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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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...
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...

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Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast
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MAPK pathway activation delays G2/M progression by destabilizing Cdc25B.

Puji Astuti1, Tanya Pike, Charlotte Widberg

  • 1Diamantina Institute for Cancer Immunology and Metabolic Medicine, University of Queensland, Brisbane 4102, Queensland, Australia.

The Journal of Biological Chemistry
|October 6, 2009
PubMed
Summary

Mitogen-activated protein kinase (MAPK) pathway activation delays cell cycle G2 phase entry and blocks G2 checkpoint exit. This occurs via MEK1-dependent destabilization of cdc25B, a key G2/M regulator.

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12:26

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

Published on: May 3, 2018

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • The role of the mitogen-activated protein kinase (MAPK) pathway in G2/M phase progression is debated.
  • Growth factors and phorbol esters activate MAPK signaling, impacting cell cycle progression.

Purpose of the Study:

  • To elucidate the specific role of the MAPK pathway in G2/M phase progression.
  • To investigate the mechanism by which MAPK activation influences entry into mitosis and G2 checkpoint control.

Main Methods:

  • Activation of the MAPK pathway using epidermal growth factor (EGF) or 12-O-tetradecanoylphorbol-13-acetate (TPA).
  • Assessment of G2 phase delay and G2 checkpoint arrest.
  • Investigation of the involvement of MAPK/extracellular signal-regulated kinase kinase 1 (MEK1).
  • Analysis of cdc25B stability and function.

Main Results:

  • MAPK pathway activation induced a G2 phase delay independent of known checkpoint pathways but dependent on MEK1.
  • MAPK signaling blocked exit from G2 checkpoint arrest.
  • MEK1-dependent destabilization of cdc25B mediated the G2 delay and blocked checkpoint exit.
  • Reintroduction of cdc25B rescued the MEK1-dependent G2 delay.

Conclusions:

  • MEK1 has a novel function in controlling G2/M progression by regulating cdc25B stability.
  • MAPK signaling influences mitotic entry timing and G2 checkpoint exit via cdc25B destabilization.
  • This study reveals a new mechanism for MAPK pathway involvement in cell cycle control.