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Documentos Principais

KAA002

Sigma-Aldrich

Cellular Senescence Assay

Cellular Senescence Assay Kits provide all the reagents required to efficiently detect SA-β-gal activity at pH 6.0 in cultured cells & tissue sections.

Sinônimo(s):

Senescence Detection Kit

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About This Item

Código UNSPSC:
12161503
eCl@ss:
32161000
NACRES:
NA.84

Nível de qualidade

fabricante/nome comercial

Chemicon®

técnica(s)

cell based assay: suitable

método de detecção

colorimetric

Condições de expedição

wet ice

Descrição geral

Cellular senescence is one of the most fundamental aspects of cell behavior, and is thought to play a critical role in regulating cellular lifespan both in vitro and in vivo [1-3]. Primary somatic cells grown in vitro do not proliferate indefinitely. Instead, after a period of rapid proliferation, cell division rate slows, and ultimately ceases altogether, with the cells becoming unresponsive to mitogenic stimuli. This process is termed cellular senescence, and senescent cells have a well-defined accompanying phenotype - increased cell size, distinctive flat morphology, accumulated lipofuscin granules, wide changes in gene expression, and activity of senescence-associated β-galactosidase (SA-β-gal) [2,3].

It is generally believed that cellular senescence reflects some of the changes that occur during the aging of organisms, and senescent cells have been detected in vivo at sites of age-related pathology, such as benign hyperplastic prostate [4] and atherosclerotic lesions [5]. Recent studies have also provided convincing demonstrations of cellular senescence occurring in vivo in response to internally- and externally-induced stress signals [6,7]. In all of these studies, senescence was characterized by the appearance of senescence-associated β-galactosidase (SA-β-gal) activity, in common with the senescent phenotype in vitro.

Cellular senescence has become an increasingly important target in the development of novel therapeutics. Emerging data implicates senescence bypass in the development of cancer and suggests that senescence may represent a tumor suppressor mechanism. The demonstration that tumor cells can be induced to undergo replicative senescence following the introduction of negative cell-cycle regulators, anti-telomerase peptides, or drug treatment suggests that induction of senescence can be exploited as a basis for cancer therapy [8,9].

For Research Use Only; Not for use in diagnostic procedures

Test Principle:
As outlined above, a classic characteristic of the senescent phenotype is the induction of senescence-associated β-galactosidase (SA-β-gal) activity. SA-β-gal is present only in senescent cells, not in presenescent, quiescent, or proliferating cells. Chemicon′s Cellular Senescence Assay Kit provides all the reagents required to efficiently detect SA-β-gal activity at pH 6.0 in cultured cells and tissue sections. In this assay, SA-β-gal catalyzes the hydrolysis of X-gal, which results in the accumulation of a distinctive blue color in senescent cells. Each kit provides sufficient quantities of reagents to perform at least 50 assays in 35 mm wells.

Aplicação

Cellular Senescence Assay Kits provide all the reagents required to efficiently detect SA-β-gal activity at pH 6.0 in cultured cells & tissue sections.

Componentes

100X Fixing Solution: (Part No. 2004755) One 1.5 mL vial

10X Staining Solution A: (Part No. 2004756) One 15 mL bottle

10X Staining Solution B: (Part No. 2004754) One 15 mL bottle

X-gal Solution: (Part No. 2004752) Two 1.5 mL vials

Armazenamento e estabilidade

Store X-gal solution protected from light at -20°C, and other kit components at 4°C. All components supplied are stable for 1 year.

Precautions:
Please refer to the Material Safety Data Sheet at www.chemicon.com for any necessary precautions.

Informações legais

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Exoneração de responsabilidade

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Palavra indicadora

Danger

Classificações de perigo

Acute Tox. 4 Dermal - Acute Tox. 4 Inhalation - Acute Tox. 4 Oral - Aquatic Acute 1 - Aquatic Chronic 2 - Eye Dam. 1 - Flam. Liq. 3 - Repr. 1B - Resp. Sens. 1 - Skin Corr. 1B - Skin Sens. 1 - STOT SE 3

Órgãos-alvo

Respiratory system

Perigos de suplementos

Código de classe de armazenamento

3 - Flammable liquids

Ponto de fulgor (°F)

135.5 °F

Ponto de fulgor (°C)

57.5 °C


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E L Duncan et al.
Biogerontology, 1(2), 103-121 (2001-11-16)
Following a limited number of population doublings (PD), human diploid somatic cells enter the terminal proliferation arrest state of senescence. This is an intrinsic mechanism which involves p53- and pRB/p16INK4-mediated pathways. The most popular candidate for the counting mechanism which
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p53 and INK4a/ARF mutations promote tumorigenesis and drug resistance, in part, by disabling apoptosis. We show that primary murine lymphomas also respond to chemotherapy by engaging a senescence program controlled by p53 and p16(INK4a). Hence, tumors with p53 or INK4a/ARF
Goberdhan P Dimri
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Cancer therapeutics are primarily thought to work by inducing apoptosis in tumor cells. However, various tumor suppressors and oncogenes have been shown to regulate senescence in normal cells, and senescence bypass appears to be an important step in the development
E Vasile et al.
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VPF/VEGF acts selectively on the vascular endothelium to enhance permeability, induce cell migration and division, and delay replicative senescence. To understand the changes in gene expression during endothelial senescence, we investigated genes that were differentially expressed in early vs. late
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Anti-silencing function 1a (ASF1a) is a histone H3-H4 chaperone isoform involved in chromatin assembling and transcription regulation. Recently, ASF1a has been shown to be up-regulated in certain human malignancies and required for the expression of telomerase reverse transcriptase (TERT), a

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