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34 results about "Wild type mice" patented technology

FcRn-based therapeutics for the treatment of auto-immune disorders

InactiveUS20020138863A1Increased catabolismShort livedDepsipeptidesAntibody ingredientsDiseaseTransgenic knockout
Disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene, wherein said homozygous disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse in which exogenously administered IgG1 exhibits a substantially shorter half-life, as compared to the half-life of exogenously administered IgG1 in a wild-type mouse. Also disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene, wherein said homozygous disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse which is unable to absorb maternal IgG in the prenatal or neonatal stage of development Methods of using the transgenic knockout mouse, and cells derived therefrom, are also disclosed.
Owner:JACKSON LAB THE

Novel application of inhibitor for protein HSD17B13 or coding genes thereof

The invention discloses a novel application of an inhibitor for protein HSD17B13 or coding genes thereof. The novel application provided by the invention particularly means the application of the inhibitor for the protein HSD17B13 or the coding genes thereof in preparation of products for preventing and / or treating fatty liver. Proved by experiments, through immunizing a C57 wild-type mouse by using a recombinant adenovirus carrying an HSD17B13 gene, the condition that the liver of the mouse is subjected to obvious fatty change can be observed, oil red of a slice of the liver is stained and shows the accumulation of a lot of fat, and the content of triglyceride and cholesterol in liver tissues is increased remarkably, so that the HSD17B13 possibly participates in the formation process of fatty liver. The novel application has an important significance in prevention and / or treatment of fatty liver.
Owner:JIANGSU MEIDISEN BIOLOGICAL MEDICINE

Construction method and application of SDK2 gene mutation mice mice

The invention provides a construction method of an SDK2 gene mutation mice model. The mice model comprises the following steps of designing and constructing sgRNA capable of specifically identifying an SDK2 gene on the basis of a CRISPR/Cas9 system, injecting the sgRNA and a targeting vector constructed on the basis of the sgRNA into a mice fertilized egg; and after embryo transplantation, screening out F0-generation mice with SDK2 gene mutation from the output mice, and hybridizing the F0-generation mice with wild type mice to obtain an F1-generation mice model with SDK2 gene mutation. The mice model constructed by the method can be stably passaged, the action mechanism of the SDK2 gene in mice hereditary cataract can be conveniently researched in practical application, and under the condition that human patient research materials are not easy to obtain and are restricted by medical ethics, the SDK2 gene can be stably cloned. The mice model provided by the invention can become an important tool in the research of hereditary cataract, and a research model capable of realizing stable heredity is provided in the research of pathogenesis, treatment methods, drug screening, cataract surgery and the like.
Owner:BEIJING TONGREN HOSPITAL AFFILIATED TO CAPITAL MEDICAL UNIV

Functions and application of responsive to centrifugal force and shear stress gene 1 (RECS1) to treatment of restenosis after vascular injury

ActiveCN104198697APromote restenosisPro-restenosisGenetic material ingredientsSurgeryCell phenotypeDisease
The invention discloses functions and application of responsive to centrifugal force and shear stress gene 1 (RECS1) to treatment of restenosis after vascular injury. An RECS1 knockout mouse and a wild type mouse are taken as experimental subjects, and detection on mouse internal membrane regeneration, vessel wall cell proliferation level and smooth muscle cell phenotype transformation is carried out by a vascular injury model. Detection results prove that by virtue of RECS1 knockout, internal membrane regeneration and cell proliferation can be obviously inhibited, and smooth muscle cells are inhibited to be transformed into synthetic phenotype from contractile phenotype. Therefore, the functions of the RECS1 to the restenosis after vascular injury are mainly embodied in that internal membrane regeneration, cell proliferation and smooth muscle cell phenotype transformation are promoted by the RECS1. Aiming at the functions of the RECS1, the RECS1 can be used as a drug target for screening medicines for preventing, relieving and / or treating the disease of restenosis after vascular injury; an inhibitor of the RECS1 can be used for preparing medicines and arterial stents for preventing, relieving and / or treating the restenosis after vascular injury.
Owner:武汉惠康基因科技有限公司

Function of tumor progress site 2 in treatment of fatty liver and type 2 diabetes as well as application thereof

InactiveCN106512014AWith deteriorating fatty liverType 2 diabetes mellitusMetabolism disorderDigestive systemIntraperitoneal routeHepatic dysfunction
The invention discloses a function of tumor progress site 2 in treatment of fatty liver and type 2 diabetes as well as an application thereof. According to the invention, TPL2 gene knockout mice and wild type mice are taken as the experiment objects, through a high-fat diet-induced obesity mice model, the result shows that compared with the wild type C 57 mice, body weight of the TPL2 gene knockout mice is mitigated, the fasting blood glucose level is lower than that of a control group WT mice, and the hepatic dysfunction is obviously mitigated. Through intraperitoneal glucose tolerance experiment, the endurance of the TPL2 gene knockout mice on glucose is obviously enhanced. the mice liver tissue cholesterol content change result instructs that TPL2-KO mice fatty liver pathology of a HFD group (High fat diet) is obviously mitigated, and the lipid accumulation is obviously reduced. TPL2 can be taken as a drug target for treating fatty liver and / or type 2 diabetes, and its inhibitor can be used for preparing a drug to treating fatty liver and / or type 2 diabetes.
Owner:WUHAN UNIV

