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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...
Replication in Eukaryotes01:29

Replication in Eukaryotes

In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
Many Proteins Orchestrate Replication at the Origin
Eukaryotic replication follows many of the same...
Replication in Eukaryotes02:31

Replication in Eukaryotes

Overview
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.

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Related Experiment Video

Updated: May 12, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

YAP/TEAD-mediated transcription controls cellular senescence.

Qi Xie1, Jing Chen, Han Feng

  • 1State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.

Cancer Research
|April 12, 2013
PubMed
Summary

Yes-associated protein (YAP) regulates cellular senescence. YAP deficiency induces senescence, while its expression suppresses it, offering potential cancer therapy targets.

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Last Updated: May 12, 2026

Techniques to Induce and Quantify Cellular Senescence
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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

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Yes-associated protein (YAP) is a key transcription coactivator regulating cell proliferation and apoptosis.
  • The role of YAP in cellular senescence remains largely unexplored.

Purpose of the Study:

  • To elucidate the role of YAP in regulating cellular senescence.
  • To identify downstream targets of YAP involved in senescence.
  • To explore the therapeutic potential of targeting YAP in cancer.

Main Methods:

  • Replication-induced senescence in IMR90 cells.
  • YAP silencing and ectopic expression.
  • TEAD, Rb/p16/p53 pathway analysis.
  • Cdk6 expression and functional assays.
  • Chemotherapeutic agent treatment in tumor cells.

Main Results:

  • YAP protein levels decrease during replication-induced senescence.
  • YAP silencing inhibits proliferation and induces premature senescence.
  • Senescence induced by YAP deficiency is TEAD- and Rb/p16/p53-dependent.
  • Cdk6 is a direct downstream target of YAP, mediating senescence.
  • YAP or Cdk6 expression rescues YAP knockdown-induced senescence.
  • Downregulation of YAP enhances chemotherapy-induced senescence in tumor cells.

Conclusions:

  • YAP plays a critical role in regulating cellular senescence.
  • The YAP-TEAD complex regulates Cdk6 expression, impacting senescence.
  • Targeting YAP or Cdk6 presents a potential therapeutic strategy for tumor suppression via senescence induction.