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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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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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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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Related Experiment Video

Updated: Aug 31, 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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Protein Kinase C Inhibitors Reduce SARS-CoV-2 Replication in Cultured Cells.

Changbai Huang1,2, Fei Feng3, Yongxia Shi4

  • 1Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.

Microbiology Spectrum
|August 24, 2022
PubMed
Summary

Protein Kinase C (PKC) inhibitors significantly reduce SARS-CoV-2 replication by targeting an early infection stage. This discovery highlights PKCs as crucial host factors and PKC inhibitors as promising COVID-19 therapeutics.

Keywords:
PKCSARS-CoV-2replicontranslation

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Area of Science:

  • Virology
  • Cell Biology
  • Pharmacology

Background:

  • Severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) infection presents a significant global health challenge.
  • The urgent need for effective therapeutics against SARS-CoV-2 necessitates exploring novel antiviral strategies.

Purpose of the Study:

  • To investigate the role of protein kinases C (PKCs) in SARS-CoV-2 infection.
  • To evaluate the antiviral potential of PKC inhibitors against SARS-CoV-2.

Main Methods:

  • Testing the efficacy of pan-PKC inhibitors (Go 6983, bisindolylmaleimide I, enzastaurin, sotrastaurin) and a PKCδ-specific inhibitor (rottlerin) on SARS-CoV-2 replication in cell culture models (BHK-21, Huh7, ACE2-expressing A549 cells).
  • Assessing the stage of viral infection targeted by PKC inhibitors.

Main Results:

  • Several PKC inhibitors, including pan-PKC and PKCδ-specific agents, demonstrated significant reduction in SARS-CoV-2 replication.
  • PKC inhibitors were found to interfere with an early step in the SARS-CoV-2 infection cycle.
  • Inhibition of viral replication was confirmed in ACE2-expressing A549 cells using wild-type SARS-CoV-2.

Conclusions:

  • The PKC signaling pathway plays a critical role in SARS-CoV-2 infection.
  • PKC inhibitors exhibit potent antiviral activity against SARS-CoV-2, acting early in the infection process.
  • PKC inhibitors represent promising therapeutic candidates for treating COVID-19.