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Menin binds on the promoter of Inhbb (show INHBB ELISA Kits) gene where it favours the recruitment of Ezh2 (show EZH2 ELISA Kits) via an indirect mechanism involving Akt (show AKT1 ELISA Kits)-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 (show INS ELISA Kits) resistance, but via increased glucagon (show GCG ELISA Kits) 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 (show GRN ELISA Kits) 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 (show NOL3 ELISA Kits) 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 (show NOL3 ELISA Kits).
The study characterized the binding position of Ezh2 (show EZH2 ELISA Kits) 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.
Data show that menin, encoded by the MEN1 gene, inhibits the transcriptional activity of nuclear receptor liver X receptor alpha (LXRalpha (show NR1H3 ELISA Kits)).
Conditional knockout of beta-catenin (show CTNNB1 ELISA Kits) suppresses the tumorigenesis and growth of Men1-deficient pancreatic neuroendocrine tumors.
miR (show MLXIP ELISA Kits)-802 expression levels are increased in lung carcinoma tissues and targets the tumor suppressor menin and downregulates its expression.
Multiple endocrine neoplasia type 1-related primary hyperparathyroidism patients experienced more common kidney complications but less skeletal issues, and a milder biochemical manifestation compared with SHPT patients. MEN1 mutation detection rate was 79.4% and 9 of the identified mutations were novel.
miR (show MLXIP ELISA Kits)-24-dependent expression of menin may be important in the regulation of nonmalignant and cholangiocarcinoma proliferation.
rs2959656, a nonsynonymous variant in MEN1, is associated with the development of clinically active pituitary adenoma.
Study acts as a further supplement of the genetic features of neuroendocrine tumors. Somatic mutations of three potential tumor-related genes (HRAS (show HRAS ELISA Kits), PAK1 (show PAK1 ELISA Kits) and MEN1) might contribute to the tumorigenesis of thymic neuroendocrine tumors with EAS.
The results and clinical course of disease in this case indicate the potential role of menin in the development of non-endocrine or atypical-endocrine tumors in MEN1 patients.
cellular staining for menin also reveals the distribution of menin in the cell membrane and the punctate-like cell organelles
study to evaluate frequency of Multiple Endocrine Neoplasia type 1 (MEN1) in patients with pituitary adenoma and to perform genetic analysis and familial screening of those with MEN1; genetic analysis showed MEN1 mutations in 4 index cases: IVS4+1 G>A, IVS3-6 C>T, c.1547insC and a new D180A mutation
Study reports the coexistence of a germline intronic heterozygote variation at the MEN1 gene (IVS4+1G>T) and a germline mutation of exon 11 of RET proto-oncogene (show RET ELISA Kits) (K666M) in a large Italian family and describes clinical manifestations in the carriers.
novel MEN1 c.8251G>A mutation in a family with multiple endocrine neoplasia type 1
progenitors. Our findings define SON as a fine-tuner of the MLL (show MLL ELISA Kits)-menin interaction and reveal short SON overexpression as a marker indicating aberrant transcriptional initiation in leukemia.
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 1
, multiple endocrine neoplasia I
, multiple endocrine neoplasia protein