Genome wide expression analysis in AtT-20 cells following Dnmt1 knockdown
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE10552 | GEO | 2008/12/31
SECONDARY ACCESSION(S): PRJNA107919
REPOSITORIES: GEO
Similar Datasets
Project description:Efficient and sustained knockdown of DNMT1 transcript and protein was achieved using a consecutive transfection protocol in the mouse pituitary adenoma cell line, AtT-20. Genome wide microarray analysis identified 91 transcripts that were significantly differentially expressed relative to cells treated with a non-targeting control. Keywords: Differential expression AtT-20 cells were repeatedly treated with 20 nM siRNA (siDNMT1 or siNT) over an eight day period. After eight days total RNA was extracted and prepared for microarray analysis. The procedure was repeated three times independently.
2008-12-30 | E-GEOD-10552 | biostudies-arrayexpress
Project description:As the Crh-system and the HPA-axis are known to be crucially involved in the onset, development and maintainance of psychiatric disorders like anxiety and depression and regulate the behavioural and endocrine stress responses the further analysis of Crhr1-dependent signaling cascades is essential to understand the molecular mechanisms behind these psychiatric diseases. In this project, new candidate genes involved in Crhr1-dependent signaling cascades were dissected in the cell line model of AtT-20 cells by transcriptional profiling of mouse pituitary corticotroph cells comparing control untreated AtT-20 cells with AtT-20 cells treated with 100 nM Crh at 1, 3, 6, 12 and 24 hours. Keywords: time course, treatment response
2009-01-31 | GSE13156 | GEO
Project description:While the hypothalamo-pituitary-adrenal axis (HPA) activates a general stress response by increasing glucocorticoid (Gc) synthesis, biological stress resulting from infections triggers the inflammatory response through production of cytokines. The pituitary gland integrates some of these signals by responding to the pro-inflammatory cytokines IL6 and LIF and to a negative Gc feedback loop. The present work used whole-genome approaches to define the LIF/STAT3 regulatory network and to delineate cross-talk between this pathway and Gc action. Genome-wide ChIP-chip identified 3 449 STAT3 binding sites, whereas 2 396 genes regulated by LIF and/or Gc were found by expression profiling. Surprisingly, LIF on its own changed expression of only 85 genes but the joint action of LIF and Gc potentiated the expression of more than a thousand genes. Accordingly, activation of both LIF and Gc pathways also potentiated STAT3 and GR recruitment to many STAT3 targets. Our analyses revealed an unexpected gene cluster that requires both stimuli for delayed activation: 83% of the genes in this cluster are involved in different cell defense mechanisms. Thus, stressors that trigger both general stress and inflammatory responses lead to activation of a stereotypic innate cellular defense response. Experiment Overall Design: 1) Pituitary corticotrophs cell line (AtT-20) response to glucocorticoids and LIF: Experiment Overall Design: AtT-20 cells mRNA extracted after treatment with PBS as control, LIF for 18h, Dex+LIF for 3h and Dex+LIF for 18h. Each treatment were made in duplicate. [GSM471246-GSM471253] Experiment Overall Design: 2) Pituitary corticotrophs cell line (AtT-20) response to LIF after 3h treatment: Experiment Overall Design: AtT-20 cells mRNA extracted after treatment with PBS as control or LIF for 3h. Each treatment were made in duplicate. [GSM471254-GSM471257] Experiment Overall Design: 3) Pituitary corticotrophs cell line (AtT-20) response to Dex after 3h treatment: Experiment Overall Design: AtT-20 cells mRNA extracted after treatment with PBS as control or Dex for 3h. Each treatment were made in duplicate. [GSM471258-GSM471261] Experiment Overall Design: 4) Pituitary corticotrophs cell line (AtT-20) response to Dex after 18h treatment: Experiment Overall Design: AtT-20 cells mRNA extracted after treatment with PBS as control or Dex for 18h. Each treatment were made in duplicate. [GSM471262-GSM471269]
2009-11-23 | E-GEOD-19042 | biostudies-arrayexpress
Project description:As the Crh-system and the HPA-axis are known to be crucially involved in the onset, development and maintainance of psychiatric disorders like anxiety and depression and regulate the behavioural and endocrine stress responses the further analysis of Crhr1-dependent signaling cascades is essential to understand the molecular mechanisms behind these psychiatric diseases. In this project, new candidate genes involved in Crhr1-dependent signaling cascades were dissected in the cell line model of AtT-20 cells by transcriptional profiling of mouse pituitary corticotroph cells comparing control untreated AtT-20 cells with AtT-20 cells treated with 100 nM Crh at 1, 3, 6, 12 and 24 hours. Keywords: time course, treatment response Two condition experiment: untreated vs. 100 nM Crh treated AtT-20 cells with a time curve of 1, 3, 6, 12, 24 hours. Technical replicates: 6 for each time point, including dye-swap each with 3 replicates
2010-05-06 | E-GEOD-13156 | biostudies-arrayexpress
Project description:Deployment of a cell-specifying enhancer repertoire by the pioneer factor Pax7 The establishment and maintenance of cell identity depends on implementation of stable cell-specific chromatin landscapes. Pioneer transcription factors establish new cell fate competences by triggering chromatin remodeling during development. Here, we used pituitary cell specification to define the salient features of pioneer action. Comparison of purified pituitary cells of different lineages showed that chromatin accessibility differs at enhancers rather than promoters. The pioneer factor Pax7 specifies one pituitary lineage identity by opening a specific repertoire of enhancers that are distinct from the myogenic targets of Pax7. Pax7 binds its pioneer targets rapidly and days before chromatin remodeling and gene activation. Finally, enhancers opened by Pax7-dependent chromatin remodeling exhibit loss of DNA methylation and they acquire long term epigenetic memory. The present work identifies enhancer pioneering as a critical feature for cell fate specification and maintenance.
