mL using mouse cells and tissues
neutralization: suitable
western blot: 0.1-0.2 μg/mL
UniProt accession no.
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
mouse ... Tnf(21926)
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General description
Tumor Necrosis Factor-α (TNF-α) is a protein produced by lipopolysaccharide-stimulated macrophages and causes tumor necrosis. It also facilitates many functions like stimulate growth of human fibroblasts and other cell lines, activate polymorphonuclear neutrophils and osteoclasts and collagenase production. Anti-Tumor Necrosis Factor-α antibody can be used for neutralizing the biological activity of recombinant mouse TNF-α. It can also be used in indirect immunofluorescence. Goat anti-Tumor Necrosis Factor-α antibody reacts specifically with recombinant mouse TNF-α.
Specificity
The antibody neutralizes the biological activity of recombinant mouse TNF-α.
Immunogen
recombinant mouse TNF-α
Application
Anti-Tumor Necrosis Factor-α antibody can be used in ELISA capture and flow cytometry. It can also be used in immunoblotting.
Physical form
Lyophilized from 0.2 μm filtered solution in phosphate buffered saline with 5% trehalose.
Preparation Note
Purified using mouse TNF-α affinity chromatography.
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
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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E A Carswell et al.
Proceedings of the National Academy of Sciences of the United States of America, 72(9), 3666-3670 (1975-09-01)
In studying "hemorrhagic necrosis" of tumors produced by endotoxin, it was found that the serum of bacillus Calmette--Guerin (BCG)-infected mice treated with endotoxin contains a substance (tumor necrosis factor; TNF) which mimics the tumor necrotic action of endotoxin itself. TNF-positive
D R Bertolini et al.
Nature, 319(6053), 516-518 (1986-02-06)
When leukocytes are exposed to mitogens or antigens in vitro, they release bone-resorbing activity into the culture supernatants which can be detected by bioassay. Like many lymphocyte-monocyte products, this activity has been difficult to purify because of its low abundance
J M Dayer et al.
The Journal of experimental medicine, 162(6), 2163-2168 (1985-12-01)
Cachectin/TNF (tumor necrosis factor), an endotoxin-induced murine macrophage hormone implicated in the pathogenesis of cachexia and shock, has been found capable of stimulating collagenase and prostaglandin E2 (PGE2) production by isolated human synovial cells and dermal fibroblasts. This bioactivity associated
B J Sugarman et al.
Science (New York, N.Y.), 230(4728), 943-945 (1985-11-22)
Modulation of the growth of human and murine cell lines in vitro by recombinant human tumor necrosis factor-alpha (rTNF-alpha) and recombinant human interferon-gamma (rIFN-gamma) was investigated. rTNF-alpha had cytostatic or cytolytic effects on only some tumor cell lines. When administered
Jianhua Liu et al.
Frontiers in physiology, 8, 611-611 (2017-10-11)
Objective: This study aimed to investigate the effect of osmotin on myocardial ischemia/reperfusion (I/R), as well as the underlying mechanisms. Methods:In vitro I/R injury model was established on rat cardiac myoblast H9c2 cells by oxygen and glucose deprivation followed by
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