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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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.
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...
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...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

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Related Experiment Video

Updated: Jun 23, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Origin licensing and p53 status regulate Cdk2 activity during G(1).

Kathleen R Nevis1, Marila Cordeiro-Stone, Jeanette Gowen Cook

  • 1Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA.

Cell Cycle (Georgetown, Tex.)
|May 15, 2009
PubMed
Summary
This summary is machine-generated.

Origin licensing, crucial for DNA replication, prevents rereplication. Inhibiting licensing factors Cdc6 or Cdt1 in normal cells causes G1 arrest, while cancer cells undergo apoptosis, revealing cell-type specific responses.

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Related Experiment Videos

Last Updated: Jun 23, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Area of Science:

  • Cell Cycle Regulation
  • DNA Replication Licensing
  • Molecular Biology

Background:

  • DNA replication origins are licensed by prereplication complexes during G1 phase.
  • Regulatory mechanisms prevent new licensing after the G1/S transition to avoid rereplication.
  • Coordination between S phase entry and origin licensing completion is not fully understood.

Purpose of the Study:

  • To investigate the role of origin licensing factors Cdc6 and Cdt1 in cell cycle progression.
  • To elucidate the mechanisms coordinating S phase entry with origin licensing.
  • To compare the effects of licensing inhibition in normal versus cancer cells.

Main Methods:

  • Depletion of essential licensing factors Cdc6 or Cdt1 in normal human fibroblasts.
  • Analysis of cell cycle arrest, cyclin E/Cdk2 activity, and Rb phosphorylation.
  • Comparison of licensing inhibition effects in HeLa and U2OS cancer cell lines.
  • Co-depletion of Cdc6 and p53 in normal cells to assess p53's role.

Main Results:

  • Depletion of Cdc6 or Cdt1 in normal fibroblasts induced G1 arrest, inhibited cyclin E/Cdk2 activity, and caused Rb hypophosphorylation.
  • Inhibition of licensing in cancer cells led to apoptosis, without affecting Cdk2 or Rb phosphorylation.
  • Co-depletion of Cdc6 and p53 in normal cells restored Cdk2 activation and Rb phosphorylation, allowing S phase entry with DNA damage.

Conclusions:

  • Origin licensing is essential for multiple G1 progression events in normal cells.
  • A mechanism preventing premature S phase entry relies on origin licensing and p53.
  • This mechanism functions in normal cells but is impaired in p53-deficient cancer cells.