41 results about "Transgenic Model" patented technology

The invention discloses a detection method for the expression of a GPR120 gene based on eGFP. The detection method comprises the following steps: inserting an eGFP fragment to the specific site TAA of the termination codon of the GPR120 gene by using CRISPR/Cas 9 technology so as to obtain a transgenic model mouse with eGFP-labeled GPR120 positive cells; and carrying out excitation by using a fluorescence analyzer and determining the fluorescence intensity of the positive cells of the mouse. The method carries out real-time monitoring on the expression of the GPR120 gene so as to control and reduce errors among groups, guarantee the reliability of results and compensate for and overcome the problems of variability caused by comparison of different groups of histocytes and incapability of monitoring the changes of gene expression at a living cell level in the prior art. According to the invention, the expression level of the GPR120 gene can be immediately determined after collection of cells, and operations and reactions like RNA extraction, inverse transcription and PCR are omitted, so detection of the expression of the GPR120 gene is simpler.

The invention provides a mammalian cDNA which encodes a mammalian Ras association domain containing protein. It also provides for the use of the cDNA, fragments, complements, and variants thereof and of the encoded protein, portions thereof and antibodies thereto for diagnosis and treatment of cell proliferative and inflammatory disorders, particularly thymus hyperplasia, allergies, asthma, and hypereosinophilia. The invention additionally provides expression vectors and host cells for the production of the protein and a transgenic model system.

In accordance with the present invention, it is demonstrated that selected mutations such as an Asp -> Ala (D664A) mutation in APP (which prevents cleavage at the caspase cleavage site) prevent both hippocampal synaptic loss and dentate gyral atrophy, even though such mutations do not interfere with the production of Ass or the formation of amyloid plaques in a transgenic model of Alzheimer's disease. Accordingly, in view of this finding, methods have been developed for the identification of agents which block cleavage at Asp664 of APP, including transgenic animals which are useful for such purpose, as well as methods for the use thereof for the treatment of neurodegenerative diseases.

The invention relates to a construction method and application of a humanized mouse model, in particular to a construction method and application of a transgenic mouse model of a human Nbs1<c.657del5> gene. The method includes: constructing a 5bp deletion mutation-containing BAC carrier in the human Nbs1 gene, conducting pronuclei microinjection, and performing screening to obtain 3 stable transgenic lines for high expression and low expression of the human Nbs1 gene. The transgenic mouse involved in the invention has the phenotypes of delayed puberty, uniform shortening of body length and bone dysplasia at certain proportion in one of the lines, and a new mouse model is established for Nijmegen breakage syndrome diseases. At the same time, as the Nbs1 gene function impairment is closely related to cancers, the transgenic model can be applied to short-term carcinogenic tests in drug pre-clinical safety evaluation, thus providing a potential substitution model for traditional biennium carcinogenic tests and also providing an effective tool for research of carcinogenesis mechanisms.

The invention provides a building method of a Drosophila melanogaster model for screening and researching mitochondria disease virulence gene, and an application of the same. In the method, first fluorescent protein is represented by a mitochondria in a wing nerve cell in a Drosophila melanogaster model; second fluorescent protein is represented by in a wing nerve cell film in the Drosophila melanogaster model; the mitochondria is labeled via the first fluorescent protein positioned by the mitochondria; the nerve cell is labeled by the second fluorescent protein positioned by the nerve cell film; and research to mitochondria functions in a nervous system can be achieved in vivo. The Drosophila melanogaster transgene model built by the method can simply and conveniently screen and research mitochondria disease virulence genes; and demands for high flux, strong economic property and short time during mitochondria disease virulence gene screening can be met.

The invention provides a mammalian cDNA which encodes a mammalian AQP8V. It also provides for the use of the cDNA, fragments, complements, and variants thereof and of the encoded protein, portions thereof and antibodies thereto for diagnosis and treatment of pancreatic disorders, particularly type I diabetes. The invention additionally provides expression vectors and host cells for the production of the protein and a transgenic model system.

