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Title:ATP regulates sodium channel kinetics in pancreatic islet beta cells
Authors:ID Zou, Na (Author)
ID Rupnik, Marjan (Author)
Files:URL http://link.springer.com/content/pdf/10.1007%2Fs00232-012-9506-7.pdf
Work type:Not categorized
Typology:1.01 - Original Scientific Article
Organization:MF - Faculty of Medicine
Abstract:Pancreatic beta cells act as glucose sensors, in which intracellular ATP ([ATP](i)) are altered with glucose concentration change. The characterization of voltage-gated sodium channels under different [ATP](i) remains unclear. Here, we demonstrated that increasing [ATP](i) within a certain range of concentrations (2-8 mM) significantly enhanced the voltage-gated sodium channel currents, compared with 2 mM cytosolic ATP. This enhancement was attenuated by even high intracellular ATP (12 mM). Furthermore, elevated ATP modulated the sodium channel kinetics in a dose-dependent manner. Increased [ATP](i) shifted both the current-voltage curve and the voltage-dependent inactivation curve of sodium channel to the right. Finally, the sodium channel recovery from inactivation was significantly faster when the intracellular ATP level was increased, especially in 8 mM [ATP](i), which is an attainable concentration by the high glucose stimulation. In summary, our data suggested that elevated cytosolic ATP enhanced the activity of Na(+) channels, which may play essential roles in modulating cell excitability and insulin release when blood glucose concentration increases.
Keywords:Langerhansovi otočki, trebušna slinavka
Year of publishing:2013
Number of pages:str. 101-107
Numbering:Vol. 246, iss. 2
PID:20.500.12556/DKUM-50505 New window
ISSN on article:0022-2631
COBISS.SI-ID:512288568 New window
Publication date in DKUM:10.07.2015
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Record is a part of a journal

Title:The journal of membrane biology
Shortened title:J. membr. biol.
COBISS.SI-ID:25763840 New window


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