Iyanna Boston
MIT Department: Biology
Faculty Mentor: Prof. Richard Young
Research Supervisor: Alessandra Dall’Agnese
Undergraduate Institution: North Carolina Central University
Hometown: Plymouth, North Carolina
Website: LinkedIn
Biography
Iyanna Boston is a rising sophomore at North Carolina Central University, pursuing a degree in Biomedical Science. Passionate about healthcare and driven by personal experiences, she is dedicated to becoming a physician-scientist specializing in Obstetrics and Gynecology, inspired by her mother’s resilience through numerous medical challenges. Completing her first year of college was a transformative journey. Initially focused on academic achievement, she learned that success lies not just in grades, but in understanding and building connections. With a lifelong love for science, she is currently interning at the Whitehead Institute (MIT), where she researches chronic disease cellular mechanisms under Professor Richard Young. Aspiring to empower women by facilitating informed healthcare decisions, her goal is to offer compassionate OB/GYN care. Pursuing a biomedical science degree, she aims to deepen her knowledge through clinical rotations and research, contributing to women’s health and advancements. In her free time, she enjoys cooking, shopping, watching Disney, and spending time with loved ones, which allows her to unwind.
Abstract
Proteolethargy is a pathogenic mechanism in chronic disease
Iyanna Boston1, Richard A. Young2, Alessandra Dall’Agnese3
1Department of Biological and Biomedical Sciences, North Carolina Central University
2Department of Biology, Whitehead Institute
3Department of Biology, Massachusetts Institute of Technology; Whitehead Institute
Chronic diseases, leading causes of global mortality, often stem from dysregulated cellular signaling pathways. Our study focuses on ‘Proteolethargy,’ a term that describes decreased protein mobility. The Young lab has found that pathogenic signaling decreases the movement of essential proteins within cells, compromising their functionality and contributing to the pathogenesis of chronic diseases such as diabetes, dyslipidemia, and inflammation, among others. This decrease in protein is associated with disordered redox environments affecting oxidation-responsive cysteines. Our research aims to explain Proteolethargy’s role in chronic diseases and devise strategies to treat these diseases and diminish associated mortality rates. By leveraging insights into pathogenic signaling, we aim to identify potential therapeutic targets and advance diagnostic approaches. We seek to unveil how pathogenic signaling alters protein dynamics and function through state-of-the-art methodologies in engineered HepG2 cells, such as single particle tracking (SPT), fluorescence recovery after photobleaching (FRAP), and immunofluorescence. This study’s findings promise to deepen our understanding of Proteolethargy and its implications for chronic diseases, offering new avenues for therapeutic development and healthcare improvement. The impact of this research extends to enhancing patient outcomes and alleviating the socioeconomic burden of chronic diseases globally.
