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Related Concept Videos

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.
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.
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...
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...

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Related Experiment Video

Updated: May 9, 2026

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

Targeting Transcriptional Cyclin-Dependent Kinases in Cancer.

Aleksandra Kolodziejczyk1,2, Piotr Sicinski1,2

  • 1Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.

Molecular Cancer Therapeutics
|July 15, 2025
PubMed
Summary

Transcriptional cyclin-dependent kinases (tCDKs) are crucial for cancer growth. Inhibiting tCDKs shows promise in preclinical cancer models by selectively targeting cancer cells, offering a new therapeutic avenue.

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Last Updated: May 9, 2026

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

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Published on: May 3, 2018

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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A Murine Cell Line Based Model of Chronic CDK9 Inhibition to Study Widespread Non-Genetic Transcriptional Elongation Defects (TEdeff) in Cancers
10:49

A Murine Cell Line Based Model of Chronic CDK9 Inhibition to Study Widespread Non-Genetic Transcriptional Elongation Defects (TEdeff) in Cancers

Published on: September 26, 2019

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Pharmacology

Background:

  • Cyclin-dependent kinases (CDKs) are vital for cell cycle and transcription.
  • Dysregulated CDKs are common in cancer.
  • Transcriptional CDKs (tCDKs) are emerging as key therapeutic targets.

Purpose of the Study:

  • To explore the therapeutic potential of targeting transcriptional CDKs (tCDKs) in cancer treatment.
  • To highlight the role of tCDKs in tumor growth and survival.
  • To discuss challenges and future directions in tCDK inhibitor development.

Main Methods:

  • Review of preclinical studies on tCDK inhibitors.
  • Analysis of the mechanisms underlying tCDK selectivity in cancer cells.
  • Exploration of emerging strategies like targeted protein degradation.

Main Results:

  • tCDK inhibitors demonstrate efficacy in preclinical cancer models.
  • Selectivity is observed due to cancer cells' heightened dependence on transcription (oncogene addiction).
  • tCDKs regulate critical processes like RNA polymerase activation and transcriptional elongation.

Conclusions:

  • Targeting tCDKs is a promising strategy for cancers with high transcriptional activity.
  • Challenges include inhibitor specificity and understanding broader biological impacts.
  • Further research and novel strategies like targeted degradation are needed for clinical translation.