The present invention relates to a method for generating sterile Zeugodacus scutellata males by emitting an electron beam at a dose of 150 Gy (inclusive) to 250 Gy (exclusive) to pupae of Zeugodacus scutellata and a method for controlling Zeugodacus scutellata by releasing the generated sterile males and normal males at a ratio of 9:1. In the present invention, electron beams are used instead of radioactive beams and suitable doses of electron beams are determined to generate sterile males of domestic native Zeugodacus scutellata. The generated sterile Zeugodacus scutellata males and normal males are released at a ratio of 9:1 to effectively control Zeugodacus scutellata through a sterile insect release technique (SIT).

Descried in certain example embodiments herein are engineered fish, particularly engineered catfish, that are engineered to contain modified myostatin, melanocortin-4 receptor, and/or one or more n-3 fatty acid biosynthesis pathway genes and/or gene products.

The present invention pertains to a non-human genetically modified animal with increased susceptibility to infection with a human virus. The invention suggests to genetically impair the expression of newly identified viral infection repression factors CD302, Cr11, Ndufc2, AW112010, Scarb2 and Zc3hav1, which markedly improves infection with human viruses in none-human hosts. Furthermore provided are methods for the generation of the animal of the invention, methods for increasing or reducing the susceptibility of a cell to viral infection, methods for screening novel modulators of viral infection as well as new therapy options for the treatment of viral diseases, in particular hepatitis C.

The present disclosure provides, among other things, genetically modified non-human animals whose germline genome comprises an engineered endogenous immunoglobulin κ light chain locus comprising a single rearranged human immunoglobulin λ light chain variable region operably linked to a non-human Cλ gene segment, where the single rearranged human immunoglobulin λ light chain variable region comprises a human Vλ gene segment and a human Jλ gene segment. All immunoglobulin λ light chains expressed by B cells of the genetically modified non-human animal include human immunoglobulin λ light chain variable domains expressed from the single rearranged human immunoglobulin λ light chain variable region or a somatically hypermutated version thereof. Such animals, tissues from such animals, and cells from such animals represent an effective platform for producing antibodies, e.g., bispecific antibodies.

The present invention generally pertains to methods of treating X-linked juvenile retinoschisis and animal models thereof. In particular, the present invention pertains to the use of RS1 gene supplementation therapy by subretinal administration to treat X-linked juvenile retinoschisis and models thereof caused by one or more missense mutations of the RS1 gene.

Disclosed herein are nucleic acids encoding for and proteins expressing chimeric C1q polypeptides, non-human animals comprising said nucleic acids, and methods of making or using said non-human animals.

Described herein are donor vectors and systems for use in dual recombinase-mediated cassette exchange. Also described herein are animal models and human cells for consistent, rigorous, and facile investigation of transgene expression. Further described herein are methods of screening for therapeutic drugs using these animal models, and methods of treatment.

The present invention describes transgenic animals with human(ized) immunoglobulin loci and transgenes encoding human(ized) Igα and/or Igβ sequences. Of particular interest are animals with transgenic heavy and light chain immunoglobulin loci capable of producing a diversified human(ized) antibody repertoire that have their endogenous production of Ig and/or endogenous Igα and/or Igβ sequences suppressed. Simultaneous expression of human(ized) immunoglobulin and human(ized) Igα and/or Igβ results in normal B-cell development, affinity maturation and efficient expression of human(ized) antibodies.

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.

This invention relates to inhibition of the complement signaling using an anti-C5 antibody or fusion protein thereof. Specifically, the invention relates to methods of treating a complement-mediated disease or complement-mediated disorder in an individual by contacting the individual with an anti-C5 antibody fusion protein thereof.