The invention discloses an application of noble dendrobium total alkali in preparing a drug for atherosclerosis and belongs to the technical field of biomedicine. According to the application of nobledendrobium total alkali in preparing the drug for atherosclerosis, the noble dendrobium is biennial noble dendrobium and the dosage of the noble dendrobium total alkali is 20-180 mg/kg per day. The invention further explicits the degreasing action of noble dendrobium total alkali DNLA and a probable action mechanism thereof. By adopting an experimental rat atherosclerosis model and an ApoE-/- mouse transgenic model, influence of the DNLA on hyperlipidemia atherosclerosis of blood vessels is observed, and the action mechanism thereof is analyzed, finding that the DNLA has preventing and treating action on the rat atherosclerosis model and the action mechanism is partially related to down-regulation of expression of MCP-1/CCR2, MCPIP and CRP genes, thereby providing a basic pharmacologicalbasis for clinical treatment of HLP and As by DENLA.

In some aspects, the present invention provides chimeric transferrin receptor (TfR) polynucleotides and polypeptides. In other aspects, this invention provides chimeric TfR transgenic animal models and methods of using the animal models to identify therapeutics that can cross the blood-brain barrier.

Tricyclic pyrone compounds having high oral bioavailability, excellent blood-brain barrier permeability, and low toxicity are presented. Administration of the compounds to Alzheimer's Disease transgenic models resulted in substantially reduced soluble and insoluble Aβ species in the brain without affecting general behavior and motor coordination. Furthermore, in addition to blocking the toxicity and formation of both intraneuronal and extracellular Aβ aggregates, the compounds also increase cellular cholesterol efflux, restore axonal trafficking, and enhance hippocampal synaptic plasticity.

The invention discloses an application of luteolin in antagonizing the accumulation of beta-amyloid protein, improving cognitive memory and reducing senile plaques. The Alzheimer's disease (AD) is a neurodegenerative disease characterized by neurofibrillary tangles, beta-amyloid (A beta) plaque deposition, and cognitive decline, The accumulation of extracellular toxicity of A beta protein is considered as one of the main links in the pathogenesis of AD. The luteolin can significantly inhibit the accumulation of beta-amyloid protein 1-42 monomers to form fibers, inhibits the formation of a betasecondary structure, and improves the spatial memory learning ability of AD mice and significantly eliminates amyloid plaques in the brain tissue of APP/PS1 double transgenic AD model mice. The luteolin can be applied to the treatment of Alzheimer's disease and related drug development.

Disclosed is a vector pair for screening tau oligomer formation, a mouse embryo introduced with the vector pair, a transgenic model mouse of neurological disease, obtained from the mouse embryo, and a method of screening a tau oligomer formation inhibitor candidate using the transgenic model mouse. More specifically, the present invention provides vector pair for screening tau oligomer formation, comprising: a first vector comprising a first tau gene, a first fluorescence protein gene and a first neuron-specific promoter; and a second vector comprising a second tau gene, a second fluorescence protein gene and a second neuron-specific promoter, wherein a protein expressed from the first fluorescence protein gene and a protein expressed from the second fluorescence protein gene bind to each other to display fluorescence, by association between a protein expressed from the first tau gene and a protein expressed from the second tau gene.

The invention provides a rapid screening method applied to model animal zebrafish transgenosis. The method includes the following steps of 1, building a gene expression vector containing a strong promoter, an objective gene and a label gene; 2, designing a specific target spot aiming at a target gene, and obtaining a targeted SgRNA sequence; 3, based on the specific target spot, building a homologous recombinant vector; 4, injecting a homologous recombinant vector section, mRNA obtained through in-vitro transcription synthesis of the SgRNA sequence and nCas9-mRNA obtained through in-vitro transcription synthesis together into a zebrafish zygote; 5, firstly, screening out zebrafishes lack of a target gene function, then conducting second screening through the label gene, obtaining a label gene expression individual, and therefore obtaining the expression individual which expresses the objective gene. Through the method, early juvenile zebrafishes can be screened, and the purpose of quickly establishing a transgenic model is achieved.

The present invention relates generally to transgene constructs, transgenic non-human animals comprising transgene constructs, methods of making and methods of using the transgenic non-human animals comprising transgene constructs. An embodiment of the invention relates to methods of assaying the activation of GPCR ligands non-invasively in whole animals, tissue slices, or in native cells using a transgenic model containing a bioluminescent transgene reporter system that is responsive to pathway modulation following ligand binding of GPCR receptors.

