The invention relates to a metabolic enzyme-disrupted aerobic strain and a method for culturing the strain. The present invention provides, for example, a culture comprising a culture medium that has been cultured under an aerobic condition, wherein the culture medium contains an aerobe, wherein the aerobe has a disrupted gene encoding a metabolic enzyme of glycolysis selected from the group consisting of the metabolic enzymes of glycolysis except hexokinase, thereby suppressing metabolism from a carbon source (e.g., glucose) to the TCA cycle in the aerobe.

The present invention relates to a mutant microorganism in which a gene that encodes phosphofructokinase-2 is disrupted or deleted to reduce glycolytic flux to thereby improve the ability of the microorganism to produce N-acetylglucosamine, and to a method of producing N-acetylglucosamine using the mutant microorganism. The mutant microorganism according to the present invention has advantages in that it has high resistance to various chemical substances, grows rapidly, is easily cultured, and produces N-acetylglucosamine with high efficiency, indicating that it is useful for production of a large amount of N-acetylglucosamine.

The present invention relates to a mutant microorganism in which a gene that encodes phosphofructokinase-2 is disrupted or deleted to reduce glycolytic flux to thereby improve the ability of the microorganism to produce N-acetylglucosamine, and to a method of producing N-acetylglucosamine using the mutant microorganism. The mutant microorganism according to the present invention has advantages in that it has high resistance to various chemical substances, grows rapidly, is easily cultured, and produces N-acetylglucosamine with high efficiency, indicating that it is useful for production of a large amount of N-acetylglucosamine.

Methods of treating ischemia by modulating ischemic cell bioenergetics are described. For example, the methods include the administration of small molecule, polypeptide, and/or genetic agents that modulate oxidative metabolism and/or glycolytic metabolism in ischemic cells, such as ischemic muscle cells. In some embodiments, the agent is adapted to deliver Cox6a2 or PFKFB3 to the cell. Also described are related pharmaceutical compositions and kits for the treatment of ischemia and ischemic injury related to, for instance, such as peripheral arterial disease, stroke, myocardial infarction, and diabetes.

The present invention relates to methods and pharmaceutical compositions for the treatment of retinal degenerative diseases. The inventors identified a new key actor of the mechanism underlying the protective role of RdCVF: 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2). The inventors showed that PFKFB2 is expressed by cones in a rod-dependant manner. In particular, they showed that its expression follows the viability of cones: its expression is lost in an animal model retinitis pigmentosa. The inventors accumulated evidences that PFKFB2, especially its kinase domain, is involved in the mechanism of action of RdCVF. More particularly they showed that transduction of a polynucleotide encoding for PFKFB2 increases cone survival. In particular, the present invention relates to a method of treating a retinal degenerative disease in a subject in need thereof comprising administering to the subject a therapeutically effective amount of a polynucleotide encoding for the PFKFB2 kinase domain.