In one aspect, the invention provides a transgenic non-human animal model having germ cells and somatic cells containing an endogenous MMTV-SV40-Spy1A gene sequence introduced into said animal model or an ancestor of said animal model at an embryonic stage, wherein said gene sequence comprises a mouse mammary tumor virus gene (MMTV), a functionally disrupted SV40 gene (SV40) and a human Spy1A gene. In another aspect, the present invention provides a transgenic non-human animal model whose germ cells and somatic cells contain an endogenous Spy1A-pTRE-Tight gene sequence introduced into said animal model or an ancestor of said animal model at an embryonic stage. Preferably, the Spy1A-pTRE-Tight animal model expresses the Spy1A gene and develop cancer, preferably breast cancer, when administered with tetracycline, preferably doxycycline.

Provided is a pharmaceutical composition for treating a degenerative brain disease, including a glycine transporter as an active ingredient. A composition including, as an active ingredient, a glycine transporter protein, a fragment thereof or a nucleic acid molecule encoding the protein or the fragment thereof, a vector including the nucleic acid molecule, or a cell transformed with the vector including the nucleic acid molecule, according to an embodiment, not only can achieve excellent effect(s) of inhibiting amyloid-beta aggregation and/or degrading aggregated amyloid-beta, but also degrades tau protein (and/or inhibition of the aggregation thereof), inhibits the hyperphosphorylation of tau protein, and has excellent blood-brain barrier permeability, thus making it possible to successively act on brain tissues. Therefore, the composition can be effectively applied to the prevention and/or treatment of various degenerative brain diseases associated with amyloid-beta aggregation, tau protein aggregation, and/or hyperphosphorylated tau protein.

Nucleic acids encoding modified myosin heavy-chain-associated RNA transcripts are provided. The modified myosin heavy-chain-associated RNA transcripts belongs to a cluster of long noncoding RNAs (lncRNA) and bind to chromatin remodeler Brg1 to inhibit Brg1's genomic targeting and gene regulation function. The modified myosin heavy-chain-associated RNA transcripts expressed in an individual inhibit Brg1's gene regulation function and protect the heart of the individual from myopathy and failure. One of the modified heavy-chain-associated RNAs is a 400 base pair fragment segmented from a natural 779 base pair sequence of Mhrt (Mhrt779) and has the same cardioprotective effects as the Mhrt779.

The present invention relates to a HSP27 mutation (S135F) mediated Charcot-Marie-Tooth disease (CMT) animal model. Particularly, the vector expressing mutant HSP27 protein wherein the 135.sup.th serine is substituted with phenylalanine has been injected in the mouse zygote and then the mouse harboring the expression vector was selected. The selected mouse was confirmed to display Charcot-Marie-Tooth disease phenotype, so that the animal model was expected to be efficiently used for the evaluation of the effect of Charcot-Marie-Tooth disease treating material candidates.

Provided herein are methods and compositions related to non-human animals that express exogenous Terminal Deoxynucleotidyltransferase (TdT).

A non-human transgenic animal expressing ApoL1 is provided as well as a method for generating the same. Also provided is a method for identifying an agent capable of reducing the progression of an ApoL1 mediated nephropathy. Furthermore, an isolated antibody is provided which binds to the human variants of ApoL1.

The present disclosure relates to transgenic Caenorhabditis elegans including, in sensory neurons, Channelrhodopsin 2 (ChR2)::Green Fluorescence Protein (GFP) DNA in which the ChR2 gene and the GFP gene are linked, a method of producing the same, a method of regulating the lifespan thereof, and a method of screening an aging regulation candidate by using the same. The present disclosure may also provide an animal model for research into prevention/treatment of aging-related diseases by regulating the lifespan of an animal on a subject level and a method of screening a drug candidate for prevention/treatment of aging-related diseases.

This invention is intended to develop a promoter that can strongly induce marker gene expression throughout an embryo, so as to simply, efficiently, and accurately identify a transgenic insect at an early developmental stage, and to provide a gene expression vector into which such promoter has been incorporated as a transformant discrimination marker. Such exogenous gene expression vector comprises a polynucleotide comprising the nucleotide sequence as shown in SEQ ID NO: 1 as a promoter.

The invention relates to a downmodulator of CUB domain-containing protein 1 (CDCP1), for use in a method of treating a patient suffering from castrate-resistant prostate cancer. The invention further relates to a pharmaceutical composition, comprising a downmodulator of CDCP1 and a senolytic compound, and to methods of selecting a patient with prostate cancer eligible for treatment with a combination of downmodulator of CDCP1 and a senolytic compound.

The present disclosure relates to the field of commercial scale production and processing of pharmaceutical liquid or solid compositions derived from insects, wherein the compositions include a purified recombinant protein, vaccine, antibody, peptide, or chemical. Systems and methods to produce the insects and a purified insect-derived recombinant protein, vaccine, antibody, peptide, insecticide, fungicide, or chemical within a bioreactor are also described.