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Menin functions as an oncogenic regulatory factor that is critical for MYC (Montrer MYC Protéines)-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 (Montrer AIP Protéines)) 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 (Montrer RET Protéines) and MEN2B (Montrer RET Protéines) are due to pathogenic RET (Montrer RET Protéines) variants (10q11.21), MEN4 (Montrer CDKN1B Protéines) is due to pathogenic CDKN1B (Montrer CDKN1B Protéines) variants (12p13.1), and the HPT-JT syndrome is due to pathogenic CDC73 (Montrer CDC73 Protéines) 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.
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 (Montrer TGFB1 Protéines) and the activation of TGF-beta (Montrer TGFB1 Protéines)/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 (Montrer CXCL10 Protéines) 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 (Montrer MLXIP Protéines)-24 increases menin and TGF-beta1 (Montrer TGFB1 Protéines) expression, subsequently increasing hepatic fibrosis in FVB/NJ WT and Mdr2 (Montrer ABCB4 Protéines)(-/-) mice.
Menin and PRMT5 (Montrer PRMT5 Protéines) suppress GLP1R (Montrer GLP1R Protéines) transcript levels and PKA-mediated phosphorylation of FOXO1 (Montrer FOXO1 Protéines) and CREB (Montrer CREB1 Protéines).
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 (Montrer CD8A Protéines)(+) T cells that are activated upon infection; study uncovered an important role for menin in the immune response of CD8 (Montrer CD8A Protéines)(+) T cells to infection
Our data further confirms that deletion of Men1 alone does not favour carcinoid development, but rather cooperates with additional loci.
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