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Merck

T3564

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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UNSPSC Code:
51111800
NACRES:
NA.32
MDL number:
Form:
lyophilized powder
Assay:
>97% (SDS-PAGE)
Biological source:
mouse
Recombinant:
expressed in E. coli
Mol wt:
21 kDa
Servicio técnico
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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

mouse ... Tnfrsf1a(21937)

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.


Clase de almacenamiento

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable



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Contenido relacionado


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