Clavia Ruth Wooton-Kee

Wooton-Kee

Clavia Ruth Wooton-Kee, Ph.D.

Assistant Professor

(713) 798-0372

Positions

Assistant Professor
Pediatrics
Nutrition
Baylor College of Medicine
Houston, TX, US
Faculty Senator
Baylor College of Medicine
Houston, Texas
Assistant Professor
Molecular and Cellular Biology - Secondary Appointment
Baylor College of Medicine
Assistant Professor
Pediatrics - Secondary Appointment
Gastroenterology, Hepatology, and Nutrition
Baylor College of Medicine

Addresses

Children's Nutrition Research Center (CNRC) (Lab)
1100 Bates
Office: 9070
Houston, TX, 77030
United States
Phone: (713) 798-0372
wootenke@bcm.edu

Education

BSc from Union College
05/1996 - Barbourville, Kentucky, United States
Biology and Chemistry
MS from University of Louisville, School of Medicine
12/1999 - Louisville, Kentucky, United States
Biochemistry
PhD from University of Kentucky, College of Medicine
12/2008 - Lexington, Kentucky, United States
Toxicology

Professional Statement

The overall goal of my research program is to understand the role of nuclear receptors in hepatic metabolism and chronic liver disease. Our previous and current studies have utilized a mouse model for Wilson’s disease (Atp7b-/- mouse). Wilson’s disease results from mutations in the Atp7b transporter, which leads to excessive hepatic copper levels and progressive liver disease. Wilson’s disease patients and Atp7b-/- mice have profound mitochondria and nuclear ultrastructural changes that are likely due to copper induction of redox stress in the hepatocyte. Atp7b-/- mice also develop spontaneous hepatic nodules between 10-16 months of age. Our lab identified that excessive copper concentrations decreased metabolic nuclear receptor activity (FXR - farnesoid X receptor, HNF4a – hepatocyte nuclear factor, and LRH-1 – liver receptor homolog-1) in vivo and in Atp7b-/- mice (Wooton-Kee, et. al, JCI, 2015). We also found that Atp7b-/- mice exhibited reduced adiposity and hepatic steatosis and were more insulin sensitive compared with wild-type mice (Wooton-Kee, et. al, PNAS, 2020).
Our current projects aim to understand the mechanisms driving metabolic and hepatocellular changes in Atp7b-/- mice and whether ligand activation of nuclear receptors may lessen the hepatocellular dysfunction in Wilson’s disease. Future studies will address whether transcriptomic and proteomic signatures in Wilson’s disease overlap other chronic liver diseases.

Professional Development

Career Advancement Series
Workshop (Participant, 2017)
Sponsor: Baylor College of Medicine

Selected Publications

Memberships

American Association for the Study of Liver Diseases
Texas Medical Digestive Disease Center
Dan L Duncan Comprehensive Cancer Center

Funding

• Nuclear Receptor Dysfunction Reprograms Metabolism and Cellular Proliferation in Wilson's Disease
#R01DK129579-01A1
(07/18/2022 - 05/31/2027)
Grant funding from NIH/NIDDK
Unraveling the Complexities of Lactation: Exploring Gene-Variant Networks, Hypothalamic Regulation, and Metabolic Adaptations of the Liver-Gut Axis
#3092-51000-062-03S
(10/01/2024 - 09/30/2027)
Grant funding from USDA/CRIS
• Metabolic adaptations that occur during lactation
#3092-51000-062-03S
(12/01/2021 - 12/31/2022)
Grant funding from USDA/CRIS
Copper Disruption of Nuclear Receptors and Zinc Therapy
#P30 DK056338
(02/28/2014 - 02/28/2015)
Grant funding from Texas Medical Center Digestive Diseases Center, NIH/NIDDK
Nuclear Receptors as Novel Therapeutic Targets for Wilson's Disease
#1K01DK111716-01
(02/17/2017 - 01/31/2022)
Grant funding from NIH/NIDDK
NIH K01 Career Development Award
Excessive Copper Levels Disrupt Hepatic Nuclear Receptor Function
#F32 DK089689-01A1
(10/01/2010 - 10/31/2012)
Grant funding from NIH/NIDDK
Ruth L. Kirschstein National Research Service Award for Individual Postdoctoral Fellow - F32 Award

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