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accession-icon SRP071973
Integrated transcriptional analysis unveils the dynamics of cellular differentiation in the developing mouse hippocampus
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The ability to assign expression patterns to individual cell types that constitute a tissue is a major challenge in RNA expression analysis. This especially applies to brain given the plethora of different cells coexisting in that tissue. Here, we derived cell-type specific transcriptome signatures from existing single cell RNA data and integrated these signatures with a newly generated dataset of expression (bulk RNA-seq) of the postnatal developing hippocampus. This integrated analysis allowed us to provide a comprehensive and unbiased prediction of the differentiation drivers for 10 different hippocampal cell types and describe how the different cell types interact to support crucial developmental stages. Our integrated analysis provides a reliable resource of predicted differentiation drivers and insight into the multifaceted aspects of the cells in hippocampus during development. Overall design: 21 RNA-seq samples. For the stages E15, P1, P7, P15, and P30, there are respectively 3, 4, 3, 3, and 6 RNA-seq biological replica (total 19). One RNA-seq sample has two technical replica.

Publication Title

Integrated transcriptional analysis unveils the dynamics of cellular differentiation in the developing mouse hippocampus.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE66468
Opposite phenotypic effects and genetic dosage in mouse models of 16p11.2 deletion and duplication syndromes
  • organism-icon Mus musculus
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

The 16p11.2 deletion and duplication syndromes have been associated with developmental delay and autism spectrum disorders, and a reciprocal effect on body mass index. Here we explored these links with new engineered mouse models carrying a deletion (Del/+) and duplication (Dup/+) of the whole 16p11.2 homologous Sult1a1-Spn region. On a pure genetic background, compared to wild-types, Del/+ mice carrying the deletion showed weight and adipogenesis deficits, hyperactivity, repetitive behaviors, and recognition memory deficits, whereas Dup/+ mice showed the opposite phenotypes and Del/Dup individuals displayed no changes. Alterations in social interaction were also observed in Del/+ and Dup/+ animals on a mixed genetic background.

Publication Title

Reciprocal Effects on Neurocognitive and Metabolic Phenotypes in Mouse Models of 16p11.2 Deletion and Duplication Syndromes.

Sample Metadata Fields

Sex, Specimen part

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accession-icon E-MEXP-1597
Transcription profiling by array of mouse FLA2 cells (high frequency of leukemia stem cells) and FLB1 cells (low frequency of leukemia stem cells)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Expression profile of FLA2 (highest LSC frequency) and FLB1 (lowest LSC frequency) leukemias.

Publication Title

A role for GPx3 in activity of normal and leukemia stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE84015
UTX controls lineage-specific epigenetic program of iNKT cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

iNKT cells are innate-like lymphocytes that protect against infection, autoimmune disease, and cancer. However, little is known about epigenetic regulation of iNKT cell development. Here, we show that the H3K27me3 histone demethylase UTX is an essential cell-intrinsic factor that controls an iNKT lineage specific gene expression program and epigenetic landscape in a demethylase activity dependent manner. UTX deficient iNKT cells exhibit impaired expression of iNKT signature genes due to a decrease in activation-associated H3K4me3 and an increase in repressive H3K27me3 marks within the promoters that UTX occupies. Notably, we identified JunB as a novel regulator of iNKT development that partners with UTX to establish an iNKT lineage specific gene expression program. Moreover, we demonstrate that UTX-mediated regulation of super-enhancer accessibility is a key mechanism for iNKT lineage commitment. These findings uncover how UTX regulates iNKT cell development through multiple epigenetic mechanisms.

Publication Title

The histone demethylase UTX regulates the lineage-specific epigenetic program of invariant natural killer T cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE87228
Transcriptional and genome organization changes in HT1080 cells after overexpression of tissue-specific nuclear transmembrane proteins (NETs)
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Tissue-specific NETs alter genome organization and regulation even in a heterologous system.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE87150
Transcriptome analysis of human HT1080 cells overexpressing full length or soluble nucleoplasmic fragment of NET29/TMEM120A, NET39/PPAPDC3 and NET47/TM7SF2
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

The nuclear transmembrane proteins (NETs) NET29/TMEM120A, NET39/PPAPDC3 and NET47/TM7SF2 are able to reposition chromosomes towards/away from the nuclear envelope when overexpressed or knocked down in HT1080 cells. In this study we wanted to investigate the transcriptome changes after transfection of the full length NETs or a nucleoplasmic soluble fragment that does not localise to the nuclear envelope.

