The present disclosure relates to a composition for treating or diagnosing osteoarthritis targeting activin A receptor type 2B (ACVR2B). More specifically, the present disclosure provides ACVR2B as a biomarker for diagnosing osteoarthritis because it was found that expression and activity of ACVR2B were increased at an early stage of osteoarthritis, expression of Mmp3, Mmp13, and Cox2 that induce destruction of cartilage was increased thereby, and expression of the genes was suppressed by inhibition of ACVR2B expression. In addition, since it was found that osteoarthritis was alleviated by suppressing the expression of ACVR2B, the present disclosure provides an ACVR2B expression or activity inhibitor as a therapeutic agent for osteoarthritis.

The present invention relates to a medical diagnostic device with a cellular biosensor which detects urea and uric acid by means of a synthetic genetic circuit essentially consisting of transcriptional regulator and bio-sensing module.

The technology described herein is directed to methods of treating and diagnosing bronchial premalignant lesions, e.g. by determining the lesion subtype using one or more biomarkers described herein.

Provided are methods and compositions for identifying inhibitors of an interaction between the oncogenic transcription factor MYC and its cofactor TRRAP. The methods involve both cell-based and in vitro approaches for probing an interaction between MYC and TRRAP and for identifying inhibitors of a MYC-TRRAP interaction. Also provided are compounds for use as inhibitors of an interaction between MYC and TRRAP, and methods for developing a cancer therapeutic from such compounds, including methods for derivatizing such inhibitors and for testing the inhibitors and derivatized inhibitors for an ability to treat cancer in a subject. The methods, compounds, and compositions provided herein can provide various advantages, such as a means to target the oncogenic transcription factor MYC in cancer.

The present invention relates inter alia to the treatment or prevention of influenza virus infection (including subtypes influenza A virus, influenza B virus, avian strain H5N1, A/H1N1, H3N2 and/or pandemic influenza) using compounds which inhibit the activity of p59-HCK and to a method of screening for a candidate drug substance intended to prevent or treat influenza virus infection in a subject, said method comprising identifying a test substance capable of inhibiting p59-HCK activity.

The present invention provides a screening method for a pain suppressor, which method comprises using FLRT3 to select a substance capable of inhibiting FLRT3 expression or a substance capable of inhibiting FLRT3 transport to the spinal cord. In addition, the present invention provides a pharmaceutical composition for prevention or treatment of pain, which pharmaceutical composition comprises, as an active ingredient, a substance capable of inhibiting FLRT3 expression or a substance capable of inhibiting FLRT3 transport to the spinal cord.

Methods for the detection, enumeration and analysis of circulating tumor cells expressing insulin-like growth factor-1 receptors (IGF-1R) are disclosed. These methods are useful for cancer screening and staging, development of treatment regimens, and for monitoring for treatment responses, cancer recurrence or the like. Test kits that facilitate the detection, enumeration and analysis of such circulating tumor cells are also provided.

The present invention relates to the use of the editing profile of PDE8A pre-mRNA as a specific bio marker of ADARs activities in evolved primate, particularly in Human tissues. The present invention also relates to an in vitro method for predicting in Human an alteration of the mechanism of the ADARs catalysed pre-mRNA editing of target genes, by analysing the PDE8A pre-mRNA editing profile in a peripheral tissue sample containing cells expressing said PDE8A pre-mRNA, such as blood sample. The present invention is also directed to an in vitro method for the screening of potential therapeutic compound and to predict and assess therapeutic efficacy and/or efficiency or to diagnose potential severe brain or peripheral drug side effects implementing said PDE8A pre-mRNA editing profile as specific biomarker. The present invention is further directed to a method for determining the PDE8A pre-mRNA editing profile in Human, particularly by capillary electrophoresis single-strand conformation polymorphism (CE-SSCP) method after amplification by a nested PCR. Finally the invention relates to particular nucleic acid primers implemented in said nested PCR and kit comprising such sets of primers and human cells capable of expressing PDE8A and ADARs.

Disclosed are multimeric compounds of K1 domains from the Hepatocyte Growth Factor/Scatter Factor (HGF/SF) being able to induce activation of the tyrosine kinase receptor MET and their uses.

Certain embodiments of the invention provide a method of detecting and/or quantitating nonsense mediated RNA decay (NMD) activity in a cell, comprising 1) detecting an altered level of RNA expression of a NMD-sensitive isoform in a cell, as compared to a control cell; and 2) detecting an unaltered level of RNA expression of a corresponding NMD-insensitive isoform in the cell, as compared to a control cell, wherein the isoforms are derived from an endogenously expressed, alternatively spliced gene.