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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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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

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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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Positive Regulator Molecules01:45

Positive Regulator Molecules

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To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
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M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

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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...
6.0K
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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DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

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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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Related Experiment Video

Updated: Nov 18, 2025

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
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Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

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CDK1/2/5 blockade: killing two birds with one stone.

Jiao Liu1, Rui Kang2, Daolin Tang1,2

  • 1Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.

Oncoimmunology
|February 4, 2021
PubMed
Summary

Dinaciclib, a CDK1/2/5 inhibitor, combats immune-resistant pancreatic cancer. It reduces immune checkpoints and induces immunogenic cell death, transforming cold tumors into hot ones and improving survival in mouse models.

Keywords:
ApoptosisCDKdinaciclibhistoneimmune checkpointimmunogenic cell deathimmunotherapypancreatic cancer

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is a highly immune-resistant malignancy.
  • The tumor microenvironment in PDAC is often characterized as "cold," limiting therapeutic efficacy.

Purpose of the Study:

  • To investigate the therapeutic potential of dinaciclib, a CDK1/2/5 inhibitor, in overcoming immune resistance in PDAC.
  • To elucidate the mechanisms by which dinaciclib modulates the tumor immune microenvironment.

Main Methods:

  • Treatment of PDAC mouse models with dinaciclib.
  • Analysis of immune checkpoint expression.
  • Assessment of histone-dependent immunogenic cell death.
  • Evaluation of tumor microenvironment changes and overall survival.

Main Results:

  • Dinaciclib effectively blocks immune checkpoint expression in PDAC.
  • The drug treatment triggers histone-dependent immunogenic cell death.
  • This dual action converts the "cold" tumor microenvironment to a "hot" one.

Conclusions:

  • Dinaciclib exhibits a dual mechanism of action against PDAC by modulating immune checkpoints and inducing cell death.
  • This approach shows promise in transforming the tumor microenvironment and improving survival in PDAC mouse models.