MPO1 and MPO2 can be regulated for either decreasing or increasing alkaloid levels in plants, in particular in Nicotiana plants. In particular, suppressing or overexpressing one or more of MPO1 and MPO2 may be used to decrease or increase nicotine and nicotinic alkaloid levels in tobacco plants. Suppression or overexpression of one or more of MPO1 and MPO2 may be used in combination with modification of expression of other genes encoding enzymes on the nicotinic alkaloid biosynthetic pathway such as A622, NBB1, PMT, and QPT.

Provided is an amino acid dehydrogenase mutant. The amino acid sequence of the mutant is obtained by mutating the amino acid sequence shown in SEQ ID NO:1. The mutation includes at least one of the following mutation sites: 64th, 94th, 133rd, 137th, 148th, 168th, 173rd, 183 rd, 191st, 207th, 229th, 248th, 255th and 282nd sites; or the amino acid sequence of the amino acid dehydrogenase mutant is an amino acid sequence having the mutation sites in the mutated amino acid sequence and having a 80% or more homology with the mutated amino acid sequence. The mutant enzyme activity is more than 50 times higher than that of wild amino acid dehydrogenase, and the enzyme specificity is also correspondingly improved.

The invention relates to a novel inhibitor pharmacophore of PCSK9 and heteroaryl compounds that bind the PCSK9 protein.

A method for producing an objective substance such as vanillin and vanillic acid is provided. An objective substance is produced from a carbon source or a precursor of the objective substance by using a microorganism that is able to produce the objective substance, which microorganism has been modified so that the activity of an enzyme involved in SAM cycle (SAM cycle enzyme) is increased.

MPO1 and MPO2 can be regulated for either decreasing or increasing alkaloid levels in plants, in particular in Nicotiana plants. In particular, suppressing or overexpressing one or more of MPO1 and MPO2 may be used to decrease or increase nicotine and nicotinic alkaloid levels in tobacco plants. Suppression or overexpression of one or more of MPO1 and MPO2 may be used in combination with modification of expression of other genes encoding enzymes on the nicotinic alkaloid biosynthetic pathway such as A622, NBB1, PMT, and QPT.

Provides an artificial enzyme obtained by improving upon a sequence of a natural nicotine dehydrogenase, wherein the improvement comprises replacing at least one amino acid hindering product release with an amino acid with smaller side chains, thereby improving a catalytic rate.

The present invention relates to the preparation of amines from aldehydes and ketones by reductive amination with enzymes having a reductive aminase activity on aldehydes and ketones devoid of any carboxyl group gamma of the carbonyl group. The invention also relates to the enzymes per se and their uses in biocatalysis. The enzymes are derived from Mycobacterium smegmatis and vaccae, Cystobacter fuscus, Microbacterium sp. and Aminomonas paucivorans.

Provided is an amino acid dehydrogenase mutant. The amino acid sequence of the mutant is obtained by mutating the amino acid sequence shown in SEQ ID NO:1. The mutation includes at least one of the following mutation sites: 64th, 94th, 133rd, 137th, 148th, 168th, 173rd, 183 rd, 191st, 207th, 229th, 248th, 255th and 282nd sites; or the amino acid sequence of the amino acid dehydrogenase mutant is an amino acid sequence having the mutation sites in the mutated amino acid sequence and having a 80% or more homology with the mutated amino acid sequence. The mutant enzyme activity is more than 50 times higher than that of wild amino acid dehydrogenase, and the enzyme specificity is also correspondingly improved.

The present disclosure relates generally to compositions and methods for treating, preventing, inhibiting, or delaying central nervous system degeneration. The disclosure relates to a recombinant gene therapy vector comprising a PARK2, PINK1, DJ-1, LRRK2, SCNA, c-Rel, ATG7, VMAT2, or GBA gene, or functional fragment or variant thereof. The disclosure also relates to CRISPR/Cas-based gene editing systems for treating, preventing, inhibiting, or delaying central nervous system degeneration.

The invention relates to a novel inhibitor pharmacophore of PCSK9 and heteroaryl compounds that bind the PCSK9 protein.