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Receptor Tyrosine Kinases01:26

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Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...
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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
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Updated: May 14, 2025

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Cellular Receptor Tyrosine Kinase Signaling Plays Important Roles in SARS-CoV-2 Infection.

Shania Sanchez1, Brigitte H Flannery1, Hannah Murphy1

  • 1Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, MN 55108, USA.

Pathogens (Basel, Switzerland)
|May 7, 2025
PubMed
Summary
This summary is machine-generated.

Targeting host receptor tyrosine kinases (RTKs) with inhibitors like Lapatinib shows promise for developing new SARS-CoV-2 antivirals, potentially overcoming drug resistance in COVID-19 treatment.

Keywords:
SARS-CoV-2antiviral therapeutichost signalingreceptor tyrosine kinase (RTK)

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Area of Science:

  • Virology
  • Molecular Biology
  • Drug Discovery

Background:

  • Antiviral drugs targeting viral components risk resistance.
  • Targeting host cell pathways offers a novel strategy for next-generation antivirals.
  • Receptor tyrosine kinases (RTKs) are implicated in coronavirus replication.

Purpose of the Study:

  • To investigate the role of RTKs in SARS-CoV-2 replication.
  • To evaluate the efficacy of RTK inhibitors against SARS-CoV-2.
  • To identify potential host-targeted antiviral therapies for COVID-19.

Main Methods:

  • Utilized A549-ACE2 and Vero-E6 cell lines for SARS-CoV-2 infection models.
  • Administered chemical inhibitors targeting HER2 (Lapatinib), TrkA (GW441756), and EGFR (Gefitinib).
  • Assessed viral replication and therapeutic index (CC50/EC50); conducted time-of-addition experiments.

Main Results:

  • Lapatinib significantly reduced SARS-CoV-2 replication in both cell lines.
  • GW441756 was effective in A549-ACE2 cells but not Vero-E6 cells.
  • Lapatinib indicated early-stage inhibition (entry), while GW441756 affected post-entry steps.

Conclusions:

  • HER2 and TrkA signaling pathways are crucial for SARS-CoV-2 infection in human lung epithelial cells.
  • RTK inhibitors, particularly Lapatinib, demonstrate potential as novel COVID-19 therapeutics.
  • Further research into RTK inhibitors is warranted for developing effective antiviral strategies against SARS-CoV-2.