A modified melanoma cell line capable of quantification of the effects of MEK inhibitors and CDK4/6 inhibitors in a quantitative, temporal and non-invasive manner both in vitro and in vivo.

The invention relates to compounds that specifically bind a T1R1/T1R3 or T1R2/T1R3 receptor or fragments or sub-units thereof. The present invention also relates to the use of hetero-oligomeric and chimeric taste receptors comprising T1R1/T1R3 and T1R2/T1R3 in assays to identify compounds that respectively respond to umami taste stimuli and sweet taste stimuli. Further, the invention relates to the constitutive of cell lines that stably or transiently co-express a combination of T1R1 and T1R3; or T1R2 and T1R3; under constitutive or inducible conditions. The use of these cells lines in cell-based assays to identify umami and sweet taste modulatory compounds is also provided, particularly high throughput screening assays that detect receptor activity by use of fluorometric imaging.

The present invention provides an aptamer that binds to IL-21, an aptamer that binds to IL-21 and inhibits the binding of IL-21 and a receptor thereof, and an aptamer that binds to IL-21 and contains a nucleotide sequence represented by the formula (1): CGRYKACY wherein R is A or G, Y is C or U, and K is G or U.

A method of predicting the likelihood of success of a gene therapy procedure includes inducing DNA damage in a cell sample from an individual. The ability of the individual's cells in the sample to repair the DNA damage is then assessed to determine whether the individual could tolerate DNA damage caused by a gene therapy vector. In preferred embodiments, the ability of the individual's cells to repair DNA damage is assessed by detecting, and monitoring the subsequent disappearance of, a marker of DNA damage repair (such as gamma H2AX or phosphorylated 53BP1) in the sample.

The invention provides methods, compositions, and kits for characterizing open chromatin by dual DNA/protein tagging.

The present invention relates to cells and methods for detecting compounds that affect G protein coupled receptor mediated conditions. The invention also relates to methods for treating adverse drug reactions, autoimmune disorders, and pruritus.

The invention relates to compounds and methods for restoring or preserving cholesterol efflux in a cell infected with Human Immunodeficiency Virus (HIV) by preventing or decreasing an interaction between Negative Regulatory Factor (Nef) protein and Calnexin protein, and methods for screening for such compounds.

This invention provides modified IGFBP-derived peptides—collectively termed “immodulator peptides”—and related compositions and methods. Chemical modifications to peptides using small molecules, and sequence extensions to immodulator core sequences exhibit new and surprising biological activities. The invention builds the combinatorial power of the immodulator peptide class further by demonstrating which core sequences bind metal or glycosaminoglycans such as heparin. The invention discloses some surprising biological properties of compositions derived from these modifications, including a host of new therapeutic and diagnostic utilities (e.g. immune modulation of TLR signaling, enhanced collagen synthesis by skin fibroblasts, and synergy with a RIG-1 agonist in killing melanoma cells). The invention also teaches methods for enhancing previously disclosed uses of immodulator peptides by showing how the modifications of the invention can boost the efficacy of immodulator peptides in a model of burn trauma.

A method for determining the presence of a molecule coupled to the cytoplasmic side of a cellular membrane is disclosed. The method is implemented in a microfluidic setting and is particularly suitable for determining the presence and/or the activity of a G protein or an arrestin protein in a cell.

The present application relates to novel therapeutic agents, particularly to agents capable of activating (GPR)124/RECK/Frizzled/lipoprotein receptor-related protein (LRP)-mediated Wnt signaling, wherein said agents do not activate Frizzled/LRP -mediated Wnt signaling in the absence of RECK and/or GPR124. The present agents are particularly useful for the prevention or treatment of neurovascular disorders or central nervous system (CNS) disorders comprising neurovascular dysfunction.