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T3564

Sigma-Aldrich

Tumor Necrosis Factor Soluble Receptor I (TNF sRI) from mouse

>97% (SDS-PAGE), recombinant, expressed in E. coli, lyophilized powder, suitable for cell culture

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About This Item

MDL number:
UNSPSC Code:
51111800
NACRES:
NA.32

biological source

mouse

Quality Level

recombinant

expressed in E. coli

Assay

>97% (SDS-PAGE)

form

lyophilized powder

potency

0.5-1.5 μg/mL ED50

mol wt

21 kDa

packaging

pkg of 50 μg

storage condition

avoid repeated freeze/thaw cycles

technique(s)

cell culture | mammalian: suitable

impurities

endotoxin, tested

UniProt accession no.

storage temp.

−20°C

Gene Information

Application

Tumor Necrosis Factor Soluble Receptor I (TNF sRI) from mouse plays a pivotal role in the signaling of apoptosis and NF-κB activation because of its “death domain” present at the intracellular portion.

Biochem/physiol Actions

Tumor Necrosis Factor Soluble Receptor I (TNF sRI) from mouse belongs to TNF family of receptors and has a pivotal role in neutralizing the biological activities of both TNF-α and TNF-β. Soluble tumor necrosis factor receptor along with intrathecal interleukin-1 receptor antagonist shows an anti-allodynic action in rat L5 spinal nerve transection model of neuropathic pain.

Physical form

Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline with 2.5 mg bovine serum albumin

Analysis Note

The biological activity is measured by its ability to inhibit the recombinant mouse TNF-α mediated cytotoxicity in mouse L929 cells, in the presence of the metabolic inhibitor actinomycin D.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Matthews, N. et al. et al.
Lymphokines and Interferons, A Practical Approach, 221-221 (1987)
S Sweitzer et al.
Neuroscience, 103(2), 529-539 (2001-03-14)
The expression of interleukin-1beta and tumor necrosis factor has previously been shown to be up-regulated in the spinal cord of several rat mononeuropathy models. This present study was undertaken to determine whether blocking the action of central interleukin-1beta and tumor

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