The present invention refers to a fluorescent fusion polypeptide capable of changing its localization within the cell from the cell cytoplasmic membrane to the retention vesicles, upon an increase in the concentration of second messengers within the cell cytoplasm, comprising a membrane localization peptide, a second messenger transduction protein binding peptide, a reticulum retention signal and a fluorescent peptide wherein: a. the membrane localization peptide is located at the N-terminus of the fluorescent fusion polypeptide and is physically bound, optionally through a linker, to the fluorescent peptide, which in turn is physically bound, optionally through a linker, to the second messenger transduction protein binding peptide; and b. the second messenger transduction protein binding peptide is physically bound, optionally through a linker, to the reticulum retention signal, which in turn is located at the C-terminus of the fluorescent fusion polypeptide.

The present invention includes a high throughput screen for an active agent for the treatment of comprising: plating cells at least one pathophysiologically relevant mislocated mutant form of a peroxisomal enzyme; adding a control and compound to each plate from a library of compounds; fixing the cells; contacting the cells with an agent that detects the mislocated mutant form of a peroxisomal enzyme; and imaging the cells in the wells.

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.

Provided herein are compositions and methods for assessing arrestin-dependent signaling. The provided compositions include fusion proteins comprising arrestin polypeptides that bind strongly to G protein-coupled receptors (GPCRs). In some instances, the fusion proteins may also bind to non-GPCR proteins, such as single transmembrane receptors and non-receptor proteins. Also provided are nucleic acids, vectors, constructs, and host cells that encode or express such fusion proteins. Also provided are methods of using such fusion proteins to assess arrestin trafficking, localization, and other functions including, for example, arrestin-mediated GPCR signaling as well as non-GPCR protein activity or signaling.

The present invention relates to an in vitro method for analysing liquid samples as to the presence, identity and properties of a virus comprising: a) analyzing said liquid samples for a virus spectroscopically by means of spontaneous Raman spectroscopy; and b) comparing the spectroscopic data to a database and identifying said virus. The present invention further relates to an in vitro method for analyzing exosomes in a liquid sample of a subject comprising: a) isolating exosomes from the liquid sample; b) analyzing said exosomes spectroscopically by means of spontaneous Raman spectroscopy; and c) obtaining a Raman spectrum for said exosomes. The present invention also refers to a device for analysing a liquid sample as to the presence, identity and properties of viruses; and to a device for analyzing exosomes in a liquid sample. Also envisaged are a method for monitoring a viral infection in a cell or group of cells and a method of monitoring the antiviral treatment effect in a virus infected cell or group of cells, as well as a system comprising said device and a module comprising a database comprising reference values of Raman spectra.

Current application relates to the field of neurodegenerative diseases. More specifically, the present invention relates to screening methods to identify compounds that can reduce the production of amyloidogenic Amyloid beta fragments. Said compounds can be used in treatments of for example Alzheimer's disease.

Disclosed herein are isolated and purified Staphylococcus aureus bi-component leukocidin, referred to herein as LukAB, and its components LukA and LukB, antibodies specific to LukA, antibodies specific to LukB, therapeutic compositions containing LukA and/or LukB, or anti-LukA and/or anti-LukB antibodies, uses of the compositions to treat acute inflammatory conditions or S. aureus infection, methods for identifying inhibitors of LukAB-mediated cytotoxicity of human phagocytes, and methods for using LukAB as a marker to predict severity of S. aureus infection.

Compounds of the present invention and pharmaceutically acceptable compositions thereof, are useful as modulators of ATP-Binding Cassette (“ABC”) transporters or fragments thereof, including Cystic Fibrosis Transmembrane Conductance Regulator (“CFTR”). The present invention also relates to methods of treating ABC transporter mediated diseases using compounds of the present invention.

Methods, devices and kits for the detection and quantification of XBP1s and XBP1u are described.

Compounds of the present invention and pharmaceutically acceptable compositions thereof, are useful as modulators of ATP-Binding Cassette (“ABC”) transporters or fragments thereof, including Cystic Fibrosis Transmembrane Conductance Regulator (“CFTR”). The present invention also relates to methods of treating ABC transporter mediated diseases using compounds of the present invention.