Associated Papers
Alternative splicing generates isoform diversity in MEN1.
Ramachandran A et al.
Endocrine Oncology (bristol, England), 2024
39649118 (PubMed )
Supplement: supplementary_table_3.xlsx › Supplementary_Table_3
Multi-omics analyses of MEN1 missense mutations identify disruption of menin-MLL and menin-JunD interactions as critical requirements for molecular pathogenicity.
Dreijerink KMA et al.
Epigenetics & Chromatin, 2022
35941657 (PubMed )
Supplement: 13072_2022_461_MOESM5_ESM.xlsx › Database_van_mutaties
Integrated Whole-Exome and Transcriptome Sequencing of Sporadic Parathyroid Adenoma.
Hu Y et al.
Frontiers in Endocrinology, 2021
34054720 (PubMed )
Supplement: Table_1.xlsx › Sheet1
Identification of pathogenic missense mutations using protein stability predictors.
Gerasimavicius L et al.
Scientific Reports, 2020
32958805 (PubMed )
Supplement: 41598_2020_72404_MOESM2_ESM.xlsx › gnomAD
Exome sequencing in families with chronic central serous chorioretinopathy.
Schellevis RL et al.
Molecular Genetics & Genomic Medicine, 2019
30724488 (PubMed )
Supplement: MGG3-7-na-s005.xlsx › Family_17
Assessment of pancreatic neuroendocrine tumor cytologic genotype diversity to guide personalized medicine using a custom gastroenteropancreatic next-generation sequencing panel.
Gleeson FC et al.
Oncotarget, 2017
29212165 (PubMed )
Supplement: oncotarget-08-93464-s001.pdf
MEN1 mutations and potentially MEN1-targeting miRNAs are responsible for menin deficiency in sporadic and MEN1 syndrome-associated primary hyperparathyroidism.
Grolmusz VK et al.
Virchows Archiv : an International Journal of Pathology, 2017
Correlation of mutant menin stability with clinical expression of multiple endocrine neoplasia type 1 and its incomplete forms.
Shimazu S et al.
Cancer Science, 2011
Characteristics of the Danish families with multiple endocrine neoplasia type 1.
Jäger AC et al.
Molecular and Cellular Endocrinology, 2006
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