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accession-icon GSE18778
Comparison of gene expression between wild-type and PTIP deficient chicken DT40 B cells
  • organism-icon Gallus gallus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

PTIP (Pax2 transactivation domain-interacting protein) is a nuclear protein containing six BRCT domains. It has been shown that PTIP affects gene expression by controlling the activity of the transcription factor Pax2 and histone H3 lysine 4 methyltransferase complexes. In addition to its role in transcriptional regulation, PTIP has been implicated in DNA damage response. To ask if the depletion of PTIP affects the expression level of genes encoding DNA damage response factors , we compared the whole transcripts between wild-type and PTIP deficient chicken DT40 B cell lines.

Publication Title

PTIP promotes DNA double-strand break repair through homologous recombination.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE12599
Transcriptional profiling of mouse glomerulus in lipopolysaccharide-induced proteinuria model
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The pathogenic mechanisms of common kidney glomerular diseases, including the vast majority of cases of proteinuria, remain unknown.

Publication Title

Glomerular transcriptome changes associated with lipopolysaccharide-induced proteinuria.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE40296
Essential roles of the histone methyltransferase ESET in the epigenetic control of neural progenitor cells during development
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In the developing brain, neural progenitor cells (NPCs) switch the differentiation competency via changing gene expression profiles that are governed partly by epigenetic control such as histone modification, although the precise mechanism is unknown. Here we found that ESET/Setdb1/KMT1E, a histone H3 Lys-9 (H3K9) methyltransferase, was highly expressed at early stages of brain development but down-regulated over time, and that ablation of ESET led to decreased H3K9 trimethylation and misregulation of genes, resulting in severe brain defects and early lethality. In the mutant brain, endogenous retrotransposons were derepressed, and non-neural gene expression was activated. Furthermore, early neurogenesis was most severely impaired, while astrocyte formation was enhanced. We conclude that there is an epigenetic role of ESET in temporal and tissue-specific gene regulation in the developing brain.

Publication Title

Essential roles of the histone methyltransferase ESET in the epigenetic control of neural progenitor cells during development.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE16007
miR-140 deficiency effect on the chondrocytes
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Analysis of mouse chondrocytes lacking the microRNA-140. MicroRNAs are genomically encoded small RNAs to regulate the gene expression. miR-140 shows high expression in cartilage. Results provide insight into the molecular mechanisms underlying miR-140 function in chondrocytes.

Publication Title

MicroRNA-140 plays dual roles in both cartilage development and homeostasis.

Sample Metadata Fields

Specimen part

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accession-icon GSE61697
Gene expressions of CD4+ T cells in each developmental stages
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The development of T cells has been characterized as taking place over three stages: nave (Tn), central memory (Tcm), and effector memory (Tem) cells.

Publication Title

Polarization diversity of human CD4+ stem cell memory T cells.

Sample Metadata Fields

Sex, Age

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accession-icon SRP186367
Loss of RNA-binding protein Sfpq causes long-gene transcriptopathy in skeletal muscle and severe muscle mass reduction with metabolic myopathy (skeletal muscle, mRNA-seq)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Growing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle. Overall design: We analyzed polyA-tailed RNA profiles including transcribing RNAs in gastrocnemius skeletal muscle ( from 3 control and 3 Sfpq-/- P35 male mice) using Ion-proton.

Publication Title

Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon SRP124852
Loss of RNA-binding protein Sfpq causes long-gene transcriptopathy in skeletal muscle and severe muscle mass reduction with metabolic myopathy (Primary culture, rRNA depleted RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Growing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle. Overall design: We analyzed rRNA-depleted RNA profiles including transcribing RNAs in primary myoblasts obtained from skeletal muscles of 1-month-old SfpqSM-KO (n=1) and control (n=1) mice under differentiated condition using Ion-proton.

Publication Title

Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.

Sample Metadata Fields

Subject

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accession-icon SRP073310
Differential expression of Hdc-/- VS WT hematopoietic stem and progenitor cells (HSPC) from bone marrow.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The gene expression of bone marrow Hdc-/- and WT (LSK, Lin-c-kit+Sca-1+) hematopoetic stem and progenitor cells were isolated from Hdc-/- or WT mice. Cells were sorted by the cell surface markers of LSK total RNA was isolated from sorted 2,000 HSPCs using the ARCTURUS PicoPure RNA isolation kit (Life Technologies). cDNA was amplified and libraries were constructed by using the SMARTer Ultra Low Input RNA kit (Clontech Laboratories) and the Nextera XT DNA Library Preparation kit (Illumina) according to the respective manufacturer's instructions. Sequencing was performed on the Illumina HiSeq2500 platform. Overall design: a. Hdc-/- bone marrow HSPC (n=4) b. WT bone marrow HSPC (n=4)

Publication Title

Histidine decarboxylase (HDC)-expressing granulocytic myeloid cells induce and recruit Foxp3<sup>+</sup> regulatory T cells in murine colon cancer.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE79728
Differential expression of Hdc-GFP+/hiCD11b+Gr1+ vs Hdc-GFP-/loCD11b+Gr1+ myeloid cells from mouse bone marrow
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Bone marrow Hdc-GFP+/hi and Hdc-GFP-/loCD11b+Gr1+ cells were isolated from bones from histidine decarboxylase (Hdc) green fluorescent protein (Hdc-GFP) mice Hdc-GFP+/hiCD11b+Gr1+ cells and Hdc-GFP-/loCD11b+Gr1+ cells were sorted by combinations of GFP and myeloid cell surface markers CD11b and Gr1 and their differential mRNA expression compared with Affymetrix microarrays.

Publication Title

Histidine decarboxylase (HDC)-expressing granulocytic myeloid cells induce and recruit Foxp3&lt;sup&gt;+&lt;/sup&gt; regulatory T cells in murine colon cancer.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE43563
Expression data of GMP and MDP from wild-type and Trib1-/- mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Trib1 is critical for some myeloid cell differentiation.

Publication Title

Critical role of Trib1 in differentiation of tissue-resident M2-like macrophages.

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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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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