The present invention relates to an enzyme-catalyzed process for producing UDP-N-acetyl-α-D-glucosamine (UDP-GlcNAc) from low-cost substrates uridine monophosphate and N-acetyl-D glucosamine in a single reaction mixture with immobilized or preferably co-immobilized enzymes. Uridine may be used as starting material instead of uridine monophosphate as well. Further, said process may be adapted to produce GlcNAcylated molecules and biomolecules including saccharides, particularly human milk oligosaccharides (HMO), proteins, peptides, glycoproteins, particularly antibodies, or glycopeptides, and bioconjugates, particularly carbohydrate conjugate vaccines and antibody-drug conjugates.

A lentiviral vector system for expressing a lentiviral particle is disclosed. The lentiviral vector system includes a therapeutic vector, an envelope plasmid, and at least one helper plasmid. The lentiviral vector system can produce a lentiviral particle for inhibiting PARP expression in neuron cells of a subject afflicted with Parkinson's disease.

A genetically modified plant or plant cell with reduced α1,3-fucosyltransferase and β1,2-xylosyltransferase activity compared to a wild type plant or plant cell, wherein less than 10% of the total glycan on a protein produced by the plant or plant cell is α1,3-fucosylated glycan and less than 3% of the total glycan on the protein is β1,2-xylosylated glycan is provided. In one embodiment, the plant or plant cell comprises three T-DNA insertions expressing five copies of RNAi targeting α1,3-fucosyltranserase and three copies of RNAi targeting β1,2xylosyltransferase.

This disclosure relates to methods of treating cancer or initiating, enhancing, or prolonging an anti-tumor response in a subject in need thereof comprising administering to the subject an effective amount of a checkpoint inhibitor in combination with a purine cleaving enzyme or a vector encoding expression thereof, and a prodrug cleaved by said purine cleaving enzyme. In certain embodiments, this disclosure relates to methods of treating cancer or initiating, enhancing, or prolonging an anti-tumor response in a subject in need thereof comprising administering to the subject an effective amount of a checkpoint inhibitor in combination with a purine cleaving enzyme, or a vector encoding expression thereof, in the absence of a prodrug cleaved by said purine cleaving enzyme.

The present disclosure provides an innovative method for improving the enzyme activity of an NMN biosynthetic enzyme Nampt, and relates to the technical field of genetic engineering. A mutant protein of the present disclosure is obtained by firstly analyzing a target protein Nampt using two softwares FoldX and DeepDDG, and then predicting multiple key sites influencing the enzyme functions and finally performing the semi-rational design of the enzyme. In the examples of the present disclosure, 10 mutant strains are constructed using the designed primers according to the principle of point mutation, and 8 of the mutants have higher activity than a wild-type strain, in which the NMN yield of the mutant Nampt-V365L is increased by 62%, and the NMN yields of the mutants Nampt-S248A, Nampt-N164L, Nampt-S382M, Nampt-A245T and Nampt-A208G are increased by 34%, 27%, 27%, 22% and 17% respectively.

The present invention addresses the problem of providing a method for producing nicotinamide mononucleotide, that produces nicotinamide mononucleotide using a single enzyme and using nucleoside monophosphate, pyrophosphate, and nicotinamide as starting materials. This problem is solved by a nicotinamide mononucleotide production method that includes at least the following steps 1) and 2): 1) a first step of producing phosphoribosyl diphosphate by the action of substantially one enzyme on nucleoside monophosphate and pyrophosphate; and 2) a second step of producing nicotinamide mononucleotide by the action of only substantially the aforementioned one enzyme on nicotinamide and the phosphoribosyl diphosphate that is the product of the first step.

Aspects of the disclosure relate to biosynthesis of histidine in host cells. For example, host cells may comprise: a promoter; a ribosome binding site (RBS); and a nucleic acid comprising: hisG; hisD; hisC hisB; hisH; hisA; hisF; and/or hisI. Host cells may further comprise a nucleic acid encoding a ribose phosphate pyrophosphokinase (RPPK), optionally comprising one or more amino acid substitutions relative to the sequence of wildtype E. coli RPPK. Host cells of the disclosure may comprise a nucleic acid encoding a 5,10-methylene-tetrahydrofolate dehydrogenase/5,10-methylene-tetrahydrofolate cyclohydrolase (MTHFDC) enzyme. Further aspects of the disclosure relate to production of purine pathway metabolites and/or plasmid DNA in host cells.

Disclosed herein are prokaryotic and eukaryotic microbes, including E. coli and S. cerevisiae, genetically altered to biosynthesize tryptamine and tryptamine derivatives. The microbes of the disclosure may be engineered to contain plasmids and stable gene integrations containing sufficient genetic information for conversion of an anthranilate or an indole to a tryptamine. The fermentative production of substituted tryptamines in a whole-cell biocatalyst may be useful for cost effective production of these compounds for therapeutic use.

The present disclosure relates to a microorganism having increased glycine productivity and a method for producing a fermented composition using the microorganism, and more specifically, to a microorganism of the genus Corynebacterium having increased glycine productivity due to the introduction of a mutation in HisG, a method for preparing a fermented composition comprising glycine and glutamic acid using the microorganism of the genus Corynebacterium, and the fermented composition.

Provided is a method for tumor treatment, comprising administering immune effector cells and a PARP inhibitor to an individual suffering from a tumor, the immune effector cell expresses a receptor for identifying a tumor antigen. Further provided is a kit for tumor treatment.