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.

Nucleic acid molecules and compositions, and methods using the same are provided herein for intraocular gene-based delivery and expression of two or more proneural bHLH transcription factors in the retina. The nucleic acid molecules, compositions and methods disclosed herein stimulate regeneration of retinal interneurons from retinal Müller glia (MG) and reprogram the MG into bipolar, amacrine, horizontal, and/or ganglion cells. Such methods and nucleic acid molecules are used for vision restoration and/or treatment of a range of ocular diseases involving retinal degeneration after injury, disease, or vison loss.

Disclosed herein are rodents (such as, but not limited to, mice and rats) genetically modified to comprise a humanized Tslp gene, a humanized Tslpr gene, a humanized 117ra gene, or a combination thereof. Compositions and methods for making such genetically modified rodents, as well as methods of using such genetically modified rodents as an animal model for diseases such as allergic diseases and cancer are provided.

Inhibitors of miRNA-128 capable of promoting cardiomyocyte mitotic cell proliferation and methods effective for regeneration of heart tissue.

The invention provides non-human cells and mammals having a genome encoding chimeric antibodies and methods of producing transgenic cells and mammals. Certain aspects of the invention include chimeric antibodies, humanized antibodies, pharmaceutical compositions and kits. Certain aspects of the invention also relate to diagnostic and treatment methods using the antibodies of the invention.

A method of producing a non-erythroid protein in erythrocytes of a transgenic animal using an erythroid-specific promoter includes synthesizing an erythroid-specific globin gene promoter and globin gene locus control region and cloning the promoter and the globin gene locus control region and a gene encoding a non-erythroid protein into a vector to obtain a transgene; introducing the transgene in pronuclear embryos collected from a mammalian animal in vitro; transplanting the pronuclear embryos containing the transgene into oviduct of a female recipient of the mammalian animal to obtain a transgenic animal which then expresses the non-erythroid protein in progenitor cells of erythrocytes; and collecting blood from the transgenic animal and isolating the non-erythroid protein from the erythrocytes. Further disclosed are a transgenic animal expressing a non-erythroid protein in progenitor cells of erythrocytes and an isolated erythrocyte of a non-human transgenic animal containing a human non-erythroid protein encoded by a transgene.

The present disclosure relates methods and compositions useful for prevention of porcine reproductive and respiratory syndrome virus (PRRSv) in animals, including animals of the species Sus scrofa. The present teachings relate to swine wherein at least one allele of a CD163 gene has been inactivated, and to specific methods and nucleic acid sequences used in gene editing to inactivate the CD163 gene. Swine wherein both alleles of the CD163 gene are inactivated are resistant to porcine reproductive and respiratory syndrome virus (PRRSv). Elite lines comprising homozygous CD163 edited genes retain their superior properties

Methods of treating traumatic brain injury (TBI) are provided according to aspects of the present disclosure including: converting reactive astrocytes to functional neurons by providing exogenous neurogenic differentiation 1 (NeuroD1, also called ND1 herein) to at least one reactive astrocyte in a damaged region of a subject's brain, such as the brain of a human subject with a TBI. According to aspects, presence of non-functional neurons and reactive astrocytes in the damaged region of the subject's brain are not primarily due to bleeding and/or ischemia in the damaged region. According to aspects of the present disclosure, the traumatic brain injury causes a period of astrogliosis in the damaged region of the subject's brain, and the exogenous NeuroD1 is provided to reactive astrocytes in the damaged region of the subject's brain during the period of astrogliosis or within four weeks after the period of astrogliosis.

The invention discloses methods for the generation of chimaeric human-non-human antibodies and chimaeric antibody chains, antibodies and antibody chains so produced, and derivatives thereof including fully humanised antibodies; compositions comprising said antibodies, antibody chains and derivatives, as well as cells, non-human mammals and vectors, suitable for use in said methods.