Compositions and methods for detecting nucleic acid-protein interactions, or more generally interactions between a nucleic acid and another molecule. A Cas protein (e.g., a catalytically dead Cas13) is fused to a proximity tagging enzyme (e.g., a Pup ligase) and thus brings the proximity tagging enzyme to the proximity of a protein that binds to a nucleic acid, when the Cas protein recognizes the nucleic acid, e.g., through a guide RNA. The proximity tagging enzyme then tags the protein enabling it to be identified as a protein that interacts with the nucleic acid.

The present application discloses methods of correcting a gene defect in a cell, methods of treating a patient having a disease or disorder characterized by a gene defect, methods of preparing a chimeric antigen receptor T cell, as well as systems for correcting a gene defect in a cell, ex vivo modified cells, and related compositions.

The invention provides methods for reprogramming somatic cells to generate multipotent or pluripotent cells. Such methods are useful for a variety of purposes, including treating or preventing a medical condition in an individual. The invention further provides methods for identifying an agent that reprograms somatic cells to a less differentiated state.

Provided is an application of a non-IGF1R-binding substance in the prevention and/or treatment of inflammatory diseases. Specifically, provided is use of a non-IGF1R-binding substance. The non-IGF1R-binding substance is used for preparing a composition or formulation, and the composition or formulation is used for preventing and/or treating inflammatory diseases.

This application relates to therapeutic siRNA agents and methods of making and using the agents.

This invention relates to the finding that testis development related protein (TDRP; also termed Immunomoodulin or Imood herein) is a circulatory anxiogenic factor that modulates anxiety-like behaviour in mammalian models through the regulation of the immune system. Methods of treatment of mental disorders, such as anxiety, and TDRP antagonists for use in such methods are provided. Methods of diagnosing or monitoring a mental disorder in an individual by determining levels of TDRP in a sample and methods of screening for compounds that reduce levels of TDRP are provided.

Transgenic non-human animal models for cellular senescence are provided herein, as are methods and materials for making and using the transgenic non-human animal models. For example, a p21-Cre mouse model for cellular senescence is provided herein.

The present disclosure provides a promoter having at least the core components of a duck retinoic acid-inducible gene I (RIG-I) promoter, as well as expression constructs having the duck RIG-I promoter operably linked to a gene product-encoding nucleic acid (e.g., an avian RIG-I protein), and recombinant host cells containing the duck RIG-I promoter, e.g., in such expression constructs. The present disclosure also provide animals genetically modified to have a gene encoding a duck RIG-I promoter operably linked to a gene product-encoding nucleic acid (e.g., an avian RIG-I protein, such as a duck RIG-I protein).

Non-human animal cells and non-human animals comprising CRISPR/Cas synergistic activation mediator system components and methods of making and using such non-human animal cells and non-human animals are provided. Methods are provided for using such non-human animals to increase expression of target genes in vivo and to assess CRISPR/Cas synergistic activation mediator systems for the ability to increase expression of target genes in vivo.

An auxin-inducible degron system kit that controls degradation of a target protein in a non-plant-derived eukaryotic cell, the kit containing a first nucleic acid that encodes a mutant TIR1 family protein having a mutation at an auxin-binding site, an auxin analog that has an affinity to the mutant TIR1 family protein and a second nucleic acid that encodes a degradation tag containing at least a part of an Aux/IAA family protein and having an affinity to a complex of the mutant TIR1 family protein and the auxin analog.