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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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Development and Application of Rapamycin-regulated Tyrosine Phosphatases
06:56

Development and Application of Rapamycin-regulated Tyrosine Phosphatases

Published on: September 6, 2024

Cdk5 regulates Rap1 activity.

Elias Utreras1, Daniel Henriquez, Erick Contreras-Vallejos

  • 1Laboratory of Cellular and Neuronal Dynamics, Department of Biology, Faculty of Sciences, Universidad de Chile, Chile.

Neurochemistry International
|February 19, 2013
PubMed
Summary
This summary is machine-generated.

Cyclin-dependent kinase 5 (Cdk5) phosphorylates C3G, influencing Rap1 protein stability and activity. This Cdk5-mediated phosphorylation of C3G impacts neuronal functions like migration and differentiation.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Signaling

Background:

  • Rap1 signaling pathways are crucial for fundamental neuronal processes including migration, differentiation, and polarity.
  • Cyclin-dependent kinase 5 (Cdk5) plays a significant role in neuronal development and migration.
  • Cdk5 activity is regulated by its activator p35, and its inhibition affects Rap1 levels.

Purpose of the Study:

  • To investigate the potential link between Cdk5-dependent phosphorylation of C3G and its regulation of Rap1 expression and activity.
  • To elucidate the molecular mechanism by which Cdk5 influences Rap1 signaling.

Main Methods:

  • Co-transfection of C3G and a tet-OFF system for p35 (Cdk5 activator) in COS-7 cells.
  • Immunoprecipitation and Western blot analysis to assess C3G phosphorylation and Rap1 protein levels.
  • Utilized roscovitine (Cdk5 inhibitor) and MG-132 (proteasome inhibitor) to modulate signaling pathways.
  • Analysis of Cdk5(-/-) and Cdk5(+/+) mouse brains to confirm in vivo findings.

Main Results:

  • Overexpression of p35 increased serine phosphorylation of C3G, while its inhibition or Cdk5 inhibition decreased it.
  • Proteasome inhibition rescued Rap1 protein levels when Cdk5 activity was inhibited.
  • C3G phosphorylation and Rap1 protein levels were reduced in Cdk5 knockout brains.
  • p35 overexpression enhanced Rap1 activity, whereas inhibition of p35 or Cdk5 reduced Rap1 activity.

Conclusions:

  • Cdk5-mediated serine phosphorylation of C3G is a key regulator of Rap1 protein stability and activity.
  • This regulatory mechanism involving Cdk5, C3G, and Rap1 signaling has significant implications for neuronal functions such as migration, differentiation, and polarity.