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Merck
CN

F0552

Fas Ligand from mouse

>95% (SDS-PAGE), recombinant, expressed in mouse NSO cells, lyophilized powder

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关于此项目

UNSPSC Code:
12352200
NACRES:
NA.32
MDL number:
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产品名称

Fas Ligand from mouse, >95% (SDS-PAGE), recombinant, expressed in mouse NSO cells, lyophilized powder

recombinant

expressed in mouse NSO cells

assay

>95% (SDS-PAGE)

form

lyophilized powder

mol wt

monomer calculated mol wt ~18 kDa
28-32 kDa by SDS-PAGE

impurities

endotoxin, tested

UniProt accession no.

storage temp.

−20°C

Quality Level

Gene Information

mouse ... Fasl(14103)

Analysis Note

Measured by its ability to induce apoptosis in Jurkat cells.

Application

Fas Ligand (FASLG) from mouse has been used for-
  • the induction of apoptosis in PC12 cells and
  • the induction of migration in BV-2 murine microglial cells.

Biochem/physiol Actions

FASLG (Fas ligand) and Fas receptor constitute the basic elements in apoptosis. Interaction of FASLG with Fas receptor leads to activation of caspase-8. This caspase in turn leads to activation of effector caspases such as caspase-3, -6 and -7. This cascade results in the hydrolysis of nuclear and cytoplasmic components. Expression of FASLG is induced by nuclear factor-κB (NFκB). NFκB/FASLG pathway facilitates the suppression of p,p′-DDT (dichlorodiphenoxytrichloroethane)-induced cell toxicity by vitamin C and E. In CD4+ T cells, this protein is expressed on stimulus by T-cell receptor (TCR), both during normal and pathological conditions, such as alcohol exposure.
Fas ligand, a protein belonging to the tumor necrosis factor (TNF) family of cytokines, induces apoptosis in cells expressing the cell membrane receptor Fas (CD95/Apo-1).
Protein belonging to the tumor necrosis factor (TNF) family of cytokines; induces apoptosis in cells expressing the cell membrane receptor Fas (CD95/Apo-1).

General description

FASLG (Fas ligand) acts as a ligand for Fas receptor, and is a major protein involved in programmed cell death, apoptosis. Soluble Fas (sFAS) is usually detected in plasma prior to apoptosis.

Other Notes

Mouse Fas Ligand, N-terminal 6X histidine-tagged, encodes amino acid residues 132-279.

Physical form

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

存储类别

10 - Combustible liquids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

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分析证书(COA)

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Aleksander Szymanowski et al.
Atherosclerosis, 233(2), 616-622 (2014-02-19)
Apoptosis of natural killer (NK) cells is increased in patients with coronary artery disease (CAD) and may explain why NK cell levels are altered in these patients. Soluble forms of Fas and Fas ligand (L) are considered as markers of
Xiaoting Jin et al.
PloS one, 9(12), e113257-e113257 (2014-12-03)
Dichlorodiphenoxytrichloroethane (DDT) is a known persistent organic pollutant and liver damage toxicant. However, there has been little emphasis on the mechanism underlying liver damage toxicity of DDT and the relevant effective inhibitors. Hence, the present study was conducted to explore
Ying-mei Lu et al.
Journal of neuroinflammation, 9, 172-172 (2012-07-14)
The cerebral microvascular occlusion elicits microvascular injury which mimics the different degrees of stroke severity observed in patients, but the mechanisms underlying these embolic injuries are far from understood. The Fas ligand (FasL)-Fas system has been implicated in a number
Nicole Suyun Liu et al.
PloS one, 7(8), e43180-e43180 (2012-08-21)
Diva is a member of the Bcl2 family but its function in apoptosis remains largely unclear because of its specific expression found within limited adult tissues. Previous overexpression studies done on various cell lines yielded conflicting conclusions pertaining to its
Smita S Ghare et al.
Journal of immunology (Baltimore, Md. : 1950), 193(1), 412-421 (2014-06-06)
Activation-induced Fas ligand (FasL) mRNA expression in CD4+ T cells is mainly controlled at transcriptional initiation. To elucidate the epigenetic mechanisms regulating physiologic and pathologic FasL transcription, TCR stimulation-responsive promoter histone modifications in normal and alcohol-exposed primary human CD4+ T

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