I joined the Nichols lab in 2016 after completing my PhD in Prof Stephen Tucker’s lab at the University of Oxford, where I focussed on the structure, function and pharmacology of TREK K2P potassium channels. Since then I have boldly diversified by turning my attention to the structure, function and pharmacology of other potassium channels… I am interested in the role of KATP channel dysfunction in the cardiovascular system, with particular emphasis on the rare, complex disorder, Cantu Syndrome. Here I use electrophysiological and biophysical techniques to investigate the effects of KATP channel mutations on channel regulation, pharmacology and physiology in recombinant expression systems and novel mouse models of CS.

I graduated from Bradley University in 2013 with a B.S. in Biology. As an undergraduate, I worked in a stem cell research lab where I focused on optimizing the differentiation of human-induced pluripotent stem cells into cardiomyocytes. I began my PhD in Developmental, Regenerative, and Stem Cell Biology at Washington University in St. Louis in the fall of 2013. I am co-mentored by Dr. Colin Nichols and Dr. Stacey Rentschler, and my thesis work focuses on understanding the role of the highly conserved signaling pathway, Notch, in arrhythmogenesis through its aberrant activation in diseased/injury states and subsequent electrical remodeling of cardiomyocytes. To study this, I utilize inducible transgenic mouse lines in which I conditionally activate Notch signaling within adult cardiomyocytes. In particular, I examine how Notch effects transcription and protein regulation through molecular assays and immunohistochemistry, as well as electrophysiologic function through sharp microlectrode recordings of intact hearts.

I joined the Nichols lab in the summer of 2016 after my first year of med school at WashU. My main focus in the lab has been electrophysiologic characterization of the functional effects of KATP channels containing Cantú Syndrome-associated mutations. I am spending my years as a PhD student investigating the unique physiological manifestations of Cantú Syndrome.

I joined Nichols lab in 2018 as a Master's student in BME, with no background in electrophysiology or ion channels. By retooling an old patch-clamp rig, I was able to understand the mechanism of recording channel activity. Using this rig, I characterized KATP channels in the zebrafish cardiovascular system. Captivated by ion channel research, I committed myself to pursue a Ph.D. in Nichols lab, starting in Fall 2019. Currently, I'm working with droplet interface bilayers to understand how membrane asymmetry affects Kir channel activity.

I completed my PhD at the University of Wisconsin – Madison, where I studied the role of oxytocin receptor in the retina and its regulation if Kir7.1. After joining the Nichols lab in 2018 I have focused on the impact KATP channels in intestinal smooth muscle and GI function, specifically looking at the disruption of GI transit in mouse models of Cantu syndrome.

I joined the Nichols lab in the summer of 2018 after spending my sophomore year in the Norimatsu lab at A.T. Still University, where I gained my first experience with molecular biology techniques. In the Nichols lab I’ve put those skills to use, carrying out molecular biology tasks in support of the work being done on KATP-related disorders, and I’ve learned some electrophysiology along the way. Additionally I’ve worked closely with Conor McClenaghan, studying the pharmacologic reversal of cardiac abnormalities in a mouse model of Cantú syndrome. More recently we’ve begun drug-screening in mouse and zebrafish models of AIMS syndrome in hopes of reversing myopathy and fatiguability phenotypes.