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expression increa (show MLXIP ELISA Kits)sed in late-stage primary scleros (show TGFB1 ELISA Kits)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 (show CTNNB1 ELISA Kits) and inhibition of Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling.
knockdown of RPA2 (show RPA2 ELISA Kits) promoted formation of the menin-p65 (show GORASP1 ELISA Kits) complex and repressed the expression of NF-kappaB (show NFKB1 ELISA Kits)-mediated genes. RPA2 (show RPA2 ELISA Kits) expression was induced via an E2F1 (show E2F1 ELISA Kits)-dependent mechanism in MCF7 and MDA-MB-231 cells treated with NF-kappaB (show NFKB1 ELISA Kits) activators, TNF-alpha (show TNF ELISA Kits) or lipopolysaccharide (LPS (show IRF6 ELISA Kits)).
Loss of Menin is an early event in pancreatic neuroendocrine tumorigenesis and that ATRX (show ATRX ELISA Kits)/DAXX (show DAXX ELISA Kits) loss and alternative lengthening of telomeres are relatively late events.
The lack of somatic CDKN1B (show CDKN1B ELISA Kits) mutations in our samples points to a rare involvement in parathyroid adenomas, despite the frequent loss of nuclear p27 (show PAK2 ELISA Kits) expression. MEN1 biallelic inactivation seems to be directly related to down-regulation of p27 (show PAK2 ELISA Kits) expression through the inhibition of CDKN1B (show CDKN1B ELISA Kits) 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 (show DAXX ELISA Kits), 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.
miR-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.
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 (show MLXIP ELISA Kits)-24 increases menin and TGF-beta1 (show TGFB1 ELISA Kits) expression, subsequently increasing hepatic fibrosis in FVB/NJ WT and Mdr2 (show ABCB4 ELISA Kits)(-/-) mice.
Menin and PRMT5 (show PRMT5 ELISA Kits) suppress GLP1R (show GLP1R ELISA Kits) transcript levels and PKA-mediated phosphorylation of FOXO1 (show FOXO1 ELISA Kits) and CREB (show CREB1 ELISA Kits).
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 (show CD8A ELISA Kits)(+) T cells that are activated upon infection; study uncovered an important role for menin in the immune response of CD8 (show CD8A ELISA Kits)(+) 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 (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 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.
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