1998-039 – Through the use of gene targeting in mouse embryonic stem (ES) cells we have successfully generated a line of mice deficient in eosinophil granule major basic protein-1 (mMBP-1). These mice would be useful in drug discovery programs directed toward developing treatments for asthma, allergy, inflammation and a variety of eosinophil-related disorders. PMID: 11067904
2014-430 – Mouse model for human progeroid syndrome. Genotype/Phenotype: Sprtn hypomorphic, premature aging (progeria with humans). Utility: disease model for progeria. PMID: 25501849
2014-330 – An adult hypomorphic model of Propionic acidemia (PA) in Pcca− mice using a transgene bearing an A138T mutant of the human PCCA protein. Pcca−/−(A138T) mice have 2% of wild-type PCC activity, survive to adulthood, and have elevations in propionylcarnitine, methylcitrate, glycine, alanine, lysine, ammonia, and markers associated with cardiomyopathy similar to those in patients with PA. Data... Read More
2014-148 – The SR4G transgenic zebrafish stress response reporter line utilizes a tandem array of glucocorticoid response element sequences to drive expression of a short half-life green fluorescent protein when bound by active glucocorticoid receptors. High-resolution imaging and qRT-PCR have been used to characterized the spatiotemporal responses of this reporter line following exposure to exogenous... Read More
2014-055 – Exon 41 of LRRK2 is floxed, thus LRRK2 can be removed by cre-mediated deletion. Genotype/Phenotype: homozygous LRRK2loxp/ LRRK2loxp, phenotype would be dependent on which cells express Cre after crossing. Utility: Parkinson’s Disease Research PMID: 22647713
2010-196 – iPhil mouse line permitting inducible loss of eosinophils to study eosinophil-related diseases. Genotype/Phenotype: Inducible ablation of eosinophils is accomplished through expression of the human diptheria toxin receptor exclusively in cells of the eosinophil lineage. Diptheria toxin exposure completely eliminates circulating osinophils without affecting other cell types. Depletion is... Read More
2010-142 – Conditional NKAP knockout mouse. Genotype/Phenotype: NKAP is a transcriptional repressor of the Notch signaling pathway. The cre-lox system was used to remove exon 3 of NKAP and disrupt repressor function of NKAP. Loss of NKAP function early in T cell development resulted in a severe block in T cell development. Utility: Mouse model for examining NKAP function and the role of NKAP in T... Read More
2010-040 – Mouse overexpressing PAPP-A in arterial smooth muscle for the study of atherosclerotic lesion development. Genotype/Phenotype: A modified SM22alpha promoter with a deleted repressor element drives smooth muscle overexpression. Upon crossbreeding with ApoE knockout mice, PAPP-A transgenic mice develop larger atherosclerotic lesions than ApoE knockout mice. Utility: Model for examining the... Read More
2009-216 – Mouse expressing human rab9 GTPase. Genotype/Phenotype: Mice demonstrate a dramatic reduction in storage of gangliosides and an approximately 22% increase in lifespan relative to controls. Utility: Useful for studies of secretion in the intestine and/or liver. Possible application to other lysosomal storage diseases. Model for in vivo studies of rab9 regulation and activity. PMID:... Read More
2007-110 – Genotype/Phenotype: Mice expressing human MUC1 (mucin) were mated with mice expressing elastase-driven SV40 T antigen. The resulting mice spontaneously develop pancreatic tumors that express high levels of the MUC1. Utility: Useful for investigating immune responses during tumor progression. PMID link: 10975866
2007-016 – Mouse expressing the human alpha-synuclein gene for the study of Parkinson’s disease. Genotype/Phenotype: These mice express the human alpha-synuclein gene, under the control of its endogenous human promoter and regulatory elements. Genomic multiplication of this locus in humans results in Parkinson’s disease with subsequent dementia, with post-mortem transitional or diffuse Lewy body... Read More
2006-116 – Mice expressing multiple human HLA class II molecules for the study of immune response to bacterial superantigens. Genotype/Phenotype: Mice express multiple varieties of human HLA class II molecules. Utility: Model systems for studying bacterial superantigens. PMID: 16428778 PMID: 18501769 PMID: 18086265
2003-128 – Human brain tumors that show invasive behavior in the brains of immunocompromised mice. Numerous, well-characterized tissue grafts are available.
2000-020 – Mouse strain allowing inducible gene expression in the heart. Genotype/Phenotype: Utilizes a tetracycline- inducible cardiac-specific promoter (a-MHC) to drive a transactivator activating expression of any target gene. Utility: System for modulating gene expression in cardiac tissue. This technology uses the TET-ON/TET-OFF System®. PMID publication: 11437283
2013-287 – Researchers at Mayo Clinic have generated immortalized osteocytes derived from sclerostin (Sost-/-) knock out and wild-type (Sost+/+) mice. Clonal populations of cells were immortalized with SV40 T-antigen-containing viral constructs and maintained on collagen coated plates. Clone 8 (derived from Sost knock out mice) and clone 12 (derived from Sost wild-type mice) expressed mRNAs for... Read More
2013-107 – The generation of a mouse strain with knockout of B7-H1 gene.
