Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Quantitative analysis of AP-1 dependent gene expression in CRISPR/Cas9 negative control and AP-1 depleted human uterine smooth muscle cells (HUtSMCs).

ABSTRACT: Down-regulation of genes belonging to the JUN, FOS, and ATF families of transcription factors has previously been described. In this study, we demonstrate that the loss of AP-1 subunit gene expression leads to a decrease in AP-1 enhancer occupancy. CRISPR/Cas9 mediated depletion of AP-1 subunits demonstrates that loss of AP-1 subunit gene expression results in a perturbation of extracellular matrix-associated gene expression. This work establishes AP-1 as an important transcription factor in uterine leiomyoma gene transcription.

ORGANISM(S): Homo sapiens

PROVIDER: GSE139581 | GEO | 2020/01/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Quantitative analysis of AP-1 dependent gene expression in negative control and AP-1 knockdown myometrium primary cells derived from 2 patient tissue samples.

Project description:Down-regulation of genes belonging to the JUN, FOS, and ATF families of transcription factors has previously been described. In this study, we demonstrate that the loss of AP-1 subunit gene expression leads to a decrease in AP-1 enhancer occupancy. Knockdown of AP-1 subunits demonstrates that loss of AP-1 subunit gene expression results in a perturbation of extracellular matrix-associated gene expression. This work establishes AP-1 as an important transcription factor in uterine leiomyoma disease pathogenesis.

2020-01-01 | GSE128237 | GEO

Genome-wide map of H3K27Ac chromatin state in CRISPR/Cas9 negative control and AP-1 depleted human uterine smooth muscle cells (HUtSMCs).

Project description:We report that the loss of AP-1 subunit gene expression leads to alterations in enhancer H3K27Ac enrichment. Altered distal enhancer regions are shown to overlap significantly with AP-1 DNA binding motifs.

2020-01-01 | GSE139582 | GEO

AP-1 subunits converge promiscuously at enhancers to potentiate transcription

Project description:The AP-1 transcription factor dimer contributes to many biological processes and environmental responses. The many ways that AP-1 subunits can dimerize has posed a challenge to understanding its regulatory function. To determine patterns of AP-1 dimerization genome-wide, we definitively establish the genome-wide binding patterns and the enhancer function of five AP-1 subunits. We find limited evidence for strong dimerization preferences between specific subunits. In particular, our analysis suggests that canonical AP-1 motifs have the potential to recruit all AP-1 subunits to genomic sites that also have hallmarks of strong enhancer activity. We term those sites AP-1 hotspots. AP-1 hotspots function as a ‘hub' for AP-1 subunit binding that elicits changes in cell-type specific AP-1-mediated gene expression. AP-1 hotspots are more predictive of genomic responses to glucocorticoid signaling than super enhancers, and are particularly enriched in disease-associated genetic variants. Together, these results support a model that promiscuous convergence of many subunits to common genomic locations potentiates AP-1-mediated transcription in a cell-type specific fashion.

2021-03-04 | GSE153254 | GEO

Expression profiling of long noncoding RNAs and mRNAs in uterine leiomyoma

Project description:Global protein coding gene and miRNA expression profiling studies in uterine leiomyoma showed their aberrant expression and involvement in the pathogenesis of uterine leiomyoma. But the global expression patterns and potential clinical value of long noncoding RNA (lncRNA) in uterine leiomyoma have not been explored.In this study, we performed lncRNA expression profiles analysis of uterine leiomyoma using microarray(Arraystar Human LncRNA Array v2.0) to evaluate the genome-wide expression of lncRNAs and mRNAs and their potential role in the pathogenesis of uterine leiomyoma.

2014-08-14 | GSE52618 | GEO

Multi-omics analysis of MEN1 missense mutations identifies disruption of menin-MLL and menin-JunD interactions as critical requirements for molecular pathogenicity

Project description:Loss-of-function mutations of the multiple endocrine neoplasia type 1 (MEN1) gene are causal to the MEN1 tumor syndrome, but they are also commonly found in sporadic pancreatic neuroendocrine tumors and other types of cancers. The MEN1 gene product, menin, is involved in transcriptional and chromatin regulation, most prominently as an integral component of KMT2A/MLL1 and KMT2B/MLL2 containing COMPASS-like histone H3K4 methyltransferase complexes. In a mutually exclusive fashion, menin also interacts with the JunD subunit of the AP-1 and ATF/CREB transcription factors. After in silico screening of 253 disease-related MEN1 missense mutations, we selected a set of nine menin mutations in surface-exposed residues. The protein interactomes of these mutants were assessed by quantitative mass spectrometry, which indicated that seven of the nine mutants disrupt interactions with both MLL1/2 and JunD complexes in the nucleus. We identified three missense mutations, R52G, E255K and E359K, which display predominant reduction in interaction with MLL1 compared to JunD. This observation was supported by a pronounced loss of binding of the R52G, E255K and E359K mutant proteins at unique MLL1 genomic binding sites with less effect on unique JunD sites. These findings support the general importance of the menin-MLL1 and menin-JunD interactions in MEN1 gene-associated pathogenic conditions.

2022-10-14 | PXD031928 | Pride

3-AP and Gemcitabine in Treating Patients With Advanced Solid Tumors or Lymphoma

Project description:This phase I trial is studying the best dose of 3-AP and the side effects of giving 3-AP together with gemcitabine in treating patients with advanced solid tumors or lymphoma. Drugs used in chemotherapy, such as 3-AP and gemcitabine (GEM), work in different ways to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. 3-AP may help gemcitabine kill more cancer cells by making the cells more sensitive to the drug. 3-AP may also stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

| 2026481 | ecrin-mdr-crc

Role of AP-2a/AP-2b transcription factors in the adult epidermis.

Project description:To investigate the effects of inactivation of the transcription factors AP-2a and/or AP-2b in the adult mouse skin.

2023-12-20 | GSE248372 | GEO

Expression profiling of long noncoding RNAs and mRNAs in uterine leiomyoma

2014-08-14 | E-GEOD-52618 | biostudies-arrayexpress

Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer (ChIP-Seq)

Project description:Analysis of genes regulated by RU486 (an progesterone antagonist) in human breast cancer T47D cells and human uterine leiomyoma smooth muscle cells. The hypothesis is that RU486 inhibits tumor growth by inactivating the transcription of multiple genes which trigger critical signaling pathways to induce tumorigenesis in both breast caner and uterine leomyoma. Tissue-specific and common patterns of gene regulation may determine the therapeutic effects of antiprogestins in uterine leiomyoma and breast cancer. We applied ChIP-seq to identify PR-interaction sites in T47D breast cancer cells and primary uterine leiomyoma cells treated with RU486.

2012-09-11 | E-GEOD-40724 | biostudies-arrayexpress

Quantitative analysis of AP-1 dependent gene expression in CRISPR/Cas9 negative control and AP-1 depleted human uterine smooth muscle cells (HUtSMCs).

Project description:Quantitative analysis of AP-1 dependent gene expression in CRISPR/Cas9 negative control and AP-1 depleted human uterine smooth muscle cells (HUtSMCs).

| PRJNA580366 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data