ArticleThe FEBS journal2006
The catalysis of the SARS 3C-like protease is under extensive regulation by its extra domain.
Article in The FEBS journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 170 citations in OpenAlex.
- Statistical crystallography reveals an allosteric network in SARS-CoV-2 MCommunications biology · 2026Article
- Cooperativity and communication between the active sites of the dimeric SARS-CoV-2 main protease.Science advances · 2026Article
- Exploring covalent inhibitors of SARS-CoV-2 main protease: from peptidomimetics to novel scaffolds.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Unveiling the mechanism of action of a novel natural dual inhibitor of SARS-CoV-2 Mpro and PLpro with molecular dynamics simulations.Natural products and bioprospecting · 2025Article
- Computational Insights into Acrylamide Fragment Inhibition of SARS-CoV-2 Main Protease.Current issues in molecular biology · 2024Article
- Allostery in homodimeric SARS-CoV-2 main protease.Communications biology · 2024Article
- 3-chymotrypsin-like protease in SARS-CoV-2.Bioscience reports · 2024Review
- Review
- On Inactivation of the Coronavirus Main Protease.Journal of chemical information and modeling · 2024Article
- The SARS-CoV-2 MACS synthetic biology · 2024Article
- Bayesian Inference Elucidates the Catalytic Competency of the SARS-CoV-2 Main Protease 3CLAnalytical chemistry · 2023Article
- Paxlovid (Nirmatrelvir/Ritonavir): A new approach to Covid-19 therapy?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Review
- Lessons Learnt from COVID-19: Computational Strategies for Facing Present and Future Pandemics.International journal of molecular sciences · 2023Review
- Unveiling the Potentiality of Shikonin Derivatives Inhibiting SARS-CoV-2 Main Protease by Molecular Dynamic Simulation Studies.International journal of molecular sciences · 2023Article
- The Discovery of Small Allosteric and Active Site Inhibitors of the SARS-CoV-2 Main Protease via Structure-Based Virtual Screening and Biological Evaluation.Molecules (Basel, Switzerland) · 2022Article
- A new glimpse on the active site of SARS-CoV-2 3CLpro, coupled with drug repurposing study.Molecular diversity · 2022Article
- Autoprocessing and oxyanion loop reorganization upon GC373 and nirmatrelvir binding of monomeric SARS-CoV-2 main protease catalytic domain.Communications biology · 2022Article
- Allosteric Hotspots in the Main Protease of SARS-CoV-2.Journal of molecular biology · 2022Article
- Review
- Allosteric inhibitors of the main protease of SARS-CoV-2.Antiviral research · 2022Article
28 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 3C-like protease of the severe acute respiratory syndrome (SARS) coronavirus has a C-terminal extra domain in addition to the chymotrypsin-fold adopted by picornavirus 3C proteases hosting the complete catalytic machinery. Previously we identified the extra domain to be involved in enzyme dimerization which has been considered essential for the catalytic activity. In an initial attempt to map out the extra-domain residues critical for dimerization, we have systematically generated 15 point mutations, five deletions and one triple mutation and subsequently characterized them by enzymatic assay, dynamic light scattering, CD and NMR spectroscopy. The results led to identification of four regions critical for enzyme dimerization. Interestingly, Asn214Ala mutant with a significant tendency to form a monomer still retained approximately 30% activity, indicating that the relationship between the activity and dimerization might be very complex. Very surprisingly, two regions (one over Ser284-Thr285-Ile286 and another around Phe291) were discovered on which Ala-mutations significantly increased the enzymatic activities. Based on this, a super-active triple-mutant STI/A with a 3.7-fold activity enhancement was thus engineered by mutating residues Ser284, Thr285 and Ile286 to Ala. The dynamic light scattering, CD and NMR characterizations indicate that the wild-type (WT) and STI/A mutant share similar structural and dimerization properties, thus implying that in addition to dimerization, the extra domain might have other mechanisms to regulate the catalytic machinery. We rationalized these results based on the enzyme structure and consequently observed an interesting picture: the majority of the dimerization-critical residues plus Ser284-Thr285-Ile286 and Phe291 are clustered together to form a nano-scale channel passing through the central region of the enzyme. We therefore speculate that this channel might play a role in relaying regulatory effects from the extra domain to the catalytic machinery.
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