KAA002
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.
Synonym(s):
Senescence Detection Kit
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About This Item
UNSPSC Code:
12161503
eCl@ss:
32161000
NACRES:
NA.84
Recommended Products
Quality Level
manufacturer/tradename
Chemicon®
technique(s)
cell based assay: suitable
detection method
colorimetric
shipped in
wet ice
General description
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.
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.
Application
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.
Components
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
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
Storage and Stability
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.
Precautions:
Please refer to the Material Safety Data Sheet at www.chemicon.com for any necessary precautions.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
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.
Signal Word
Danger
Hazard Statements
Precautionary Statements
Hazard Classifications
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
Target Organs
Respiratory system
Supplementary Hazards
Storage Class Code
3 - Flammable liquids
Flash Point(F)
135.5 °F
Flash Point(C)
57.5 °C
Certificates of Analysis (COA)
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Clemens A Schmitt et al.
Cell, 109(3), 335-346 (2002-05-23)
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
Grégoire Le Gac et al.
Anesthesia and analgesia, 125(5), 1600-1609 (2017-09-01)
Hepatocellular carcinoma (HCC) is an aggressive cancer with limited therapeutic options. Retrospective studies have shown that the administration of local anesthetics (LAs) during cancer surgery could reduce cancer recurrence. Besides, experimental studies reported that LAs could inhibit the growth of
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
Goberdhan P Dimri
Cancer cell, 7(6), 505-512 (2005-06-14)
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
A Satyanarayana et al.
The EMBO journal, 22(15), 4003-4013 (2003-07-26)
Telomere shortening limits the regenerative capacity of primary cells in vitro by inducing cellular senescence characterized by a permanent growth arrest of cells with critically short telomeres. To test whether this in vitro model of cellular senescence applies to impaired
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