Sruthi Selvakumar


Sruthi Selvakumar
Mentor: Dr. Michael Bubb
College of Medicine
 
"I got involved with research for a variety of reasons. I have always been a curious and inquisitive person by nature, and once I came to college, I was awestruck by the numerous research opportunities that undergraduate students have. I knew then that I wanted to work in a lab and experience learning beyond the standard classroom setting. Research has been a way for me to broaden my horizons and develop a deeper and extensive understanding of concepts, and it has been just as rewarding to my college experience as I had expected."

Major

Biomedical Engineering

Minor

N/A

Research Interests

  • Cancer Biology
  • Biochemistry
  • Peptide Inhibiton

Academic Awards

  • Asian American Heritage Council Student Achiever
  • Florida Academic Scholars Bright Futures Award
  • Dean's List 2015, 2016
  • University Scholars Program 2016

Organizations

  • Interfaith Ambassadors
  • MentorUF Team
  • Hindu Society of Central Florida

Volunteer

  • Shands Niche Program volunteer
  • Hindu Society of Central Florida Youth volunteer
  • UF Chemistry Club Science Outreach Volunteer

Hobbies and Interests

  • Singing
  • Reading
  • Badminton
  • Watching movies

Research Description

Peptide Inhibition of Myristoylated Alanine-Rich C-kinase Substrate (MARCKS) to Demonstrate Akt Activation and Define the Role of MARCKS in Akt Inhibition
Akt, or protein kinase B, is a serine/threonine-specific protein kinase associated with tumor cell survival and proliferation. The activation of Akt often accompanies cancinogenesis. The development of a better understanding regarding the Akt pathway and its inhibition will likely lead to novel therapies for cancer. In the laboratory, research will be focused on MARCKS protein and protein kinase B (Akt). We will be cloning, purifying, and evaluating a peptide that corresponds to a proposed auto-inhibitory domain of MARCKS. Through laboratory experiments, we will test the hypothesis that this peptide segment functions as an inhibitor of MARCKS. We hypothesize that a peptide corresponding to the auto-inhibitory domain will release MARCKS from PIP2 and allow the localization of Akt on cell membrane; this would signify that the peptide segment is, in fact, an inhibitor of MARCKS and that the addition of this peptide will result in Akt activation. The testing of this hypothesis will provide further insight regarding the clinical relevance of the MARCKS protein, and the relationship between the protein and the functioning of the PI3K-Akt pathway can be observed.