Disclosed are gene engineering bacteria for producing L-arginine and a construction method and an application of the gene engineering bacteria. According to the method, genes encoding a carbamoyl phosphate synthetase and a gene encoding an L-arginine biosynthesis pathway enzyme are integrated into Escherichia coli; the present invention has analyzed and reconstructed the arginine synthetic pathway and the metabolic flow related to arginine in the entire amino acid metabolic network in E. coli and finally obtained a genetically engineered bacterial strain which has a clear genetic background, carries no plasmids, undergoes no mutagenesis and is capable of stably and efficiently producing L-arginine.

The present invention relates to the treatment of respiratory viral infections, including those caused by coronaviruses.

The present invention provides an engineered cell, such as a T-cell, which expresses a chimeric antigen receptor (CAR) or an engineered T-cell receptor (TCR) and one or more enzymes which, when secreted or expressed at the cell surface causes depletion of a molecule extracellular to the engineered cell; wherein said molecule is selected from: an amino acid; a nucleotide or nucleoside; or a lipid.

The invention provides a method for treating acute myeloid leukemia (AML) in a subject in need thereof, said method comprising administering a therapeutically effective amount of an arginine-depleting agent to the subject, wherein the AML is of the French-American-British (FAB) subtype M0 (undifferentiated acute myeloblastic leukemia), M2 (acute myeloblastic leukemia with maturation), M4 (acute myeloblastic leukemia with maturation), M4 eos (acute myelomonocytic leukemia with eosinophilia), M5 (acute monocytic leukemia), M6 (acute erythroid leukemia) or M7 (acute megakaryoblastic leukemia).

Provided herein, among other things, is an engineered non-plant cell that produces a tropane alkaloid product, a precursor of a tropane alkaloid product, or a derivative of a tropane alkaloid product. A method for producing a tropane alkaloid, a precursor of a tropane alkaloid product, or a derivative of a tropane alkaloid product that makes use of the cell is also described.

A method for producing an active-form mutant enzyme, by specifying a protein of which a native form exhibits an enzyme activity but which has 10% or less enzyme activity of the native form when a gene of the protein is expressed to provide an inactive-form enzyme; determining a sequence conservation of amino acid residues in an amino acid sequence of the inactive-form enzyme and specifying amino acid residue(s) for which sequence conservation in the inactive-form enzyme is lower than sequence conservation of other amino acid(s) of the same residue; preparing a gene having a base sequence that codes for the amino acid sequence of the inactive-form enzyme in which at least one said specified amino acid residue is substituted by another amino acid with a higher sequence conservation; and expressing the gene to obtain an enzyme that exhibits an enzyme activity of the native form protein.

The present invention relates to a combination therapy for the treatment of cancer, particularly to combinations of oligo(2-(2-ethoxy)ethoxy ethyl guanidinium chloride), poly(hexamethylendiamine guanidiniumchloride), polyetheramines, triethyleneglycol diamine, enzymes, PGPR, amino acids, antioxidants like humic acids and some natural products like phytotherapeutic plant extracts. The combination therapy of the present invention shows enhanced anti-cancerous therapeutic effects compared to the effect of each of the components administered alone. In some embodiments, the combination therapy provide for a synergistic anti-cancer effect. A liposomal drug composition comprising; A dimeric or polymeric guanidine derivative or polyetheramines, triethyleneglycol diamine, enzymes, PGPR, amino acids, antioxidants like humic acids and some natural products like phytotherapeutic plant extracts a pharmaceutically acceptable salt thereof as drug substance, and a lipid modified by polyethylene glycole (PEG).

The present disclosure provides methods for inducing intermittent fasting and modulating autophagy in cells or organs in a subject via periodic administration of arginine-depleting agents. Induction of intermittent fasting and modulation of autophagy are useful in preventing and/or treating diseases, including those associated with deficits in autophagy, promoting the clearance of intracellular pathogens and protein aggregates, and promoting regeneration and longevity. The methods can be used alone or in combination with other agents to enhance intermittent fasting and autophagy activity to potentiate the health benefit(s).

The present disclosure relates to compositions and methods of using the same for the treatment of various metabolic diseases and related disorders (e.g. diabetes mellitus, NAFLD, obesity, metabolic syndrome). The compositions and methods of the disclosure relate to the administration of an arginine-degrading enzyme.

A method for producing an active-form mutant enzyme, by specifying a protein of which a native form exhibits an enzyme activity but which has 10% or less enzyme activity of the native form when a gene of the protein is expressed to provide an inactive-form enzyme; determining a sequence conservation of amino acid residues in an amino acid sequence of the inactive-form enzyme and specifying amino acid residue(s) for which sequence conservation in the inactive-form enzyme is lower than sequence conservation of other amino acid(s) of the same residue; preparing a gene having a base sequence that codes for the amino acid sequence of the inactive-form enzyme in which at least one said specified amino acid residue is substituted by another amino acid with a higher sequence conservation; and expressing the gene to obtain an enzyme that exhibits an enzyme activity of the native form protein.