Associated Papers
Identification of Variants Responsible for Monogenic Forms of Diabetes in Brazil.
Abreu GM et al.
Frontiers in Endocrinology, 2022
Evolution- and structure-based computational strategy reveals the impact of deleterious missense mutations on MODY 2 (maturity-onset diabetes of the young, type 2).
George DC et al.
Theranostics, 2014
24578721 (PubMed )
Supplement: thnov04p0366s1.pdf
Incidental mild hyperglycemia in children: two MODY 2 families identified in Brazilian subjects.
Caetano LA et al.
Arquivos Brasileiros De Endocrinologia E Metabologia, 2012
Detection of glucokinase gene defects in non-obese Japanese children diagnosed with diabetes by school medical examinations.
Yokota I et al.
Endocrine Journal, 2011
Maturity-onset diabetes of the young in children with incidental hyperglycemia: a multicenter Italian study of 172 families.
Lorini R et al.
Diabetes Care, 2009
G/A polymorphism at -258 of the hepatic glucokinase promoter is not associated with decreased birth weight in preterm neonates.
Pawlowski M et al.
Neonatology, 2008
Hyperinsulinism in infancy: from basic science to clinical disease.
Dunne MJ et al.
Physiological Reviews, 2004
Glucokinase (GCK) mutations in hyper- and hypoglycemia: maturity-onset diabetes of the young, permanent neonatal diabetes, and hyperinsulinemia of infancy.
Gloyn AL
Human Mutation, 2003
Pancreas duodenum homeobox-1 regulates pancreas development during embryogenesis and islet cell function in adulthood.
Hui H et al.
European Journal of Endocrinology, 2002
Single-strand conformation polymorphism analysis of the glucose transporter gene GLUT1 in maturity-onset diabetes of the young.
Baroni MG et al.
Journal of Molecular Medicine (berlin, Germany), 2001
Three novel missense mutations in the glucokinase gene (G80S; E221K; G227C) in Italian subjects with maturity-onset diabetes of the young (MODY). Mutations in brief no. 162. Online.
Guazzini B et al.
Human Mutation, 1998
Select a paper to view details