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Animal Models

Animal Models 

Browse through our UMassMed Animal Models inventions by scrolling though the listings below.

Core facilities: 

1. Drosophila Resource Facility
2. Animal Medicine  
3. Animal Pathology Services 
4. Mutagenesis Core 
5. Transgenic Animal Modeling
6. Mouse Phenotyping 
7. Mouse Metabolic Phenotyping Center

Browse Our Animal Models Innovations:




Title: Genetically Modified Non-Human Animals and Methods Relating to Complement Dependent Cytotoxicity. UMMS16-63; Patent Pending. 

  • The present invention provides a genetically modified immunodeficient mouse, wherein the genome of the mouse comprises a repaired C5 complement component structural gene such that the 5 genetically modified immunodeficient mouse expresses the C5 complement component structural gene and is characterized by an intact complement system. The present invention relates to immunodeficient non-obese diabetic (NOD), A/J, A/He, AKR, DBA/2, NZB/B1N, BlO.D2/oSn and other mouse strains genetically modified to restore complement-dependent cytotoxicity which is lacking in the unmodified immunodeficient mice.

Title: In vitro and in vivo Transduction of Intact Pre-implantation Mammalian Embryos. UMMS16-29; Patent Pending.

  • This invention simplifies genetic engineering in mammalian (does it matter which ones?) research and commercial settings by introducing nucleic acids into mammalian embryos without the need for conventional mechanical methods, microinjection or electroporation, which can be lethal. The new transgenic platform works simply by exposing AAV viral particles to an “intact” pre-implantation embryo. Using this method minimizes the need for labor-intensive embryo harvesting and transferring into pseudopregnant females.

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Title: SerpinA1 Null Mouse as a Model for Alpha-one Antitrypsin Deficiency and Lung Conditions. UMMS15-62; Patent Pending. 

  • The invention provides a novel mouse model with alpha-one antitrypsin deficiency for use as a tool to study lung conditions including emphysema. With the use of the recently developed CRISPR technology, the inventors designed and implemented a strategy to delete all five copies of the SerpinA1 gene at once overcoming previous technical limitations preventing development of SerpinA1 null mice.

Title: Creation of RIPK3 Reporter and Conditional Deletion Mouse Model. UMMS15-05; Patent Pending. 

  • This invention allows investigators to track endogenous RIPK3 expression in live cells and enables tissue-specific inactivation of RIPK3.  Specifically, the last coding exon of the mouse RIPK3 gene is fused in-frame to the enhanced green fluorescent protein (GFP). LoxP sites flank the last coding exon of RIPK3. Crossing the RIPK3-GFP “floxed” mice to transgenic mice expressing Cre recombinase under the control of tissue-specific promoter enables conditional deletion and inactivation of RIPK3 in distinct tissues.

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Title: Conditional ASC-citrine Expressing Inflammasome Reporter Mouse. UMMS14-64. Related Publication.

  • To facilitate the study of inflammasome activation in vivo, this transgenic mouse expresses fluorescent ASC in the Rosa26 locus. This system contains a knock-in of ASC-citrine gene and a proximal floxed stop site enabling conditional expression in a lineage specific manner by breeding mice with different cre expressing lines.

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Title: Development of NOD.Cg-Prkdc<scid> Il2rg<tm1Wjl> Tlr4lps-del Sz/Sz ("NSG Tlr4 Mice"). UMMS13-61. 

  • This invention provides a immunodeficient mouse model based on the NOD strain (referred to as NSG and NRG mice) that can be engrafted with functional human immune systems, including adaptive and innate immune systems. These mice completely lack adaptive immune cells such as T and B cells, as well as NK cells.  To study the response of human innate immune cells to the TLR agonist LPS in the absence of a murine innate immune response, these NSG mice completely lack TLR4 on their innate immune cells.


  • This invention provides a patented chimeric mouse model for Facioscapulohumeral muscular dystrophy (FSHD) that can be used to further characterize the disease or identify potential therapeutic agents. In a related pending patent application, the invention further discloses inhibitory nucleic acids targeting one or more of SLC34A2, TRIM49, TRIM43, CD177, NAAA, HSPA6, TC2N, or CD34 to treat FSHD.

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Title: Transgenic Non-Human Animal and Methods for Stem Cell Engraftment. UMMS10-43; Patent Pending. 

  • A transgenic immunodeficient non-obese diabetic (NOD) mouse homozygous for the SCID mutation and having an IL2 receptor gamma chain deficiency. Administration of human stem cells to the mouse in the absence of conditioning by irradiation results in similar or greater levels of engraftment of human stem cells compared to a non-obese diabetic (NOD) mouse homozygous. 

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  • The technology utilizes methods of implementing viral vectors harboring a transgene(s) in combination with tissue specific anti-miRNA sequences to minimize off-target effects. In addition, this method allows for production of somatic transgenic animal models by targeted destruction of specific cell types.