Senescence Map Selection Guide

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

Product Cellular Senescence Detection Kit - SPiDER-βGal Cellular Senescence Plate Assay Kit - SPiDER-βGal DNA Damage Detection Kit – γH2AX *Please Contact Us Nucleolus Bright Green / Red
Detection Fluorescence Fluorescence Fluorescence Fluorescence



500 - 540 nm / 530 - 570 nm 535 nm / 580 nm Green: 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
Indicator SA-β-gal activity SA-β-gal activity Changes in DNA Damage Changes in the Nucleolus
Detection method Imaging
Substrate: SPiDER-βGal
Plate Assay
Substrate: SPiDER-βGal
Imaging Detection of γH2AX
secondary antibody method
Imaging Detection of the
Nucleolus by RNA staining reagent
Instrument  Fluorescence
 Microscopy                           Flow cytometry
Plate Reader  Fluorescence                 Microscopy  Fluorescence           Microscopy
Sample Live Cells, Fixed Cells Live cells(Lysis of live cells) Fixed cells Fixed cells
Item# SG03 SG05 Green: G265 / Red:G266
Deep Red: G267
Green: N511 / Red: N512



Feature of Cellular Senescence


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.



Fluctuation of factors involved in cellular senescence



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 Reports2017, 18(9), 2148.
② L. Garcia-Prat, M. Martinez-Vicente and P. Munoz-Canoves, “Autophagy: a decisive process for stemness”Oncotarget2016, 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 Rep2015, 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 Cells2016, 34(12), 2840.

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