Patent classifications
A01K2207/05
SYSTEM FOR MODULATING ACTIVITY OF CELL AND METHOD FOR MODULATING ACTIVITY OF CELL
The system for modulating the activity of cells according to an exemplary embodiment of the present invention may include a rotating magnetic field generating device which has an internal space in which a magnetic force generating unit and a living body can be disposed and forms a rotating magnetic field which satisfies Relationship Formulas 1 and 2 below; and magnetic particles disposed in the living body and capable of binding to a bioactive material and generating a torque when a rotating magnetic field is applied to transmit the torque to the bioactive material.
|M.sub.c|≥1 mT [Relationship Formula 1]
|M.sub.75−M.sub.c|/D.sub.75≤5.0 T/m [Relationship Formula 2]
In Relationship Formulas 1 and 2 above, M.sub.c is the strength of the magnetic field at the position of the rotation axis, D.sub.75 is the distance from the rotation axis to the 75% position of the distance to the magnetic force generating unit, and M.sub.75 is the strength of the magnetic field at the position D.sub.75.
Method for Producing Virus-Infected Cell Line and Animal Model
Disclosed herein are methods for producing virus-infected cell lines or animal models, wherein an enveloped virus including a lipid bilayer is mixed with a bile acid or a bile acid derivative, which allows the lipid bilayer to be replaced with a lipid bilayer derived from a target animal. Also disclosed herein are the virus-infected cell lines or animal models so produced and methods of screening a therapeutic candidate for a viral disease using the same.
Methods for treating hepatitis B infection
This application relates to potent oligonucleotides useful for reducing HBsAg expression and treating HBV infections.
SCREENING METHOD FOR SELECTED AMINO-LIPID-CONTAINING COMPOSITIONS
The invention features a method of identifying therapeutically relevant compositions which include a therapeutic agent and 2,2-dimethylaminomethyl-[1-3]-dioxolane by screening for an effect of the agent on the liver of a model subject.
COMBINATION OF ANTISENSE RNA SEQUENCES AND USE IN THE PRODUCTION OF ABORTIVE TILAPIA
The present disclosure provides a combination of antisense RNA sequences and use thereof in the production of abortive tilapia, belonging to the technical field of molecular biology and reproductive biology, the combination of antisense RNA sequences includes antisense RNA of steroidgenic factors SF1-1 and SF1-2; the nucleotide sequences of Anti-SF1-1-I, Anti-SF1-1-II, Anti-SF1-2-I and Anti-SF1-2-II are set forth in SEQ ID NO. 1-SEQ ID NO. 4 respectively. The method of the present disclosure introduces antisense RNA fragments into the eggs through the fertilization hole to realize effective and accurate targeted intervention for regulating the gene expression, and the method has the advantages of simple operation, minimal egg damage, high success rate, stable phenotype after breeding, and excellent application prospects.
Protein having nuclease activity, fusion proteins and uses thereof
The present invention relates to a nucleic acid molecule encoding (I) a polypeptide having the activity of an endonuclease, which is (a) a nucleic acid molecule encoding a polypeptide comprising or consisting of the amino acid sequence of SEQ ID NO: 1; (b) a nucleic acid molecule comprising or consisting of the nucleotide sequence of SEQ ID NO: 2; (c) a nucleic acid molecule encoding an endonuclease, the amino acid sequence of which is at least 70% identical to the amino acid sequence of SEQ ID NO: 1; (d) a nucleic acid molecule comprising or consisting of a nucleotide sequence which is at least 50% identical to the nucleotide sequence of SEQ ID NO: 2; (e) a nucleic acid molecule which is degenerate with respect to the nucleic acid molecule of (d); or (f) a nucleic acid molecule corresponding to the nucleic acid molecule of any one of (a) to (e) wherein T is replaced by U; (II) a fragment of the polypeptide of (I) having the activity of an endonuclease. Also, the present invention relates to a vector comprising the nucleic acid molecule and a protein encoded by said nucleic acid molecule. Further, the invention relates to a method of modifying the genome of a eukaryotic cell and a method of producing a non-human vertebrate or mammal.
Method for preparing fish skin mucous gland bioreactor and application thereof
A method for preparing a fish skin mucous gland bioreactor and its application, including: identifying genes specifically expressed in fish skin mucinous gland cells, promoters and secreted protein signal peptides, constructing transgenic expression vectors that can specifically express endogenous or heterologous biologically active substances in fish skin and mucous gland cells, developing stable genetic and transgenic fish that secrete bioactive substances into fish mucus, and using bioactive substances secreted by mucus glands for animal and plant growth, stress resistance and disease resistance, human health care and disease prevention, and commercial enzymes. The fish skin mucous gland bioreactor developed by the invention has the characteristics of easy breeding and expansion, more skin mucus secretion, convenient mucus collection, and easy purification of bioactive substances, and can realize the large-scale production of fish skin mucous gland bioreactor and efficient application.
METHODS OF GENETIC MEDIATED ENGINEERING OF RNAi MODELS
Provided herein are systems and methods for Inducible and conditional CRISPR/Cas9 and RNAi. From animal model creation and the efficiency of CRISPR-based targeting, the present invention comprises developing RNAi models that enable inducible and reversible gene silencing to simulate new therapeutic regimes.
METHODS FOR TREATING HEPATITIS B INFECTION
This application relates to potent oligonucleotides useful for reducing HBsAg expression and treating HBV infections.
CORRECTION OF DYSTROPHIN EXON 43, EXON 45, OR EXON 52 DELETIONS IN DUCHENNE MUSCULAR DYSTROPHY
Duchenne muscular dystrophy (DMD), which affects 1 in 5,000 male births, is one of the most common genetic disorders of children. This disease is caused by an absence or deficiency of dystrophin protein in striated muscle. The major DMD deletion “hot spots” are found between exon 6 to 8, and exons 45 to 53. Here, three DMD mouse models are provided that can be used to test a variety of DMD exon skipping and refraining strategies. Among these are, CRISPR/Cas9 oligonucleotides, small molecules or other therapeutic modalities that promote exon skipping or exon refraining or micro dystrophin mini genes or cell based therapies. Methods for restoring the reading frame of exon 43, exon 45, and exon 52 deletion via CRISPR-mediated exon skipping and refraining in the humanized DMD mouse model, in patient-derived iPSCs and ultimately, in patients using various delivery systems are also contemplated. The impact of CRISPR technology on DMD is that gene editing can permanently correct mutations.