Sulfonylurea receptor 1 mutations that cause opposite insulin secretion defects with chemical chaperone exposure

Journal of Biological Chemistry

Volumn 284, Issue 12, 2009, Pages 7951-7959

  Pratt, Emily B ^a   Yan, Fei Fei ^a   Gay, Joel W ^a   Stanley, Charles A ^b   Shyng, Show Ling ^a  

^a OREGON HEALTH AND SCIENCE UNIVERSITY   (United States)

^b CHILDREN S HOSPITAL OF PHILADELPHIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CELL EXCITABILITY; CELL SURFACES; CHANNEL FUNCTIONS; CHEMICAL CHAPERONE; ENDOPLASMIC RETICULUM; EXPRESSION LEVELS; GLUCOSE METABOLISM; HYPERPOLARIZED; HYPOGLYCEMIC DRUG; INSULIN SECRETION; INTRACELLULAR ATP; MEMBRANE POTENTIALS; NORMAL CONDITION; POTASSIUM CHANNELS; SMALL MOLECULES; SULFONYLUREA RECEPTORS; SULFONYLUREAS; SURFACE EXPRESSION; WILD TYPES;

DEFECTS; GLUCOSE; INSULIN; PHYSIOLOGY; POTASSIUM;

CELL MEMBRANES;

ADENOSINE TRIPHOSPHATE; CHAPERONE; INSULIN; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR6.2; NUCLEOTIDE; SULFONYLUREA DERIVATIVE; SULFONYLUREA RECEPTOR 1; ABC TRANSPORTER; DRUG RECEPTOR; GLUCOSE; INWARDLY RECTIFYING POTASSIUM CHANNEL; SULFONYLUREA RECEPTOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL MEMBRANE POTENTIAL; CELL SURFACE; CONTROLLED STUDY; DIABETES MELLITUS; DRUG MECHANISM; ENDOPLASMIC RETICULUM; HYPERINSULINISM; HYPERPOLARIZATION; INSULIN RELEASE; MISSENSE MUTATION; MUTATIONAL ANALYSIS; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; RAT; AMINO ACID SUBSTITUTION; ANIMAL; CELL LINE; DRUG POTENTIATION; GENETICS; HUMAN; METABOLISM; MUTATION; PANCREAS ISLET BETA CELL; PERSISTENT HYPERINSULINEMIC HYPOGLYCEMIA OF INFANCY; SECRETION;

ADENOSINE TRIPHOSPHATE; AMINO ACID SUBSTITUTION; ANIMALS; ATP-BINDING CASSETTE TRANSPORTERS; CELL LINE; DIABETES MELLITUS; GLUCOSE; HUMANS; INSULIN; INSULIN-SECRETING CELLS; MOLECULAR CHAPERONES; MUTATION; MUTATION, MISSENSE; PERSISTENT HYPERINSULINEMIA HYPOGLYCEMIA OF INFANCY; POTASSIUM CHANNELS, INWARDLY RECTIFYING; RATS; RECEPTORS, DRUG; SULFONYLUREA COMPOUNDS;

EID: 65549138897     PISSN: 00219258     EISSN: 1083351X     Source Type: Journal    
DOI: 10.1074/jbc.M807012200     Document Type: Article

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