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accession-icon GSE39233
Placental PPARg-Regulated Genes
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Robust identification of placental PPARg target genes via mutliple PPARg-dependence criteria.

Publication Title

Placental PPARγ regulates spatiotemporally diverse genes and a unique metabolic network.

Sample Metadata Fields

Specimen part

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accession-icon GSE24817
Regulation of early folliculogenesis by Sohlh1 and Sohlh2 in mouse ovary
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE21525
Expression data from testis of day-7 Sohlh1 knock-out mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Sohlh1 and Sohlh2 encode a germ cell-specific basic helix-loop-helix transcriptional regulator critical in spermatogonial differentiation. Seven-day-old Sohlh1 or Sohlh2 knockout and wild-type testes were arrayed on the Affy 430 2.0 platform.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE24816
Transcriptional changes in Sohlh1 knockout and Sohlh2 knockout mouse newborn ovaries
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Sohlh1 and Sohlh2 are germ cell-specific basic helix-loop-helix transcription factors critical in early folliculogenesis. We discovered that Sohlh1 and Sohlh2 knockout females lose oocytes after birth and few remains by postnatal day 14. Here, we show that many genes preferentially expressed in the oocytes are misregulated by Sohlh1 and/or Sohlh2 deficiency.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE24815
Transcriptional changes in Sohlh1/Sohlh2 double knockout newborn mouse ovaries
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Sohlh1 and Sohlh2 are germ cell-specific basic helix-loop-helix transcription factors critical in early folliculogenesis. Differential genes expression by both Sohlh1 and Sohlh2 deficiency in mouse newborn ovaries was accessed using microarray. RNA samples from Sohlh1/ Sohlh2 double knockout and wild-type newborn ovaries were arrayed on the Illumina beadchip mouse WG-6 2.0.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE72688
RNA expression in MDA-MB-231 cells treated for 24h with SAHA, Pargyline, or both [HG-U133A_2]
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Abnormal activities of histone lysine demethylases (KDMs) and lysine deacetylases (HDACs) are associated with aberrant gene expression in breast cancer development. However, the precise molecular mechanisms underlying the crosstalk between KDMs and HDACs in chromatin remodeling and regulation of gene transcription are still elusive. In this study, we showed that treatment of human breast cancer cells with inhibitors targeting the zinc cofactor dependent class I/II HDACs, but not NAD+ dependent class III HDACs, led to significant increase of H3K4me2 which is a specific substrate of histone lysine-specific demethylase 1 (LSD1) and a key chromatin mark promoting transcriptional activation. We also demonstrated that inhibition of LSD1 activity by a pharmacological inhibitor, pargyline, or siRNA resulted in increased acetylation of H3K9 (AcH3K9). However, siRNA knockdown of LSD2, a homolog of LSD1, failed to alter the level of AcH3K9, suggesting that LSD2 activity may not be functionally connected with HDAC activity. Combined treatment with LSD1 and HDAC inhibitors resulted in enhanced levels of H3K4me2 and AcH3K9, and exhibited synergistic growth inhibition of breast cancer cells. Finally, microarray screening identified a unique subset of genes whose expression was significantly changed by combination treatment with inhibitors of LSD1 and HDAC. Our study suggests that LSD1 intimately interacts with histone deacetylases in human breast cancer cells. Inhibition of histone demethylation and deacetylation exhibits cooperation and synergy in regulating gene expression and growth inhibition, and may represent a promising and novel approach for epigenetic therapy of breast cancer.

Publication Title

Inhibitors of histone demethylation and histone deacetylation cooperate in regulating gene expression and inhibiting growth in human breast cancer cells.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE72687
RNA expression in MDA-MB-231 cells transfected with scramble, LSD1 or HDAC5 shRNA (HG-U133A_2)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

We performed gene expression microarray to examine the potential effect that depletion of HDAC5 (an important HDAC isozyme) or LSD1 (an FAD-dependent histone lysine demethylase) has on the triple-negative breast cancer transcriptome.

Publication Title

HDAC5-LSD1 axis regulates antineoplastic effect of natural HDAC inhibitor sulforaphane in human breast cancer cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE108714
RNA expression in MDA-MB-231 cells with stable knockdown or overexpression of LSD2 (KDM1B).
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Abnormal activities of histone lysine demethylases (KDMs) are associated with aberrant gene expression in breast cancer development. However, the precise molecular mechanisms in chromatin remodeling and regulation of gene transcription are still elusive. In this study, we performed Gene Expression Microarray (HG-U133A_2) using RNA from the aggressive breast cancer cell line MDA-MB-231 expressing stable knockdown or overexpression of LSD2. The goal of this study is to identify genes and pathways differentially expressed in triple negative breast cancer cells with genetically modified LSD2 expression.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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accession-icon GSE71620
The effects of aging on circadian patterns of gene expression in the human prefrontal cortex
  • organism-icon Homo sapiens
  • sample-icon 419 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

With aging, significant changes in circadian rhythms occur, including a shift in phase toward a morning chronotype and a loss of rhythmicity in circulating hormones. However, the effects of aging on molecular rhythms in the human brain have remained elusive. Here we employed a previously-described time-of-death analyses to identify transcripts throughout the genome that have a significant circadian rhythm in expression in the human prefrontal cortex (Brodmanns areas (BA) 11 and 47). Expression levels were determined by microarray analysis in 146 individuals. Rhythmicity in expression was found in ~10% of detected transcripts (p<0.05). Using a meta-analysis across the two brain areas, we identified a core set of 235 genes (q<0.05) with significant circadian rhythms of expression. These 235 genes showed 92% concordance in the phase of expression between the two areas. In addition to the canonical core circadian genes, a number of other genes were found to exhibit rhythmic expression in the brain. Notably, we identified more than one thousand genes (1186 in BA11; 1591 in BA47) that exhibited age-dependent rhythmicity or alterations in rhythmicity patterns with aging. Interestingly, a set of transcripts gained rhythmicity in older individuals, which may represent a compensatory mechanism due to a loss of canonical clock function. Thus, we confirm that rhythmic gene expression can be reliably measured in human brain and identified for the first time significant changes in molecular rhythms with aging that may contribute to altered cognition, sleep and mood in later life.

Publication Title

Effects of aging on circadian patterns of gene expression in the human prefrontal cortex.

Sample Metadata Fields

Sex, Age, Specimen part, Race

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accession-icon GSE87610
Gene expression of L3 and L5 pyramidal neurons in the DLPFC comparing schizophrenia from bipolar major depressive disorders and unaffected subjects.
  • organism-icon Homo sapiens
  • sample-icon 286 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Impairments in certain cognitive processes (e.g., working memory) are typically most pronounced in schizophrenia (SZ), intermediate in bipolar disorder (BP) and least in major depressive disorder (MDD).

Publication Title

Transcriptome Alterations in Prefrontal Pyramidal Cells Distinguish Schizophrenia From Bipolar and Major Depressive Disorders.

Sample Metadata Fields

Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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