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Related Concept Videos

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...
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...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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...
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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...

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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Published on: June 6, 2017

Interference between p53 and cdc25C in cell cycle regulation.

Sandra L Ruppenthal1, Andreas Noll, Claudia Götz

  • 1Medical Biochemistry and Molecular Biology, University of the Saarland, D-66424 Homburg, Germany.

International Journal of Oncology
|July 6, 2007
PubMed
Summary

The tumor suppressor p53 inhibits the phosphatase cdc25C, regulating entry into mitosis. This binding interaction is crucial for cell cycle control in mammalian cells, unlike in yeast.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • The eukaryotic cell cycle is tightly regulated by protein kinases and phosphatases.
  • The tumor suppressor p53 is linked to cell cycle regulation through various mechanisms.
  • cdc25C is a key phosphatase controlling entry into mitosis.

Purpose of the Study:

  • To investigate the interaction between p53 and cdc25C in mammalian cells.
  • To determine if cdc25C overexpression can suppress p53-induced growth arrest in mammals.
  • To elucidate the role of p53 in regulating cdc25C phosphatase activity.

Main Methods:

  • Co-immunoprecipitation assays to detect p53-cdc25C interaction.
  • Overexpression studies of cdc25C in mammalian cells.
  • Enzyme activity assays to measure cdc25C phosphatase activity in the presence of p53.

Main Results:

  • Overexpression of cdc25C did not suppress p53-induced growth arrest in mammalian cells.
  • p53 was found to co-immunoprecipitate with cdc25C.
  • p53 inhibited cdc25C phosphatase activity in a dose-dependent manner.

Conclusions:

  • p53 directly interacts with cdc25C.
  • p53 regulates entry into mitosis by inhibiting cdc25C phosphatase activity.
  • This mechanism highlights a conserved role for p53 in cell cycle control.