2013-105 – The ε4 allele of the apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD) compared to the more common ε3 allele. Studies in animal models and humans suggest that apoE4 exhibits both loss-of-function and gain-of-toxic-function compared to apoE3. In regulating amyloid pathology, apoE4 is less efficient than apoE3 in mediating the clearance of... Read More
2013-102 – The Hdac3 conditional knockout mouse model made with Osx-Cre is a useful tool to study the molecular and physiological mechanisms by which factors (e.g., OPG and others) produced in the skeleton, particularly by immature osteoblasts and osteoblast progenitor cells, influence energy metabolism and prevent diseases like type 2 diabetes.
Genetically Engineered Mouse Model of Multiple Myeloma Without IoxP Sites (Vk*MYCwoLoxP) and Transplantable Cell Lines
2013-058 – A transgenic mouse model of multiple myeloma. Vk*MYCwoLoxP mice have conditional MYC activation in germinal center B cells. Mice progress to indolent myeloma with features highly characteristic of human disease. These mice can be used to study the biology and drug treatment of multiple myeloma, and can be crossed with conditional mice strains expressing Cre recombinase. Transplantable... Read More
2012-144 – The knock-in mouse model mimics an incompletely penetrant genetic mutation found in patients with atypical autosomal dominant polycystic kidney disease (ADPKD). The model was established to investigate the pathogenic mechanism of this particular mutation (PKD1 R3277C). As in patients, mice carrying the mutation together with a PKD1 truncating change develop severe, early onset disease,... Read More
2012-123 – This mouse model contains TFPIFlox allele with LoxP sites flanking exon 4 of the TFPi gene. When bred to mice that express Cre recombinase, the resulting off spring will have the sequences encoding the Kuntz1 domain of the TFPI protein deleted in cre-expressing tissues. As the TFPI-K1 domain is necessary for TFPI inhibition of the tissue factor coagulation pathway, these mice may be useful... Read More
2012-122 – A transgenic mouse model having vascular smooth muscle cell directed overexpression of a mouse tissue factor pathway inhibitor cDNA sequence encoding the TFPI alpha isoform. These mice may be useful in studying the role of vascular TFPI expression in intravascular thrombosis, the tissue factor pathway in vascular disease, coagulation, innate immunity, angiogenesis and lipid metabolism.
2012-084 – A homozygous transgenic mouse model expressing mutant M377V human TDP-43 cDNA encoding the TAR-bindign protein 43kD - 6 fold endogenous levels (Xu et al, Molecular Neurodegeneration, 2011).
2011-075 – This invention includes the development of Inducible transgenic mice expressing human TDP-cDNA encoding the TAR-binding protein 43kD utilizing the MoPrpTta promoter.
2011-030 – Studies from our laboraties have shown that deleted in breast cancer 1 (DBC1) is an important negative regulator of SIRT1 in vivo. Deletion of DBC1 in mice results in higher SIRT1 activity in various moust tissues, and these mice are protected from metabolic diseases, such as high fat diet-induced liver disease. Therefore, DBC1 knockout mice will be a valuble tool to study SIRT1 function and... Read More
2009-296 – Mouse model of recessive polycystic Kidney Disease (ARPKD)
2009-126 – This invention includes the developement of inducible transgenic mice expressing human TDP-43 cDNA encoding the TAR-binding protein 43kD.
2009-125 – This invention includes the development of a homozygous transgenic mouse model expressing wild-type human TDP-43 cDNA encoding the TAR-binding protein 43kD endogenous levels.
2008-035 – Mice lacking 53BPI were developed at Mayo to study DNA damage responses and tumor suppression. See Ward et al. (2003) Mol Cell Biol 23(7):2556-2563
2007-330 – We created mice that contain human LRRK2 cDNA encoding either the wild-type or G2019S mutant form of the gene (hereafter termed “responder line(s).” The cDNA in these animals has been placed behind a minimal CMV promoter containing TetO and will only produce human LRRK2 protein when combined (in bigenic mice) with tTA. We have demonstrated in COS7 cells that the human LRRK2 expression from... Read More
2007-288 – Mice in which the endogenous leucine-rich repeat kinase 2 gene (LRRK2) has been ablated. Exon 41 has been flanked with loxP sites to alow Cre-mediated deletion. The region deleted contains the serion/threonine protein kinase catalytic domain. Splicing of exon 40 to 42 causes a frameshift mutation with the introduction of an early stop codon (TGA).
2007-230 – We have replace the mouse islet amyloid polypeptide (IAPP, amylin) gene with the human IAPP gene. Human IAPP is readily converted to amyloid fibrils. Amyloids have been associated with a large number of human diseases that are associated with cell death. Mouse IAPP is non-amyloidogenic. By replacing the mouse IAPP with the human IAPP gene we have created a physiologic model of hman IAPP... Read More
2007-027 – Mice that over-express the human wild-type and mutant leucine-rich repeat kinase 2 gene (LRRK2).
2005-316 – These mice do not express the gene for CD229.
