The present disclosure provides methods of correcting gene variants associated with Parkinson's Disease in pluripotent stem cells, and methods of lineage specific differentiation of such corrected pluripotent stem cells into floor plate midbrain progenitor cells, determined dopamine (DA) neuron progenitor cells, and/or DA neurons, or into glial cells, such as microglial cells, astrocytes, oligodendrocytes, or ependymocytes. Also provided are compositions uses thereof, such as for treating neurodegenerative diseases and conditions, including Parkinson's disease.

Methods of treating and preventing diseases associated with fibrosis are disclosed, as well as agents for use in such methods. The methods comprise inhibiting at least one of ITFG1, MFAP4, GRHPR, ABCC4, PAK3, TRNP1, APLN, KIF20A, and/or LTB. In one embodiment, the disease is a liver disease or condition. Also disclosed are methods of promoting regeneration of cells, such as hepatocytes.

RNA virus vectors comprising a gene encoding the DNA-dependent activator of interferon-regulatory factors (DAI) protein, and optionally further comprising a gene encoding the receptor-interacting serine; threonine-protein kinase 3 (RIPK3) may be used therapeutically to induce cell death, as well as an inflammatory immune response, against tumors and virally-infected cells.

In one aspect, the invention provides a peptide comprising a chaperone-mediated autophagy (CMA)-targeting signal domain; a protein-binding domain that selectively binds to a target cytosolic protein; and a cell membrane penetrating domain (CMPD). In another aspect, the invention provides methods for reducing the intracellular expression level of an endogenous target protein in vitro and in an animal, wherein the method involves administration of the peptide. Methods are also provided for treating a pathological condition in an animal, the methods comprising administering the peptide to the animal. In one embodiment, the pathological condition is a neurodegenerative disease. In another embodiment of the invention, the target cytosolic protein is death associated protein kinase 1 and the CMPD is protein transduction domain of the HIV-1 Tat protein.

The present invention relates to a method for treating breast cancer in a subject having a breast cancer of the estrogen receptor (ERα) negative type, which method comprises the step of administering to said subject a therapeutically effective amount of a modulator of the Large Tumor Suppressor Kinase (LATS). Also provided are a siRNA decreasing or silencing the expression of the Large Tumor Suppressor Kinase (LATS), and an antibody specifically binding to the Large Tumor Suppressor Kinase (LATS), for use to treat breast cancer of the estrogen receptor (ERα) negative type.

Methods for reducing MSK1 levels in a plurality of cells are disclosed. For example, the methods include providing to the cells a curcumin composition that is at least 5% curcumin III. Methods for inhibiting MSK1 serine.sup.376 phosphorylation in a plurality of cells are also disclosed, which include providing to the cells a curcumin composition that is at least 5% curcumin III. In addition, methods for ameliorating inflammation in a subject are disclosed, which include providing to a subject a curcumin composition that is at least 5% curcumin III. Still further, methods for ameliorating symptoms in a subject having glucocorticoid-resistant inflammatory disease are disclosed, which include providing to a subject a curcumin composition that is at least 5% curcumin III. In addition, compositions are disclosed that include a curcumin composition consisting of at least 5% curcumin III; glucocorticoids; and a pharmaceutically acceptable solvent, filler, or carrier.

Described herein is a previously unknown function of XBP1 in triple-negative breast cancer (TNBC). It is shown that XBP1 is preferentially spliced and activated in TNBC, and that deletion of XBP1 significantly blocks triple negative breast tumor growth. Strikingly, XBP1 is required for the self-renewal of breast tumor initiating cells (TICs). Genome-wide mapping of the XBP1 transcriptional regulatory network identified a fundamental role for XBP1 in regulating the response to hypoxia via the transcription factor hypoxia-inducible factor 1α (HIF1α). Importantly, activation of this pathway appears to carry prognostic implications, as expression of the XBP1-dependent signature is associated with shorter survival times in human TNBC.

Provided are methods and compositions which are useful for separating, isolating, detecting, and quantifying compounds of interest which have been modified chemically, enzymatically or catalytically from other compounds which have not been so modified. The modifications may take the form of functional groups which are gained, lost or retained by the compounds of interest.

The present invention relates to compositions and methods for the treatment of myotonic dystrophy.

Disclosed herein are compounds, compositions, and methods of their use for the treatment of diabetes.