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anti-Human MEN1 Antikörper:
anti-Mouse (Murine) MEN1 Antikörper:
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Human Polyclonal MEN1 Primary Antibody für 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
expression increa (zeige MLXIP Antikörper)sed in late-stage primary scleros (zeige TGFB1 Antikörper)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 (zeige CTNNB1 Antikörper) and inhibition of Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling.
knockdown of RPA2 (zeige RPA2 Antikörper) promoted formation of the menin-p65 (zeige GORASP1 Antikörper) complex and repressed the expression of NF-kappaB (zeige NFKB1 Antikörper)-mediated genes. RPA2 (zeige RPA2 Antikörper) expression was induced via an E2F1 (zeige E2F1 Antikörper)-dependent mechanism in MCF7 and MDA-MB-231 cells treated with NF-kappaB (zeige NFKB1 Antikörper) activators, TNF-alpha (zeige TNF Antikörper) or lipopolysaccharide (LPS (zeige IRF6 Antikörper)).
Loss of Menin is an early event in pancreatic neuroendocrine tumorigenesis and that ATRX (zeige ATRX Antikörper)/DAXX (zeige DAXX Antikörper) loss and alternative lengthening of telomeres are relatively late events.
The lack of somatic CDKN1B (zeige CDKN1B Antikörper) mutations in our samples points to a rare involvement in parathyroid adenomas, despite the frequent loss of nuclear p27 (zeige PAK2 Antikörper) expression. MEN1 biallelic inactivation seems to be directly related to down-regulation of p27 (zeige PAK2 Antikörper) expression through the inhibition of CDKN1B (zeige CDKN1B Antikörper) 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 (zeige DAXX Antikörper), 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 (zeige MLXIP Antikörper)-24 increases menin and TGF-beta1 (zeige TGFB1 Antikörper) expression, subsequently increasing hepatic fibrosis in FVB/NJ WT and Mdr2 (zeige ABCB4 Antikörper)(-/-) mice.
Menin and PRMT5 (zeige PRMT5 Antikörper) suppress GLP1R (zeige GLP1R Antikörper) transcript levels and PKA-mediated phosphorylation of FOXO1 (zeige FOXO1 Antikörper) and CREB (zeige CREB1 Antikörper).
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 (zeige CD8A Antikörper)(+) T cells that are activated upon infection; study uncovered an important role for menin in the immune response of CD8 (zeige CD8A Antikörper)(+) 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 (zeige INHBB Antikörper) gene where it favours the recruitment of Ezh2 (zeige EZH2 Antikörper) via an indirect mechanism involving Akt (zeige AKT1 Antikörper)-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 (zeige INS Antikörper) resistance, but via increased glucagon (zeige GCG Antikörper) 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