Disclosed is a vector pair for screening tau oligomer formation, a mouse embryo introduced with the vector pair, a transgenic model mouse of neurological disease, obtained from the mouse embryo, and a method of screening a tau oligomer formation inhibitor candidate using the transgenic model mouse. More specifically, the present invention provides vector pair for screening tau oligomer formation, comprising: a first vector comprising a first tau gene, a first fluorescence protein gene and a first neuron-specific promoter; and a second vector comprising a second tau gene, a second fluorescence protein gene and a second neuron-specific promoter, wherein a protein expressed from the first fluorescence protein gene and a protein expressed from the second fluorescence protein gene bind to each other to display fluorescence, by association between a protein expressed from the first tau gene and a protein expressed from the second tau gene.

A genetically modified mouse is provided that comprises a conditional Acvr1 allele that comprises a mutated exon that, upon induction, converts to a mutant exon phenotype, wherein the mutant exon phenotype includes ectopic bone formation. Mice comprising a mutant Acvr1 exon 5 in antisense orientation, flanked by site-specific recombinase recognition sites, are provided, wherein the mice further comprise a site-specific recombinase that recognizes the site-specific recombinase recognitions sites, wherein the recombinase is induced upon exposure of the mouse to tamoxifen. Upon exposure to tamoxifen, the recombinase is expressed and acts on the RRS-flanked mutant exon 5 and places the mutant exon 5 in sense orientation and deletes the wild-type exon.

A simulation method for a chronic atrophic gastritis (CAG) lesion includes: (1) taking a metaplasia lesion stage as a simulation object, (2) selecting a simulation form of spasmolytic polypeptide-expressing metaplasia (SPEM), and (3) conditionally deleting gene associated with retinoid-IFN-induced mortality-19 (GRIM-19) from gastric mucosal parietal cells. The present disclosure successfully simulates the SPEM, an initial metaplasia response after a gastric mucosal injury and the initial metaplasia response can progress into intestinal metaplasia (IM) and even gastric cancer (GC) under the continuous stimulation of chronic inflammation. The simulation of this pathological formation provides a basis for research on early prevention and control of intestinal GC and effective suppression of a precancerous lesion of gastric cancer (PLGC), provides a research basis for screening and development of drugs for preventing and treating CAG, and provides an important experimental tool for the implementation of anti-inflammatory and anti-cancer drug tests.

The present disclosure provides a method for genetic analysis of gene variants as well as a system for implementing such analysis.

A genetically modified mouse is provided that comprises a conditional Acvr1 allele that comprises a mutated exon that, upon induction, converts to a mutant exon phenotype, wherein the mutant exon phenotype includes ectopic bone formation. Mice comprising a mutant Acvr1 exon 5 in antisense orientation, flanked by site-specific recombinase recognition sites, are provided, wherein the mice further comprise a site-specific recombinase that recognizes the site-specific recombinase recognitions sites, wherein the recombinase is induced upon exposure of the mouse to tamoxifen. Upon exposure to tamoxifen, the recombinase is expressed and acts on the RRS-flanked mutant exon 5 and places the mutant exon 5 in sense orientation and deletes the wild-type exon.

A genetically modified mouse is provided that comprises a conditional Acvr1 allele that comprises a mutated exon that, upon induction, converts to a mutant exon phenotype, wherein the mutant exon phenotype includes ectopic bone formation. Mice comprising a mutant Acvr1 exon 5 in antisense orientation, flanked by site-specific recombinase recognition sites, are provided, wherein the mice further comprise a site-specific recombinase that recognizes the site-specific recombinase recognitions sites, wherein the recombinase is induced upon exposure of the mouse to tamoxifen. Upon exposure to tamoxifen, the recombinase is expressed and acts on the RRS-flanked mutant exon 5 and places the mutant exon 5 in sense orientation and deletes the wild-type exon.

This invention relates to the engineering of animal cells, preferably mammalian, more preferably rat, that are deficient due to the disruption of tumor suppressor gene(s) or gene product(s). In another aspect, the invention relates to genetically modified rats, as well as the descendants and ancestors of such animals, which are animal models of human cancer and methods of their use.

The invention provides compositions and methods for manufacturing pluripotent cells. In particular, the invention provides improved culture platforms for manufacturing pluripotent cells with ground state pluripotency.

The invention provides for AAV vectors expressing the ANO5 gene and antioxidant therapy as methods of inducing muscle regeneration and a method of treating muscular dystrophy.

This invention relates to glaucoma, and more particularly to use of VE-PTP-null allele to rescue from the glaucoma symptom of elevated intraocular pressure. This invention also relates to conditional knockout of VE-PTP to rescue from the glaucoma symptom of elevated intraocular pressure expressed in an Angiopoietin 1 and Angiopoietin 2 conditional knockout mouse. This invention also relates to the use of VE-PTP-null alleles.