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Related Concept Videos

S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

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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).
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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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The DNA Replication Fork01:02

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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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Inhibition of Cdk Activity02:34

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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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Positive Regulator Molecules02:39

Positive Regulator Molecules

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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.
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Negative Regulator Molecules01:23

Negative Regulator Molecules

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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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Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
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Cyclin E/CDK2: DNA Replication, Replication Stress and Genomic Instability.

Rafaela Fagundes1, Leonardo K Teixeira1

  • 1Group of Cell Cycle Control, Program of Immunology and Tumor Biology, Brazilian National Cancer Institute (INCA), Rio de Janeiro, Brazil.

Frontiers in Cell and Developmental Biology
|December 13, 2021
PubMed
Summary
This summary is machine-generated.

The Cyclin E/CDK2 complex is crucial for normal DNA replication and cell cycle progression. Its oncogenic activation causes replication stress, DNA damage, and genomic instability, contributing to human cancer.

Keywords:
CCNECDK2DNA replicationcancercell cyclecyclin Egenomic instabilityreplication stress

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Cell cycle progression, including DNA replication, is tightly regulated by Cyclin-Dependent Kinases (CDKs) and their cyclin partners.
  • E-type cyclins (Cyclin E1 and Cyclin E2, encoded by CCNE1 and CCNE2 genes) complex with CDK2 to drive the G1/S phase transition.

Purpose of the Study:

  • To review the essential functions of the Cyclin E/CDK2 complex in normal DNA replication.
  • To elucidate the molecular mechanisms underlying replication stress and genomic instability induced by oncogenic Cyclin E/CDK2 activation in human cancers.

Main Methods:

  • Literature review focusing on Cyclin E/CDK2 functions.
  • Analysis of molecular mechanisms linking Cyclin E/CDK2 to replication stress.
  • Examination of the role of Cyclin E/CDK2 in genomic instability and carcinogenesis.

Main Results:

  • Cyclin E/CDK2 complex regulates cell cycle and DNA replication via substrate phosphorylation.
  • Aberrant Cyclin E/CDK2 activity disrupts normal DNA replication, leading to replication stress and DNA damage.
  • Replication stress induced by oncogenic Cyclin E/CDK2 contributes to genomic instability and cancer development.

Conclusions:

  • The Cyclin E/CDK2 complex plays a dual role in cell cycle regulation, being essential for normal progression but also a driver of cancer when aberrantly activated.
  • Understanding the mechanisms of Cyclin E/CDK2-mediated replication stress is critical for developing targeted cancer therapies.