Transient neonatal diabetes mellitus is associated with a recurrent (R201H) KCNJ11 (KIR6.2) mutation

[1] Relapsing diabetes can result from moderately activating mutations in KCNJ11 [J]. HUMAN MOLECULAR GENETICS, 2005, 14 (07) : 925 - 934

[2] Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2004, 350 (18) : 1838 - 1849

[3] The identification of a R201H mutation in KCNJ11, which encodes Kir6.2, and successful transfer to sustained-release sulphonylurea therapy in a subject with neonatal diabetes:: evidence for heterogeneity of beta cell function among carriers of the R201H mutation [J]. DIABETOLOGIA, 2005, 48 (05) : 1029 - 1031

[4] KCNJ11 activating mutations in Italian patients with permanent neonatal diabetes [J]. HUMAN MUTATION, 2005, 25 (01) : 22 - 27

[5] Polak Michel, 2004, Semin Neonatol, V9, P59, DOI 10.1016/S1084-2756(03)00064-2

[6] Glucose-sensing in glucagon-like peptide-1-secreting cells [J]. DIABETES, 2002, 51 (09) : 2757 - 2763

[7] Permanent neonatal diabetes due to mutations in KCNJ11 encoding Kir6.2 -: Patient characteristics and initial response to sulfonylurea therapy [J]. DIABETES, 2004, 53 (10) : 2713 - 2718

[8] Kir6.2 mutations are a common cause of permanent neonatal diabetes in a large cohort of French patients [J]. DIABETES, 2004, 53 (10) : 2719 - 2722

[9] Glibenclamide treatment in permanent neonatal diabetes mellitus due to an activating mutation in Kir6.2 [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (11) : 5504 - 5507

[1] Relapsing diabetes can result from moderately activating mutations in KCNJ11 [J]. HUMAN MOLECULAR GENETICS, 2005, 14 (07) : 925 - 934

[2] Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2004, 350 (18) : 1838 - 1849

[3] The identification of a R201H mutation in KCNJ11, which encodes Kir6.2, and successful transfer to sustained-release sulphonylurea therapy in a subject with neonatal diabetes:: evidence for heterogeneity of beta cell function among carriers of the R201H mutation [J]. DIABETOLOGIA, 2005, 48 (05) : 1029 - 1031

[4] KCNJ11 activating mutations in Italian patients with permanent neonatal diabetes [J]. HUMAN MUTATION, 2005, 25 (01) : 22 - 27

[5] Polak Michel, 2004, Semin Neonatol, V9, P59, DOI 10.1016/S1084-2756(03)00064-2

[6] Glucose-sensing in glucagon-like peptide-1-secreting cells [J]. DIABETES, 2002, 51 (09) : 2757 - 2763

[7] Permanent neonatal diabetes due to mutations in KCNJ11 encoding Kir6.2 -: Patient characteristics and initial response to sulfonylurea therapy [J]. DIABETES, 2004, 53 (10) : 2713 - 2718

[8] Kir6.2 mutations are a common cause of permanent neonatal diabetes in a large cohort of French patients [J]. DIABETES, 2004, 53 (10) : 2719 - 2722

[9] Glibenclamide treatment in permanent neonatal diabetes mellitus due to an activating mutation in Kir6.2 [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (11) : 5504 - 5507