Sitsapesan, Rebecca - University of Oxford - Department of Pharmacology

个人简介

Rebecca Sitsapesan holds a BSc in Pharmacology (Aberdeen), an MSc in Cardiovascular Studies (Leeds) and a PhD in Cardiac Physiology and Pharmacology (Strathclyde). Her post-doctoral research into ion-channel biophysics began at the University of Glasgow and continued at the National Heart & Lung Institute at Imperial College, London. In 1991 she was awarded a British Heart Foundation Basic Science Lectureship to investigate the function of cardiac intracellular Ca2+-release channels and a University Lectureship at Imperial College. Rebecca Sitsapesan moved to Bristol in 2001 and was promoted to Professor of Pharmacology in 2011. In August 2013, she became Professor of Pharmacology at the University of Oxford.

研究领域

The release of Ca2+ from intracellular stores is of fundamental importance in cell biology, initiating and regulating a wide variety of cellular functions including muscle contraction, fertilisation, cell division and neurotransmitter release. The focus of our laboratory is the study of intracellularly located ion-channels, particularly those that are involved in the control and regulation of Ca2+-release from intracellular stores in cardiac muscle. Our research is funded by the British Heart Foundation. Research focuses on the biophysical properties and putative physiological roles of ion-channels present on intracellular Ca2+-stores. Although we are particularly interested in their relevance in the heart, these ion-channels are also crucial to the normal physiology of many other organs, including the lungs, kidney, brain, vascular smooth muscle and skeletal muscle. We are interested in the function of the ryanodine receptor Ca2+-release channel (RyR) and how the regulation of this channel is altered in heart failure. In collaboration with Antony Galione, Oxford, we are also characterising the single-channel behaviour of putative Ca2+-release channels present on acidic lysosomal stores, such as the two-pore channels (TPC1, TPC2 & TPC3). There are other ion-channels that support the process of Ca2+-release but whose exact physiological roles have not been fully identified. These include the two sub-types of trimeric intracellular cation channel (TRIC-A and TRIC-B) that are present in the SR of most cells. Abnormalities in TRIC-A and/or TRIC-B are associated with severe disease including embryonic heart failure, respiratory failure, hypertension and the disease, osteogenesis imperfecta. We are working closely with Hiroshi Takeshima (Kyoto, Japan) to examine the relationships between structure and function of the TRIC channels and to relate our understanding of the gating and conducting properties of the channels to their physiological roles in the heart and other organs. We expect our investigations to expose many novel sites on intracellular Ca2+-stores as targets for therapeutic intervention.

近期论文

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Pitt, SJ, Lam, AKM, Rietdorf, K, Galione, A, and Sitsapesan, R (2014) Reconstituted Human TPC1 Is a Proton-Permeable Ion Channel and Is Activated by NAADP or Ca2+. Venturi, E, Matyjaszkiewicz, A, Pitt, SJ, Tsaneva-Atanasova, K, Nishi, M, Yamazaki, D, Takeshima, H, and Sitsapesan, R (2013) TRIC-B channels display labile gating: evidence from the TRIC-A knockout mouse model. Venturi, E, Sitsapesan, R, Yamazaki, D, and Takeshima, H (2013) TRIC channels supporting efficient Ca(2+) release from intracellular stores. Galfre, E, Pitt, SJ, Venturi, E, Sitsapesan, M, Zaccai, NR, Tsaneva-Atanasova, K, O'Neill, S, and Sitsapesan, R (2012) FKBP12 activates the cardiac ryanodine receptor Ca2+-release channel and is antagonised by FKBP12.6. Venturi, E, Mio, K, Nishi, M, Ogura, T, Moriya, T, Pitt, SJ, Okuda, K, Kakizawa, S, Sitsapesan, R, Sato, C, and Takeshima, H (2011) Mitsugumin 23 forms a massive bowl-shaped assembly and cation-conducting channel. Carter, S, Pitt, SJ, Colyer, J, and Sitsapesan, R (2011) Ca(2)+-dependent phosphorylation of RyR2 can uncouple channel gating from direct cytosolic Ca(2)+ regulation.