BSc (Hons), MSc, PhD
I work on genetic mutations in troponin and tropomyosin that cause hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). In particular, I work on the development of myofilament specific genetically encoded calcium sensors to study subcellular calcium dynamics in cardiomyocytes. My current research also focuses on the development of novel compounds, which alter calcium sensitivity in cardiomyocytes that can be used to treat the cellular dysfunction in HCM.
I completed my PhD at the University of Nottingham in developmental biology where I studied the role of LIM kinase and metanephric mesenchymal cell migration in the developing kidney.
Hypertrophic cardiomyopathy mutations increase myofilament Ca2+ buffering, alter intracellular Ca2+ handling and stimulate Ca2+ dependent signalling.
Robinson P. et al, (2018), J Biol Chem
LIM kinase function and renal growth: Potential role for LIM kinases in fetal programming of kidney development.
Sparrow AJ. et al, (2017), Life Sci, 186, 17 - 24
Acetylsalicylic acid interferes with embryonic kidney growth and development by a prostaglandin-independent mechanism.
Welham SJM. et al, (2017), World J Nephrol, 6, 21 - 28
Excess maternal salt intake produces sex-specific hypertension in offspring: putative roles for kidney and gastrointestinal sodium handling.
Gray C. et al, (2013), PLoS One, 8