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Merck

F0552

Sigma-Aldrich

Fas Ligand from mouse

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

Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez


About This Item

MDL-szám:
UNSPSC kód:
12352200
NACRES:
NA.32

rekombináns

expressed in mouse NSO cells

Minőségi szint

Teszt

>95% (SDS-PAGE)

Forma

lyophilized powder

molekulatömeg

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

szennyeződések

endotoxin, tested

UniProt elérési szám

tárolási hőmérséklet

−20°C

Géninformáció

mouse ... Fasl(14103)

Általános leírás

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.

Alkalmazás

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.

Biokémiai/fiziológiai hatások

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).

Egyéb megjegyzések

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

Fizikai forma

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

Analízis megjegyzés

Measured by its ability to induce apoptosis in Jurkat cells.

Tárolási osztály kódja

10 - Combustible liquids

WGK

WGK 3

Lobbanási pont (F)

Not applicable

Lobbanási pont (C)

Not applicable


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Analitikai tanúsítványok (COA)

Lot/Batch Number

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Dokumentumtár megtekintése

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
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
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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