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Merck

T5944

Sigma-Aldrich

Tumor Necrosis Factor-α from rat

≥98% (SDS-PAGE and HPLC), recombinant, expressed in E. coli, powder, suitable for cell culture

Synonym(e):

Cachectin, TNF-α

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About This Item

MDL-Nummer:
UNSPSC-Code:
12352202
NACRES:
NA.77

product name

Tumor Necrosis Factor-α from rat, TNF-α, recombinant, expressed in E. coli, powder, suitable for cell culture

Biologische Quelle

rat

Qualitätsniveau

Rekombinant

expressed in E. coli

Assay

≥98% (SDS-PAGE and HPLC)

Form

powder

Qualität

endotoxin tested

Mol-Gew.

predicted mol wt ~17 kDa

Verpackung

pkg of 10 μg
pkg of 50 μg

Lagerbedingungen

avoid repeated freeze/thaw cycles

Methode(n)

cell culture | mammalian: suitable

Verunreinigungen

<1 EU/μgtested (LAL test)

Farbe

white

Löslichkeit

water: soluble

UniProt-Hinterlegungsnummer

Lagertemp.

−20°C

Angaben zum Gen

rat ... Tnf(24835)

Allgemeine Beschreibung

The Tnf (tumor necrosis factor) gene is mapped to rat chromosome 20p12.

Anwendung

TNF-α influences the growth and function of both normal and neoplastic cells. TNF-α causes cytolysis or cytostasis of certain transformed cells being synergistic with γ-interferon in its cytotoxicity.
Tumor Necrosis Factor-α from rat has been used:
  • To stimulate inducible nitric oxide synthase (iNOS) expression in the macrophages as an indication of M1 macrophage activation
  • To study its effect on pancreatic β cell apoptosis
  • To evaluate the effect of progesterone on the expression of tumor necrosis factor (TNF)-α in synovial membrane
  • As a blocking antigen in the control, for immunohistochemical analysis

Biochem./physiol. Wirkung

Tumor necrosis factor-α (TNF-α), also known as cachectin, plays roles in antitumor activity, immune modulation, inflammation, anorexia, cachexia, septic shock, viral replication, and hematopoiesis. TNF-α is expressed by a variety of cells, with numerous inductive and suppressive agents. It is primarily produced by macrophages in response to immunological challenges such as bacteria (lipopolysaccharides), viruses, parasites, mitogens, and other cytokines. TNF-α is cytotoxic for many transformed cells (its namesake activity) but in normal diploid cells, it can stimulate proliferation (fibroblasts), differentiation (myeloid cells) or activation (neutrophils). TNF-α also shows antiviral effects against both DNA and RNA viruses and it induces production of several other cytokines. TNF-α and the related molecule TNF-β (LT-α) share close structural homology with 28% amino acid sequence identity and both activate the same TNF receptors, TNFR1 and TNFR2.

Physikalische Form

Lyophilized from an 0.2 μm-filtered buffered solution with bovine serum albumin as a carrier.

Hinweis zur Analyse

The biological activity is measured in a cytotoxic assay using a TNF-susceptible mouse L929 cell line in the presence of actinomycin D.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

Endothelin system mRNA variation in the heart of Zucker rats: Evaluation of a possible balance with natriuretic peptides
Cabiati M, et al.
Nutrition, Metabolism, and Cardiovascular Diseases, 24(11), 1166-1173 (2014)
Progesterone attenuates temporomandibular joint inflammation through inhibition of NF-kappa pathway in ovariectomized rats
Xue XT, et al.
Scientific Reports, 7(1), 15334-15334 (2017)
Melissa M Gresle et al.
Glia, 63(6), 1005-1020 (2015-02-03)
In order to further investigate the molecular mechanisms that regulate oligodendrocyte (OC) survival, we utilized microarrays to characterize changes in OC gene expression after exposure to the cytokines neurotrophin3, insulin, or leukemia inhibitory factor (LIF) in vitro. We identified and
Estradiol promotes M1-like macrophage activation through cadherin-11 to aggravate temporomandibular joint inflammation in rats
Kou XX, et al.
Journal of Immunology, 1303188-1303188 (2015)
Chronic intermittent hypoxia induces local inflammation of the rat carotid body via functional upregulation of proinflammatory cytokine pathways
Lam SY, et al.
Histochemistry and Cell Biology, 137(3), 303-317 (2012)

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