Cellular Senescence Detection Comparison

Cellular senescence is considered crucial to many different research areas, especially since the recent discovery of the senescence-associated secretory phenotype (SASP). SASP is a known risk factor for malignant transformation and exploration into stem cell research has found a link between SASP and the aging phenomenon. The features of cellular senescence were summarized based on modern publications that have a high number of citations.

Various Senescent Cell from Various Indicators

ProductCellular Senescence Detection Kit – SPiDER-ßGalCellular Senescence Plate Assay Kit – SPiDER-ßGalDNA Damage Detection Kit – γH2AX * Coming SoonNucleolus Bright Green / Red
DetectionFluorescenceFluorescenceFluorescenceFluorescence
Wavelength
(Ex/Em)
500 – 540 nm / 530 – 570 nm535 nm / 580 nmGreen: 494 nm / 518 nm
Red: 550 nm / 566 nm
Deep Red: 646 nm / 668 nm
Green: 513 nm / 538 nm
Red: 537 nm / 605 nm
IndicatorSA-ß-gal activitySA-ß-gal activityChanges in DNA damageChanges in the Nucleolus
Detection methodImaging
Substrate:SPiDER-ßGal
Plate assay
Substrate:SPiDER-ßGal
Imaging Detection of γH2AX by secondary antibody method Imaging Detection of the Nucleolus by RNA staining reagent
InstrumentFluorescence microscopy
Flow cytometry
Plate readerFluorescence microscopyFluorescence microscopy
SampleLive cells Fixed cellsLive cells
(lysis of live cells)
Fixed cellsFixed cells
data
Item#SG04SG05Green: G265
Red: G266
Deep Red: G267
Green: N511
Red: N512

Feature of Cellular Senescence


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Evaluate senescent cells from various makers

In WI-38 cells at different passages SA-ß-Gal activity, mitochondrial membrane potential, and cellular metabolism (Glucose and Lactate) were evaluated using each specific kit. In senescent cells, SA-ß-Gal activity was enhanced and mitochondrial membrane potential was reduced. Consumption of Glucose and lactate level in the supernatant measured as an indicator of metabolism was increased.

Publications

① H. Tanaka, S. Takebayashi, A. Sakamoto, N. Saitoh, S. Hino and M. Nakao, “The SETD8/PR-Set7 Methyltransferase Functions as a Barrier to Prevent Senescence-Associated Metabolic Remodeling.”, Cell Reports, 2017, 18(9), 2148.
② L. Garcia-Prat, M. Martinez-Vicente and P. Munoz-Canoves, “Autophagy: a decisive process for stemness”, Oncotarget, 2016, 7(11), 12286.
③ M. Bitar, S. Abdel-Halim and F. Al-Mulla, “Caveolin-1/PTRF upregulation constitutes a mechanism for mediating p53-induced cellular senescence: implications for evidence-based therapy of delayed wound healing in diabetes”, Am J Physiol Endocrinol Metab., 2013, 305(8), E951.
④ C. Wiley, M. Velarde, P. Lecot, A. Gerencser, E. Verdin, J. Campisi, et. al., “Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype”, Cell Metab., 2016, 23(2), 303.
⑤ E. Liao, Y. Hsu, Q. Chuah, Y. Lee, J. Hu, T. Huang, P-M Yang & S-J Chiu, “Radiation induces senescence and a bystander effect through metabolic alterations.”, Cell Death Dis., 2014, 5, e1255.
⑥ K. Nishimura, T. Kumazawa, T. Kuroda, A. Murayama, J. Yanagisawa and K. Kimura, “Perturbation of Ribosome Biogenesis Drives Cells into Senescence through 5S RNP-Mediated p53 Activation”, Cell Rep. 2015, 10(8), 1310.
⑦ M. J. Son, Y. Kwon, T. Son and Y. S. Cho, “Restoration of Mitochondrial NAD+ Levels Delays Stem Cell Senescence and Facilitates Reprogramming of Aged Somatic Cells”, Stem Cells. 2016, 34(12), 2840.

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