Publication Title

Tissue-specific NETs alter genome organization and regulation even in a heterologous system.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP056833
Conditional depletion of intellectual disability and Parkinsonism candidate gene ATP6AP2 in fly and mouse induces cognitive impairment and neurodegeneration
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

ATP6AP2 is an essential accessory component of the vacuolar H+ ATPase (V-ATPase) and has been associated with intellectual disabilities (ID) and Parkinsonism. ATP6AP2 has been implicated in several signaling pathways, but little is known about its role in the nervous system. To decipher its function in behaviour and cognition, we generated and characterized conditional ATP6AP2 Drosophila and mouse models in the nervous system. In Drosophila, knockdown of ATP6AP2 induced defective phototaxis and vacuolisation of photoreceptor neurons and pigment cells when deleted in eyes and alteration of short- and long-term memory when deleted in the mushroom body. In mouse, conditional Atp6ap2 deletion in glutamatergic neurons (Atp6ap2Camk2aCre/0 mice) caused increased spontaneous locomotor activity and altered memory for fear. Both Drosophila ATP6AP2 knockdown and Atp6ap2Camk2aCre/0 mice presented with presynaptic transmission defect, abnormal number and morphology of synapses, and alteration of axonal transport in fly. In addition, Atp6ap2Camk2aCre/0 mice showed autophagy defect leading to axonal and neuronal degeneration in the cortex and the hippocampus. Surprisingly, myelinisation of axons was affected in our mutant mice. In accordance with the identified phenotypes across species, genome-wide transcriptome profiling of Atp6ap2Camk2aCre/0 mouse hippocampi revealed dysregulated genes involved in myelination, action potential, membrane bound vesicles and adult behaviour. In summary, disruption of ATP6AP2 in mouse and fly leads to cognitive impairment and neurodegeneration, mimicking aspects of the neuropathology associated with ATP6AP2 mutations in humans. Our results identify ATP6AP2 as an essential gene for the nervous system. Overall design: 4 samples, 2 wt and 2 Atp6ap2Camk2aCre/0

Publication Title

Conditional depletion of intellectual disability and Parkinsonism candidate gene ATP6AP2 in fly and mouse induces cognitive impairment and neurodegeneration.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE94972
Genome reorganisation and transcriptional changes during activation of the human T-cell line Jurkat
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Constrained release of lamina-associated enhancers and genes from the nuclear envelope during T-cell activation facilitates their association in chromosome compartments.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE94970
Transcriptome analysis of human T-cell Jurkat cell line in resting cells (t0) and at 8h, 24h and 48h post-activation using Raji B-cells conjugated with superantigen (SEE)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Activation of T-cells induces dramatic changes in genome organisation and gene transcription. Here we identify changes in transcriptional profiles at 8h, 24h and 48 post activation

Publication Title

Constrained release of lamina-associated enhancers and genes from the nuclear envelope during T-cell activation facilitates their association in chromosome compartments.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon SRP098701
RNA editing is the essential function of ADAR1 and, in the absence of MDA5, is dispensable for normal adult homeostasis [mmPCR-seq]
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Adenosine-to-Inosine (A-to-I) editing of dsRNA by ADAR proteins is a pervasive feature of the epitranscriptome. There are estimated to be over 100 million potential A-to-I editing sites in humans and A-to-I editing can have varying consequences for gene expression. Whilst editing resulting in protein recoding defines the role of ADAR2, ADAR1 has been proposed to have both editing-dependent and -independent functions. The relative contribution of these putative functions to ADAR1 biology is unclear. We demonstrate that the absence of ADAR1-mediated editing is well tolerated when the cytosolic dsRNA sensor MDA5 is deleted. These mice have normal hematopoiesis, tissue patterning and life span. A direct comparison of the complete deletion of ADAR1 and the specific loss of A-to-I editing activity demonstrates that RNA editing is the only essential function of ADAR1 in adult mice. Therefore, preventing MDA5 substrate formation by endogenous RNA is the essential in vivo function of ADAR1-mediated editing. Overall design: Microfluidics-based multiplex PCR and deep sequencing (mmPCR-seq) identification of A-to-I editing sites in 8 tissues from 12 week old mice in a E861A point mutant of ADAR on a MDA5 knockout background

Publication Title

Protein recoding by ADAR1-mediated RNA editing is not essential for normal development and homeostasis.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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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