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accession-icon GSE109112
Multi-brain-region transcriptional organization linking sleep and affective functions
  • organism-icon Mus musculus
  • sample-icon 380 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Sleep and affective behaviors are highly interrelated phenotypes, commonly altered in a variety of neuropsychiatric diseases, including major depressive disorder (MDD). To understand the transcriptomic organization underlying sleep and affective function, we studied a population of (C57BL/6J x 129S1/SvImJ) F2 mice by measuring 283 affective and sleep phenotypes and profiling gene expression across four brain regions, including the frontal cortex, hippocampus, thalamus, and hypothalamus. We identified converging molecular bases for sleep and affective phenotypes at both the single-gene and gene-network levels. Utilizing publicly available transcriptomic datasets collected from sleep-deprived mice and major depressive disorder (MDD) patients, we identified three cortical gene networks altered by sleep/wake changes and depression. The network-level actions of sleep loss and depression were opposite to each other, providing a mechanistic basis for the sleep disruptions commonly observed in depression as well as the reported acute antidepressant effects of sleep deprivation. We highlight one particular network composed of circadian rhythm regulators and neuronal activity-dependent immediate-early genes. The key upstream driver of this network, Arc, may act as a nexus linking sleep and depression. Our data provide mechanistic insights into the role of sleep in affective function and MDD.

Publication Title

Cross-species systems analysis identifies gene networks differentially altered by sleep loss and depression.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP192714
RNA-seq transcript and gene data on zika exposed and zika naïve samples
  • organism-icon Homo sapiens
  • sample-icon 1021 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

RNA-seq count data at 3 timepoints was generated for Zika-exposed and Zika-naïve individuals in order to assess associated signatures Overall design: RNA-seq count data at 3 timepoints was generated for Zika-exposed and Zika-naïve individuals, extracted from PAXgene RNA blood solution with the PAXgene Blood RNA Kit using DNase digestion and an additional clean-up using RNEasy MinElute kit.

Publication Title

Comprehensive Immunoprofiling of Pediatric Zika Reveals Key Role for Monocytes in the Acute Phase and No Effect of Prior Dengue Virus Infection.

Sample Metadata Fields

Sex, Age, Subject, Time

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accession-icon SRP069789
Distinct and shared functions of ALS-associated TDP-43, FUS, and TAF15 revealed by comprehensive multi-system integrative analyses [RNA-Seq_Stability]
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

TDP-43, FUS, and TAF15 are implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. We integrate CLIP-seq and RNA Bind-N-Seq technologies to discover that TAF15 binds to ~4,900 RNAs enriched for GGUA motifs. In the mouse brain, TAF15 and FUS, but not TDP-43, exhibit strikingly similar RNA binding profiles, yet they alter the expression of distinct mRNA populations upon their individual depletions. TAF15 has a minimal role in alternative splicing and instead affects RNA turnover, consistent with an enrichment of TAF15 binding sites in 3’ untranslated regions. In human stem cell-derived motor neurons, loss of both TAF15 and FUS affected mRNAs distinct from those altered by loss of either protein alone, revealing redundant roles for TAF15 and FUS in maintaining mRNA levels. Furthermore, concomitant rather than individual depletion of TAF15 and FUS more closely resembles RNA profiles of motor neurons derived from FUS R521G ALS patients or from late-stage, sporadic ALS patients. Our study reveals convergent and divergent mechanisms by which FUS, TAF15 and TDP-43 affects RNA metabolism in neurological disease. Overall design: RNA-seq, CLIP-seq and arrays in mouse and human against TAF15 knockdowns This Series represents RNA-seq sample(s).

