Non-human animals comprising a human or humanized IL-4 and/or IL-4Rα nucleic acid sequence are provided. Non-human animals that comprise a replacement of the endogenous IL-4 gene and/or IL-4Rα gene with a human IL-4 gene and/or IL-4Rα gene in whole or in part, and methods for making and using the non-human animals, are described. Non-human animals comprising a human or humanized IL-4 gene under control of non-human IL-4 regulatory elements is also provided, including non-human animals that have a replacement of non-human IL-4-encoding sequence with human IL-4-encoding sequence at an endogenous non-human IL-4 locus. Non-human animals comprising a human or humanized IL-4Rα gene under control of non-human IL-4Rα regulatory elements is also provided, including non-human animals that have a replacement of non-human IL-4Rα-encoding sequence with human or humanized IL-4Rα-encoding sequence at an endogenous non-human C IL-4Rα locus. Non-human animals comprising human or humanized IL-4 gene and/or IL-4Rα sequences, wherein the non-human animals are rodents, e.g., mice or rats, are provided.

The present disclosure provides formulations and therapies for treating subjects with elevated levels of TIM-3 using gene-based cytotoxic immunostimulant therapy alone or with other immunotherapies.

The present invention provides a novel modified protein which is to be used, as a novel detection tool relating to gene expression, for detecting a chromatin open structure more easily at a higher sensitivity than by the conventional technique. The present invention relates to: a nucleic acid binding fluorescent protein, said protein containing a DNA binding domain in which 3 or more TAL-repeats are repeatedly connected, characterized by binding independently from base sequences; and a method for fluorescent labeling of an open chromatin in a vital cell, said method comprising a step for transferring a gene encoding a nucleic acid binding protein into the vital cell, characterized in that the nucleic acid binding protein is a protein comprising a DNA binding domain, in which 3 or more TAL-repeats are repeatedly connected, and a fluorescent protein directly or indirectly bound thereto and the DNA binding domain binds to a nucleic acid independently from base sequences.

A protein selected from the group consisting of Chrdl1, Fam3c, Fam3b and a fragment thereof, or a polynucleotide encoding therefor, for use in treating or reducing the risk of heart disease.

The present invention to a method for expressing an exogenous gene specifically in cells of the retinal pigment epithelium of a primate, this method comprising the step of delivering an isolated nucleic acid molecule comprising, or consisting of, the nucleic acid sequence of SEQ ID NO:1, or consisting of a nucleic acid sequence of at least 400 bp having at least 80% overall identity to the sequence of SEQ ID NO:1, to cells of the retinal pigment epithelium of the primate, wherein this isolated nucleic acid molecule specifically leads to the expression of an exogenous gene in cells of the retinal pigment epithelium of primates when a nucleic acid sequence coding for the exogenous gene is operatively linked to this isolated nucleic acid molecule.

Nonsense-mediated mRNA decay (NMD) polypeptides, nucleic acids encoding NMD polypeptides, and methods of using such polypeptides and nucleic acids in the treatment of ALS and in screening for agents for the treatment of ALS are described.

Provided are a targeting vector, a nucleic acid composition, and a method for constructing a liver-injured mouse model. The targeting vector includes a first expression cassette and a second expression cassette located downstream of the first expression cassette, the first expression cassette has the following elements connected in series in sequence: a liver-specific promoter, a tetracycline transcription activation regulating factor, and a first polyA; and the second expression cassette has the following elements connected in series in sequence: a second polyA, a mouse prourokinase activator encoding gene, and a tetracycline-inducible promoter. The liver-injured mouse model constructed with this targeting vector has the phenotype of spontaneously generating the liver injury and aggravating the liver injury by induction, which provides liver-injured mouse models for studies of liver diseases.

The invention provides a method of modulating electrophysiological activity of an excitable cell. The method involves causing exogenous expression of a glycine receptor (GlyR) protein in an excitable cell of a subject. Thereafter, the excitable cell is exposed to an allosteric modulator of the GlyR protein. Modulation of the exogenous GlyR protein (an ion channel) in response to the allosteric modulator modulates the electrophysiological activity of the excitable cell. The method can be used to control pain in a subject. The invention further provides a replication-defective HSV vector comprising an expression cassette encoding a GlyR protein, stocks and pharmaceutical compositions containing such vectors, and a transgenic animal.

The present disclosure relates to genetically modified non-human animals that express a human or chimeric (e.g., humanized) CD47, and methods of use thereof.

The present invention provides methods for generating a mouse model that produces anti-polyethylene glycol (PEG) antibodies. Also provided are mice generated by said methods and methods of using these mice to screen PEG-containing products in vivo.