Grant R. MacGregor, D.Phil.

  • Mouse Reproduction, Development and Homeostasis
  • Functions of FNDC3 proteins
  • Improved Mouse Models of Late Onset Alzheimer’s Disease

Since 1993 the MacGregor laboratory has investigated the molecular basis for mammalian reproduction and development, using the mouse as a model genetic system. With our collaborators, these studies have made new contributions to our understanding of mechanisms of germline development, skeletogenesis, programmed cell death, post-translational modification of microtubules, and mitochondrial genetics and biology.

Functions for FNDC3 proteins

A current research goal is to identify the roles of the novel Fndc3 gene family in mammalian reproduction, development and homeostasis, and to understand how FNDC3 proteins function. We do so because mice with altered Fndc3 function display pathology found in several common human health conditions that have significant societal and economic impact. These include bone fragility, infertility, lactational insufficiency, cardiac development, neonatal acute respiratory distress, non-alcoholic fatty liver disease, obesity, and abnormal skeletogenesis. FNDC3B is also frequently amplified and over-expressed in both liver and brain cancer, and knockdown of FNDC3B can inhibit metastasis in vivo. We predict that understanding how FNDC3 proteins function will provide insight into mechanisms that contribute to human birth defects and adult disease.

Improved Mouse Models of Late Onset Alzheimer’s Disease

The lab is part of the UC Irvine component of the NIA / NIH funded Model Organism Development & Evaluation for Late-Onset Alzheimer’s Disease (MODEL-AD) program. The goals of MODEL-AD are to develop and validate improved mouse models that can be used to investigate mechanisms of late-onset Alzheimer’s Disease (LOAD). Using open-science practices, all data and mouse models generated by MODEL-AD are available for use by both academia and for-profit industry without restrictions.

Publications (from Pub Med)

https://www.ncbi.nlm.nih.gov/myncbi/12KCbtzdjYm5t/bibliography/public/

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