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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...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
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.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.

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Related Experiment Video

Updated: May 10, 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

The tumor suppressor CDKN3 controls mitosis.

Grzegorz Nalepa1, Jill Barnholtz-Sloan, Rikki Enzor

  • 1Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

The Journal of Cell Biology
|June 19, 2013
PubMed
Summary

The tumor suppressor CDKN3 is crucial for cell division (mitosis) and early cell growth. This phosphatase regulates the cell cycle by dephosphorylating CDC2, impacting cancer therapeutics.

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Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
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Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1

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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
08:33

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

Published on: December 5, 2017

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Last Updated: May 10, 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

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
13:15

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1

Published on: February 25, 2016

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
08:33

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

Published on: December 5, 2017

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Mitosis is a tightly regulated process involving intricate networks of kinases and phosphatases.
  • Understanding the roles of specific phosphatases in mitosis is critical for deciphering cell cycle control and identifying potential therapeutic targets.

Purpose of the Study:

  • To comprehensively screen human phosphatases for their roles in mitosis.
  • To investigate the function of the tumor suppressor CDKN3 in cell cycle regulation and mitosis.
  • To identify downstream targets and signaling pathways regulated by CDKN3 during mitosis.

Main Methods:

  • Genome-wide small interfering RNA (siRNA) screen of human phosphatases.
  • Cell cycle analysis and assessment of mitotic progression.
  • Western blotting to detect phosphorylated CDC2 (pThr-161).
  • Phosphokinome-wide mass spectrometry to identify CDKN3 signaling effectors.
  • Immunofluorescence microscopy to visualize protein localization.
  • Analysis of CDKN3 protein levels in brain tumor samples.

Main Results:

  • Identified four candidate spindle checkpoint phosphatases, including CDKN3.
  • Demonstrated that CDKN3 is essential for normal mitosis and the G1/S cell cycle transition.
  • Showed that CDKN3 dephosphorylates CDC2 at threonine-161 during mitotic exit.
  • Identified CKβ phosphorylated at serine 209 as a downstream target of the CDKN3-CDC2 axis, localizing to mitotic centrosomes and controlling the spindle checkpoint.
  • Observed down-regulation of CDKN3 protein in brain tumors.

Conclusions:

  • CDKN3 plays a vital role in regulating mitosis and cell cycle progression through the CDC2 signaling pathway.
  • The findings highlight CDKN3's function in maintaining genomic stability and its potential as a therapeutic target in cancers, particularly brain tumors.