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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...
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.
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...

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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

Cdk activity couples epigenetic centromere inheritance to cell cycle progression.

Mariana C C Silva1, Dani L Bodor, Madison E Stellfox

  • 1Instituto Gulbenkian de Ciência, 2780-156 Oeiras, Portugal.

Developmental Cell
|December 16, 2011
PubMed
Summary

Centromere identity is epigenetically maintained by CENP-A nucleosomes. Inhibiting Cdk1/Cdk2 activity triggers CENP-A assembly cell-wide, revealing cell cycle regulation of this crucial process.

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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
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Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
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Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

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Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
05:35

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Published on: March 3, 2016

Area of Science:

  • Cell Biology
  • Epigenetics
  • Molecular Biology

Background:

  • Centromeres are critical chromosomal regions for accurate cell division.
  • Epigenetic maintenance of centromeres relies on the histone H3 variant CENP-A.
  • CENP-A chromatin assembly is tightly regulated and uncoupled from DNA replication.

Purpose of the Study:

  • To investigate the cell cycle regulation of CENP-A assembly.
  • To identify factors controlling CENP-A localization during the cell cycle.
  • To elucidate the mechanism coupling CENP-A assembly to cell division.

Main Methods:

  • Cell cycle synchronization and inhibition of Cyclin-dependent kinases (Cdks) Cdk1 and Cdk2.
  • Immunofluorescence microscopy to assess CENP-A and Mis18BP1 localization.
  • Western blotting to analyze protein phosphorylation states.

Main Results:

  • Inhibition of Cdk1 and Cdk2 activity induced CENP-A assembly outside of mitotic exit.
  • The key assembly factor Mis18BP1 (HsKNL2) phosphorylation is cell cycle-dependent, controlling its centromeric localization.
  • Cdk activity maintains the CENP-A assembly machinery in an inactive, non-centromeric state during S, G2, and M phases.

Conclusions:

  • CENP-A assembly is poised for activation throughout the cell cycle.
  • Cdk activity acts as a gatekeeper, restricting CENP-A assembly to G1 phase.
  • This regulation ensures proper coordination between DNA replication, cell division, and centromere maturation.