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accession-icon GSE42987
Hippocampal expression data from WT, KO, R270X, and G273X mice at 4 and 9 weeks
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Mecp2 loss-of-function has been associated with altered gene expression in many tissues. We characterized gene expression changes within the hippocampi of 3 different Mecp2 loss-of-function mouse models.

Publication Title

An AT-hook domain in MeCP2 determines the clinical course of Rett syndrome and related disorders.

Alternate Accession IDs

E-GEOD-42987

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE23089
Molecular Determinants of Dorsal Spinal Cord Interneurons Specified by Atoh1 (Math1)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Neural basic helix-loop-helix (bHLH) transcription factors are important for the differentiation and cell type specification of neurons. They are thought to share direct downstream targets in their common role as neuronal differentiation factors, but have distinct targets with respect to their cell type specific roles. Little is known about distinct cell-type specific bHLH targets as previous work did not distinguish these from common targets. Based on previous genetic evidence, we hypothesize that bHLH transcription factors have unique targets for their function in regulating neuronal sub-type specification. Atoh1 (Math1) is a bHLH transcription factor that specifies different cell types of the proprioceptive pathway in mammals such as the dorsal interneuron 1 population of the developing neural tube. Using microarray analyses of neighboring specific bHLH sorted populations from developing mouse neural tubes, we determine transcripts unique to the Atoh1-derived population and not those common to bHLH transcription factors in related neural progenitor populations. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) experiments of native tissue followed by enhancer reporter analyses identified five direct cell-type specific targets of Atoh1 in vivo: Klf7, Rab15, Rassf4, Selm, and Smad7, along with their Atoh1-responsive enhancers. These Atoh1 targets were found from native tissue in the appropriate developmental context and have diverse functions that range from transcription factors to regulators of endocytosis and signaling pathways. Only Rab15 and Selm are expressed across several different Atoh1-specified cell types including external granule cells (EGL) in the developing cerebellum, hair cells of the inner ear, and Merkel cells, demonstrating that even within Atoh1 lineages, not all Atoh1 specific targets are shared. Our work establishes on a molecular level that the neuronal differentiation bHLH transcription factors also have distinct targets for their roles in neuronal sub-type specification. From this work, we can begin to address how bHLH transcription factors are able to specify unique cell types and initiate programs that organize neuronal diversity.

Publication Title

In vivo neuronal subtype-specific targets of Atoh1 (Math1) in dorsal spinal cord.

Alternate Accession IDs

E-GEOD-23089

Sample Metadata Fields

Specimen part

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accession-icon GSE11115
Selective estrogen receptor-beta agonists repress transcription of proinflammatory
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

In addition to their role in the development and function of the reproductive system, estrogens have significant anti-inflammatory properties. Although both estrogen receptors (ERs) can mediate anti-inflammatory actions, ERbeta is a more desirable therapeutic target because ERalpha mediates the proliferative effects of estrogens on the mammary gland and uterus. In fact, selective ERbeta agonists have beneficial effects in preclinical models involving inflammation without causing growth-promoting effects on the uterus or mammary gland. However, their mechanism of action is unclear. The purpose of this study was to use microarray analysis to determine whether ERbeta-selective compounds produce their anti-inflammatory effects by repressing transcription of proinflammatory genes. We identified 49 genes that were activated by TNF-alpha in human osteosarcoma U2OS cells expressing ERbeta. Estradiol treatment significantly reduced the activation by TNF-alpha on 18 genes via ERbeta or ERalpha. Most repressed genes were inflammatory genes, such as TNF-alpha, IL-6, and CSF2. Three ERbeta-selective compounds, ERB-041, WAY-202196, and WAY-214156, repressed the expression of these and other inflammatory genes. ERB-041 was the most ERbeta-selective compound, whereas WAY-202196 and WAY-214156 were the most potent. The ERbeta-selective compounds repressed inflammatory genes by recruiting the coactivator, SRC-2. ERB-041 also repressed cytokine genes in PBMCs, demonstrating that ERbeta-selective estrogens have anti-inflammatory properties in immune cells. Our study suggests that the anti-inflammatory effects of ERB-041 and other ERbeta-selective estrogens in animal models are due to transcriptional repression of proinflammatory genes. These compounds might represent a new class of drugs to treat inflammatory disorders.

Publication Title

Selective estrogen receptor-beta agonists repress transcription of proinflammatory genes.

Alternate Accession IDs

E-GEOD-11115

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE44285
Atxn1L is a novel regulator of Hematopoietic Stem Cell Quiescence
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We compared gene expression differences in Atxn1L knockout vs wildtype HSCs

Publication Title

Ataxin1L is a regulator of HSC function highlighting the utility of cross-tissue comparisons for gene discovery.

Alternate Accession IDs

E-GEOD-44285

Sample Metadata Fields

Specimen part

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accession-icon GSE9914
Expression data from early symptomatic Sca1154Q/2Q and Sca7266Q/5Q knock-in cerebellum
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Comparative analysis of cerebellar gene expression changes occurring in Sca1154Q/2Q and Sca7266Q/5Q knock-in mice

Publication Title

The insulin-like growth factor pathway is altered in spinocerebellar ataxia type 1 and type 7.

