Mindy Wang

Mindy Wang
Mentor: Dr. Yehia Daaka
College of Medicine
 
"Research challenges and offers me intellectual vitality that cannot be found in the classroom. Conducting research allows me to network with and learn from knowledgeable peers and scientists. Moreover, research allows me to contribute my work and results to the scientific world, in hopes of improving our society. Through the University Scholars program, I aim to network with successful undergraduate students conducting research and learn from the diverse research fields offered at the University of Florida to become a well-rounded scientist."
 

Major

Biochemistry, Interdisciplinary Biological and Medical Sciences

Minor

N/A

Research Interests

  • Biochemistry
  • Cancer
  • Urology

Academic Awards

  • Howard Hughes Medical Institute (HHMI) Science for Life Intramural Award
  • Hazen E. Nutter Scholarship
  • Presidential Service Award
  • Wentworth Freshman Scholar

Organizations

  • Arts in Health at UF
  • American Medical Student Association
  • Gator Pre-medical Guide

Volunteer

  • Shands Hospital
  • Arts in Medicine
  • Relay for Life

Hobbies and Interests

  • UF Century Tower Carillon
  • Piano Performance
  • Reading
  • Cooking

Research Description

α-Adrenergic Receptor Agonist-mediated Stress Model in Benign Prostatic Hyperplasia
Benign Prostatic Hyperplasia (BPH) is a common disease in men which involves the enlargement of the prostate as a result of signal transduction initiated by α-Adrenergic Receptors (α-AR). When bound by ligands, α-AR stimulate the mitogenic extracellular signal-regulated kinases 1 and 2 (ERK) signaling pathway, which ultimately sends signals to the cell nucleus that cause growth of both stromal and epithelial prostate cells. However, just how α-AR promote the prostate cell growth remains incomplete. In this study, BPH-1 cells were treated with α-AR agonist phenylephrine for various periods of time to observe the time dependent increase in ERK activation. Results show two time dependent increases in ERK phosphorylation, suggesting that different signal pathways could be responsible for the growth of BPH-1 cells after the activation of ERK. Further experiments were done to confirm the role of b-arrestin proteins in ERK phosphorylation.