Provided are a fusion protein including glutathione-S-transferase and a protein having binding affinity for a target cell or a target protein, and use thereof as a drug delivery carrier and a pharmaceutical composition. The fusion protein and the drug delivery carrier including the same according to an aspect may sustain an in vivo residence time, and may also have improved target cell-targeting ability, and thus may be effectively delivered to target cells. Accordingly, it may be usefully applied to a targeted therapeutic agent.

The disclosure relates to a method for the generation of plants, such as Euphorbia pulcherrima, having a dysfunctional glutathione S-transferase (GST), and the seeds, plant parts or plant cells derived therefrom. The disclosure further relates to a molecular marker capable of identifying a dysfunctional GST gene, to isolated DNA encoding such a dysfunctional GST gene and to the use of such DNA for the preparation of a molecular marker and for use in methods of targeted mutagenesis to inactivate the GST gene to generate plants with a white foliage phenotype.

The invention relates to the field of cell culture technology. It concerns the knockdown, using RNA interference, or gene knockout, of activating transcription factor 6 beta (ATF6B), or the combination of ceramide synthase 2 (CERS2) and TBC1 domain family member 20 (TBC1 D20) proteins, which play central roles in the cellular secretion pathway. This downregulation leads to improved secretion of biopharmaceutically relevant products produced in mammalian cells. The invention specifically relates to mammalian cells having enhanced secretion of a recombinant therapeutic protein compared to a control cell, a method of producing said mammalian cell, a method for the production of a recombinant secreted therapeutic protein and the use of said mammalian cell for increasing the yield of a recombinant secreted therapeutic protein.

The present invention provides a drug that makes it possible to effectively inhibit cancer cell growth. In particular, the present invention provides: a cell growth inhibitor for cancers in which the RAS/RAF/MEK/ERK signaling cascade has been activated, the cell growth inhibitor combining a drug that inhibits GSTP1 and a drug that inhibits the RAS/RAF/MEK/ERK signaling cascade; and a cell growth inhibitor for cancers in which the RAS/RAF/MEK/ERK signaling cascade has been activated, the cell growth inhibitor including a drug that inhibits interaction between GSTP1 and CRAF.

A method for providing a sub-population of stem cell or plurality of stem cells by determining or modulating GSTT1 expression level or genotype is disclosed together with uses of the stem cells.

The present disclosure concerns agents and their use in the treatment of endocrine, nutritional and/or metabolic diseases in a mammal. The disclosure furthermore concerns novel peptides.

This invention provides methods and compositions for preventing, treating or ameliorating one or more symptoms of a malignant tumor associated with KRAS mutation in a mammal in need thereof, by identifying a tumor cell in the mammal, the tumor cell comprising at least one of: (i) a mutation of the KRAS gene, and (ii) an aberrant expression level of KRAS protein; and administering to the mammal a therapeutically effective amount of a composition comprising one or more RNAi molecules that are active in reducing expression of GST-.

The present invention generally relates to systems and methods for treating certain oxidative stress conditions. In one aspect, compositions and methods of the invention can be used to treat a subject having an oxidative stress condition, for example, a subject having pulmonary fibrosis. In some embodiments, an inhibitor of ERp57 (for example, thiomuscimol) and/or an inhibitor of GSTP (for example, TLK-199) may be used to treat the subject. Also provided in certain aspects of the present invention are kits for such therapies, methods for promoting such therapies, and the like.

The invention relates to the field of cell culture technology. It concerns the knockdown, using RNA interference, or gene knockout, of activating transcription factor 6 beta (ATF6B), or the combination of ceramide synthase 2 (CERS2) and TBC1 domain family member 20 (TBC1 D20) proteins, which play central roles in the cellular secretion pathway. This downregulation leads to improved secretion of biopharmaceutically relevant products produced in mammalian cells. The invention specifically relates to mammalian cells having enhanced secretion of a recombinant therapeutic protein compared to a control cell, a method of producing said mammalian cell, a method for the production of a recombinant secreted therapeutic protein and the use of said mammalian cell for increasing the yield of a recombinant secreted therapeutic protein.

This invention provides formulations for use in distributing RNAi molecules targeted to a human GST- for treating a malignant tumor in a subject. The formulation can include nanoparticles composed of an ionizable lipid, a DSPE lipid, and additional lipids. A drug product can be made by lyophilization of the formulation. This invention further provides methods for ameliorating or treating a malignant tumor by administering a therapeutically effective amount of a formulation containing the RNAi agents.