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Our study provides important insights into the role of menin in DNA methylation (显示 HELLS ELISA试剂盒) 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 increa (显示 MLXIP ELISA试剂盒)sed in late-stage primary scleros (显示 TGFB1 ELISA试剂盒)ing cholangitis
The results provide novel molecular insights into the tumor suppressor activity of menin, which is partly mediated by proteasomal degradation of beta-catenin (显示 CTNNB1 ELISA试剂盒) and inhibition of Wnt (显示 WNT2 ELISA试剂盒)/beta-catenin (显示 CTNNB1 ELISA试剂盒) signaling.
knockdown of RPA2 (显示 RPA2 ELISA试剂盒) promoted formation of the menin-p65 (显示 GORASP1 ELISA试剂盒) complex and repressed the expression of NF-kappaB (显示 NFKB1 ELISA试剂盒)-mediated genes. RPA2 (显示 RPA2 ELISA试剂盒) expression was induced via an E2F1 (显示 E2F1 ELISA试剂盒)-dependent mechanism in MCF7 and MDA-MB-231 cells treated with NF-kappaB (显示 NFKB1 ELISA试剂盒) activators, TNF-alpha (显示 TNF ELISA试剂盒) or lipopolysaccharide (LPS (显示 IRF6 ELISA试剂盒)).
Loss of Menin is an early event in pancreatic neuroendocrine tumorigenesis and that ATRX (显示 ATRX ELISA试剂盒)/DAXX (显示 DAXX ELISA试剂盒) loss and alternative lengthening of telomeres are relatively late events.
The lack of somatic CDKN1B (显示 CDKN1B ELISA试剂盒) mutations in our samples points to a rare involvement in parathyroid adenomas, despite the frequent loss of nuclear p27 (显示 PAK2 ELISA试剂盒) expression. MEN1 biallelic inactivation seems to be directly related to down-regulation of p27 (显示 PAK2 ELISA试剂盒) expression through the inhibition of CDKN1B (显示 CDKN1B ELISA试剂盒) gene transcription.
This result shows a novel mechanism whereby menin, a RNA-binding protein, facilitates the processing of its specific miRNA by regulating the dynamics of the menin-miR-24 Gene Regulatory Network at the level of pri-miRNA processing.
findings reveal a previously unappreciated cross-talk between two crucial tumor suppressor genes, MEN1 and DAXX (显示 DAXX ELISA试剂盒), thought to work by independent pathways
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.
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 (显示 MLXIP ELISA试剂盒)-24 increases menin and TGF-beta1 (显示 TGFB1 ELISA试剂盒) expression, subsequently increasing hepatic fibrosis in FVB/NJ WT and Mdr2 (显示 ABCB4 ELISA试剂盒)(-/-) mice.
Menin and PRMT5 (显示 PRMT5 ELISA试剂盒) suppress GLP1R (显示 GLP1R ELISA试剂盒) transcript levels and PKA-mediated phosphorylation of FOXO1 (显示 FOXO1 ELISA试剂盒) and CREB (显示 CREB1 ELISA试剂盒).
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 (显示 CD8A ELISA试剂盒)(+) T cells that are activated upon infection; study uncovered an important role for menin in the immune response of CD8 (显示 CD8A ELISA试剂盒)(+) 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 (显示 INHBB ELISA试剂盒) gene where it favours the recruitment of Ezh2 (显示 EZH2 ELISA试剂盒) via an indirect mechanism involving Akt (显示 AKT1 ELISA试剂盒)-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 (显示 INS ELISA试剂盒) resistance, but via increased glucagon (显示 GCG ELISA试剂盒) 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.
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