Publication Title

Distinct and shared functions of ALS-associated proteins TDP-43, FUS and TAF15 revealed by multisystem analyses.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP069787
Distinct and shared functions of ALS-associated TDP-43, FUS, and TAF15 revealed by comprehensive multi-system integrative analyses [RNA-Seq_human]
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

TDP-43, FUS, and TAF15 are implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. We integrate CLIP-seq and RNA Bind-N-Seq technologies to discover that TAF15 binds to ~4,900 RNAs enriched for GGUA motifs. In the mouse brain, TAF15 and FUS, but not TDP-43, exhibit strikingly similar RNA binding profiles, yet they alter the expression of distinct mRNA populations upon their individual depletions. TAF15 has a minimal role in alternative splicing and instead affects RNA turnover, consistent with an enrichment of TAF15 binding sites in 3’ untranslated regions. In human stem cell-derived motor neurons, loss of both TAF15 and FUS affected mRNAs distinct from those altered by loss of either protein alone, revealing redundant roles for TAF15 and FUS in maintaining mRNA levels. Furthermore, concomitant rather than individual depletion of TAF15 and FUS more closely resembles RNA profiles of motor neurons derived from FUS R521G ALS patients or from late-stage, sporadic ALS patients. Our study reveals convergent and divergent mechanisms by which FUS, TAF15 and TDP-43 affects RNA metabolism in neurological disease. Overall design: RNA-seq, CLIP-seq and arrays in mouse and human against TAF15 knockdowns This Series represents RNA-seq sample(s).

Publication Title

Distinct and shared functions of ALS-associated proteins TDP-43, FUS and TAF15 revealed by multisystem analyses.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP069788
Distinct and shared functions of ALS-associated TDP-43, FUS, and TAF15 revealed by comprehensive multi-system integrative analyses [RNA-Seq_mouse]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

TDP-43, FUS, and TAF15 are implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. We integrate CLIP-seq and RNA Bind-N-Seq technologies to discover that TAF15 binds to ~4,900 RNAs enriched for GGUA motifs. In the mouse brain, TAF15 and FUS, but not TDP-43, exhibit strikingly similar RNA binding profiles, yet they alter the expression of distinct mRNA populations upon their individual depletions. TAF15 has a minimal role in alternative splicing and instead affects RNA turnover, consistent with an enrichment of TAF15 binding sites in 3’ untranslated regions. In human stem cell-derived motor neurons, loss of both TAF15 and FUS affected mRNAs distinct from those altered by loss of either protein alone, revealing redundant roles for TAF15 and FUS in maintaining mRNA levels. Furthermore, concomitant rather than individual depletion of TAF15 and FUS more closely resembles RNA profiles of motor neurons derived from FUS R521G ALS patients or from late-stage, sporadic ALS patients. Our study reveals convergent and divergent mechanisms by which FUS, TAF15 and TDP-43 affects RNA metabolism in neurological disease. Overall design: RNA-seq, CLIP-seq and arrays in mouse and human against TAF15 knockdowns This Series represents RNA-seq sample(s).

Publication Title

Distinct and shared functions of ALS-associated proteins TDP-43, FUS and TAF15 revealed by multisystem analyses.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE100833
A functional genomics predictive network model identifies regulators of inflammatory bowel disease: Microarray Analysis of Human Blood and Intestinal Biopsy Samples from a Phase 2b, Double-blind, Placebo-controlled Study of Ustekinumab in Crohn's Disease
  • organism-icon Homo sapiens
  • sample-icon 477 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Microarray Analysis of Human Whole Blood and Intestinal Biopsy Samples from a Phase 2b, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group Study of Ustekinumab in Crohns Disease

Publication Title

A functional genomics predictive network model identifies regulators of inflammatory bowel disease.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Treatment

View Samples
accession-icon SRP077046
A functional genomics predictive network model identifies regulators of inflammatory bowel disease: Mount Sinai Hospital (MSH) Population Specimen Collection and Profiling of Inflammatory Bowel Disease
  • organism-icon Homo sapiens
  • sample-icon 125 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

