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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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Related Experiment Video

Updated: Feb 28, 2026

Growth-based Determination and Biochemical Confirmation of Genetic Requirements for Protein Degradation in Saccharomyces cerevisiae
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HTD1265 Disrupts GimC-Dependent Cellular Processes in Saccharomyces cerevisiae.

Kaori Itto-Nakama1, Naoya Hosoyamada1, Shinsuke Ohnuki1

  • 1Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5 Kashiwano-ha, Kashiwa 277-8562, Chiba, Japan.

Pathogens (Basel, Switzerland)
|February 27, 2026
PubMed
Summary

The antifungal compound HTD1265 disrupts GimC-dependent pathways, affecting fungal cell structure and growth. This mechanism offers a new strategy for combating challenging non-albicans Candida species.

Keywords:
Candida kruseiGimC (prefoldin)Saccharomyces cerevisiaeantifungal agents

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Area of Science:

  • Mycology
  • Molecular Biology
  • Cell Biology

Background:

  • Candida krusei is a challenging non-albicans fungal pathogen.
  • Understanding antifungal mechanisms is crucial for developing new treatments.

Purpose of the Study:

  • To elucidate the mechanism of action of the novel antifungal compound HTD1265.
  • To investigate HTD1265's effects on fungal cellular processes.

Main Methods:

  • Integrative phenotypic analysis in Saccharomyces cerevisiae.
  • High-resolution morphological profiling.
  • Pathway inference and genetic validation.

Main Results:

  • HTD1265 treatment caused nuclear positioning defects and impaired mitotic spindle elongation.
  • The compound induced hallmarks of GimC (prefoldin) deficiency.
  • HTD1265 demonstrated antifungal activity by disrupting GimC-dependent processes, not directly targeting tubulin.

Conclusions:

  • HTD1265 targets GimC-dependent cellular processes, highlighting cytoskeletal and cell wall regulation as a fungal vulnerability.
  • HTD1265 serves as a valuable tool for studying GimC-dependent pathways in fungi.