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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE139582 | GEO | 2020/01/01

REPOSITORIES: GEO

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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: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.

2020-01-01 | GSE139581 | 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:Genome-wide map of H3K27Ac chromatin state in CRISPR/Cas9 negative control and AP-1 depleted human uterine smooth muscle cells (HUtSMCs).

| PRJNA580365 | ENA

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).

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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

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

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.

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AP-1 family members act at DNA targets in conjunction with Sox9 to promote chondrocyte hypertrophy

Project description:A comprehensive analysis of Sox9 binding profiles in developing chondrocytes identified marked enrichment of an AP-1-like motif (Ohba et al. 2015). Here, we have explored the functional interplay between Sox9 and AP-1 in mammalian chondrocyte development. Among AP-1 family members, Jun and Fosl2 were highly expressed within prehypertrophic and early hypertrophic chondrocytes. Chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) showed a striking overlap in Jun- and Sox9-bound regions throughout the chondrocyte genome, a reflection of direct binding of each factor to target motifs in shared enhancers, and physical interactions of AP-1 with Sox9. In vitro expression analysis indicates that direct co-binding of Sox9 and AP-1 at target motifs enhanced target gene expression, while protein-protein interactions suppressed AP-1- and Sox9-driven transcription. Analysis of prehypertrophic chondrocyte removal of Sox9 demonstrated Sox9 was essential for hypertrophic chondrocyte development, while in vitro and ex vivo analyses showed AP-1 promotes chondrocyte hypertrophy. Sox9 and Jun co-bound and co-activated a Col10a1 enhancer in Sox9 and AP-1 motif-dependent manners consistent with their combined action promoting hypertrophic gene expression. Together, the data support a model where AP-1-family members promote Sox9-action in the transition of chondrocytes to a terminal hypertrophic program. Intersection of ChIP-seq data from Sox9 and AP-1 factor Jun, RNA-seq data from developing rib chondrocytes and Col10a1mCherry positive hypertrophic chondrocytes in neonatal mice to uncover regulation of Sox9 by AP-1 factors during chondrocyte hypertrophy.

2016-02-29 | E-GEOD-73372 | biostudies-arrayexpress

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

Generation of a new mouse model of glaucoma characterized by reduced expression of the AP-2 and AP-2

Project description:This study reports on the generation of a transgenic mouse which is characterized by early-onset angle-closure glaucoma. The phenotype is due to the transgene insertion site which is proximal to the genes encoding AP-2 and AP-2, two proteins present in the retina and corneal epithelium. This leads to a reduction in AP-2 levels, which is likely to are responsible for the glaucomatous phenotype. Here we provide paired-end raw DNA-Seq reads of the transgenic mouse genome.

2017-03-10 | E-MTAB-5502 | biostudies-arrayexpress

Insights into the invasiveness of triple negative breast cancer from genome-wide profiling of transcription factor AP-1 (expression)

Project description:Triple negative breast cancer (TNBC) is an aggressive clinical phenotype, and accounts for 15% to 20% of all breast cancers. The molecular determinants of malignant cell behaviors in TNBC remain largely unknown. We find that the AP-1 transcription factor component, Fra-1, is overexpressed in basal-like breast tumors, and its expression level has high prognostic significance. Depletion of Fra-1 or its heterodimeric partner c-Jun inhibits the proliferative and invasive phenotypes in TNBC cells. To gain insights into the transcriptional regulatory networks of AP-1 in TNBC cells, we combine genome-wide ChIP-seq with loss-of-function transcriptome analyses. We observe dysregulation of direct targets of the Fra-1/c-Jun heterodimer involved in cell proliferation, cell adhesion, and cell-cell contact. Intriguingly, we find that AP-1 mediates downregulation of E-cadherin through direct transcriptional induction of ZEB2. This work sheds light on the mechanisms and pathways by which TNBC acquires invasiveness and proliferative propensity. BT549 cells grown in complete medium were transfected with a control siRNA, siRNA targeting Fra-1 or siRNA targeting c-Jun for 72 h, and then global gene expression profiles were assessed. Three or four biological replicates were used for each group.

2014-06-30 | E-GEOD-46440 | biostudies-arrayexpress

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