Depletion of SK1 channel subunits leads to constitutive insulin secretion

FEBS Letters

Volumn 583, Issue 2, 2009, Pages 369-376

  Andres, Marilou A ^a   Baptista, Nicholas C ^a   Efird, Jimmy T ^a,b,d   Ogata, Kathleen K ^b,c   Bellinger, Frederick P ^b   Zeyda, Thomas ^b  

^a UNIVERSITY OF HAWAII   (United States)

^b UNIVERSITY OF HAWAII   (United States)

^c Kapiolani Community College   (United States)

^d CINCINNATI CHILDREN'S HOSPITAL MEDICAL CENTER   (United States)

Author keywords

Afterhyperpolarization; Beta cell; Diabetic; Heteromeric channel; Insulin secretion; SK potassium channel

Indexed keywords

GLUCOSE; INSULIN; POTASSIUM CHANNEL SK1; POTASSIUM CHANNEL SK2; POTASSIUM CHANNEL SK3; POTASSIUM CHANNEL SK4; SMALL CONDUCTANCE CALCIUM ACTIVATED POTASSIUM CHANNEL; UNCLASSIFIED DRUG;

ACTION POTENTIAL; ANIMAL CELL; ARTICLE; CONTROLLED STUDY; GENE EXPRESSION; INSULIN RELEASE; MEMBRANE STEADY POTENTIAL; NONHUMAN; PANCREAS ISLET BETA CELL; POTASSIUM CONDUCTANCE; PRIORITY JOURNAL; RAT;

ACTION POTENTIALS; ANIMALS; APAMIN; CELL LINE, TUMOR; HYPERINSULINISM; INSULIN; INSULIN-SECRETING CELLS; MEMBRANE POTENTIALS; PROTEIN SUBUNITS; RATS; SMALL-CONDUCTANCE CALCIUM-ACTIVATED POTASSIUM CHANNELS; TRANSCRIPTION, GENETIC;

RATTUS;

EID: 58149503733     PISSN: 00145793     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.febslet.2008.12.024     Document Type: Article

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