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Related Concept Videos

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...
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Positive Regulator Molecules02:39

Positive Regulator Molecules

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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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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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Anaphase Promoting Complex00:50

Anaphase Promoting Complex

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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...
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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Related Experiment Video

Updated: Jan 8, 2026

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

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Recent Developments in Cyclin-Dependent Kinase (CDK) PROTAC in Cancer Therapy.

Arijit Nandi1, Anwesha Das2, M Rhia L Stone1

  • 1Centre for Superbug Solutions, Institute for Molecular Bioscience, The University of Queensland, Brisbane 4067, Queensland Australia.

ACS Medicinal Chemistry Letters
|December 17, 2025
PubMed
Summary

Cyclin-dependent kinase (CDK)-based Proteolysis Targeting Chimeras (PROTACs) show promise for cancer treatment. This review covers 2024 advancements in CDK-targeting PROTACs, including computational screening, linker strategies, and E3 ligase applications.

Keywords:
chimeraheterobifunctionalserine-threonine kinasetargeted protein degradationternary complex

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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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Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
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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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Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
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Area of Science:

  • Oncology
  • Medicinal Chemistry
  • Drug Discovery

Background:

  • Proteolysis Targeting Chimeras (PROTACs) represent a novel therapeutic modality.
  • Cyclin-dependent kinases (CDKs) are crucial regulators of the cell cycle and are frequently dysregulated in cancer.
  • Targeting CDKs with small molecules has been a long-standing strategy in oncology.

Purpose of the Study:

  • To provide a comprehensive overview of the current landscape of anti-cancer PROTAC development targeting the CDK family.
  • To highlight recent advancements and emerging strategies in CDK-based PROTAC design and application as of 2024.

Main Methods:

  • Review of recent scientific literature and patent filings related to CDK-targeting PROTACs.
  • Analysis of computational screening approaches for PROTAC design.
  • Discussion of structure-activity relationships (SAR) and linker optimization strategies.
  • Exploration of alternative degradation strategies and novel E3 ligase utilization.

Main Results:

  • Significant progress has been made in developing CDK-targeting PROTACs for various cancers.
  • Computational screening aids in identifying potential PROTAC candidates.
  • Diverse linker chemistries and E3 ligases are being explored to optimize degradation efficiency and selectivity.
  • Strategies to improve pharmacokinetic properties of heterobifunctional molecules are under investigation.

Conclusions:

  • CDK-based PROTACs are a rapidly advancing field with substantial therapeutic potential in oncology.
  • Continued innovation in linker technology, E3 ligase recruitment, and molecular design is key to realizing their full clinical benefit.
  • Further research is needed to optimize drug-like properties and clinical efficacy for patient benefit.