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accession-icon GSE79276
Detection of differentially expressed genes in broiler Pectoralis major muscle affected by White Striping Wooden Breast myopathies
  • organism-icon Gallus gallus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Gene 1.1 ST Array (chigene11st)

Description

White Striping and Wooden Breast (WS/WB) are abnormalities increasingly occurring in the fillets of high breast yield and growth rate chicken hybrids. These defects lead to consistent economic losses for poultry meat industry, as affected broilers fillets present an impaired visual appearance that negatively affects consumers acceptability. Previous studies have highlighted in affected fillets a deeply damaged muscle, showing profound inflammation, fibrosis and lipidosis. The present study investigated the differentially expressed genes and pathways linked to the compositional changes observed in WS/WB breast muscles, in order to outline a more complete framework of the gene networks related to the occurrence of this complex pathological picture. The biochemical composition was performed on 20 Pectoralis major samples obtained from high breast yield and growth rate broilers (10 affected vs. 10 normal) and 12 out of the 20 samples were used for the microarray gene expression profiling (6 affected vs. 6 normal). The obtained results indicate strong changes in muscle mineral composition, coupled to an increased deposition of fat. In addition, 204 differentially expressed genes (DEG) were found: 102 up-regulated and 102 down-regulated in affected breasts. The gene expression pathways found more altered in WS/WB muscles are those related to muscle development, polysaccharide metabolic processes, proteoglycans synthesis, inflammation and calcium signaling pathway. On the whole, the findings suggest that a multifactorial and complex etiology is associated with the occurrence of WS/WB muscle abnormalities, contributing to further define the transcription patterns associated to these myopathies.

Publication Title

Detection of differentially expressed genes in broiler pectoralis major muscle affected by White Striping - Wooden Breast myopathies.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP131095
Transcriptional changes after overexpression of proliferation drivers in human mammary epithelial cells.
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Genomics has provided a detailed structural description of the cancer genome. Identifying oncogenic drivers that work primarily through dosage changes is a current challenge. Unrestrained proliferation is a critical hallmark of human cancer. We constructed modular, barcoded libraries of human open reading frames (ORFs) and performed screens for proliferation regulators in multiple cell types. Approximately 10% of genes tested regulate proliferation, many performing in an unexpectedly highly tissue-specific manner. Proliferation drivers in a given cell type showed specific enrichment in SCNAs (somatic copy number changes) from cognate tumors and helped predict aneuploidy patterns in those tumors, implying that tissue type-specific genetic network architectures underlie SCNA selection in different cancers. In vivo screening confirmed these results. We report a substantial contribution to the catalog of SCNA-associated cancer drivers, identifying 147 amplified and 107 deleted genes as potential drivers, and derive new insights about the genetic network architecture of aneuploidy in tumors. KRTAPs are a class of human genes that promote proliferation in mammary epithelial cells (HMEC), but the mechanism is not understood. We performed RNAseq to study transcriptional changes associated with oeverxepression of KRTAPs and other oncogenes in hTERT-immortalized human mammary epithelial cells. GSEA analysis revealed the top enriched pathways upregulated by KRTAP expression are E2F-mediated regulation of DNA replication, G1-S specific transcription, cell cycle, translation and ribosome. KRTAP-induced mRNA changes are most closely related to those due to CCND1 expression, including induction of E2F1 transcription factor. Overall design: Analysis of whole transcriptome in HMEC overexpressing different human genes.

Publication Title

Profound Tissue Specificity in Proliferation Control Underlies Cancer Drivers and Aneuploidy Patterns.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon SRP072468
RNA-seq analysis of testis transcripts from Wt and Trf2-/- mice [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

TRF2 is a paralogue of TATA-box binding protein (TBP) with highest expression in testis. Although Trf2 inactivation in mice leads to arrested spermatogenesis, there is no direct evidence that Trf2 is recruited to chromatin to directly regulate gene expression. We used genetically modified mice where endogenous Trf2 has been modified to carry a TAP-TAG to perform ChIP-reChIP followed by deep sequencing. We found that Trf2 is recruited to all active promoters as a subunit of TFIIA/ALF complex together with TBP. To assess the effect of Trf2 inactivation on gene expression we performed RNA-seq on WT and Trf2-/- testes at 21 days of age when haploid cell gene expression is activated. Overall design: The testes from three 21 day old WT and three Trf2-/- males were taken to prepare total RNAs for deep sequencing.

Publication Title

TRF2 is recruited to the pre-initiation complex as a testis-specific subunit of TFIIA/ALF to promote haploid cell gene expression.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP049105
B cell survival and development is dependent on the coordination of NFkappaB family members RelB and cRel
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Identify genes which are induced in wild type, crel ko, and relbcrle dbko B cells under BAFF stimulation, and find the differential expressed genes which are distinct from wildtype controls. Overall design: RNA-seq analysis of wild type, crelko, relbcrel dbko follicular B cells stimulated with BAFF ligand for 6 hours and wildtype only for 27 hours

Publication Title

B-cell survival and development controlled by the coordination of NF-κB family members RelB and cRel.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20405
HDAC and aminopeptidase inhibitor treatment of myeloma cells
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

H929 human myeloma cells were exposed to aminopeptidase inhibitor (CHR-2797), HDAC inhibitor (CHR-3996), or a combinaion of the two agents, for 24 hours.

