Hypersensitive PYR/PYL receptor polypeptides comprising an amino acid substitution in a type 2 protein phosphatase (PP2C) binding interface are provided. Compositions and plants comprising the hypersensitive PYR/PYL receptor polypeptides and methods of producing plants comprising a hypersensitive PYR/PYL receptor polypeptide are also provided.

Disclosed are compositions and methods for targeted treatment of glioblastoma multiforme (GBM). In particular, chimeric antigen receptor (CAR) polypeptides are disclosed that can be used with adoptive cell transfer to target and kill Glioblastoma Stem Cells (GSCs). Also disclosed are immune effector cells, such as T cells or Natural Killer (NK) cells, that are engineered to express these CARs. Therefore, also disclosed are methods of providing an anti-tumor immunity in a subject with Glioblastoma Stem Cells (GSCs) that involves adoptive transfer of the disclosed immune effector cells engineered to express the disclosed CARs.

The present disclosure relates to a method for inhibiting a STAT3 activity, and a method for treating inflammatory bowel disease (IBD).

Mitochondria modified by a targeting protein, according to one embodiment of the present invention, can be effectively delivered to a target. In addition, when a protein of interest bound to the modified mitochondria is delivered into a cell, various activities can be exhibited. The modified mitochondria can effectively cause cancer tissue death, and thus can also be used as an anticancer agent. Furthermore, various activities are exhibited according to a protein of interest loaded on modified mitochondria, and thus the modified mitochondria can be applied in the treatment of various diseases. Additionally, a fusion protein comprising a protein of interest and a fusion protein comprising a targeting protein, according to one embodiment of the present invention, can be used in order to modify mitochondria. Moreover, mitochondria modified with the fusion proteins exhibits various effects in a target cell.

Disclosed are compositions and methods for targeted treatment of glioblastoma multiforme (GBM). In particular, chimeric antigen receptor (CAR) polypeptides are disclosed that can be used with adoptive cell transfer to target and kill Glioblastoma Stem Cells (GSCs). Also disclosed are immune effector cells, such as T cells or Natural Killer (NK) cells, that are engineered to express these CARs. Therefore, also disclosed are methods of providing an anti-tumor immunity in a subject with Glioblastoma Stem Cells (GSCs) that involves adoptive transfer of the disclosed immune effector cells engineered to express the disclosed CARs.

Described are compositions and methods relating to modified yeast that over-express protein phosphatases associated with the HOG pathway. The yeast produces an increased amount of ethanol and deceased amount of glycerol compared to parental cells. Such yeast is particularly useful for large-scale ethanol production from starch substrates.

The present disclosure relates to a method of preventing rheumatoid arthritis comprising administering a polynucleotide encoding Ssu72.

The present disclosure provides modified cells including pluripotent stem cells, hematopoietic precursor cells, and hematopoietic cells (e.g., modified Tregs) that are steroid and/or calcineurin inhibitor-resistant. The present disclosure provides methods for generating steroid and/or calcineurin inhibitor-resistant modified cells including pluripotent stem cells, hematopoietic precursor cells, and hematopoietic cells. Also provided herein are compositions and methods of treatment.

The present invention provides oligomeric compounds. Certain such oligomeric compounds are useful for hybridizing to a complementary nucleic acid, including but not limited, to nucleic acids in a cell. In certain embodiments, hybridization results in modulation of the amount activity or expression of the target nucleic acid in a cell.

The present invention provides a method of treating heart failure with reduced ejection fraction, by administering to a patient at risk of such damage, a pharmaceutically effective amount of a composition which inhibits the anchoring of PP2A to mAKAP. This composition is preferably in the form of a viral based gene therapy vector that encodes a fragment of mAKAP to which PP2A binds.