Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes

Pflugers Archiv European Journal of Physiology

Volumn 453, Issue 3, 2006, Pages 323-332

  Girard, Christophe A J ^a   Shimomura, Kenju ^a   Proks, Peter ^a   Absalom, Nathan ^a   Castano, Luis ^b   Perez De Nanclares, Guiomar ^b   Ashcroft, Frances M ^a  

^a UNIVERSITY OF OXFORD   (United Kingdom)

^b HOSPITAL DE CRUCES   (Spain)

Author keywords

ATP sensitive potassium channel; Insulin secretion; Kir6.2; Neonatal diabetes; Sulphonylureas; SUR1

Indexed keywords

ADENOSINE TRIPHOSPHATE; ADENOSINE TRIPHOSPHATE MAGNESIUM; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR6.2; ION CHANNEL; POTASSIUM CHANNEL; SULFONYLUREA; SULFONYLUREA RECEPTOR; TOLBUTAMIDE;

ANIMAL CELL; ARTICLE; BINDING SITE; CONTROLLED STUDY; DIABETES MELLITUS; DISEASE ASSOCIATION; GENE; GENE MUTATION; GENETIC ANALYSIS; GENETIC ASSOCIATION; HETEROZYGOSITY; HUMAN; HUMAN CELL; INSULIN RELEASE; KCNJ11 GENE; NEWBORN DISEASE; NONHUMAN; NUCLEOTIDE SEQUENCE; OOCYTE; PANCREAS ISLET BETA CELL; PANCREAS ISLET CELL TUMOR; PRIORITY JOURNAL; SENSITIVITY ANALYSIS; WHOLE CELL; WILD TYPE;

ADENOSINE TRIPHOSPHATE; ANIMALS; ATP-BINDING CASSETTE TRANSPORTERS; DIABETES MELLITUS; FEMALE; GENOTYPE; HUMANS; HYPOGLYCEMIC AGENTS; INFANT; INFANT, NEWBORN; INSULIN-SECRETING CELLS; MULTIDRUG RESISTANCE-ASSOCIATED PROTEINS; MUTATION; PATCH-CLAMP TECHNIQUES; POTASSIUM CHANNELS, INWARDLY RECTIFYING; RATS; TOLBUTAMIDE; TRANSFECTION; XENOPUS LAEVIS;

EID: 33751089560     PISSN: 00316768     EISSN: 14322013     Source Type: Journal    
DOI: 10.1007/s00424-006-0112-3     Document Type: Article

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