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I began my studies of ion channels as an electrophysiologist at Merck in the laboratories of Dr. Charles Cohen and Dr. Owen McManus where I characterized the pharmacological modulation of voltage gated sodium channels. David Yue. My research focused on understanding the spatial selectivity of calmodulin regulation of voltage gated calcium channels.

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Upon graduation, I elected to remain in the Calcium als lab for my post-doctoral research and later as a Research Associate, and continued my research on the mechanisms underlying calmodulin regulation of calcium channels, and how those mechanisms are disrupted in Timothy Syndrome. Limpitikul W. Circulation Research Jan 6; 1 Epub Oct Niu J. Biophysical Journal Sep 20; 6 Sang L, Dick I. Nature Communications 7 Dick I. Nature Communications 7, Adams, P. Dick, I. Scientific Reports 6, The Journal of physiology Yue and his calcium als laboratory.

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Channels 10 1 Ben-Johny M. Current molecular pharmacology 8 2 Limpitikul, W. Joshi-Mukherjee, R. Tay, L. Tadross, M. Liu, C. Brochu, R. Liang, J. Herrington, J. Priest, B. Felix, J. Smith, H. Pacific Disruption of these important regulatory processes in severe clinical phenotypes including autism, ataxia and long QT syndrome. Recent work has focused on unraveling the mechanisms leading to cardiac arrhythmias in calcium channelopathies such as Timothy Syndrome TS.

By examining the inactivation defects underlying two different L-type channel TS mutations, we uncovered a remarkable divergence in the mechanisms leading to deficits in CDI. These findings promise new insight into customized treatment for TS, and illustrate how in depth biophysical understanding can inform on therapeutic interventions in patients.

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Overall, my lab studies the mechanisms underlying the regulation of voltage-gated calcium channels, how these mechanisms are disrupted by genetic mutations, and how new therapeutic strategies can address these disruptions. Hemmeter Scholar for 3 years.

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