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Pamela V. Tran, PhD

Pam Tran portrait
Associate Professor, Anatomy and Cell Biology
ptran@kumc.edu

Professional Background

Dr. Pamela Tran received her B.Sc. (Hon.) in Biology from the University of New Brunswick in Fredericton, Canada. She obtained her Ph.D. in Biology at McGill University in Montreal, Canada, under the mentorship of Dr. Rima Rozen, studying the role of folate metabolism in neural tube defects. She then pursued postdoctoral training with mouse geneticist, Dr. David Beier, at the Brigham and Women’s Hospital/Harvard Medical School, where she positionally cloned mutations of ENU-induced mouse models of birth defects. Dr. Tran joined the Department of Anatomy and Cell Biology at the University of Kansas Medical Center in 2011 as an Assistant Professor. She is currently an Associate Professor with Tenure. Her research investigates the role of primary cilia dysfunction in Polycystic Kidney Disease and obesity.

Education and Training
  • BS, Hon., University of New Brunswick, Fredericton, NB
  • PhD, Biology, McGill University, Montreal, QC
  • Post Doctoral Fellowship, Developmental Biology and Mouse Genetics, Brigham and Women's Hospital/Harvard Medical School, Boston, MA
Professional Affiliations
  • American Society of Nephrology, Biosciences Research Advisory Group, Member, 2015 - 2016
  • American Society of Nephrology, Member, 2010 - Present

Research

Overview

Primary cilia are antenna-like, sensory organelles essential for human health. Genetic mutations that disrupt cilia function affect multiple organ systems, and include clinical manifestations such as renal cystic disease and obesity. Renal cystic diseases comprise the most commonly inherited, fatal diseases (more common than Down’s Syndrome, Cystic Fibrosis, muscular dystrophy and Huntington’s Disease combined), while 1 in 3 individuals in the United States is obese, which is associated with insulin-resistance that can lead to serious chronic diseases.

Our laboratory uses cell and mouse models to investigate the role of cilia dysfunction in renal cystic disease, and in obesity and insulin resistance. Questions that we are trying to answer include: What ciliary-mediated signaling pathways initiate or contribute to renal cystogenesis? How do mechanical forces in the tissue microenvironment affect renal cystogenesis? How does metabolism alter renal cystic disease? What ciliary-mediated pathways regulate appetite? Do ciliated and unciliated cells respond to insulin via different mechanisms?

Using candidate and genome-wide approaches, and genetic and pharmacological means, we aim to identify signaling molecules and interactions connecting cilia dysfunction to these diseases, and thereby, reveal novel therapeutic targets for these common medical burdens.

Publications
  • Tran, Pamela., V., Talbott, George., C., Turbe-Doan, Annick, Jacobs, Damon., T., Schonfeld, Michael., P., Silva, Luciane., M., Chatterjee, Anindita, Prysak, Mary, Allard, Bailey., A., Beier, David., R.. 2014. Downregulating Hedgehog Signaling Reduces Renal Cystogenic Potential of Mouse Models. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 25 (10), 2201-2212
  • Jacobs, Damon., T., Silva, Luciane., M., Allard, Bailey., A., Schonfeld, Michael., P., Chatterjee, Anindita, Talbott, George., C., Beier, David., R., Tran, Pamela., V.. 2016. Dysfunction of intraflagellar transport-A causes hyperphagia-induced obesity and metabolic syndrome. DISEASE MODELS & MECHANISMS, 9 (7), 789-798
  • Avasthi, P, Maser, R., L, Tran, P., V. 2017. Primary Cilia in Cystic Kidney Disease.. Results and problems in cell differentiation, 60, 281-321
  • Silva, Luciane., M., Jacobs, Damon., T., Allard, Bailey., A., Fields, Timothy., A., Sharma, Madhulika, Wallace, Darren., P., Tran, Pamela., V.. 2018. Inhibition of Hedgehog signaling suppresses proliferation and microcyst formation of human Autosomal Dominant Polycystic Kidney Disease cells. SCIENTIFIC REPORTS, 8
  • Silva, Luciane., M., Wang, Wei, Allard, Bailey., A., Pottorf, Tana., S., Jacobs, Damon., T., Tran, Pamela., V., Weimbs, Thomas. 2019. Analysis of primary cilia in renal tissue and cells, 205-229. http://dx.doi.org/10.1016/bs.mcb.2019.04.008
  • Jacobs, D., T, Allard, B., A, Pottorf, T., S, Silva, L., M, Wang, W, Al-Naamani, A, Agborbesong, E, Wang, T, Carr, D., A, Tran, P., V. 2020. Intraflagellar-transport A dysfunction causes hyperphagia-induced systemic insulin resistance in a pre-obese state.. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34 (1), 148-160
  • Pottorf, T., S, Fagan, M., P, Burkey, B., F, Cho, D., J, Vath, J., E, Tran, P., V. 2020. MetAP2 inhibition reduces food intake and body weight in a ciliopathy mouse model of obesity.. JCI insight, 5 (2)
  • Wang, W, Allard, B., A, Pottorf, T., S, Wang, H., H, Vivian, J., L, Tran, P., V. 2020. Genetic interaction of mammalian IFT-A paralogs regulates cilia disassembly, ciliary entry of membrane protein, Hedgehog signaling, and embryogenesis.. FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • Wang, W, Silva, L., M, Allard, B., A, Pottorf, T., S, Wang, H., H, Jacobs, D., T, Cornelius, J., T, Chaturvedi, A, Slawson, Chad, Pritchard, M., T, Sharma, M, Wallace, D., P, Calvet, J., C, Tran, P., V. 2020. Intraflagellar transport-A dysfunction attenuates ADPKD in a renal tubular- and maturation-dependent manner. [preprint]. Kidney International. https://doi.org/10.1101/2020.04.26.061796
  • Wang, W, Pottorf, T., S, Wang, H., H, Dong, R, Kavanaugh, M., A, Cornelius, J., T, Apte, U, Pritchard, M., T, Sharma, M, Tran, P., V. 2020. IFT-A deficiency in juvenile mice impairs biliary development and exacerbates ADPKD liver disease. [preprint]. J. of Pathology . https://biorxiv.org/cgi/content/short/2020.09.10.289645v1