Mutants Having a Deficit of Functional Steroid Hormone Receptors

This invention concerns "knockout" animals, including mice, which have a deficit of functional steroid hormone receptors, DNA constructs containing the mutations, and methods for producing the animals. The mutation is introduced into the animal or its ancestors at an embryonic stage. These knockout animals provide a model system for studying the biological role of hormones, including steroid hormones and sex steroids, in growth, development, morphological differentiation, and sexual and reproductive behavior and cycles, etc.

A Tet-Regulated Mouse Model for Cataract

Cataract is the most common cause of blindness worldwide, with an estimated 25 million blind and 119 million visually impaired individuals worldwide. Over 20 million adults in the US alone are currently diagnosed with cataracts making this disease a major health concern. The incidence of cataract increases with age and a number of etiologic factors have been proposed in the pathogenesis of age-related cataract in humans including genetic factors, environmental factors and metabolic and biochemical changes in the crystalline lens.

Transgenic Mouse Models for Studying HLA-B57:01 and HLA-B15:02 Linked Immune Responses and Hypersensitivity Reactions

Transgenic mouse models expressing human HLA-B57:01 and HLA-B15:02 molecules have emerged as invaluable tools for unraveling the intricacies of immune responses and hypersensitivity reactions. The major histocompatibility complex (MHC) encoded proteins play a pivotal role in the immune system by presenting peptide fragments to T lymphocytes, and HLA-B57:01 has been associated with severe hypersensitivity reactions triggered by abacavir, a widely used anti-retroviral drug.

DLX3 Knockout Mice for the Study Mouse Models of Tooth, Hair, and Epidermal Defects

This technology includes K14creDLX3 conditional knockout (cKO) mice which will be used to study ectodermal dysplasia disorders such as Amelogenesis Imperfecta, and to study molecular mechanisms of DLX3 regulation in skin and ectodermal appendages. DLX3 is expressed in the epidermis, hair matrix cells in the hair follicle and in the mesenchymal and epithelial compartment of the tooth during embryonic development. To determine the transcriptional network dependent on DLX3-function, we will generate and analyze an epithelial-specific conditional knockout of DLX3.

Oxytocin Conditional Knockout Mouse Model for Studying Behavioral Effects

This invention relates to a novel mouse model that permits temporal and spatial inactivation of the oxytocin receptor. Oxytocin is a neurohormone that has been associated with human diseases such as autism and schizophrenia. The use of animal models to study oxytocin disease progression has been invaluable. However, existing mouse models have been limited to knockouts which leads to early mortality. Researchers at the National Institute of Mental Health (NIMH) generated the conditional oxytocin receptor knockout mice using the Cre-loxP and FLP-FRT systems.

A Mouse with a Targeted Mutation in the Uncoupling Protein-3 (upc3) Gene

The NIH announces the development of a transgenic mouse with a targeted mutation in the ucp3 gene. The ucp3 gene is implicated I the function of regulating energy metabolism. This regulatory function is thought to be accomplished by changing metabolic efficiency (causing energy expended as heat rather than used for ADP/ATP conversion) and/or by participating in fat metabolism. The mutation should inactivate the ucp3 function and the mouse provided a testing vehicle for the above hypotheses.

Generation of Smad3-null Mice and Smad4-conditional Mice

SMADs are a novel set of mammalian proteins that act downstream of TGF-beta family ligands. These proteins can be categorized into three distinct functional sets, receptor-activated SMADs (SMADs 1,2,3,5, and 8), the common mediator SMAD (SMAD 4), and inhibitory SMADs (SMADs 6 and 7). SMAD proteins are thought to play a role in vertebrate development and tumorigenesis.

A Nurr1-Knockout Mouse Model for Parkinson's Disease and Stem Cell Differentiation

The researchers have generated Nurr1-knockout mice via genomic locus inactivation using homologous recombination.

Transcription factor Nurr1 is an obligatory factor for neurotransmitter dopamine biosynthesis in ventral midbrain. From a neurological and clinical perspective, it suggests an entirely new mechanism for dopamine depletion in a region where dopamine is known to be involved in Parkinson's disease. Activation of Nurr1 may be therapeutically useful for Parkinson's disease patients; therefore, the mice would be useful in Parkinson's disease research.

Method to Detect and Quantify In Vivo Mitophagy

This technology includes a transgenic reporter mouse that expresses a fluorescent protein called mt-Keima, to be used to detect and quantify in vivo mitophagy. This fluorescent protein was originally described by a group in Japan and shown to be able to measure both the general process of autophagy and mitophagy. We extended these results by creating a living animal so that we could get a measurement for in vivo mitophagy. Our results demonstrate that our mt-Keima mouse allows for a straightforward and practical way to quantify mitophagy in vivo.

Transgene Free Non-human Primate Induced Pluripotent Stem Cells (iPSCs) for Use in Pre-clinical Regenerative Medicine Research

This technology includes rhesus macaque induced pluripotent stem cells (iPSCs) lines from multiple animals and various types of cells to establish this pre-clinical model. iPSCs are a type of pluripotent stem cell that can be generated from adult somatic cells. The iPSC technology holds great potential for regenerative medicine. Before clinical application, it is critical to evaluate safety and efficacy in a clinically-relevant animal model. We propose that non-human primate models are particularly relevant to test iPSC-based cell therapies.

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