2005-016 – These transgenic mice have regulatable tau expression and profound neurofibrillary pathology, neurodegeneration and memory impairment. The key features are (1) Protein expressed is human tau P301L; (2) Expression of transgenic tau is restricted to the forebrain; (3) Mice develop memory impairment by 2.5 months; (4) Mice develop argyrophilic neurofibrillary tangles by 4 months; (5) Mice... Read More
2004-109 – This invention is a mouse line in which we disrupted the gene for FKBP52, a protein component of steroid receptor complexes. The animals are reproductively compromised. These animals can be helpful in screening for environmental compounds and drugs that might bind FKBP52 and alter FKBP52-dependent processes. Of particular interest will be compounds that may promote defects in sexual... Read More
2004-108 – The invention is a mouse line in which we disrupted the gene for FKBP51, a protein component of steroid receptor complexes. These animals can be helpful in screening for compounds and drugs that bind FKBP51 and alter FKBP51-dependent processes.
2004-022 – Mice expressing human CD46 with human-like tissue specificity and efficiency. For additional information, please see the following: Mrkic et al., (1998). Measles virus spread and pathogenesis in genetically modified mice. Journal of Virology, volume 72, number 9, 7420-7427. Mrkic et al. (2000). Lymphatic dissemination and comparative pathology of recombinant measles viruses in genetically... Read More
2003-196 – Transgenic mice were created through DNA microinjection of a construct utilizing mouse EPO derived regulatory sequences in conjunction with the Diptheria Toxin A chain (DT-A) open reading frame and a series of exons/introns derived from the human growth hormone gene to provide the necessary splicing events required for high-level expression. Assessments of circulating leukocytes and other... Read More
2003-150 – A mouse lacking both copies of the IEX-1 gene was generated. These mice have a mean arterial blood pressure that is approximately 30mm of Hg higher than that seen in wild type mice. These mice are useful for assessing compounds for the ability to reduce high blood pressure.
2001-023 – A novel expression system has been developed that selectively expresses ABeta40 or ABeta42 in the secretory pathway. This system enables expression of high levels of specific ABeta peptides. Such a system may be invaluable in developing animal models that critically determine the pathogenicity of individual ABeta peptides. In addition, the system may have general utility as a means of... Read More
2000-066 – We have created two lines of transgenic mice expressing human tau with the P301L mutation. Mice expressing the 2-3-10+ human isoform with the P301L mutation develop tau neurofibrillary tangles, motor deficits, and behavioral abnormalities. Mice expressing the longest human tau isofrom (2+3+10+) with the P301L mutation develop balloned neurons as well as neurofibrillary tangles. Motor and... Read More
2000-065 – Mouse class II-deficient HLA-DQB10302, DQA10301 (DQ8) transgenic mice are susceptible to severe collagen-induced arthritis (CIA), an animal model for rheumatoid arthritis. To examine whether polymorphism at the DRB1 locus can modulate DQ-restricted arthritis, we generated double- transgenic (DR/DQ) mice. DRB1*0301 (DR3) was introduced into CIA susceptible DQ8.Abeta transgenic mice to generate... Read More
2000-064 – We developed an HLA-DR3.Abo mouse by introducing the DR3 transgene into a H2Abo mouse, class II negative strain, by mating with BIO.M-DRB1*0301 mice. Experimental autoimmune thyroiditis (EAT) is induced in these mice when immunized with either MTg or HTg.
1998-026 – Mutations in the tau gene have been discovered that are linked to Tau pathologies. Identification of these mutations can lead to animal models of neurodegenerative diseases to be developed and provides methods for determining a diagnosis of neurodegenerative disease in a patient.
1997-112 – An inbred strain of transgenic mice that show tissue-specific expression of the human MUC1 gene. These animals express a form of the human MUC1 gene which codes for the core protein of a mucin expressed by glandular epithelia and carcinomas which develop from these tissues. The core protein is underglycosylated in these cancers and therefore represents a possible target for immunotherapy.... Read More
1997-072 – We generated mice transgenic for HLA-DQ6, an allele associated with a nonsusceptible haplotype. These mice were found to be resistant to collagen induced arthritis. These mice are a model for rheumatoid arthritis.
1997-071 – We generated an HLA-DR4ß(NT) transgene construct in which positions 110 and 139 were altered to resemble endogenous mouse H2 Aß molecules. This construct was introduced into (B10 x SWR) embryos, and DR4ß(NT) transgenic mice were produced. The transgene was transferred into B10.RFB3 (Eß0 Ealphap) mice. The transgene-encoded DR4ß molecules paired with endogenous Ealpha chains to form stable... Read More
1997-069 – We developed an HLA-DR2 mouse model by introducing a human DRB1*1502(DR2DW12) transgene into CIA susceptible BIO.RQB3 (H2A8) mice. These mice showed a significant reduction in the incidence and severity of arthritis. For further information please see Human Immunology, 1996, 50:54-60.
1996-076 – Transgenic mouse (Tg2576) carrying the Swedish mutation for Alzheimer’s Disease. This mouse was developed by Dr. Karen Hsiao Ashe at the University of Minnesota and is exclusively licensed to Mayo. This mouse develops age-related neuropathology, including development of amyloid plaques and behavioral changes, and can be used in research related to Alzheimer’s Disease and other... Read More