Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity

Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity

Abstract Background Loss-of-function mutations of the multiple endocrine neoplasia type 1 (MEN1) gene are causal to the MEN1 tumor syndrome, but they are also commonly found in sporadic pancreatic neuroendocrine tumors and other types of cancers. The MEN1 gene product, menin, is involved in transcri...

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Bibliographic Details
Main Authors: Koen M. A. Dreijerink, Ezgi Ozyerli-Goknar, Stefanie Koidl, Ewoud J. van der Lelij, Priscilla van den Heuvel, Jeffrey J. Kooijman, Martin L. Biniossek, Kees W. Rodenburg, Sheikh Nizamuddin, H. T. Marc Timmers
Format: Article
Language:English
Published: BMC 2022-08-01
Series:Epigenetics & Chromatin
Subjects:
Tumor suppressor
MEN1 syndrome
Histone H3K4 methylation
AP-1 transcription factors
ATF transcription factors
Quantitative mass spectrometry
Online Access:https://doi.org/10.1186/s13072-022-00461-8

Internet

https://doi.org/10.1186/s13072-022-00461-8

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