Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Targeted cancer therapy: the initial high concentration may slow down the selection for resistance.

Aging·2024
Same author

From osimertinib to preemptive combinations.

Oncotarget·2024
Same author

My battle with cancer. Part 1.

Oncoscience·2024
Same author

Towards disease-oriented dosing of rapamycin for longevity: does aging exist or only age-related diseases?

Aging·2023
Same author

Evaluation of off-label rapamycin use to promote healthspan in 333 adults.

GeroScience·2023
Same author

Apoptotic cell death in disease-Current understanding of the NCCD 2023.

Cell death and differentiation·2023

Related Experiment Video

Updated: Jun 22, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Rapamycin decelerates cellular senescence.

Zoya N Demidenko1, Svetlana G Zubova, Elena I Bukreeva

  • 1Oncotarget, Albany, NY, USA.

Cell Cycle (Georgetown, Tex.)
|May 28, 2009
PubMed
Summary
This summary is machine-generated.

Cellular senescence, a permanent loss of proliferation, can be reversed. Rapamycin, an mTOR inhibitor, prevents irreversible cell cycle arrest, allowing cells to regain proliferative capacity after the arrest is lifted.

More Related Videos

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs
07:39

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

Related Experiment Videos

Last Updated: Jun 22, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs
07:39

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pharmacology

Background:

  • Cellular senescence is a state of permanent growth arrest.
  • Proliferative potential is progressively lost during prolonged cell cycle arrest.
  • Senescence is characterized by cell cycle arrest without inhibiting cellular growth.

Purpose of the Study:

  • To investigate the role of cell cycle arrest duration in senescence.
  • To determine if pharmacological intervention can prevent irreversible senescence.
  • To explore the effect of rapamycin on cell cycle arrest and senescence.

Main Methods:

  • Utilized human and rodent cell lines.
  • Induced cell cycle arrest using ectopic p21, p16, and sodium butyrate.
  • Administered rapamycin (an mTOR inhibitor) during cell cycle arrest.

Main Results:

  • The duration of cell cycle arrest directly correlates with the loss of proliferative capacity.
  • Rapamycin significantly slowed the loss of proliferative potential in arrested cells.
  • Cells treated with rapamycin during arrest retained the ability to proliferate after arrest removal.

Conclusions:

  • Pharmacological suppression of senescence is achievable.
  • Rapamycin transforms irreversible cell cycle arrest into a reversible state.
  • mTOR inhibition prevents permanent loss of proliferative potential during cell cycle arrest.