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A novel MEN1 truncating mutation correlates with an aggressive evolution and behavior of MEN1 gastro-entero-pancreatic (neuro)endocrine tumours.
ATRX, DAXX or MEN1 mutant pancreatic neuroendocrine tumors are a distinct alpha-cell signature subgroup
Menin functions as an oncogenic regulatory factor that is critical for MYC-mediated gene transcription.
This novel study reveals evidence supporting a possible association between altered MEN1 promoter methylation and clinical severity of disease
De novo mutation in MEN1 is not associated with parental somatic mosaicism.(
Results revealed that the expression level of menin was lower in lung cancer. Its expression is regulated by miR24 which directly targets menin and significantly inhibit its activity, thereby promoting the growth and metastasis of lung cancer cells.
A case of dorsal pancreatic hemi-agenesis is reported in a heterozygous carrier of a novel MEN1 variant.
A missense variant in aryl hydrocarbon receptor-interacting protein (AIP) gene and a truncating mutation in multiple endocrine neoplasia I protein (MEN1) gene were both detected in the proband and his father, showing limited co-segregation with phenotype.
menin is regulated by extracellular signaling factors and has a role in nuclear receptor activation and hepatobiliary pathology in various hepatic cell types [review]
Each of these autosomal dominant syndromes results from a specific germline mutation in unique genes: MEN1 is due to pathogenic MEN1 variants (11q13), MEN2A and MEN2B are due to pathogenic RET variants (10q11.21), MEN4 is due to pathogenic CDKN1B variants (12p13.1), and the HPT-JT syndrome is due to pathogenic CDC73 variants (1q25).
Menin deficiency is the consequence of a MEN1 mutation in most menin-negative primary hyperparathyroidism tissues
Data demonstrate an essential role for MLL1 and menin in mediating tumor maintenance and posterior HOXD gene activation in Ewing sarcoma.
Data suggest that a novel germline missense mutation in MEN1 (p.Gly42Val) accounts for type 1 multiple endocrine neoplasia in a family; this mutation was found in the patient and his mother. [CASE REPORT]
Our study provides important insights into the role of menin in DNA methylation and its impact on the pathogenesis of Multiple endocrine neoplasia type 1 syndrome tumor development.
MEN1 exerts an anti-proliferative function by regulating a distinct expression signature.
expression increased in late-stage primary sclerosing cholangitis
The results provide novel molecular insights into the tumor suppressor activity of menin, which is partly mediated by proteasomal degradation of beta-catenin and inhibition of Wnt/beta-catenin signaling.
knockdown of RPA2 promoted formation of the menin-p65 complex and repressed the expression of NF-kappaB-mediated genes. RPA2 expression was induced via an E2F1-dependent mechanism in MCF7 and MDA-MB-231 cells treated with NF-kappaB activators, TNF-alpha or lipopolysaccharide (LPS).
Loss of Menin is an early event in pancreatic neuroendocrine tumorigenesis and that ATRX/DAXX loss and alternative lengthening of telomeres are relatively late events.
The lack of somatic CDKN1B mutations in our samples points to a rare involvement in parathyroid adenomas, despite the frequent loss of nuclear p27 expression. MEN1 biallelic inactivation seems to be directly related to down-regulation of p27 expression through the inhibition of CDKN1B gene transcription.
MEN1/Menin could play a regulatory role in milk protein synthesis.
Distinct pathways affected by menin versus MLL1/MLL2 in MLL-rearranged acute myeloid leukemia.
our results suggest that the influence of menin on synapse formation and synaptic plasticity occur via modulation of nAChR channel subunit composition and functional clustering.
menin maintains the T-cell functions by limiting mTORC 1 activity and subsequent cellular metabolism.
Results showed that the MEN1 gene was negatively correlated with lung fibrinogen markers and provide evidence that MEN1 plays a key role in the formation of pulmonary fibrosis by regulating the secretion of TGF-beta and the activation of TGF-beta/Smads signaling pathway.
Men1 - a tumor suppressor gene - is critical for ossifying fibroma (OF) formation. Mice with targeted disruption of Men1 in osteoblasts develop multifocal OF in the mandible with a 100% penetrance.
Men1-deficient osteocytes was expressed numerous soluble mediators such as C-X-C motif chemokine 10 (CXCL10 and a novel role for Men1 in osteocyte-osteoclast crosstalk by controlling osteoclastogenesis through the action of soluble factors.
Gastrin induces nuclear export and proteasome degradation of menin in duodenal glial cells.
gene expression analysis revealed that Menin was involved in the maintenance of the high expression of the previously identified Th2-specific genes rather than the induction of these genes. This result suggests that Menin plays a role in the maintenance of Th2 cell identity.This study confirmed the critical role of Menin in Th2 cell-mediated immune responses.
Inhibition of miR-24 increases menin and TGF-beta1 expression, subsequently increasing hepatic fibrosis in FVB/NJ WT and Mdr2(-/-) mice.
Menin and PRMT5 suppress GLP1R transcript levels and PKA-mediated phosphorylation of FOXO1 and CREB.
Inactivation of Kmt2a in Men1-deficient mice accelerated pancreatic islet tumorigenesis and shortened the average life span. Increases in cell proliferation were observed in mouse pancreatic islet tumors upon inactivation of both Kmt2a and Men1.
Data suggest that menin inhibits differentiation into terminal effectors and positively controls proliferation and survival of Ag-specific CD8(+) T cells that are activated upon infection; study uncovered an important role for menin in the immune response of CD8(+) T cells to infection
Our data further confirms that deletion of Men1 alone does not favour carcinoid development, but rather cooperates with additional loci.
Menin binds on the promoter of Inhbb gene where it favours the recruitment of Ezh2 via an indirect mechanism involving Akt-phosphorylation.
Results indicate that fasted male Men1(+/-) mice, in the early stage of development of MEN1, display glucose metabolic disorders. These disorders are caused not by direct induction of insulin resistance, but via increased glucagon secretion and the consequent stimulation of hepatic glucose production.
The inactivation of menin in the thyroid gland of young mice does not seem to change the histological pattern, but it influences the proliferation of follicular cells. Further molecular studies especially in aged mice are needed to better understand the correlation between certain oncogenes and the inactive status of menin.
Data show that progranulin is upregulated in neuroendocrine tumors (NETs) and islets of the multiple endocrine neoplasia 1 protein (MEN1) mouse as well as in the serum of patients with pancreatic NETs associated with glucagonoma syndrome.
Although mice lacking Men1 developed insulinomas as expected, elimination of ARC in this context did not significantly alter tumor load. Cellular rates of proliferation and death in these tumors were also not perturbed in the absence of ARC.
The study characterized the binding position of Ezh2 and menin at all annotated genes in embryonic stem cells and B and T lymphocytes.
Data demonstrate that loss of Men1 in pancreatic islet cells alters the epigenetic landscape of its target genes during early stages of pancreatic neuroendocrine tumor formation.
This gene encodes menin, a putative tumor suppressor associated with a syndrome known as multiple endocrine neoplasia type 1. In vitro studies have shown menin is localized to the nucleus, possesses two functional nuclear localization signals, and inhibits transcriptional activation by JunD, however, the function of this protein is not known. Two messages have been detected on northern blots but the larger message has not been characterized. Alternative splicing results in multiple transcript variants.
, multiple endocrine neoplasia protein
, multiple endocrine neoplasia 1
, multiple endocrine neoplasia I