Menin Links Estrogen Receptor Activation to Histone H3K4 Trimethylation

Dreijerink, Koen M.A.; Mulder, Klaas W.; Winkler, G. Sebastiaan; Höppener, Jo W.M.; Lips, Cornelis J.M.; Timmers, H. Th. Marc

doi:10.1158/0008-5472.can-05-4461

Cited by 183 publications

(199 citation statements)

References 45 publications

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“…A thymidine kinase (TK) promoter-luciferase construct with five Gal4 binding sites was used as a reporter gene. Similar to our previous observations, overexpression of menin increased ligand-induced transcription to almost threefold, depending on the amount of menin that was co-transfected ( Figure 2A) (Dreijerink et al, 2006). VDR binds to its response elements as a heterodimer with the retinoid X receptor (RXR) (Carlberg et al, 1993).…”

Section: Menin Can Co-activate Vdr-mediated Transcription Via a Direcsupporting

confidence: 89%

“…Construction of vectors pXJ440hVDR, pXJ440hVDR(DE), Gal4-RXRα, Gal4-DBD, pEG202NLS-menin and pBabeHygroMenin has been published (Lavigne et al, 1999, Pijnappel et al, 1993, Zwartjes et al, 2004, Hughes et al, 2004, Dreijerink et al, 2006. The menin expression vector pCDNA3.1M+ was a kind gift from G. Weber.…”

Section: Plasmids and Mutagenesismentioning

confidence: 99%

“…Cells were grown in medium containing 500 g/ml hygromycin and monoclonal cell lines were isolated. Luciferase reporter experiments in Cos7 cells were carried out as described (Dreijerink et al, 2006). In summary, DNA (750 ng per well, in a 12-well format) was transfected using FuGene 6 reagent (Roche).…”

Section: Cell Lines Stable and Transient Protein Expressionmentioning

confidence: 99%

“…Moreover, germ line mutations of the MEN1 gene have been found in patients with familial isolated hyperparathyroidism (FIHP) (Miedlich et al, 2001). We have previously reported that menin can co-activate nuclear receptor mediated gene transcription (Dreijerink et al, 2006). Reduction of menin levels led to decreased expression M a n u s c r i p t 4 of estrogen receptor alpha (ER and peroxisome proliferator-activated receptor gamma (PPAR)target genes (Dreijerink et al, 2006, Dreijerink et al, 2009.…”

Section: Introductionmentioning

confidence: 99%

“…We have previously reported that menin can co-activate nuclear receptor mediated gene transcription (Dreijerink et al, 2006). Reduction of menin levels led to decreased expression M a n u s c r i p t 4 of estrogen receptor alpha (ER and peroxisome proliferator-activated receptor gamma (PPAR)target genes (Dreijerink et al, 2006, Dreijerink et al, 2009. To investigate how loss of menin function can lead to aberrant gene expression in MEN1 tumours, we first determined global H3K4me3 staining in parathyroid tumours.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of vitamin D receptor function in MEN1-related parathyroid adenomas

Dreijerink

Varier

Nuland

et al. 2009

Molecular and Cellular Endocrinology

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Multiple endocrine neoplasia type 1 (MEN1) is heriditary syndrome characterised by the occurrence of parathyroid, gastroenteropancreatic and pituitary tumours. The MEN1 gene product, menin, co-activates gene transcription by recruiting histone methyltransferases for lysine 4 of histone H3 (H3K4). We investigated whether in MEN1 tumours global changes in H3K4 trimethylation (H3K4me3) occur or whether alterations in gene expression can be observed. By immunohistochemistry we found that global levels of H3K4me3 are not affected in MEN1-related parathyroid adenomas. Menin can interact directly with the vitamin D receptor (VDR) and enhance the transcriptional activity of VDR. Messenger RNA levels of VDR target genes CYP24 and KLK6 were significantly lower in MEN1 parathyroid adenomas compared to normal tissue. Thus, aberrant gene expression in MEN1 tumours is not caused by lower global H3K4me3, but rather by specific effects on genes that are regulated by menininteracting proteins, such as VDR.

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Section: Menin Can Co-activate Vdr-mediated Transcription Via a Direcsupporting

confidence: 89%

Section: Plasmids and Mutagenesismentioning

confidence: 99%

Section: Cell Lines Stable and Transient Protein Expressionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Regulation of vitamin D receptor function in MEN1-related parathyroid adenomas

Dreijerink

Varier

Nuland

et al. 2009

Molecular and Cellular Endocrinology

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Molecular Genetics of Kabuki Syndrome

Micale

Merla

2012

Encyclopedia of Life Sciences

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Kabuki syndrome (KS) is a rare, multiple congenital anomalies/mental retardation syndrome characterised by a peculiar face, skeletal abnormalities, cardiac anomalies, and immunological defects. Exome sequencing identified MLL2 mutations as a major cause of KS. MLL2 is a member of the Mixed Lineage Leukaemia (MLL) family of histone methyltransferases, essential in the epigenetic control of active chromatin states. MLLs act as transcriptional co‐activators in embryogenesis and development. As a significant proportion of patients do not have any MLL2 mutation, the existence of additional genes associated with this syndrome was postulated. By Comparative Genomic Hybridisation (CGH) array, de novo partial and/or complete deletions of KDM6A gene have been identified in a small group of MLL2 ‐mutation‐negative Kabuki patients. Notably, KDM6A codes a histone demethylase that interacts with MLL2. Overall, these findings suggest that Kabuki syndrome is a genetic heterogeneity disease and highlights the growing role of histone methylases and histone demethylases in multiple congenital anomalies and intellectual‐disability syndromes. Key Concepts: Kabuki syndrome is a rare, multiple malformation disorder characterised by a distinctive facial appearance, cardiac anomalies, skeletal abnormalities, and mild to moderate intellectual disability. Kabuki syndrome is an autosomal dominant condition that de novo arises in the majority of patients. It is phenotypically variable and genetically heterogeneous. Whole exome sequencing identified mutations in MLL2 gene in approximately 70% of the Kabuki patients. The MLL2 gene encodes a multiple domain‐containing protein that methylates the Lys‐4 position of histone H3 (H3K4), an epigenetic mark correlated with transcriptional active chromatin. Approximately 70% of MLL2 mutation‐positive KS patients carry truncating mutations predicted to result in haploinsufficiency or nonfunctional MLL2 protein. In a search for an additional gene causing Kabuki syndrome, microdeletions of the KDM6A gene were identified in three MLL2 ‐mutation‐negative Kabuki patients. KDM6A is a histone demethylases that interacts with MLL2. Histone methylases and histone demethylases are key‐genes involved in multiple congenital anomalies and intellectual‐disability syndromes.

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Nuclear Receptors and NR ‐coregulators: Mechanism of Action and Cell Signaling

Bhan

Mandal

2017

Gene Regulation, Epigenetics and Hormone Signaling

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Menin Links Estrogen Receptor Activation to Histone H3K4 Trimethylation

Cited by 183 publications

References 45 publications

Regulation of vitamin D receptor function in MEN1-related parathyroid adenomas

Regulation of vitamin D receptor function in MEN1-related parathyroid adenomas

Molecular Genetics of Kabuki Syndrome

Nuclear Receptors and NR ‐coregulators: Mechanism of Action and Cell Signaling

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