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Cellular Senescence Pathways Assay (CAT#: STEM-MB-0332-WXH)

Introduction

Cell Senescence is a natural aspect of life. Understanding the various mechanisms that cause the progressive decline of cellular and tissue function may aid in developing therapies to delay or treat age-related conditions and diseases. A variety of stressors, including strong mitogenic signals, DNA damage, and non-genotoxic chromatin perturbations cause cellular senescence - a state of permanent cell cycle arrest. Cellular senescence, although useful in young organisms to prevent cancer, is thought to promote aging. The most consistent determinant of life-span in eukaryotes is the mitogenic growth hormone/IGF-I pathway. However, premature aging syndromes caused by defects in the cellular response/repair to DNA damage indicate the role of accumulated damage. The complex biology of aging is impacted by both environmental and genetic factors: stochastic DNA damage causes decline of function, and genetics determines the rates of damage accumulation and functional decline.




Principle

The occurrence and development of cell senescence is a comprehensive result of multi-factor participation and coordinated regulation of a series of genes. In recent years, multiple signaling pathways related to cell senescence have been discovered, including the classic p53/pRB, insulin/IGF-1, mTOR, AMPK, Cell Senescence and other signaling pathways. These signal pathways are interconnected and influence each other, thus forming a complex cellular senescence regulatory network.

Applications

To study the regulation mechanism of cell senescence signal pathway in disease
To study the effect of each virus on cell senescence signaling pathway
To study the effects of drugs or therapies on cell senescence signaling pathways

Procedure

• Luminex Multiplex Assay
• Enzyme-linked immunosorbent assay (ELISA)
• Flow cytometry (FACS analysis) technology

Notes

Detectable targets: BAD, BAX, PIP2, IP3, STAT2, STAT3, tBID, Bcl-2, JNK, MYD88, Rac1, TLR4, Bcl-xl, APAF-1, MAPK, NAP1, Rel, TLR9, PIDD, icam1, Mda-5, NFκB, RIG-1, TRAF3, AIF, IRF9, MEKK1, p38, RIP1, TRAF5, IAPs, IRF5, MEK3, p38MAPK, SH2, TRAF6, MHC-II, IRS1, MEK6, p50, SLP76, TRAM, PSGL1, IRS2, MSK1, TLR3, Tak1, TRIF, IKB, ISGF3, MSK2, PI3K, TBK1, Vav, PMCA, ISRE, mTOR, PKR

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