Characterisation of new KATP-channel mutations associated with congenital hyperinsulinism in the Finnish population (Q44355881)

2 December 2017

Characterisation of new KATP-channel mutations associated with congenital hyperinsulinism in the Finnish population (English)

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2 December 2017

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F Reimann

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Markku Laakso

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object named as

M Laakso

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H Huopio

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M Dabrowski

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P Proks

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F M Gribble

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T Otonkoski

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F M Ashcroft

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9 January 2003

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46

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2

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241-249

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https://scigraph.springernature.com/pub.10.1007/s00125-002-1014-3

2 December 2017

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Functional analyses of novel mutations in the sulfonylurea receptor 1 associated with persistent hyperinsulinemic hypoglycemia of infancy.

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The essential role of the Walker A motifs of SUR1 in K-ATP channel activation by Mg-ADP and diazoxide

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Hyperinsulinism and hyperammonemia in infants with regulatory mutations of the glutamate dehydrogenase gene

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Acute insulin response tests for the differential diagnosis of congenital hyperinsulinism

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A point mutation inactivating the sulfonylurea receptor causes the severe form of persistent hyperinsulinemic hypoglycemia of infancy in Finland.

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Somatic deletion of the imprinted 11p15 region in sporadic persistent hyperinsulinemic hypoglycemia of infancy is specific of focal adenomatous hyperplasia and endorses partial pancreatectomy

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Nesidioblastosis of the pancreas: definition of the syndrome and the management of the severe neonatal hyperinsulinaemic hypoglycaemia

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A new ER trafficking signal regulates the subunit stoichiometry of plasma membrane K(ATP) channels

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ATP-sensitive K+ channels and insulin secretion: their role in health and disease.

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Unregulated elevation of glutamate dehydrogenase activity induces glutamine-stimulated insulin secretion: identification and characterization of a GLUD1 gene mutation and insulin secretion studies with MIN6 cells overexpressing the mutant glutamate

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Loss of functional KATP channels in pancreatic beta-cells causes persistent hyperinsulinemic hypoglycemia of infancy

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12 December 2020

Familial hyperinsulinism and pancreatic beta-cell ATP-sensitive potassium channels

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Control of rectification and gating of cloned KATP channels by the Kir6.2 subunit

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12 December 2020

Genetics of neonatal hyperinsulinism.

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12 December 2020

Defective trafficking and function of KATP channels caused by a sulfonylurea receptor 1 mutation associated with persistent hyperinsulinemic hypoglycemia of infancy

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12 December 2020

Familial hyperinsulinism caused by an activating glucokinase mutation

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Heterogeneity of persistent hyperinsulinaemic hypoglycaemia. A series of 175 cases

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Dominantly inherited hyperinsulinism caused by a mutation in the sulfonylurea receptor type 1.

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Properties of cloned ATP-sensitive K+ currents expressed in Xenopus oocytes.

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Hyperinsulinism caused by paternal-specific inheritance of a recessive mutation in the sulfonylurea-receptor gene.

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PIP2 and PIP as determinants for ATP inhibition of KATP channels

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Molecular biology of adenosine triphosphate-sensitive potassium channels

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Electrophysiology of the pancreatic beta-cell

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Involvement of the n-terminus of Kir6.2 in coupling to the sulphonylurea receptor.

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Molecular analysis of ATP-sensitive K channel gating and implications for channel inhibition by ATP.

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ATP inhibition of KATP channels: control of nucleotide sensitivity by the N-terminal domain of the Kir6.2 subunit

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Identification and pharmacological correction of a membrane trafficking defect associated with a mutation in the sulfonylurea receptor causing familial hyperinsulinism

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12 December 2020

Regulation of KATP channel activity by diazoxide and MgADP. Distinct functions of the two nucleotide binding folds of the sulfonylurea receptor

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12 December 2020

Practical management of hyperinsulinism in infancy

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12 December 2020

Successive openings of the same acetylcholine receptor channel are correlated in open time

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12 December 2020

Truncation of Kir6.2 produces ATP-sensitive K+ channels in the absence of the sulphonylurea receptor

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12 December 2020

10.1007/S00125-002-1014-3

Identifiers

DOI

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2 December 2017

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