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Related Concept Videos

S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.
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...
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...

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CDC6: from DNA replication to cell cycle checkpoints and oncogenesis.

Luis R Borlado1, Juan Méndez

  • 1DNA replication Group, Molecular Oncology Programme, Spanish National Cancer Research Centre, Melchor Fernández Almagro 3, E-28029 Madrid, Spain.

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Cell division cycle 6 (CDC6) regulates DNA replication and cell cycle checkpoints. CDC6 overexpression can lead to carcinogenesis by affecting tumor suppressor genes and promoting DNA hyperreplication.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Cell division cycle 6 (CDC6) is crucial for DNA replication initiation in eukaryotes.
  • CDC6 is known to assemble prereplicative complexes during the G1 phase.
  • Emerging evidence suggests CDC6 has roles beyond DNA replication, including in cell cycle checkpoints and potential proto-oncogenic activity.

Purpose of the Study:

  • To investigate the proto-oncogenic activity of CDC6.
  • To elucidate the mechanisms by which CDC6 overexpression contributes to carcinogenesis.
  • To understand the impact of CDC6 deregulation on tumor suppressor genes and cellular responses.

Main Methods:

  • Analysis of CDC6 function in DNA replication and cell cycle regulation.
  • Investigation of CDC6's role in checkpoint mechanisms.
  • Studies on the effects of CDC6 overexpression on INK4/ARF tumor suppressor genes.
  • Examination of epigenetic modifications at the INK4/ARF locus.
  • Assessment of DNA hyperreplication and senescence induction in primary cells.

Main Results:

  • CDC6 overexpression interferes with INK4/ARF tumor suppressor gene expression.
  • This interference occurs via epigenetic modification of chromatin at the INK4/ARF locus.
  • Overexpression of CDC6 in primary cells can lead to DNA hyperreplication.
  • CDC6 overexpression induces a senescence response, similar to oncogene activation.

Conclusions:

  • Deregulation of CDC6 expression presents a significant risk for human carcinogenesis.
  • CDC6's proto-oncogenic activity is linked to its influence on epigenetic regulation and cell cycle control.
  • Understanding CDC6's multifaceted roles is critical for cancer prevention and therapy.