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Links from GEO DataSets

Items: 20

1.

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (ChIP-Seq)

(Submitter supplied) Inactivating mutations in the MEN1 gene predisposing to the multiple endocrine neoplasia type 1 (MEN1) syndrome can also cause sporadic pancreatic endocrine tumors. MEN1 encodes menin, a subunit of MLL1/MLL2-containing histone methyltransferase complexes that trimethylate histone H3 at lysine 4 (H3K4me3). The importance of menin-dependent H3K4me3 in normal and transformed pancreatic endocrine cells is unclear. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9250
8 Samples
Download data: BED
Series
Accession:
GSE37774
ID:
200037774
2.

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL9250 GPL1261
16 Samples
Download data: BED, CEL, CHP
Series
Accession:
GSE37776
ID:
200037776
3.

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (mRNA)

(Submitter supplied) Inactivating mutations in the MEN1 gene predisposing to the multiple endocrine neoplasia type 1 (MEN1) syndrome can also cause sporadic pancreatic endocrine tumors. MEN1 encodes menin, a subunit of MLL1/MLL2-containing histone methyltransferase complexes that trimethylate histone H3 at lysine 4 (H3K4me3). The importance of menin-dependent H3K4me3 in normal and transformed pancreatic endocrine cells is unclear. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
8 Samples
Download data: CEL, CHP
Series
Accession:
GSE37775
ID:
200037775
4.

Dynamic epigenetic regulation by menin during pancreatic islet tumor formation

(Submitter supplied) loss of Men1 in mouse pancreatic islet cells alters the epigenetic landscape of a subset of target genes.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
18 Samples
Download data: BED
Series
Accession:
GSE63020
ID:
200063020
5.

Differential pancreatic islet global gene expression in young heterozygous Men1 mice and wildtype littermates

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
10 Samples
Download data: CEL
Series
Accession:
GSE29674
ID:
200029674
6.

Meg3 regulated genes in pancreatic beta cells

(Submitter supplied) Meg3 is a long non-coding RNA. It's target genes are unknown. The mouse pancreatic beta cell line MIN6-4N was used to assess the expression of genes upon stable Meg3 overexpression
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10740
6 Samples
Download data: CEL
Series
Accession:
GSE57716
ID:
200057716
7.

Loss of MEN1 activates DNMT1 implicating DNA hypermethylation as a driver of MEN1 tumorigenesis

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL11154
38 Samples
Download data: TXT
Series
Accession:
GSE64412
ID:
200064412
8.

NHGRI Menin ChIP-Chip

(Submitter supplied) Multiple endocrine neoplasia type I (MEN1) is a familial cancer syndrome characterized primarily by tumors of multiple endocrine glands. The gene for MEN1 encodes a ubiquitously expressed tumor suppressor protein called menin. Menin was recently shown to interact with several components of a trithorax family histone methyltransferase complex including ASH2, Rbbp5, WDR5, and the leukemia proto-oncoprotein MLL. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL4016
33 Samples
Download data
Series
Accession:
GSE5357
ID:
200005357
9.

2005-04-04_Human_Promo_ChIP

(Submitter supplied) Nimblegen
Organism:
Homo sapiens
1 Series
33 Samples
Download data: NDF, POS
Platform
Accession:
GPL4016
ID:
100004016
10.

Differentially regulated genes in adipocytes derived from Men1-null vs WT mouse embryonic stem cells

(Submitter supplied) MEN1 is a tumor suppressor gene loss of which causes lipoma (fatty tumors under the skin) and many other endocrine and non-endocrine tumors. It's target genes in fat cells (adipocytes) are unknown. Gene expression in adipocytes that were in vitro differentiated from mouse embryonic stem cells (mESCs) of Men1-nul l(Men1-KO) and WT mice were compared to assess the expression of genes upon menin loss in adipocytes that could lead to the deveopment of lipoma.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE65859
ID:
200065859
11.

Analysis of genome-wide occupancy of menin in T47D and MCF-10A cells

(Submitter supplied) We performed ChIP-seq using antibodies directed at menin in T47D and MCF-10A cells in order to assess the genome-wide presence of menin in these cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: BW
Series
Accession:
GSE94009
ID:
200094009
12.

