Abstract: The present invention provides a method for inducing glucose uptake in a muscle cell by inhibiting Trim32 protein in the cell and to a method for inducing glucose uptake in a muscle cell, by increasing the abundance of plakoglobin protein in the cell.

Abstract: Disclosed herein is a method for regulating the activity of NF-&kgr;B in an animal comprising contacting cells of the animal with certain proteasome inhibitors.

Abstract: Disclosed herein is a method for regulating the activity of NF-&kgr;B in an animal comprising contacting cells of the animal with certain proteasome inhibitors.

Abstract: The present invention relates to the isolation of cell- or tissue-specific F-box proteins which are involved in ubiquitin-mediated protein degradation in a specific cell- or tissue-type. Accordingly, the invention provides nucleic acids and the proteins encoded by said nucleic acids which play a role in the ubiquitinylation and subsequent degradation of substrate proteins and in regulating cell proliferation, cell differentiation, and cell survival.

Abstract: This invention is directed to treating ischemia by administering proteasome inhibitors, ubiquitin pathway inhibitors, agents that interfere with the activation of NF-&kgr;B via the ubiquitin proteasome pathway, or mixtures thereof.

Abstract: The invention is based on the discovery that the cytosolic metalloendopeptidase, thimet oligopeptidase (TOP, EC3.4.25.15) has been found to play a key role in modulating levels of MHC class I-presented peptides, and in doing so, modulates the extent of antigen presentation on cell surfaces. Thus, compositions that affect the presence and/or levels of TOP, and processes to control the presence and/or levels of TOP, can be utilized to modulate antigen presentation on cell surfaces, and thereby enhance the acquisition of cell-based immunity, or alternatively, enhance cell-mediated killing of undesirable cells.

Abstract: This invention is directed to treating ischemia by administering proteasome inhibitors, ubiquitin pathway inhibitors, agents that interfere with the activation of NF-&kgr;B via the ubiquitin proteasome pathway, or mixtures thereof.

Abstract: This invention is directed to treating ischemia by administering proteasome inhibitors, ubiquitin pathway inhibitors, agents that interfere with the activation of NF-&kgr;B via the ubiquitin proteasome pathway, or mixtures thereof.

Abstract: This invention is directed to treating ischemia by administering proteasome inhibitors, ubiquitin pathway inhibitors, agents that interfere with the activation of NF-&kgr;B via the ubiquitin proteasome pathway, or mixtures thereof.

Abstract: Methods are disclosed which employ cold-shock proteins, such as Trigger Factor, to confer cold-tolerance to cells and to enhance viability of cells at temperatures at which the cells would not normally remain viable. Proteins having peptidyl-proline isomerase activity are also disclosed as being useful to confer cold-tolerance to cells. Cells which overexpress cold-shock proteins are useful in cell-based expression systems which are intended to express proteins at low temperatures.

Abstract: The ATP-ubiquitin-dependent process has been shown to be responsible for the excessive protein degradation which occurs in conditions or disease states in which there is severe loss of body mass and negative nitrogen balance has been identified and key constituents in the process identified. A method of inhibiting the accelerated or enhanced proteolysis, a method of identifying inhibitors of the process, multipain and the proteasome inhibitor are the subject of the claimed invention.

Abstract: The ATP-ubiquitin-dependent process has been shown to be responsible for the excessive protein degradation which occurs in conditions or disease states in which there is severe loss of body mass and negative nitrogen balance has been identified and key constituents in the process identified. A method of inhibiting the accelerated or enhanced proteolysis, a method of identifying inhibitors of the process, multipain and the proteasome inhibitor are the subject of the claimed invention.

Abstract: The ATP-ubiquitin-dependent process has been shown to be responsible for the excessive protein degradation which occurs in conditions or disease states in which there is severe loss of body mass and negative nitrogen balance has been identified and key constituents in the process identified. A method of inhibiting the accelerated or enhanced proteolysis, a method of identifying inhibitors of the process, multipain and the proteasome inhibitor are the subject of the claimed invention.

Abstract: The ATP-ubiquitin-dependent process has been shown to be responsible for the excessive protein degradation which occurs in conditions or disease states in which there is severe loss of body mass and negative nitrogen balance has been identified and key constituents in the process identified. A method of inhibiting the accelerated or enhanced proteolysis, a method of identifying inhibitors of the process, multipain and the proteasome inhibitor are the subject of the claimed invention.

Abstract: This invention relates to combinations and methods for the treatment of malignant and non-malignant diseases. More particularly, this invention relates to combinations of natural or recombinant tumor necrosis factors ("TNF") and non-steroidal anti-inflammatory agents, such as indomethacin and ibuprofen, useful for the growth inhibition or killing of transformed cells. According to this invention, the non-steroidal anti-inflammatory agents are used to reduce or eliminate the toxic side effects of high doses of TNFs employed in the treatment of malignant and non-malignant neoplastic diseases. Advantageously, the combinations and methods of this invention allow the administration of higher doses of TNF than those tolerated in conventional treatment regimens based upon TNF alone.

Abstract: Proteases derived from E. coli, and a method for preparing a proteinaceous mixture having proteolytic activity.