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Related Concept Videos

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...
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.
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.
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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...

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Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
13:15

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Published on: February 25, 2016

LKB1 catalytically deficient mutants enhance cyclin D1 expression.

Kristine D Scott1, Suchita Nath-Sain, Meghan D Agnew

  • 1Department of Biochemistry and Molecular Biology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.

Cancer Research
|June 19, 2007
PubMed
Summary

Mutations in the tumor suppressor LKB1 (serine-threonine kinase) are linked to Peutz-Jeghers syndrome and cancer. Deficient LKB1 mutants promote cell cycle progression and oncogenic activity, unlike functional LKB1 which halts cell division.

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Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Cycle Regulation

Background:

  • Mutations in the serine-threonine kinase LKB1 cause Peutz-Jeghers syndrome, increasing cancer risk.
  • LKB1 mutations are also found in sporadic cancers, indicating a broader role in tumorigenesis.

Purpose of the Study:

  • To investigate the role of catalytically deficient LKB1 mutants in colorectal cancer cell cycle progression.
  • To determine if LKB1 mutants possess oncogenic properties beyond compromising tumor suppression.

Main Methods:

  • Introduction of wild-type LKB1 and catalytically deficient LKB1 mutants into DLD1p21-/-p53-/- colorectal cancer cells.
  • Analysis of cell cycle progression, including Rb, cyclin E, cyclin A2, and cyclin D1 expression.
  • Assessment of LKB1 mutant recruitment to oncogene promoter regions.

Main Results:

  • Catalytically deficient LKB1 mutants promoted cell cycle progression into S phase and increased expression of Rb, cyclin E, and cyclin A2.
  • Wild-type LKB1 induced G1 cell cycle arrest, independent of p21(WAF/CIP1) and p53.
  • LKB1 mutants activated cyclin D1 expression by binding to oncogene promoter response elements.

Conclusions:

  • LKB1's tumor-suppressor function is compromised by catalytically deficient mutants.
  • These LKB1 mutants exhibit novel oncogenic properties, contributing to cancer development.