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Related Concept Videos

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.
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...

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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

Dynamics of Cdk1 substrate specificity during the cell cycle.

Mardo Kõivomägi1, Ervin Valk, Rainis Venta

  • 1Institute of Technology, University of Tartu, Tartu 50411, Estonia. mart.loog@ut.ee

Molecular Cell
|June 11, 2011
PubMed
Summary

Cyclin-dependent kinase 1 (Cdk1) substrate specificity changes gradually with cell cycle progression, driven by both active site and cyclin docking interactions. This dynamic specificity ensures precise cell cycle timing.

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Published on: October 26, 2015

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cyclin-dependent kinases (Cdks) regulate cell cycle progression through substrate phosphorylation.
  • Cdk specificity is influenced by active site properties and cyclin docking interactions.
  • The precise roles of these factors in Cdk1 timing remain debated.

Purpose of the Study:

  • To investigate how budding yeast cyclins modulate Cdk1 substrate specificity during the cell cycle.
  • To determine the relative contributions of intrinsic Cdk1 active site and cyclin docking elements.
  • To identify specific Cdk1 targets for different cyclins.

Main Methods:

  • Analysis of budding yeast cyclins (Cln2, Clb5, Clb3, Clb2) and their interaction with Cdk1.
  • Assessing Cdk1 activity toward consensus motifs.
  • Identifying cyclin-specific docking elements and Cdk1 targets.

Main Results:

  • Cdk1 activity toward consensus motifs increased progressively with the sequence Cln2-Clb5-Clb3-Clb2, mirroring cell cycle progression.
  • A docking element was identified that enhances Cln2-Cdk1 specificity for G1 targets.
  • Cln2-Cdk1 exhibited unique consensus site specificity, indicating cyclins modulate active site preferences.
  • Specific Cdk1 targets for Cln2, Clb3, and Clb2 were identified.

Conclusions:

  • Gradual changes in Cdk1 substrate specificity, modulated by cyclins, are crucial for robust cell cycle timing and ordering.
  • Cyclins actively shape Cdk1 specificity beyond simple activation.
  • Understanding these mechanisms provides insight into cell cycle regulation.