Associated Papers
MODY Is Prevalent in Later-Onset Diabetes and Has Potential for Targeted Therapy but Is Challenging to Identify.
Sharp LN et al.
Diabetes, 2026
41288518 (PubMed )
Supplement: EMS210954-supplement-Supplementary_Materials.pdf
Common genetic variants modify disease risk and clinical presentation in monogenic diabetes.
Murray Leech J et al.
Nature Metabolism, 2025
40925988 (PubMed )
Supplement: 42255_2025_1372_MOESM1_ESM.pdf
Role of RNA Alternative Splicing in T Cell Function and Disease.
Banerjee S et al.
Genes, 2023
37895245 (PubMed )
Supplement: genes-14-01896-s001.zip › Supplementary_Table.xlsx › Supplementary_Table
Reduced penetrance of MODY-associated HNF1A/HNF4A variants but not GCK variants in clinically unselected cohorts.
Mirshahi UL et al.
American Journal of Human Genetics, 2022
36257325 (PubMed )
Supplement: mmc2.xlsx › MODY_Family_Members
Statistical evidence for high-penetrance MODY-causing genes in a large population-based cohort.
Billings LK et al.
Endocrinology, Diabetes & Metabolism, 2022
36208030 (PubMed )
Supplement: EDM2-5-e372-s001.xlsx › eTable_1
HNF1A：From Monogenic Diabetes to Type 2 Diabetes and Gestational Diabetes Mellitus.
Li LM et al.
Frontiers in Endocrinology, 2022
35299962 (PubMed )
Supplement: DataSheet_1.pdf
Mutations in the genes encoding the transcription factors hepatocyte nuclear factor 1 alpha (HNF1A) and 4 alpha (HNF4A) in maturity-onset diabetes of the young.
Ellard S et al.
Human Mutation, 2006
Select a paper to view details