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MEN1 encodes menin, a putative tumor suppressor associated with a syndrome known as multiple endocrine neoplasia type 1. Additionally we are shipping MEN1 Antibodies (107) and MEN1 Kits (1) and many more products for this protein.
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Data show that progranulin (show GRN Proteins) 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 Proteins) 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 Proteins).
The study characterized the binding position of Ezh2 (show EZH2 Proteins) 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 Proteins)).
Conditional knockout of beta-catenin (show CTNNB1 Proteins) suppresses the tumorigenesis and growth of Men1-deficient pancreatic neuroendocrine tumors.
miR (show MLXIP Proteins)-802 expression levels are increased in lung carcinoma tissues and targets the tumor suppressor menin and downregulates its expression.
CDK4 (show CDK4 Proteins) is a critical downstream target of MEN1-dependent tumor suppression and is required for tumorigenic proliferation in the pituitary and pancreatic islet, whereas CDK2 (show CDK2 Proteins) is dispensable for tumorigenesis in these neuroendocrine cell types.
This work shows that Men1 ablation in the pancreatic beta-cells leads to the inactivation of specific transcription factors, resulting in glucagon (show GCG Proteins)-expressing tumor development, which sheds light on the mechanisms of islet tumorigenesis.
Menin regulates spinal glutamate (show GRIN1 Proteins)-GABA balance through GAD65 (show GAD2 Proteins) contributing to neuropathic pain.
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 Proteins) (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 Proteins)-menin interaction and reveal short SON overexpression as a marker indicating aberrant transcriptional initiation in leukemia.
interaction between menin and Dnmt1 (show DNMT1 Proteins) reversibly regulates pancreatic cancer cell growth downstream of Hedgehog (show SHH Proteins) pathways with complex mutual modulation networks.
Molecular analysis of sporadic insulinoma (show RPS15 Proteins) revealed presence of three novel exonic mutations, two novel intronic variations, three reported exon SNPs, and one intronic SNP (rs669976).
While there appears be a modest link between MEN1 and breast cancer, causality has not so far been demonstrated.
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