Familial hyperinsulinism caused by an activating glucokinase mutation

[1] 2 REGIONS OF GLUT-2 GLUCOSE-TRANSPORTER PROTEIN ARE RESPONSIBLE FOR ITS DISTINCTIVE AFFINITY FOR GLUCOSES [J]. ENDOCRINOLOGY, 1995, 136 (10) : 4224 - 4230

[2] GLUCOKINASE GENE VARIANTS IN THE COMMON FORM OF NIDDM [J]. DIABETES, 1993, 42 (04) : 579 - 582

[3] CHARACTERIZATION OF 7 C-PEPTIDE ANTISERA [J]. DIABETES, 1978, 27 : 170 - 177

[4] Froguel P, 1997, DIABETES REV, V5, P123

[5] FAMILIAL HYPERGLYCEMIA DUE TO MUTATIONS IN GLUCOKINASE - DEFINITION OF A SUBTYPE OF DIABETES-MELLITUS [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1993, 328 (10) : 697 - 702

[6] ELISA FOR HUMAN PROINSULIN [J]. CLINICA CHIMICA ACTA, 1986, 156 (03) : 289 - 297

[7] Structural instability of mutant beta-cell glucokinase: Implications for the molecular pathogenesis of maturity-onset diabetes of the young (type-2) [J]. BIOCHEMICAL JOURNAL, 1997, 322 : 57 - 63

[8] An autosomal dominant form of familial persistent hyperinsulinemic hypoglycemia of infancy, not linked to the sulfonylurea receptor locus [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1997, 82 (04) : 1192 - 1194

[9] KUNKEL TA, 1987, METHOD ENZYMOL, V154, P367

[10] VARIABLE EFFECTS OF MATURITY-ONSET-DIABETES-OF-YOUTH (MODY)-ASSOCIATED GLUCOKINASE MUTATIONS ON SUBSTRATE INTERACTIONS AND STABILITY OF THE ENZYME [J]. BIOCHEMICAL JOURNAL, 1995, 309 : 167 - 173

[1] 2 REGIONS OF GLUT-2 GLUCOSE-TRANSPORTER PROTEIN ARE RESPONSIBLE FOR ITS DISTINCTIVE AFFINITY FOR GLUCOSES [J]. ENDOCRINOLOGY, 1995, 136 (10) : 4224 - 4230

[2] GLUCOKINASE GENE VARIANTS IN THE COMMON FORM OF NIDDM [J]. DIABETES, 1993, 42 (04) : 579 - 582

[3] CHARACTERIZATION OF 7 C-PEPTIDE ANTISERA [J]. DIABETES, 1978, 27 : 170 - 177

[4] Froguel P, 1997, DIABETES REV, V5, P123

[5] FAMILIAL HYPERGLYCEMIA DUE TO MUTATIONS IN GLUCOKINASE - DEFINITION OF A SUBTYPE OF DIABETES-MELLITUS [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1993, 328 (10) : 697 - 702

[6] ELISA FOR HUMAN PROINSULIN [J]. CLINICA CHIMICA ACTA, 1986, 156 (03) : 289 - 297

[7] Structural instability of mutant beta-cell glucokinase: Implications for the molecular pathogenesis of maturity-onset diabetes of the young (type-2) [J]. BIOCHEMICAL JOURNAL, 1997, 322 : 57 - 63

[8] An autosomal dominant form of familial persistent hyperinsulinemic hypoglycemia of infancy, not linked to the sulfonylurea receptor locus [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1997, 82 (04) : 1192 - 1194

[9] KUNKEL TA, 1987, METHOD ENZYMOL, V154, P367

[10] VARIABLE EFFECTS OF MATURITY-ONSET-DIABETES-OF-YOUTH (MODY)-ASSOCIATED GLUCOKINASE MUTATIONS ON SUBSTRATE INTERACTIONS AND STABILITY OF THE ENZYME [J]. BIOCHEMICAL JOURNAL, 1995, 309 : 167 - 173