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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...
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.
Cells Coordinate Growth and Proliferation02:36

Cells Coordinate Growth and Proliferation

Cell size is a significant factor impacting cellular design, function, and fitness. There exists some internal coordination by which cells double their masses before division, thus, achieving homeostasis. Coordination between cell growth and proliferation depends on the checkpoints in between cell cycle phases. Loss of coordination or failure in the checkpoint mechanism can drive the cell to uncontrolled growth and loss of cellular function. Like dividing cells that coordinate cellular growth,...
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

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Updated: Jul 2, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

ING1a expression increases during replicative senescence and induces a senescent phenotype.

Mohamed A Soliman1, Philip Berardi, Svitlana Pastyryeva

  • 1Department of Biochemistry and Molecular Biology, University of Calgary, Calgary, Alberta, Canada.

Aging Cell
|August 12, 2008
PubMed
Summary

The ING1a protein antagonizes apoptosis and promotes cellular senescence by altering chromatin structure. Its ratio with ING1b isoform is crucial for establishing the senescent phenotype.

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Induction and Validation of Cellular Senescence in Primary Human Cells
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Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

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Last Updated: Jul 2, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Induction and Validation of Cellular Senescence in Primary Human Cells
08:18

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The ING family of tumor suppressor proteins regulates cell growth, apoptosis, and DNA damage response by modulating chromatin structure.
  • ING1 locus has two major splicing isoforms: ING1a and ING1b, with INGlb known to induce apoptosis, while ING1a's function is unclear.

Purpose of the Study:

  • To investigate the function of the ING1a isoform and its role in cellular senescence.
  • To determine how alternative splicing of ING1 affects the ratio of ING1a to ING1b and its phenotypic consequences.

Main Methods:

  • Analysis of ING1 splicing isoform ratios in senescent versus low-passage fibroblasts.
  • Assessment of ING1a's effects on senescence-associated markers (heterochromatic foci, beta-galactosidase activity, cell morphology, cell cycle arrest).
  • Gene expression analysis (retinoblastoma, p16, PCNA) and chromatin immunoprecipitation (ChIP) to study HDAC targeting.

Main Results:

  • Alternative splicing significantly alters the ING1a:ING1b ratio in senescent cells.
  • ING1a antagonizes INGlb's apoptotic function and induces senescence hallmarks.
  • ING1a affects gene expression by increasing retinoblastoma and p16 levels and opposing PCNA expression, potentially via HDAC targeting.

Conclusions:

  • ING1a plays a novel role in promoting cellular senescence and antagonizing apoptosis.
  • Altered ratios of ING1 splicing isoforms contribute to senescence through chromatin remodeling mediated by HDAC and HAT complexes.