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Bob Cousins - University of Florida. Gainesville, FL, US

Bob Cousins

Eminent Scholar/Director | University of Florida

Gainesville, FL, UNITED STATES

Bob Cousins’ research focuses on understanding the nutritional significance of zinc and how it acts as a signaling molecule.


Bob Cousins’ research focuses on understanding the nutritional significance of zinc and how this micro-nutrient acts as a signaling molecule where specific zinc transporters target zinc to cellular sites to influence function. His laboratory makes extensive use of mutant mouse models and cell level experimentation and capitalizes on techniques of molecular biology and state-of-the-art analytical methods. Bob has trained over 75 doctoral students and postdoctoral associates. He has served as president of both the American Society for Nutrition and the Federation of American Societies for Experimental Biology. Bob is an elected member of the National Academy of Sciences and has received numerous research awards.

Areas of Expertise (4)

Food Science & Human Nutrition




Articles (5)

Mechanism of Manganese Dysregulation of Dopamine Neuronal Activity

Journal of Neuroscience

Min Lin, et al.


Manganese exposure produces Parkinson's-like neurologic symptoms, suggesting a selective dysregulation of dopamine transmission. It is unknown, however, how manganese accumulates in dopaminergic brain regions or how it regulates the activity of dopamine neurons. Our in vivo studies in male C57BLJ mice suggest that manganese accumulates in dopamine neurons of the VTA and substantia nigra via nifedipine-sensitive Ca2+ channels.

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Intestinal lncRNA H19 and miRNA-675 expression Influenced by Metal Transporter ZIP14

The FASEB Journal

Felix R. Jimenez, et al.


Zinc has been shown to influence intestinal barrier function. To function properly, zinc must be placed at specific sites of action in cells. Previously, we demonstrated that the zinc transporter Zip14 (Slc39a14) is highly expressed in the small intestine and is localized to the basolateral membrane of enterocytes. Ablation of Zip14 in mice produces a phenotype that includes increased intestinal permeability and metabolic endotoxemia.

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Intestine-specific deletion of metal transporter Zip14 (Slc39a14) causes brain manganese overload and locomotor defects of manganism

American Journal of Physiology-Gastrointestinal and Liver Physiology

Tolunay B Aydemir, et al.


Impaired manganese (Mn) homeostasis can result in excess Mn accumulation in specific brain regions and neuropathology. Maintaining Mn homeostasis and detoxification is dependent on effective Mn elimination. Specific metal transporters control Mn homeostasis. Human carriers of mutations in the metal transporter ZIP14 and whole body Zip14-knockout (WB-KO) mice display similar phenotypes, including spontaneous systemic and brain Mn overload and motor dysfunction.

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Deletion of metal transporter Zip14 (Slc39a14) produces skeletal muscle wasting, endotoxemia, Mef2c activation and induction of miR-675 and Hspb7

Scientific Reports

Jinhee Kim, et al.


Skeletal muscle represents the largest pool of body zinc, however, little is known about muscle zinc homeostasis or muscle-specific zinc functions. Zip14 (Slc39a14) was the most highly expressed zinc transporter in skeletal muscle of mice in response to LPS-induced inflammation. We compared metabolic parameters of skeletal muscle from global Zip14 knockout (KO) and wild-type mice (WT).

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Conditional mouse models support the role of SLC39A14 (ZIP14) in Hyperostosis Cranialis Interna and in bone homeostasis

PLoS Genetics

Gretl Hendrickx, et al.


Hyperostosis Cranialis Interna (HCI) is a rare bone disorder characterized by progressive intracranial bone overgrowth at the skull. Here we identified by whole-exome sequencing a dominant mutation (L441R) in SLC39A14 (ZIP14). We show that L441R ZIP14 is no longer trafficked towards the plasma membrane and excessively accumulates intracellular zinc, resulting in hyper-activation of cAMP-CREB and NFAT signaling.

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