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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...
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...
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...
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.

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Related Experiment Video

Updated: Jun 17, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Myc and a Cdk2 senescence switch.

Jan van Riggelen, Dean W Felsher

    Nature Cell Biology
    |December 23, 2009
    PubMed
    Summary

    Cyclin-dependent kinase 2 (Cdk2) unexpectedly suppresses Myc-induced senescence, a key step in cancer development. Inhibiting Cdk2 may offer a novel cancer therapy strategy by targeting this failsafe mechanism.

    Area of Science:

    • Molecular biology
    • Cellular senescence
    • Oncogenesis

    Background:

    • The oncogene c-Myc drives cell proliferation but typically induces senescence, a protective mechanism against tumor formation.
    • Cellular senescence is a critical failsafe that prevents uncontrolled cell growth and tumorigenesis.

    Discussion:

    • This study reveals an unappreciated role for Cyclin-dependent kinase 2 (Cdk2) in overcoming c-Myc-induced senescence.
    • Cdk2 activity appears essential for c-Myc to bypass senescence and promote tumor development.
    • Understanding this interaction sheds light on how cancer cells evade growth suppression.

    Key Insights:

    • Cdk2 actively suppresses the senescence response triggered by c-Myc.
    • This suppression mechanism is crucial for c-Myc-driven tumorigenesis.

    More Related Videos

    A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
    13:59

    A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

    Published on: August 12, 2018

    Related Experiment Videos

    Last Updated: Jun 17, 2026

    Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
    12:02

    Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

    Published on: June 6, 2017

    A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
    13:59

    A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

    Published on: August 12, 2018

  • Targeting Cdk2 could be a viable strategy to restore senescence and inhibit cancer progression.

    • Outlook:

    • Further investigation into the precise mechanisms of Cdk2 in senescence suppression is warranted.
    • Exploring Cdk2 inhibitors for cancer therapy holds significant therapeutic potential.
    • This finding may pave the way for novel combination therapies targeting cell cycle regulation in cancer.