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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...
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...
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...
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.

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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Replication checkpoint control by a PTK/STAT3/cyclin D1 axis.

Ben J Shields1, Tony Tiganis

  • 1Department of Biochemistry and Molecular Biology, Monash University, Victoria, Australia.

Cell Cycle (Georgetown, Tex.)
|January 24, 2009
PubMed
Summary
This summary is machine-generated.

Protein tyrosine kinases (PTKs) and phosphatases (PTPs) regulate cell cycle checkpoints. PTK-mediated STAT3 signaling and ATR cascades suppress S-phase progression, impacting genomic stability.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Tyrosine phosphorylation signaling, regulated by protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs), is crucial for cell cycle progression.
  • While traditionally linked to the G1 phase, PTKs and PTPs increasingly show roles in later cell cycle stages.

Purpose of the Study:

  • To explore the roles of PTKs and PTPs in cell cycle checkpoints.
  • To highlight recent findings on the interplay between PTK-STAT3 signaling and ATR cascades in regulating the replication checkpoint.

Main Methods:

  • Review of existing literature on PTKs, PTPs, and cell cycle checkpoints.
  • Discussion of experimental findings related to STAT3 signaling, cyclin D1 depletion, and ATR-instigated cascades.

Main Results:

  • Attenuation of PTK-mediated STAT3 signaling contributes to cyclin D1 depletion.
  • STAT3 signaling collaborates with ATR-dependent pathways to inhibit S-phase progression.
  • Oncogenic PTK pathways may circumvent the replication checkpoint, leading to genomic instability.

Conclusions:

  • PTKs and PTPs are critical regulators of cell cycle checkpoints, particularly the replication checkpoint.
  • Integrated signaling responses involving PTKs, PTPs, and ATR are essential for maintaining genomic integrity.
  • Dysregulation of PTK pathways can promote genomic instability by bypassing replication checkpoints.