Genetically modified non-human animals and methods and compositions for making and using the same are provided, wherein the genetic modification comprises a humanization of an endogenous signal-regulatory protein gene, in particular a humanization of a SIRPα gene. Genetically modified mice are described, including mice that express a human or humanized SIRPα protein from an endogenous SIRPα locus.

The invention in some aspects relates to isolated nucleic acids, compositions, and kits useful for identifying adeno-associated viruses in cells. In some aspects, the invention provides kits and methods for producing somatic transgenic animal models using recombinant AAV (rAAV) to an animal having at least one transgene that expresses a small interfering nucleic acid or at least one binding site for a miRNA.

Non-human animals and methods and compositions for making and using them are provided, which non-human animals have a genome comprising an engineered or recombinant diversity cluster within an immunoglobulin heavy chain variable region, which engineered or recombinant diversity cluster comprises an insertion of one or more D.sub.H segments that are each operably linked to a 23-mer recombination signal sequence. Methods for producing antibodies from non-human animals are also provided, which antibodies optionally contain human variable regions and rodent, e.g., constant regions.

Provided is a nonhuman animal model that is obtained by modifying a gene encoding thioredoxin and useful as a disease model of aging, kidney diseases, cardiovascular diseases, hypertension, aortic dissection, chronic obstructive lung disease, age-dependent epilepsy, abnormality of lipid metabolism, anemia, osteoporosis, abnormal immunity, etc. These variety of phenotypes are caused by the fact that a modification of a gene encoding thioredoxin induces hypofunction of thioredoxin expressed in multiple organs throughout the body. The gene encoding thioredoxin is a gene selected from among TXN, TRX, TRX1, RRDX, Txn1, Txn, Trx1 and ADF.

Non-human animals, cells, methods and compositions for making and using the same are provided, wherein the non-human animals and cells comprise a humanized a proliferation-inducing ligand gene. Non-human animals and cells that express a human or humanized a proliferation-inducing ligand protein from an endogenous a proliferation-inducing ligand locus are described.

The present disclosure relates to genetically modified non-human animals (e.g., genetically-modified mice) that express a human or chimeric (e.g., humanized) CD27. The present disclosure also relates to methods of generating the genetically-modified animals (e.g., genetically modified mice), and methods of using the genetically modified non-human animals (e.g., genetically modified mice) described herein.

The present invention relates generally to genetically modified non-human animals. The present invention relates to a genetically modified non-human animal, in which at least one copy of the endogenous nucleotide sequence encoding Protein C in the genome of said non-human animal has been replaced by a nucleotide sequence encoding human Protein C, encoding a functional fragment of human Protein C or encoding a functional variant of human Protein C. The invention also relates to vectors, cells and methods for the production of such non-human animals. The invention also relates to methods of testing agents for their ability to alter to the level and/or functional activity of human protein C and thus provides methods of testing agents for their potential therapeutic efficacy.

A liver lesion-mouse model which is a liver-specific ISX gene expression and p53 gene knockout transgenic mouse, wherein liver lesion develops after the mouse is fed with a high calorie diet.

Non-human animals, cells, methods and compositions for making and using the same are provided, wherein the non-human animals and cells comprise a humanized a proliferation-inducing ligand gene. Non-human animals and cells that express a human or humanized a proliferation-inducing ligand protein from an endogenous a proliferation-inducing ligand locus are described.

Disclosed herein, are inducible immunodeficient animals and methods to make them by adding an IL2Rg/RAG2 rescue cassette (RG-reg) or an IL2Rg/RAG2/FAH rescue cassette (FRG-reg) to a line of IL2Rg/RAG2 knockout (RG-KO) or IL2Rg/RAG2/FAH knockout (FRG-KO) swine. The rescue cassette enables line breeding of immunocompetent (regRG-KO) or (regFRG-KO) swine for rapid propagation. The rescue cassette can be excised, specifically in germ cells of regRG-KO or regFRG-KO swine, such that offspring of animals do not possess the rescue cassette and are immunodeficient. The immunodeficient swine also provide host embryos having genetic ablations to provide a niche for organ complementation by human stem cells.