Alternate Accession IDs

E-GEOD-9914

Sample Metadata Fields

Sex, Age

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accession-icon SRP126064
transcriptomic profiling of HEK293 cells upon individual knockdown of the splicing factors RBM17, U2SURP or CHERP
  • organism-icon Homo sapiens
  • sample-icon 92 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We found that the core spliceosomal proteins RBM17, U2SURP and CHERP form a protein complex regulating alternative splicing and expression of a whole network of RNA binding proteins Overall design: RNA sequencing of triplicate RNA samples from HEK293 cells treated with siRNAs against RBM17, U2SURP , CHERP or SCRAMBLE sequence

Publication Title

RBM17 Interacts with U2SURP and CHERP to Regulate Expression and Splicing of RNA-Processing Proteins.

Alternate Accession IDs

GSE107648

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP061434
Reversal of MECP2 duplication syndrome using genetic rescue and antisense oligonucleotides [Genetic Rescue Experiments]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

MECP2 duplication syndrome, a childhood neurological disorder characterized by autism, intellectual disability, motor dysfunction, anxiety and epilepsy, is caused by a duplication on chromosome Xq28 spanning the MECP2 gene that results in doubling of MeCP2 levels. MECP2 overexpression in mice causes neurobehavioral and electroencephalographic defects similar to those of human patients, but the gross anatomy of the brain remains unaffected. We hypothesized that MECP2 duplication syndrome would be reversible and tested two methods to restore MeCP2 levels to normal: conditional genetic recombination and antisense oligonucleotide therapy. Both approaches rescued molecular, physiological and behavioral features of adult symptomatic mice. Antisense therapy also restored normal MeCP2 levels in lymphoblastoid cells from MECP2 duplication patients, in a dose-dependent manner. Our data indicate that antisense oligonucleotides could provide a viable therapeutic approach for human MECP2 duplication syndrome as well as other disorders involving copy number gains. Overall design: Hippocampal mRNA profiles of conditional MECP2 overexpression and genetic rescue mice were generated by deep sequencing, in triplicate, using Illumina TruSeq.

Publication Title

Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligonucleotides.

Alternate Accession IDs

GSE71229

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP061437
Reversal of MECP2 duplication syndrome using genetic rescue and antisense oligonucleotides [ASO time point 2]
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

MECP2 duplication syndrome, a childhood neurological disorder characterized by autism, intellectual disability, motor dysfunction, anxiety and epilepsy, is caused by a duplication on chromosome Xq28 spanning the MECP2 gene that results in doubling of MeCP2 levels. MECP2 overexpression in mice causes neurobehavioral and electroencephalographic defects similar to those of human patients, but the gross anatomy of the brain remains unaffected. We hypothesized that MECP2 duplication syndrome would be reversible and tested two methods to restore MeCP2 levels to normal: conditional genetic recombination and antisense oligonucleotide therapy. Both approaches rescued molecular, physiological and behavioral features of adult symptomatic mice. Antisense therapy also restored normal MeCP2 levels in lymphoblastoid cells from MECP2 duplication patients, in a dose-dependent manner. Our data indicate that antisense oligonucleotides could provide a viable therapeutic approach for human MECP2 duplication syndrome as well as other disorders involving copy number gains. Overall design: Hippocampal mRNA profiles of WT, MECP2-TG and MECP2-TG ASO-treated treated mice 8 weeks after the initiation of the treatment, were generated by deep sequencing, in triplicate, using Illumina TruSeq.

Publication Title

Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligonucleotides.

Alternate Accession IDs

GSE71234

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP061436
Reversal of MECP2 duplication syndrome using genetic rescue and antisense oligonucleotides [ASO time point 1]
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

MECP2 duplication syndrome, a childhood neurological disorder characterized by autism, intellectual disability, motor dysfunction, anxiety and epilepsy, is caused by a duplication on chromosome Xq28 spanning the MECP2 gene that results in doubling of MeCP2 levels. MECP2 overexpression in mice causes neurobehavioral and electroencephalographic defects similar to those of human patients, but the gross anatomy of the brain remains unaffected. We hypothesized that MECP2 duplication syndrome would be reversible and tested two methods to restore MeCP2 levels to normal: conditional genetic recombination and antisense oligonucleotide therapy. Both approaches rescued molecular, physiological and behavioral features of adult symptomatic mice. Antisense therapy also restored normal MeCP2 levels in lymphoblastoid cells from MECP2 duplication patients, in a dose-dependent manner. Our data indicate that antisense oligonucleotides could provide a viable therapeutic approach for human MECP2 duplication syndrome as well as other disorders involving copy number gains. Overall design: Hippocampal mRNA profiles of WT, MECP2-TG and MECP2-TG ASO-treated treated mice 4weeks after the initiation of the treatment, were generated by deep sequencing, in triplicate, using Illumina TruSeq.

Publication Title

Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligonucleotides.

Alternate Accession IDs

GSE71233

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE32051
Capicua-dependent transcriptional changes in adult mouse cerebellum
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Analysis of cerebella from Capicua (Cic) mutant mice and wild-type controls at 28 days of age (P28). Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). The transcriptional repressor Cic binds directly to Atxn1 and plays a key role in SCA1 pathogenesis. Two isoforms of Cic, long (Cic-L) and short (Cic-S), are transcribed from alternative promoters. Using embryonic stem cells in which the Cic locus was targeted by an insertion of a genetrap cassette between exon 1 of the Cic-L isoform and exon 1 of the Cic-S isoform, we generated mice that carried this allele and backcrossed these onto a Swiss Webster (CD-1) strain for >6 generations. The resulting Cic-L-/- mice completely lack the Cic-L isoform with ~10% of Cic-S remaining. These data were used to compare with previous microarray data to determine the Cic-depedent pathogenic mechanisms in SCA1.

Publication Title

Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua.

Alternate Accession IDs

E-GEOD-32051

Sample Metadata Fields

No sample metadata fields

View Samples

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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