Engineered plasmids boost miRNA production to degrade target kinase mRNA and reduce biomolecule bioavailability in disease treatment.
Gene duplications plus HOG1, ISU1, GRE3, and IRA2 deletions let engineered yeast ferment xylose to ethanol at practical rates.
miRNA-encoding plasmids suppress overexpressed kinase mRNA through targeted degradation, helping restore cellular homeostasis in disease.
Engineered microbes use a mutant aromatic kinase to phosphorylate acetovanillone, improving lignin aromatic catabolism into useful chemicals.
Engineered Methylobacteriaceae uses glyoxylate reductase to turn methanol or formic acid into glycolic and lactic acid with less fossil reliance.
Using magnesium hydroxide or oxide to hold pH in coupled ATP regeneration and enzymatic reactions improves yield while cutting buffer load.
Artificial circRNAs bind repeat-expanded mRNAs to disrupt pathological secondary structures, restore splicing, and directly target disease mechanisms.
Recombinant prenyltransferases with tuned amino acid sequences raise cannabinoid yield and product ratio while avoiding complex, high-impact synthesis.
Targeted residue changes improve transaminase stability, activity, and substrate scope for more efficient chiral amine synthesis.
A divalent-metal basic compound maintains pH during ATP-coupled enzymatic synthesis, improving yield and productivity while easing purification.
ClpB chaperone expression helps PHA-producing microorganisms prevent protein aggregation and sustain higher polymer accumulation under stress.
Adaptive antibody dosing keeps plasma levels above 80 nM to sustain kallikrein inhibition in hereditary angioedema without dose-limiting toxicity.
Engineered AaLS protein cages use oxide-triggered open-close switching to load and release macromolecular cargo under mild physiological conditions.
Recombinant plasmids boost miRNA production to degrade kinase mRNA, lowering abnormal kinase expression and helping restore homeostasis.
Plasmid-encoded miRNA boosts intracellular silencing of kinase mRNA, improving control of disease-linked overexpression.