This study focuses on inflammatory bowel disease gene expression profiling. Surgical specimens from 134 patients undergoing bowel resection for inflammatory bowel disease (IBD) and non IBD controls at Mount Sinai Medical Center were collected as the source of tissue. Control samples (CLs) were harvested from normal non inflamed bowel located more than 10 cm away from the tumor from patients undergoing bowel resection for sporadic colon cancer. Ulcerative colitis (UC) and Crohn’s (CD) patient samples were all isolated from areas containing moderate to severe inflammation. The diagnostic pathology report for each specimen was provided by the Mount Sinai Hospital Pathology Department. Patients with UC and patients with CD shared common medications including corticosteroids, infliximab, azathioprine, and mesalamine. Overall design: Surgical specimens from 134 patients undergoing bowel resection for inflammatory bowel disease (IBD) and non IBD controls at Mount Sinai Medical Center were collected as the source of tissue. Control samples (CLs) were harvested from normal non inflamed bowel located more than 10 cm away from the tumor from patients undergoing bowel resection for sporadic colon cancer. Ulcerative colitis (UC) and Crohn’s (CD) patient samples were all isolated from areas containing moderate to severe inflammation. The diagnostic pathology report for each specimen was provided by the Mount Sinai Hospital Pathology Department. Patients with UC and patients with CD shared common medications including corticosteroids, infliximab, azathioprine, and mesalamine. The samples were collected fresh and the tissue was further processed for isolation. A representative 0.5 cm tissue fragment was isolated from the collected surgical specimen samples, flash frozen and stored at -80C. Tissue was homogenized in Trizol following the manufacturer''s protocol (Life Technologies) and RNA extraction was performed. RIN scores >7 were used for Poly A RNA-seq.

Publication Title

A functional genomics predictive network model identifies regulators of inflammatory bowel disease.

Sample Metadata Fields

Sex, Subject

View Samples
accession-icon GSE11322
Attenuated upregulation of GABAergic markers in response to BDNF in neurons lacking Xbp1
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

XBP1 is a transcription factor that is induced by unconventional splicing associated with endoplasmic reticulum stress and plays a role in development of liver and plasma cells. We previously reported that brain derived neurotrophic factor (BDNF) leads to splicing of XBP1 mRNA in neurites, and that XBP1 is required for BDNF-induced neurite extension and branching. To search for the molecular mechanisms of how XBP1 plays a role in neural development, comprehensive gene expression analysis was performed in primary telencephalic neurons obtained from Xbp1 knockout mice at embryonic day 12.5. By searching for the genes induced by BDNF in wild type neurons but this induction was reduced in Xbp1 knockout mice, we found that upregulation of three GABAergic markers, somatostatin (Sst), neuropeptide Y (Npy), and calbindin (Calb1), were compromised in Xbp1 knockout neurons. Attenuated induction of Npy and Calb1 was confirmed by quantitative RT-PCR. In neurons lacking in Xbp1, upregulation of GABAergic markers was attenuated. Impaired BDNF-induced neurite extension in Xbp1 knockout neurons might be mediated by disturbed BDNF-induced differentiation of GABAergic interneurons.

Publication Title

Attenuated BDNF-induced upregulation of GABAergic markers in neurons lacking Xbp1.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE64468
Molecular mechanism of flocculation self-recognition in yeast and its role in mating and survival
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Saccharomyces cerevisiae flocculation occurs when fermentable sugars are limiting and is therefore considered as a way to enhance the survival chance of Flo-expressing yeast cells. In this paper, the role of Flo1p in mating was demonstrated by showing that the mating efficiency, which contributes to the increased survival rate as well by generating genetic variability, is increased when cells flocculate. This was revealed by liquid growth experiments in a low shear environment and differential transcriptome analysis of FLO1 expressing cells compared to the non-flocculent wild-type cells. The results show that a floc provides a uniquely organized multicellular ultrastructure that provides a suitable microenvironment to induce and perform cell conjugation.

Publication Title

Molecular mechanism of flocculation self-recognition in yeast and its role in mating and survival.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE39857
The RALA pathway can maintain the proliferation of KRAS- and BRAF-mutated cancer cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

By silencing of RALA, a downstream member of the RAS signal transduction pathway, we aimed to determine whether genes downstream of a mutated KRAS (codon 12 or 13) or a mutated BRAF can have significant functions in colorectal cancer carcinogenesis.

Publication Title

Effects of RAL signal transduction in KRAS- and BRAF-mutated cells and prognostic potential of the RAL signature in colorectal cancer.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
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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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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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