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anti-Human MEN1 Antibodies:
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Human Polyclonal MEN1 Primary Antibody for ChIP, ICC - ABIN151584
Hughes, Rozenblatt-Rosen, Milne, Copeland, Levine, Lee, Hayes, Shanmugam, Bhattacharjee, Biondi, Kay, Hayward, Hess, Meyerson: Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus. in Molecular cell 2004
Show all 26 Pubmed References
Our study provides important insights into the role of menin in DNA methylation (show HELLS Antibodies) 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 (show MLXIP Antibodies)sed in late-stage primary scleros (show TGFB1 Antibodies)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 Antibodies) and inhibition of Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling.
knockdown of RPA2 (show RPA2 Antibodies) promoted formation of the menin-p65 (show GORASP1 Antibodies) complex and repressed the expression of NF-kappaB (show NFKB1 Antibodies)-mediated genes. RPA2 (show RPA2 Antibodies) expression was induced via an E2F1 (show E2F1 Antibodies)-dependent mechanism in MCF7 and MDA-MB-231 cells treated with NF-kappaB (show NFKB1 Antibodies) activators, TNF-alpha (show TNF Antibodies) or lipopolysaccharide (LPS (show IRF6 Antibodies)).
Loss of Menin is an early event in pancreatic neuroendocrine tumorigenesis and that ATRX (show ATRX Antibodies)/DAXX (show DAXX Antibodies) loss and alternative lengthening of telomeres are relatively late events.
The lack of somatic CDKN1B (show CDKN1B Antibodies) mutations in our samples points to a rare involvement in parathyroid adenomas, despite the frequent loss of nuclear p27 (show PAK2 Antibodies) expression. MEN1 biallelic inactivation seems to be directly related to down-regulation of p27 (show PAK2 Antibodies) expression through the inhibition of CDKN1B (show CDKN1B Antibodies) 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 Antibodies), 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 (show MLXIP Antibodies)-24 increases menin and TGF-beta1 (show TGFB1 Antibodies) expression, subsequently increasing hepatic fibrosis in FVB/NJ WT and Mdr2 (show ABCB4 Antibodies)(-/-) mice.
Menin and PRMT5 (show PRMT5 Antibodies) suppress GLP1R (show GLP1R Antibodies) transcript levels and PKA-mediated phosphorylation of FOXO1 (show FOXO1 Antibodies) and CREB (show CREB1 Antibodies).
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 Antibodies)(+) T cells that are activated upon infection; study uncovered an important role for menin in the immune response of CD8 (show CD8A Antibodies)(+) 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 Antibodies) gene where it favours the recruitment of Ezh2 (show EZH2 Antibodies) via an indirect mechanism involving Akt (show AKT1 Antibodies)-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 Antibodies) resistance, but via increased glucagon (show GCG Antibodies) 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