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Related Experiment Video

Updated: Oct 1, 2025

Author Spotlight: Identifying Compensatory Pathways in Malaria Parasites Containing Hypomorphic Allele of Essential Protein Kinases
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Covalent inhibition of Plasmodium falciparum Ubc13 impairs global protein synthesis.

Anna Truong1, Ruitian Hu1, Baiyi Quan1

  • 1Department of Chemistry, Duke University, Durham, NC 27708, USA.

Iscience
|June 10, 2025
PubMed
Summary

Ubiquitin-conjugating enzyme 13 (Ubc13) is crucial for Plasmodium falciparum. Inhibiting PfUbc13 with NSC697923 reduces parasite growth and protein synthesis, showing its potential as an antimalarial drug target.

Keywords:
Biological sciencesMicrobiologyNatural sciencesPharmacology

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Area of Science:

  • Biochemistry
  • Parasitology
  • Drug Discovery

Background:

  • Ubiquitin-conjugating enzyme 13 (Ubc13) plays a key role in protein modification.
  • Lysine 63-linked ubiquitin (K63-Ub) conjugation by Ubc13 is essential, but its function in Plasmodium parasites is poorly understood.
  • Artemisinin's antimalarial activity may involve Ubc13.

Purpose of the Study:

  • To characterize the function of Plasmodium falciparum Ubc13 (PfUbc13).
  • To evaluate the antimalarial potential of a novel PfUbc13 inhibitor, NSC697923.
  • To elucidate the role of K63-ubiquitination in Plasmodium parasites.

Main Methods:

  • Chemical characterization and deployment of NSC697923, a covalent inhibitor of PfUbc13.
  • Assessment of NSC697923's inhibitory effects on parasite life stages and drug synergy.
  • Chemoproteomic analysis to identify PfUbc13 substrates.
  • Measurement of nascent protein synthesis.

Main Results:

  • NSC697923 covalently inhibits PfUbc13 with nanomolar potency.
  • The inhibitor reduced parasite growth across multiple life stages and synergized with dihydroartemisinin.
  • NSC697923 treatment decreased K63-ubiquitination and nascent protein synthesis in blood-stage parasites.
  • 31 putative PfUbc13 substrates were identified, enriched in transcription, translation, and proteasome pathways.

Conclusions:

  • PfUbc13 and K63-ubiquitination are critical for protein translation in Plasmodium.
  • NSC697923 effectively targets PfUbc13, demonstrating its potential as a novel antimalarial drug target.
  • These findings enhance understanding of Ubc13-dependent pathways in pathogenic parasites.