Publication Title

The combination of HDAC and aminopeptidase inhibitors is highly synergistic in myeloma and leads to disruption of the NFκB signalling pathway.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP136814
RNA deep sequencing from murine BALB/c WT and IL-2-KO bulk CD8 T cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Our goal was to identify early genetic changes in the development of autoimmune dysfunction. WT and IL-2-KO CD8 T cells were sorted from the lymph node and spleen of 12-day old mice. Total RNA was isolated by Expression Analysis Inc. using Illumina TrueSeq Stranded Total RNA Sample Preparation Kit. Eight samples were sequenced (four biological replicates of IL-2-KO and WT/HET mice), producing 2X50 paired-end reads using the Illumine HiSeq 2500 platform. Raw reads were provided by Expression Analysis. We identified several genetic signatures within the bulk data including a cytolyic pattern and a novel gene expression pattern indicating a helper-like function. Overall design: WT and IL-2-KO CD8 T cells were sorted from the lymph node and spleen of 12-day old mice. Total RNA was isolated by Expression Analysis Inc. using Illumina TrueSeq Stranded Total RNA Sample Preparation Kit. Eight samples were sequenced (four biological replicates of IL-2-KO and WT/HET mice).

Publication Title

CD8 Follicular T Cells Promote B Cell Antibody Class Switch in Autoimmune Disease.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP073382
Transcriptome profiling of the human dorsal striatum in bipolar disorder
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Bipolar disorder (BD) is a highly heritable and heterogeneous mental illness whose manifestations often include impulsive and risk-taking behavior. This particular phenotype suggests that abnormal striatal function could be involved in BD etiology, yet most transcriptomic studies of this disorder have concentrated on cortical brain regions. We report the first transcriptome profiling by RNA-Seq of the human dorsal striatum comparing bipolar and control subjects. Differential expression analysis and functional pathway enrichment analysis were performed to identify changes in gene expression that correlate with BD status. Further co-expression and enrichment analyses were performed to identify sets of correlated genes that show association to BD. Overall design: Total RNA samples were isolated from 36 postmortem dorsal striatum subjects (18 bipolar and 18 control) and sequenced. One outlier sample was removed and 35 samples (18 bipolar and 17 control) were analyzed.

Publication Title

Transcriptome sequencing implicates dorsal striatum-specific gene network, immune response and energy metabolism pathways in bipolar disorder.

Sample Metadata Fields

Sex, Subject

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accession-icon GSE7187
Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for DMD
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Duchenne Muscular Dystrophy (DMD) is a fatal muscle wasting disorder caused by dystrophin deficiency. Previous work suggested that increased expression of the dystrophin-related protein utrophin in the mdx mouse model of DMD can prevent dystrophic pathophysiology. Physiological tests showed that the transgenic mouse muscle functioned in a way similar to normal muscle. More recently, it has become possible to analyse disease pathways using microarrays, a sensitive method to evaluate the efficacy of a therapeutic approach. We thus examined the gene expression profile of mdx mouse muscle compared to normal mouse muscle and compared the data with that obtained from the transgenic line expressing utrophin. The data confirm that the expression of utrophin in the mdx mouse muscle results in a gene expression profile virtually identical to that seen for the normal mouse. This study confirms that a strategy to up-regulate utrophin is likely to be effective in preventing the disease.

Publication Title

Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP091696
JNK promotes epithelial cells anoikis by transcriptional and post-translational regulation of BH3-only proteins
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Developmental morphogenesis, tissue injury, and oncogenic transformation can cause the detachment of epithelial cells. These cells are eliminated by a specialized form of apoptosis (anoikis). While the processes that contribute to this form of cell death have been studied, the underlying mechanisms remain unclear. Here we tested the role of the cJUN NH2-terminal kinase (JNK) signaling pathway using murine models with compound JNK-deficiency in mammary and kidney epithelial cells. These studies demonstrated that JNK is required for efficient anoikis in vitro and in vivo. Moreover, JNK-promoted anoikis required pro-apoptotic members of the BCL2 family of proteins. We show that JNK acts through a BAK/BAX-dependent apoptotic pathway by increasing BIM expression and phosphorylating BMF leading to death of detached epithelial cells. Overall design: In order to understand the role of the JNK pathway in anoikis, Rosa-CreER (Control) and Jnk1flox/flox Jnk2-/- Rosa-CreER (Jnk1-/-Jnk2-/-) cells were grown as attached monoloayers or suspended for 4 hours. RNA was isolated from these cells and subjected to RNASeq to measure differential gene expression. Three separate samples from each condition were analyzed.

Publication Title

JNK Promotes Epithelial Cell Anoikis by Transcriptional and Post-translational Regulation of BH3-Only Proteins.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE74600
Transcriptomic analysis and ChIP-seq in CCE-Rx cells to identify SOX2 transcription factor target genes
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Targeted resequencing identifies PTCH1 as a major contributor to ocular developmental anomalies and extends the SOX2 regulatory network.

Sample Metadata Fields

Specimen part, Time

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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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