Application of caerulin in preparing sensitizing preparation of medicaments for intervening in pancreatic cancer animal model

InactiveCN104001151AIncrease the incidence of pancreatic cancerIncrease incidenceOrganic active ingredientsPeptide/protein ingredientsNormal pancreasWild type
The invention belongs to the technical field of experimental models, relates to a medicament for intervening in an inflammation related chemically induced pancreatic cancer animal model, and in particularly relates to application of caerulin in preparing a sensitizing preparation for synergizing dimethylbenzanthracene (DMBA) to induce a pancreatic cancer animal model. According to the application, an effective sensitizing preparation is provided to a medicament DMBA for inducing a C57 wild type mouse pancreatic cancer model, and the prepared animal model is an ideal tool for further studying pancreatic precancerous lesions and pancreatic cancer; by virtue of the synergetic effect of caerulin, the experiment cycle can be shortened, the experiment efficiency can be improved, and the experiment cost can be saved; occurrence and development of multiple steps in the process of intervening in the pancreatic cancer animal model and changes of histology are extremely similar to the developing process of pancreatic cancer of human beings, so that normal pancreas ductal epithelium, atypical hyperplasia of pancreas ductal epithelium, carcinoma in situ of pancreas ductal epithelium and invasive pancreatic cancer in the pancreatic cancer developing process can reappear.
Owner:FUDAN UNIV SHANGHAI CANCER CENT

Primary mouse liver cancer model based on liver oval cell malignancy as well as establishment method and application of primary mouse liver cancer model

The invention relates to the technical field of cancer animal model establishment, in particular to a primary mouse liver cancer model based on liver oval cell malignancy and an establishment method and an application thereof. The establishment method comprises the following steps: transforming liver oval cells by using a proto-oncogene to obtain liver cancer stem cells; performing in-situ transplantation on the liver cancer stem cells to the liver of a receptor mouse to obtain a primary mouse liver cancer model; wherein the acceptor mouse is a wild type mouse subjected to X-ray irradiation treatment. According to the scheme, aiming at the limitation of the existing primary liver cancer animal model, a novel primary model for simulating the whole occurrence and development natural process of the primary liver cancer is established, so that the effect and mechanism of a specific gene in the occurrence and development of the primary liver cancer can be accurately researched, and whether the gene can be used as an effective treatment target or not is verified. By utilizing the model in the scheme, potential new targets and new drugs for treating the primary liver cancer can be screened, and conditions are created for researching and developing novel drugs or treatment methods for treating the primary liver cancer.
Owner:WEST CHINA HOSPITAL SICHUAN UNIV

Application of beta-arrestin-1 in preparing medicine for preventing or treating myocardial infarction

The invention relates to the technical field of medicines, and provides a new application of a beta-arrestin-1 protein. The new application is the application of the beta-arrestin-1 in preparing a medicine or a health care product for preventing or treating myocardial infarction. Experiments prove that the myocardial infarction area of a mouse is outstandingly increased after the beta-arrestin-1 is knockout, the myocardial infarction area is outstandingly decreased after the beta-arrestin-1 is extremely expressed; in addition, left ventricular ejection fraction and left ventricular fractional shortening are obviously lower than those of a wild type mice group after the beta-arrestin-1 is knockout, and the left ventricular ejection fraction and the left ventricular fractional shortening are outstandingly enhanced after the beta-arrestin-1 is extremely expressed. Thus, the beta-arrestin-1 plays a protective role in the prognosis of the myocardial infarction.
Owner:SECOND MILITARY MEDICAL UNIV OF THE PEOPLES LIBERATION ARMY

Method for regulating proliferation and differentiation of inner ear stem cells by using Rassf2 and application of Rassf2 in hair cell regeneration

PendingCN112877413ASeparation is accurate and largeGood research premiseMicrobiological testing/measurementGenetically modified cellsNeomycinMedicine
The invention relates to the field of inner ear stem cells, in particular to a method for regulating proliferation and differentiation of inner ear stem cells through Rassf2 and application of Rassf2 in hair cell regeneration. The regulation and control method comprises the following steps: 1, detecting expression conditions of Shh or Hippo and Rassf2 in cochlea in a wild type mouse; 2, studying the effect of Shh or Hippo and Rassf2 on proliferation and differentiation of the inner ear stem cells which are separated in a flow mode in an in-vitro experiment; 3, researching the effects of Shh or Hippo and Rassf2 on a living hair cell neomycin injury model. By using the Lgr5-EGFP-CreERT2 tool mouse, the separation of the inner ear stem cells (Lgr5 positive cells) is accurate and a large amount of the inner ear stem cells (Lgr5 positive cells) can be realized, and a relatively good research premise can be achieved: the Lgr5 positive inner ear stem cells of the mouse are sorted. Besides, after the separated inner ear stem cells are subjected to balling and differentiation experiments by researching Shh, Hippo and Rassf2 in an in-vitro experiment, the specific action mechanism of Shh, Hippo and Rassf2 in regulation and control of proliferation and differentiation of the inner ear stem cells and hair cell regeneration can be deeply explored.
Owner:SOUTHEAST UNIV
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