Expression data of siRNA interfere men1 expression in N2a cell line
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PROVIDER: PRJNA474622 | ENA |
REPOSITORIES: ENA
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Project description:Menin (MEN1) is a critical modulator of tissue development and maintenance.Although menin is abundantly expressed in the nervous system, little is known with regards to its function in the adult brain. To explore molecular mechanisms associated with the phenotypes observed upon neuronal Men1 deletion, we profiled transcriptomes from the Neuro2a(N2a) cells transfected Men1 siRNA USING NimbleGen Mouse gene expression array [100718_MM9_EXP].
2018-07-17 | GSE115344 | GEO
Project description:To analyze the role of Fus, Ewsr1, and Taf15 in alternative RNA processing, we performed exon array analysis in N2A cells using exon arrays. N2A cells were transfected with siRNA using Lipofectamine RNAiMAX (Life Technologies) according to the manufacturer’s instructions.
2020-08-10 | GSE60694 | GEO
Project description:We compared the gene expression in untransfected N2A cells and in pCDNA3.1myc/his vector transfected N2A cells 1 sample each of untransfected and transfected N2A cells were analyzed
2012-02-29 | E-GEOD-36142 | biostudies-arrayexpress
Project description:Multiple endocrine neoplasia type1 (MEN1), an inherited autosomal dominant syndrome characterized by the development of endocrine tumors including NETs, results from mutation in the MEN1 gene that encodes the protein menin. In mouse models, heterozygous loss of Men1 leads to multiple endocrine tumors with loss of heterozygocity at the Men1 locus. Men1 interacts with several partners to regulate cellular processes and gene expression through regulating histone modification. We used microarrays to detail the global gene expression change in Men1 knockout MEFs and identified up-regulated genes during this process.
2017-08-22 | GSE87733 | GEO
Project description:Multiple endocrine neoplasia type 1 (MEN1) syndrome is the result of mutations in the MEN1 gene and results in tumor formation via mechanisms that are not well understood. Using a novel genome-wide methylation analysis, we studied tissues from patients with MEN1-parathyroid tumors, tissues from Men1 knockout (KO) mouse models, and mouse Men1 null mouse embryonic fibroblast (MEF) cell lines. Tissues from KO mice were used to confirm and assess the findings from the MEN1 clinical samples and further explore the molecular mechanisms of global epigenetic changes following the inactivation of menin. We demonstrated that the inactivation of menin results in enhanced activity of DNA (cytosine-5)-methyltransferase 1 (DNMT1) by retinoblastoma-binding protein 5 (Rbbp5) activation in MEN1 tumor tissues. The increased activity of DNMT1 mediated global DNA hypermethylation, which in turn resulted in aberrant activation of the Wnt/β-catenin signaling pathway through inactivation of Sox regulatory genes. Our study provides important insights into the possible regulatory role of menin in DNA methylation and its impact on the pathogenesis of MEN1 tumor development. Global DNA methylation in tissues from patients with MEN1-parathyroid tumors. Thirty-eight human parathyroid specimens were used: 13 sporadic (non-MEN1) parathyroid adenomas, 12 MEN1-parathyroid tumors, 4 parathyroid carcinomas, and 9 normal parathyroids.
2015-12-22 | E-GEOD-64412 | biostudies-arrayexpress
Project description:APP misexpression plays a crucial role in triggering a complex pathological cascade, leading to Alzheimer’s disease (AD). The aim of this study is for determine the influence of APP ectopic expression on the miRNA profiles of neuronal exosomes. In study, miRNA sequencing was done using the exosomes derived from N2A (control) and APP-N2A (N2A with APP overexpression).
2022-03-30 | E-MTAB-11106 | biostudies-arrayexpress
Project description:Multiple endocrine neoplasia type 1 (MEN1) syndrome is the result of mutations in the MEN1 gene and results in tumor formation via mechanisms that are not well understood. Using a novel genome-wide methylation analysis, we studied tissues from patients with MEN1-parathyroid tumors, tissues from Men1 knockout (KO) mouse models, and Men1 null mouse embryonic fibroblast (MEF) cell lines. We demonstrated that the inactivation of menin (the protein product of MEN1) results in increased activity of DNA (cytosine-5)-methyltransferase 1 (DNMT1) by retinoblastoma-binding protein 5 (Rbbp5) activation in MEN1 tumor tissues. The increased activity of DNMT1 mediated global DNA hypermethylation, which in turn resulted in aberrant activation of the Wnt/β-catenin signaling pathway through inactivation of Sox regulatory genes. Our study provides important insights into the possible regulatory role of menin in DNA methylation and its impact on the pathogenesis of MEN1 tumor development.
2015-12-22 | GSE64412 | GEO
Project description:N2a cells treated with either control or siEwsr1 oligonucleotides
2022-04-13 | GSE173439 | GEO
Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Men1 in MN1 driven AML Methods: In vivo MN1 transformed cells were transduced with Cre-vector to inactivate Men1 and injected into sublethially irradiated syngeneic recipients. Men1-/- and Men1wt MN1-driven leukemic cells were isolated from moribund recipients and plated in methylcellulose for 7 days before RNA was extracted. Results: Men1-/- MN1-driven leukemic cells failed to propagate leukemia in most secondary recipients, in comparison with Men1wt MN1-driven. In vitro, cells had lost their colony forming activity. Gene expression analysis revealed a downregulation of the MN1 leukemic expression program. Conclusions: Men1 regulates long term maintenance of MN1-driven leukemia.
2020-05-09 | GSE150151 | GEO
Project description:Multiple Endocrine Neoplasia Tumor Syndrome type 1 (MEN 1) is an autosomal dominant tumor syndrome affecting individuals with a heterozygous germline mutaion of the MEN1 gene. MEN 1 carriers commonly develop parathyroid, anterior pituitary, duodenal and pancreatic endocrine tumors. The phenotype of existing mouse models for the MEN 1 syndrome, with a germline heterozygous (hz) Men1 gene inactivation, show close resemblance to the human MEN 1 syndrome. Menin, the protein encoded for by the MEN1/Men1 gene, lacks homology with known proteins, and evidence of its involvement in different cellular processes is steadily growing. Several interaction partners have been identified, involving different interaction sites on the menin protein. Accumulating evidence suggests a role for menin in transcriptional regulation, cell cycle control, apoptosis, chromatin modification and DNA damage response and repair. Loss of heterozygosity (LOH) of the MEN1 gene precedes tumor formation in the MEN 1 heterozygous pancreas. We set out to determine if there is a change in gene expression early on in the hz islet, as compared with islets in wildtype (wt) littermates, long before the LOH events occur. We performed a global mRNA expression microarray on islets from young, five-week-old, hz Men1 mice and their wt littermates, and we have subsequently corroborated a subset of the findings on the qPCR and protein level. Islets were isolated and RNA prepared from five five-week-old female mice heterozygous for the Men1 gene and five female wildtype littermates, and then a global gene expression microarray was performed.
2011-06-02 | E-GEOD-29674 | biostudies-arrayexpress