ArticleMolecular biotechnology2022
Increasing Lovastatin Production by Re-routing the Precursors Flow of Aspergillus terreus via Metabolic Engineering.
Article in Molecular biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 27 citations in OpenAlex.
- Anticancer Secondary Metabolites Produced by Fungi: Potential and Representative Compounds.International journal of molecular sciences · 2025Review
- Screening and genetic engineering of marine-derived Aspergillus terreus for high-efficient production of lovastatin.Microbial cell factories · 2024Article
- Genetic regulation of L-tryptophan metabolism in Psilocybe mexicana supports psilocybin biosynthesis.Fungal biology and biotechnology · 2024Article
- Effects of Individual and Combined Fermentation Factors on Antimicrobial Activity of Nisin by Lactococcus lactis ATCC 11454.Molecular biotechnology · 2023Article
- Whole genome sequence characterization of Aspergillus terreus ATCC 20541 and genome comparison of the fungi A. terreus.Scientific reports · 2023Article
- Co-cultivation of filamentous microorganisms in the presence of aluminum oxide microparticles.Applied microbiology and biotechnology · 2022Article
- Heterologous Synthesis of Monacolin J by Reconstructing Its Biosynthetic Gene Cluster inJournal of fungi (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lovastatin is an anti-cholesterol medicine that is commonly prescribed to manage cholesterol levels, and minimise the risk of suffering from heart-related diseases. Aspergillus terreus (ATCC 20542) supplied with carbohydrates or sugar alcohols can produce lovastatin. The present work explored the application of metabolic engineering in A. terreus to re-route the precursor flow towards the lovastatin biosynthetic pathway by simultaneously overexpressing the gene for acetyl-CoA carboxylase (acc) to increase the precursor flux, and eliminate ( +)-geodin biosynthesis (a competing secondary metabolite) by removing the gene for emodin anthrone polyketide synthase (gedC). Alterations to metabolic flux in the double mutant (gedCΔ*acc
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.