This disclosure relates to genetically modified rodent animals and rodent models of human diseases. More specifically, this disclosure relates to genetically modified rodents whose genome comprises a humanized Il1rl2 gene (coding for the IL1rl2 subunit of the IL-36R protein) and human IL-36α, β and γ ligand genes. The genetically modified rodents disclosed herein display enhanced skin and intestinal inflammation as a preclinical model of psoriasis and IBD, respectively, and serve as a rodent model of human DITRA disease.

This disclosure relates to genetically modified immunodeficient animals which express a human or chimeric (e.g., humanized) SIRPα and/or human or chimeric (e.g., humanized) CD47, and methods of use thereof.

The invention relates to a genetically modified mouse comprising a heterozygous mutation of Tardbp (TDP-43) gene in that the Asn at amino acid 390 in TDP-43 is substituted with an amino acid that is different from Asn, wherein the genetically modified mouse exhibits Amyotrophic lateral sclerosis (ALS)-like phenotypes, TDP-43 proteinopathies and/or motor neuron degeneration. The invention also so relates to an isolated spinal cord motor neuron differentiated from an embryonic stem cell (ESC) that is obtained from an offspring of a genetically modified mouse according to the invention. Methods for identifying an agent alleviating and/or suppressing ALS-TDP pathogenesis are also disclosed.

The present disclosure relates to genetically modified non-human animals that express a human or chimeric (e.g., humanized) CD40, and methods of use thereof.

The invention relates generally to genetically modified non-human animals expressing human polypeptides and their methods of use,

Provided are a humanized transgenic non-human animal, especially a rodent, in particular a transgenic mouse containing a human interleukin 17A (IL-17A) gene, a human gene 17RA (IL-17RA) and/or a human TNF-alpha gene, and a preparation method therefor and the use thereof.

Non-human animal genomes, non-human animal cells, and non-human animals comprising a humanized TTR locus comprising a V30M mutation and methods of making and using such non-human animal genomes, non-human animal cells, and non-human animals are provided. Non-human animal cells or non-human animals comprising a humanized TTR locus express a human TTR protein or a chimeric TTR protein, fragments of which are from human TTR. Methods are provided for using such non-human animals comprising a humanized TTR locus to assess in vivo efficacy of human-TTR-targeting reagents such as nuclease agents designed to target human TTR.

A method for treating a metabolic disorder associated with abnormal bodyweight in a subject is provided, the method including administering to the subject an effective amount of a compound that modulates phosphatidylinositol 5-phosphate 4-kinase beta (PI5P4Kβ) activity, wherein a PI5P4Kβ inhibitor is administered when the subject suffers from a metabolic disorder associated with an underweight bodyweight; and wherein a PI5P4Kβ agonist is administered when the subject suffers from a metabolic disorder associated with an overweight or obese bodyweight. Also provided herein are methods of increasing meat quality and/or yield in livestock or domesticated poultry by administering to an animal an effective amount of a PI5P4Kβ inhibitor, and genetically engineered animals having a substitution in PI5P4Kβ that reduces its GTP-sensing activity.

This invention relates to selective inhibition of the alternative pathway (AP) of the complement system using an anti-factor D antibody. Specifically, the invention relates to methods of treating an AP-mediated disease or AP-mediated disorder in an individual by contacting the individual with an anti-factor D antibody.

Non-human animals, tissues, cells, and genetic material are provided that comprise a modification of an endogenous non-human heavy chain immunoglobulin sequence and that comprise an ADAM6 activity functional in a mouse, wherein the non-human animals express a human immunoglobulin heavy chain variable domain and a cognate human immunoglobulin λ light chain variable domain.