Evidence indicates dysregulation. of the immunoregulatory molecule CD45 occurs in Alzheimer's disease (AD). Transgenic mice overproducing amyloid-β peptide (Aβ) and deficient in CD45 (PSAPP/CD45⁻/⁻) recapitulate AD neuropathology. Increased cerebral intracellular and extracellular soluble oligomeric and insoluble Aβ, decreased plasma soluble Aβ increased microglial neurotoxic cytokines TNF-α and IL-1β, and neuronal loss were found in PSAPP/CD45⁻/⁻ mice compared with CD45-sufficient PSAPP littermates. After CD45 ablation, in vitro and in vivo studies demonstrate a microglial phenotype whereby microglia phagocytose less Aβ but display proinflammatory properties. This microglial activation occurs with elevated Aβ oligomers and neural injury and loss as determined by decreased ratio of anti-apoptotic Bcl-xL to proapoptotic Bax, increased activated caspase-3, mitochondrial dysfunction, and loss of cortical neurons in PSAPP/CD45⁻/⁻ mice. These data show that deficiency in CD45 activity leads to brain accumulation of neurotoxic Aβ oligomers and validate CD45-mediated microglial clearance of oligomeric Aβ as a novel AD therapeutic target.

The invention discloses a construction method and a related vector of a zebra fish heart specific expression model. A homologous recombinant vector comprises an insert fragment which is inserted withan initial vector and comprises a promoter of zebra fish heart specific expression, left and right homologous arms fused with LoxP site sequences, a polyclonal site, an internal ribosome entry site, areporter gene and a transcription termination fragment, wherein the promoter is positioned at the upstream of the reporter gene, and the termination signal is positioned at the downstream of the reporter gene; the left homologous arm is positioned at the upstream of the promoter, and the right homogenous arm is positioned at the downstream of the termination signal; the inner sides of the homologous arms contain LoxP sequences; the polyclonal site is positioned between the promoter and the reporter gene; and the left and right homologous arms are targeted to the zebra fish pigment gene. The invention further provides a construction method of the zebra fish heart specific expression model, which can be used for quickly establishing a transgenic model of the zebra fish heart specific expression gene, and regulating expression of the insert fragment.

The invention aims to provide a molecular method for regulating and controlling the flowering rhythm of petunia hybrida. In the implementation method of the molecular method, the molecular method forregulating and controlling the flowering rhythm of plants by using flower specific expression promoters and circadian clock genes together is realized in combination with the means of genetic transformation. The molecular method comprises the steps of promoter synthesis, LHY gene amplification and carrier construction, genetic transformation is carried out by using the important flower petunia hybrida with simple tissue and cell operation technology, short life cycle and clear genetic background as a transgenic model plant, and finally a transgenic plant of which the flowering time changes isobtained. The expression of the circadian clock gene LHY capable of regulating and controlling the flowering rhythm in petunia hybrida is promoted by the flower specific expression promoters, and theflowering time of the obtained transgenic plant is a new product with obvious difference compared with that of a contrast plant. Through the statistics of the flowering time of the obtained positive transgenic plant, the lowering time of the transgenic plant compared with that of a check plant is delayed by nearly four hours.

The invention belongs to the field of medicines, and relates to application of andrographolide, in particular to application of triacetyl andrographolide as a medicine for regulating autophagosome degradation. The invention relates to an application of triacetyl andrographolide in preparation of a medicine for promoting autophagosome clearance. The invention also discloses application of triacetyl andrographolide as a medicine for simultaneously reducing the expression levels of LC3-II and P62 in the brain. Triacetyl andrographolide also can be used as a medicine for reducing phosphorylation levels of Akt and mTOR, improving learning and improving memory. An APP/PS1/Tau triple transgenic model mouse and an ApoE4 transgenic mouse are utilized to prove that the triacetyl andrographolide can effectively improve the learning and memory ability of a model animal and reduce the levels of A[beta]1-40 and A[beta]1-42 in the brain of a model animal. Triacetyl andrographolide can inhibit the activation of Akt-mTOR signals in both in-vivo and in-vitro models, relieve the excessive accumulation of LC3-II and P62, and reduce the aggregation of autophagosome.

The invention discloses an application of an artemisia annua extract in preparing a preparation for treating or preventing AD. The artemisia annua boiled water extract can unexpectedly improve the learning and memory ability of Alzheimer's disease transgenic model mice, prevent nerve cell death caused by oxidative damage, promote mitochondrial transmembrane potential recovery, reduce amyloid plaque deposition, nerve fiber entanglement and neuron loss, and provides an experimental basis for clinical research on treatment of the AD.