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Related Concept Videos

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 Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
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.
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...

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Updated: May 9, 2026

Studying Mitochondrial Structure and Function in Drosophila Ovaries
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Published on: January 4, 2017

MEK drives cyclin D1 hyperelevation during geroconversion.

O V Leontieva1, Z N Demidenko, M V Blagosklonny

  • 1Department of Cell Stress Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.

Cell Death and Differentiation
|July 16, 2013
PubMed
Summary

Inhibiting MEK signaling prevents cyclin D1 accumulation, a key marker of cellular senescence. This suggests that cyclin D1

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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

Area of Science:

  • Cellular senescence
  • Molecular biology
  • Cell cycle regulation

Background:

  • Cellular senescence is a state of irreversible cell cycle arrest.
  • Mechanistic Target of Rapamycin (MTOR) promotes the conversion of reversible cell cycle arrest into senescence (geroconversion).
  • Cyclin D1 is a known marker of senescence, alongside other indicators like hypertrophy and beta-Gal staining.

Purpose of the Study:

  • To investigate the role of mitogen-activated/extracellular signal-regulated kinase (MEK) signaling in cyclin D1 accumulation during senescence.
  • To determine if MEK inhibition can prevent cyclin D1 expression in different senescence models.
  • To explore the relationship between cyclin D1 expression and other senescence hallmarks.

Main Methods:

  • Induction of senescence using p21 and p16.
  • Treatment with MEK inhibitors (U0126, PD184352, siRNA) and cyclin-dependent kinase (CDK) 4/6 inhibitor (PD0332991).
  • Analysis of cyclin D1 expression and other senescence markers in various cell types (MEL10, RPE cells).

Main Results:

  • MEK inhibitors completely prevented cyclin D1 accumulation in p21- and p16-induced senescence.
  • In cells where MEK inhibitors did not affect MTOR, U0126 induced cyclin D1-negative senescence.
  • CDK4/6 inhibition induced cyclin D1-positive senescence, which was suppressed by rapamycin (MTOR inhibitor).

Conclusions:

  • MEK inhibition effectively eliminates cyclin D1, a key senescence marker, independently of MTOR activity.
  • Hallmarks of senescence can be dissociated, as cyclin D1 elevation does not always correlate with other senescence markers.
  • MEK signaling is a critical regulator of cyclin D1 expression in cellular senescence.