A method of determining enzyme activity and identifying and classifying cellular targets, enzymatic pathways, and enzymatic agents involved in regulating metabolism in order to treat pathophysiological disorders. Monitoring enzyme activity is performed via a label-free bio cellular assay or fluorescence imaging. The identified and classified agents are used, together with a therapeutic agent, in the treatment of various metabolism-related diseases.

The present invention relates to new transporter polypeptides, and genes encoding therefor, which can be used to confer upon a plant resistance to one or more biotrophic fungal pathogens.

A cell analysis system according to the present disclosure includes a motion information extracting unit and a motion characteristics calculating unit. The motion information extracting unit extracts motion information arising from a movement of ions or molecules across a cell membrane, out of a cell image obtained from imaging a cell in time series. The motion characteristics calculating unit calculates motion characteristics of the motion information.

Bioluminescence resonance energy transfer (BRET) biosensors for assessing the intracellular localization, internalization and trafficking into cellular compartments of proteins such as receptors, and other biomolecules such as second messengers, are disclosed. These biosensors, which are dependent on the concentration/density of the BRET donor and acceptor in cellular compartments rather that specific protein-protein interactions, use a Renilla GFP/Luc BRET pair, which allows the robust and reproducible monitoring of protein trafficking/localization, with a sensitivity compatible with high-throughput screening (HTS). The use of these biosensors for various applications, including assessing/monitoring protein endocytosis, recycling and intracellular trafficking, receptor maturation/rescue by pharmacological chaperones, various endocytosis/exocytosis processes, activation/inhibition, as well as biomolecule concentration/density in different cellular compartments, is also disclosed.

A cell-based quantitative high-throughput screening assay to monitor the formation of PFK1-mEGFP clusters by the action of small molecules to identify small molecules that promote intracellular PFK1 clustering in a cell cycle-dependent manner and may be used to treat cancer.

Screening methods as well as kits for identifying compounds capable of trapping proteins, e.g. proteins involved in DNA repair, are provided. The methods provide the use of live-cell imaging and local laser micro-irradiation of nuclear DNA in an assay to measure the effects of compounds on the trapping of 5 proteins on DNA. The disruption, e.g. inhibition, of specific proteins, such as poly-(ADP-ribose) polymerases or ALC1 enzyme, leads to trapping on chromatin and/or at DNA damage sites. This inhibits essential cellular functions, e.g. DNA damage repair, and can potentiate cancer cell killing.

Compositions including small molecule mitofusin activators are described. The mitofusin activators are useful for treating diseases or disorders associated with a mitochondria-associated disease, disorder, or condition such as diseases or disorders associated with mitofusin 1 (MFN1) and/or mitofusin 2 (MFN2), or mitochondrial dysfunction. Methods of treatment, pharmaceutical formulations, and screening methods for identifying compounds that activate mitochondrial fusion are also described.

The authors of the present invention designed a new fluorescent fusion polypeptide comprising a membrane localization peptide, a peptide capable of binding G-protein or tyrosine receptors following phosphorylation of these receptors by GRKs or RTKs, a vesicularization peptide and a fluorescent peptide. This biosensor is formed by two peptides targeted to two different cellular compartments, allowing the detection of the translocation of GRKs (G-protein receptor kinases) and/or beta-arrestin or Receptor tyrosine kinases (RTKs) from the cell cytoplasm to the cell cytoplasmic membrane in vivo by monitoring the distribution of the fluorescent polypeptide within the cellular cytoplasm. In this sense, the biosensor translocation within the cell shall be due to a change in its 3D conformation that hides or exposes the location signals in both ends of the polypeptide triggered by the binding of the peptide capable of binding G-protein or tyrosine receptors following phosphorylation of these receptors to the phosphorylated G-protein or tyrosine receptors.

The present application provides a diagnosis and treatment method for chronic inflammation. The technical solution provided by the present application is an application of a reagent in preparing a product for preventing and/or treating chronic inflammation diseases: the reagent is a substance for inhibiting the activity of an abnormal content of IFP35 and/or NMI which is secreted outside the cell as an inflammatory factor. Experiments prove that using antibodies and the like to inhibit the activity of an abnormal content of IFP35 and/or NMI which is secreted outside the cell as an inflammatory factor can effectively treat chronic inflammation diseases. In the present application, IFP35 and/or NMI are also used as a target spot, providing a diagnosis/auxiliary diagnosis and treatment method and tool for infection of viruses, particularly novel coronavirus-19 (COVID-19).

The present disclosure provides methods for identifying agents that are candidate agents for treating atopic dermatitis. The present disclosure provides methods for diagnosing atopic dermatitis. The present disclosure provides compositions and methods for treating atopic dermatitis.