10 results about "Knockout animal" patented technology

The application discloses an IGFBP-2 derived polypeptide and application thereof in preparation of an antidepressant, and relates to the technical field of biological medicines. The amino acid sequence of the polypeptide is Pro-Lys-Lys-Leu-Arg-Pro, the N terminal of which is acetylated and the C terminal of which is amidated, and the amino acid sequence is shown as SEQ ID NO:1. The polypeptide has a small molecular weight, can easily penetrate the blood-brain barrier, and has good stability after terminal modification. Animal experiments prove that the polypeptide can significantly improve the depressive behavior of Shank3 gene knockout mice, including improving the spatial cognitive ability, enhancing the social interaction and curiosity, and relieving the anxiety behavior. Cell experiments prove that the polypeptide can significantly improve the viability of hippocampal neuron cells from Shank3 gene knockout mice, and up-regulate the expression level of synaptic plasticity related proteins GluA1 and SYN1. The polypeptide can be prepared by a chemical synthesis method, has low cost, and can be used for preparing a medicine for preventing or treating depression (especially depression related to Shank3 gene mutation).

This invention belongs to the field of biomedical technology and discloses a method for constructing and applying a podocyte-specific S1PR1 gene knockout mouse model. Podocyte-specific S1PR1 knockout mice were constructed using the Cre-LoxP system, and then an FSGS model was established via doxorubicin injection. The model was validated using urine, serum, histopathological, and molecular mechanism detection methods. The study found that decreased S1PR1 expression induces podocyte senescence and FSGS progression by downregulating Xab2, leading to abnormal POLR2A splicing and reduced expression. This invention is the first to construct such a model, revealing the regulatory role of the S1PR1-Xab2-POLR2A pathway in podocyte senescence, providing a reliable tool for studying the pathogenesis of FSGS, clarifying the potential of S1PR1 as a therapeutic target, and enabling drug screening for FSGS treatment. It has significant clinical translational value.

This invention discloses a mouse experimental method for detecting the tissue distribution of exogenous oxytocin, belonging to the field of biotechnology. Specifically, oxytocin is injected into or nasally sprayed into oxytocin knockout mice, and body tissues, including but not limited to brain tissue, mammary gland tissue, blood, heart tissue, uterine tissue, bone tissue, and muscle tissue, are collected at different time points. The tissue distribution and content of oxytocin are then detected using liquid chromatography-mass spectrometry (LC-MS / MS). This experimental method allows for a wider range of experimental samples, not just focusing on brain tissue and blood; it also has higher sensitivity and stronger specificity; and by utilizing oxytocin gene knockout mice, it eliminates the influence of endogenous oxytocin, providing certain assistance for subsequent animal experiments and clinical research on oxytocin.

This invention discloses a DC-specific knockout animal model of the Adamdec1 gene, its construction method, and its applications. The method involves inserting Loxp sites at both ends of exons 2–10 of the Adamdec1 gene to obtain the Adamdec1 gene. flox / flox Mice, then with Cd11c cre / + Mouse hybridization and screening to obtain Cd11c cre / + Adamdec1 flox / flox In mice, the Adamdec1 gene was specifically knocked out in dendritic cells. This model, induced by 3% DSS, exhibited a more severe colitis phenotype and can be used to establish a stable and reliable research model for acute colitis. This invention provides a precise tool for studying the function of Adamdec1 in intestinal immune regulation and has significant scientific and translational value.

This invention discloses the application of NLRX1 protein inhibitors in the preparation of products with protective effects against pulmonary fibrosis, belonging to the field of biomedical technology. This invention, through the use of an NLRX1 gene knockout mouse model and siRNA silencing technology, demonstrates that inhibiting NLRX1 can significantly alleviate bleomycin-induced pulmonary fibrosis pathological damage. Its protective mechanisms include promoting the proliferation of type II alveolar epithelial cells, inhibiting their damage and apoptosis, and reducing myofibroblast infiltration and extracellular matrix deposition. Based on this, this invention provides for the first time a therapeutic strategy targeting the inhibition of the NLRX1 protein. Related products include recombinant vectors containing RNA molecules encoding NLRX1 expression inhibitors or other drugs capable of inhibiting NLRX1 expression. This invention provides new targets and drug development directions for the treatment of fibrotic diseases, especially pulmonary fibrosis.

This invention discloses a method for constructing a type I classical dendritic cell-specific knockout Dyrk1a gene mouse model and its application. The method includes the following steps: (1) [The text abruptly ends here, likely due to an incomplete sentence or missing information.] flox / + Donor mice were crossed with XCR1-Cre positive tool mice, and the genotype Dyrk1a was obtained through screening. flox / + XCR1-Cre+ and Dyrk1a flox / + (2) The F1 generation hybrid offspring of XCR1-Cre- were crossbred; (3) The F1 generation hybrid offspring obtained in step (1) were crossbred with siblings or backcrossed to obtain the F2 generation population; (4) The F2 generation population obtained in step (2) was identified and screened for genotype Dyrk1a. flox / flox Individuals with XCR1-Cre+ are thus established. This invention overcomes the embryonic lethality limitation caused by whole-body Dyrk1a knockout, and for the first time achieves in-depth research on the long-term regulatory mechanism of Dyrk1a in the cDC1 subpopulation in adult live mice. This effect is achieved through the conditional design of the Cre-loxP system, avoiding early developmental disorders and providing a reliable genetic tool for elucidating immune system function, significantly expanding the applicability of the research.

This invention provides a method for creating liver cancer cell lines with clearly defined driver genes based on transposon systems and their applications. Specifically, this invention provides a method based on the SB transposon system, which successfully establishes liver cancer cell lines with stable proliferation capacity by stably introducing oncogenes into wild-type or p53 knockout mouse primary liver cells. These cell lines provide important experimental tools for liver-related research, drug screening, and the study of liver cancer mechanisms.

This invention discloses SFMBT2 The application of genes and bromocriptine in repairing damaged cartilage and preventing osteoarthritis. Experiments have found that the gene expressed in chondrocytes... SFMBT2 The gene helps maintain the normal phenotype of chondrocytes and can mediate the axial regulation of downstream ATF3-PI3K / AKT signaling. Cartilage tissue-specific knockout mice of this gene exhibit a significant spontaneous osteoarthritis phenotype and exacerbate the progression of DMM surgery-induced PTOA. Gene complementation targeting SMBT2 can significantly activate chondrocyte activity. Among various small molecule drugs targeting SMBT2 protein predicted using docking models, bromocriptine can significantly promote the repair of damaged cartilage by activating the biological function of chondrocytes.

The application provides an application of vascular endothelial cell histone methyltransferase Ezh2 in preparation of a medicine for preventing and treating sepsis-associated encephalopathy and model construction, relates to the field of biomedical technology, and has the primary purpose of providing a drug target for preventing and treating SAE, namely, EZH2 in vascular endothelial cells. The application also provides an endothelial cell specific Ezh2 gene conditional knockout mouse model, the model has a high sensitivity and a high stability of BBB damage phenotype, and can be used for SAE pathogenesis research and drug screening. The application further has the purpose of providing SAE treatment drugs, diagnostic markers and screening methods based on the new target and the new model. In the application, a mouse Ezh2 gene conditional knockout and an induced conditional knockout-CLP high-sensitivity SAE model are successfully constructed. The model not only overcomes the problem of systemic knockout lethality, but also has a BBB damage and neuroinflammation phenotype which is much more serious and stable than that of a traditional CLP model, thereby providing an irreplaceable tool for drug research and development.