Zobrazeno 1 - 10
of 18
pro vyhledávání: '"Iain D. Dukes"'
Autor:
Mark Yeager, Rashmi S. Nunn, Brian D. Adair, Iain D. Dukes, Louis H. Philipson, Shannon Lewis
Publikováno v:
Biophysical Journal. 94:2106-2114
Kv2.1 channels are widely expressed in neuronal and endocrine cells and generate slowly activating K+ currents, which contribute to repolarization in these cells. Kv2.1 is expressed at high levels in the mammalian brain and is a major component of th
Autor:
Harvey W. Mohrenweiser, Carolyn M. Hustad, Grischa Chandy, K. George Chandy, George A. Gutman, B. F. Brandriff, K. Kalman, Michael D. Cahalan, Iain D. Dukes, Julie Tseng-Crank, Nancy A. Jenkins, Neal G. Copeland, Angela Nguyen
Publikováno v:
Journal of Biological Chemistry. 273:5851-5857
We report the isolation of a novel mouse voltage-gated Shaker-related K+ channel gene, Kv1.7 (Kcna7/KCNA7). Unlike other known Kv1 family genes that have intronless coding regions, the protein-coding region of Kv1.7 is interrupted by a 1.9-kilobase p
Publikováno v:
Current Opinion in Endocrinology and Diabetes. 4:262-271
The critical event in physiologic glucose-stimulated insulin secretion is the rise, often oscillatory, in intracellular Ca2+ concentration. This has been assumed to be derived exclusively from variations in Ca2+ influx through voltage-dependent Ca2+
Autor:
Robert J. Mertz, Nathaniel T. Blair, W. Ronald Shehee, Sam M. Witherspoon, Michael W. Roe, Jennings F. Worley, Andrey V. Kuznetsov, M S McIntyre, Anshu A. Mittal, Mary E. Lancaster, Sarmila DasGupta, Iain D. Dukes, Louis H. Philipson
Publikováno v:
Journal of Biological Chemistry. 271:32241-32246
Voltage-dependent delayed rectifier K+ channels regulate aspects of both stimulus-secretion and excitation-contraction coupling, but assigning specific roles to these channels has proved problematic. Using transgenically derived insulinoma cells (βT
Publikováno v:
Journal of Biological Chemistry. 271:4838-4845
The energy requirements of most cells supplied with glucose are fulfilled by glycolytic and oxidative metabolism, yielding ATP. In pancreatic β-cells, a rise in cytosolic ATP is also a critical signaling event, coupling closure of ATP-sensitive K+ c
Publikováno v:
Journal of Biological Chemistry. 269:32055-32058
Glucose stimulation of beta-cell insulin secretion is initiated by membrane depolarization coupled with an elevation in intracellular Ca2+ concentration ([Ca2+]i). Both depolarization-dependent Ca2+ entry and intracellular Ca2+ store release contribu
Autor:
Robert J. Mertz, Mary E. Lancaster, C.J. Frangakis, B. Spencer, A. Kuznetsov, Louis H. Philipson, J.F. Worley rd, M.W. Roe, Iain D. Dukes
Publikováno v:
Journal of Biological Chemistry. 269:18279-18282
Non-insulin-dependent diabetes mellitus (NIDDM) is a metabolic disease associated with abnormal insulin secretion, the underlying mechanisms of which are unknown. Glucose-dependent signal transduction pathways were investigated in pancreatic islets d
Publikováno v:
American Journal of Physiology-Endocrinology and Metabolism. 266:E852-E862
Stimulation of pancreatic islets of Langerhans with glucose results in changes in intracellular Ca2+ concentration ([Ca2+]i). With the use of mouse islets loaded with fura 2, the earliest glucose-induced alteration of [Ca2+]i was a pronounced decline
Publikováno v:
Journal of Biological Chemistry. 269:14359-14362
Glucose stimulation of islet beta-cell insulin secretion is initiated by membrane depolarization and an elevation in intracellular free calcium concentration ([Ca2+]i) from a combination of influx through depolarization-activated Ca2+ channels and in
Autor:
Robert J. Mertz, M.W. Roe, Iain D. Dukes, Louis H. Philipson, M S McIntyre, J.F. Worley rd, B. Spencer
Publikováno v:
Journal of Biological Chemistry. 269:10979-10982
An increase in cytosolic ATP following glucose metabolism by pancreatic beta-cells is the key signal initiating insulin secretion by causing blockade of ATP-dependent K+ channels (KATP). This induces membrane depolarization, leading to an elevation i