Genome-wide changes in FOXA1 binding after MEN1 silencing in MCF-7 cells

(Submitter supplied) We performed ChIP-seq using FOXA1 antibodies in MCF-7 cells after induction of small hairpin RNA's directed at the MEN1 mRNA or a control sequence. We demonstrate that at menin-bound loci FOXA1 binding is disrupted by MEN1 silencing.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: BW
Series
Accession:
GSE94001
ID:
200094001
13.

Messenger RNA expression after silencing or inhibition of MEN1in MCF-7 breast cancer cells

(Submitter supplied) We performed RNA-seq in MCF-7 cells after silencing of MEN1 using small hairpin RNA's directed at the MEN1 mRNA or chemical inhibition of the MEN1 gene product, menin. We demonstrate that a selected group of transcripts is affected by reduced menin function.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
12 Samples
Download data: TXT
14.

Analysis of genome-wide occupancy of menin, MLL1 and MLL2 in MCF-7 cells

(Submitter supplied) We performed ChIP-seq using antibodies directed at menin, MLL1 and MLL2 in MCF-7 cells in order to assess the genome-wide presence of these proteins in MCF-7 cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
7 Samples
Download data: BED, BW
Series
Accession:
GSE85317
ID:
200085317
15.

Genome-wide changes in H3K4me3 after MEN1 silencing in MCF-7 cells

(Submitter supplied) We performed ChIP-seq using H3K4me3 antibodies in MCF-7 cells after induction of small hairpin RNA's directed at the MEN1 mRNA or a control sequence. We demonstrate that at a selected group of loci H3K4me3 is affected by MEN1 silencing.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL15520
6 Samples
Download data: BED, BW
Series
Accession:
GSE85315
ID:
200085315
16.

Gene expression changes in Mammary Luminal Progenitor cells after MEN1 silencing

(Submitter supplied) Female patients with multiple endocrine neoplasia type 1 are at increased risk to develop breast cancer. We analyzed gene expression after silencing of the MEN1 gene in primary human mammary luminal progenitor cells to identify menin target genes involved in mammary tumorigenesis.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
4 Samples
Download data: CEL
Series
Accession:
GSE85099
ID:
200085099
17.

Hlxb9 regulated genes in pancreatic beta cells

(Submitter supplied) Hlxb9 is a differentiation factor important for neuronal, and pancreatic beta cell differentiation. It is a transcription factor that represses transcription. It's target genes are unknown. The mouse pancreatic beta cell line MIN6 was used to assess the expression of genes de-repressed upon Hlxb9 knockdown.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE32653
ID:
200032653
18.

Menin deficiency induces autism-like behaviors by regulating Foxg1 transcription and participates in Foxg1-related encephalopathy

(Submitter supplied) FOXG1 syndrome is a developmental encephalopathy with a high phenotypic variability, which results from FOXG1 mutations. However, the upstream transcriptional regulation of Foxg1 expression remains unclear. Here we report that both deficiency and overexpression of Men1 (protein: menin, a pathogenic gene of MEN1 syndrome) result in autism-like behaviors, including social defects, increased repetitive behaviors and cognition impairments. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL24247
3 Samples
Download data: BW
Series
Accession:
GSE261274
ID:
200261274
19.

Mll2 branch of the COMPASS family regulates bivalent promoters in mouse embryonic stem cells

(Submitter supplied) Promoters of many developmentally regulated genes, in the embryonic stem cell state, have a bivalent mark of H3K27me3 and H3K4me3, proposed to confer precise temporal activation upon differentiation. Although Polycomb repressive complex 2 is known to implement H3K27 trimethylation, the COMPASS family member responsible for H3K4me3 at bivalently marked promoters was previously unknown. Here, we identify Mll2 (KMT2b) as the enzyme catalyzing H3K4 trimethylation at bivalently marked promoters in embryonic stem cells. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL13112
28 Samples
Download data: BIGWIG
Series
Accession:
GSE48172
ID:
200048172
20.

Expression of genes in adult hepatocytes and fetal hepatoblasts

(Submitter supplied) To analyze stem/progenitor cell function, we purified hepatocytes derived from adult livers and fetal hepatoblasts derived from embryonic day 13 livers.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
4 Samples
Download data: TXT
Series
Accession:
GSE56734
ID:
200056734
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