2018-01-24 | GSE87178 | GEO
Project description:Deployment of a cell-specifying enhancer repertoire by the pioneer factor Pax7 The establishment and maintenance of cell identity depends on implementation of stable cell-specific chromatin landscapes. Pioneer transcription factors establish new cell fate competences by triggering chromatin remodeling during development. Here, we used pituitary cell specification to define the salient features of pioneer action. Comparison of purified pituitary cells of different lineages showed that chromatin accessibility differs at enhancers rather than promoters. The pioneer factor Pax7 specifies one pituitary lineage identity by opening a specific repertoire of enhancers that are distinct from the myogenic targets of Pax7. Pax7 binds its pioneer targets rapidly and days before chromatin remodeling and gene activation. Finally, enhancers opened by Pax7-dependent chromatin remodeling exhibit loss of DNA methylation and they acquire long term epigenetic memory. The present work identifies enhancer pioneering as a critical feature for cell fate specification and maintenance.
2018-01-24 | GSE87181 | GEO
Project description:Deployment of a cell-specifying enhancer repertoire by the pioneer factor Pax7 The establishment and maintenance of cell identity depends on implementation of stable cell-specific chromatin landscapes. Pioneer transcription factors establish new cell fate competences by triggering chromatin remodeling during development. Here, we used pituitary cell specification to define the salient features of pioneer action. Comparison of purified pituitary cells of different lineages showed that chromatin accessibility differs at enhancers rather than promoters. The pioneer factor Pax7 specifies one pituitary lineage identity by opening a specific repertoire of enhancers that are distinct from the myogenic targets of Pax7. Pax7 binds its pioneer targets rapidly and days before chromatin remodeling and gene activation. Finally, enhancers opened by Pax7-dependent chromatin remodeling exhibit loss of DNA methylation and they acquire long term epigenetic memory. The present work identifies enhancer pioneering as a critical feature for cell fate specification and maintenance.
2018-01-24 | GSE87180 | GEO
Project description:Deployment of a cell-specifying enhancer repertoire by the pioneer factor Pax7 The establishment and maintenance of cell identity depends on implementation of stable cell-specific chromatin landscapes. Pioneer transcription factors establish new cell fate competences by triggering chromatin remodeling during development. Here, we used pituitary cell specification to define the salient features of pioneer action. Comparison of purified pituitary cells of different lineages showed that chromatin accessibility differs at enhancers rather than promoters. The pioneer factor Pax7 specifies one pituitary lineage identity by opening a specific repertoire of enhancers that are distinct from the myogenic targets of Pax7. Pax7 binds its pioneer targets rapidly and days before chromatin remodeling and gene activation. Finally, enhancers opened by Pax7-dependent chromatin remodeling exhibit loss of DNA methylation and they acquire long term epigenetic memory. The present work identifies enhancer pioneering as a critical feature for cell fate specification and maintenance.
2018-01-24 | GSE87184 | GEO
Project description:To identify the target genes of Dnmt1 in skeletal muscle satellite cells, we generated satellite cell specific Dnmt1 KO using Pax7-CreERT2 and Dnmt1 flox mice. After Tamoxifen (cKO) or vehicle (Control) treatment for 5 consecutive days, mice were euthanized and muscle satellite cells were collected by FACS sorting and total RNA were extracted.
2021-01-08 | GSE156978 | GEO
Project description:While the hypothalamo-pituitary-adrenal axis (HPA) activates a general stress response by increasing glucocorticoid (Gc) synthesis, biological stress resulting from infections triggers the inflammatory response through production of cytokines. The pituitary gland integrates some of these signals by responding to the pro-inflammatory cytokines IL6 and LIF and to a negative Gc feedback loop. The present work used whole-genome approaches to define the LIF/STAT3 regulatory network and to delineate cross-talk between this pathway and Gc action. Genome-wide ChIP-chip identified 3 449 STAT3 binding sites, whereas 2 396 genes regulated by LIF and/or Gc were found by expression profiling. Surprisingly, LIF on its own changed expression of only 85 genes but the joint action of LIF and Gc potentiated the expression of more than a thousand genes. Accordingly, activation of both LIF and Gc pathways also potentiated STAT3 and GR recruitment to many STAT3 targets. Our analyses revealed an unexpected gene cluster that requires both stimuli for delayed activation: 83% of the genes in this cluster are involved in different cell defense mechanisms. Thus, stressors that trigger both general stress and inflammatory responses lead to activation of a stereotypic innate cellular defense response.
2009-11-16 | GSE19042 | GEO