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accession-icon SRP067502
Homo sapiens Raw sequence reads
  • organism-icon Homo sapiens
  • sample-icon 591 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

MicroRNA down-regulation and noise regulation

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP115462
Homo sapiens 3'' end sequencing with A-seq
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The processing of 3' untranslated regions of messenger RNAs changes widely in relation to the cellular state, yet the key regulators remain largely unknown. To uncover sequence elements that drive the choice of polyadenylation (poly(A)) sites in specific conditions, we have developed KAPAC, a method to infer activities of oligomeric sequence motifs on polyadenylation site choice. We demonstrate that KAPAC readily uncovers the sequence elements, targets and binding site position-dependent activity of the mammalian cleavage factor I which regulates the length of 3' untranslated regions.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment

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accession-icon SRP013842
Homo sapiens Variation
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2000

Description

This project aims to discover canonical gene fusion events from mixed human tissue cell lines.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3249
Analysis of RPE65 loss of function in mouse retina
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To characterize gene response in RPE65-/- mouse model of Lebers congenital amaurosis during progression of the disease, we analyzed differential gene expression in retinae early in the development of the disease, namely before and at the onset of photoreceptor cell death in knock-out mice of 2, 4 and 6 months of age.

Publication Title

Biological characterization of gene response in Rpe65-/- mouse model of Leber's congenital amaurosis during progression of the disease.

Sample Metadata Fields

Age, Specimen part

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accession-icon E-MEXP-3260
Muscle Gene Expression Is a Marker of Amyotrophic Lateral Sclerosis Severity
  • organism-icon Homo sapiens
  • sample-icon 37 Downloadable Samples
  • Technology Badge IconUNKNOWN

Description

This study was designed to identify gene expression changes in skeletal muscle that could define reliably the degree of the severity of Amyotrophic lateral sclerosis (ALS). All samples were from human biopsies, either from healthy muscles or from muscle whose patients were clearly diagnosed as having Amyotrophic Lateral Sclerosis (ALS)

Publication Title

Muscle Gene Expression Is a Marker of Amyotrophic Lateral Sclerosis Severity

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

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accession-icon GSE51191
Transcriptional network analysis in muscle reveals AP-1 as a partner of PGC-1 in the regulation of the hypoxic gene program
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II, Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional network analysis in muscle reveals AP-1 as a partner of PGC-1α in the regulation of the hypoxic gene program.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE80618
Loss of renal tubular PGC-1 exacerbates diet-induced renal steatosis and age-related urinary sodium excretion in mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The kidney has a high energy demand and is dependent on oxidative metabolism for ATP production. Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor coactivator 1 (PGC-1) is highly expressed in kidney, its role in renal physiology is so far unclear. Here we show that PGC-1 is a central transcriptional regulator of mitochondrial metabolic pathways in the kidney. Moreover we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1 in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Overall, PGC-1 seems largely dispensable for basal renal physiology. However, the central role of PGC-1 in renal mitochondrial biogenesis indicates that activation of PGC-1 in the context of renal disorders could be a valid therapeutic strategy to ameliorate renal mitochondrial dysfunction.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE80265
PGC-1a Determines Light Damage Susceptibility of the Murine Retina
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The peroxisome proliferator-activated receptor c coactivator 1 (PGC-1) proteins are key regulators of cellular bioenergetics and are accordingly expressed in tissues with a high energetic demand. For example, PGC-1a and PGC-1b control organ function of brown adipose tissue, heart, brain, liver and skeletal muscle. Surprisingly, despite their prominent role in the control of mitochondrial biogenesis and oxidative metabolism, expression and function of the PGC-1 coactivators in the retina, an organ with one of the highest energy demands per tissue weight, are completely unknown. Moreover, the molecular mechanisms that coordinate energy production with repair processes in the damaged retina remain enigmatic. In the present study, we thus investigated the expression and function of the PGC-1 coactivators in the healthy and the damaged retina. We show that PGC-1a and PGC-1b are found at high levels in different structures of the mouse retina, most prominently in the photoreceptors. Furthermore, PGC-1a knockout mice suffer from a striking deterioration in retinal morphology and function upon detrimental light exposure. Gene expression studies revealed dysregulation of all major pathways involved in retinal damage and apoptosis, repair and renewal in the PGC-1a knockouts. The light-induced increase in apoptosis in vivo in the absence of PGC-1a was substantiated in vitro, where overexpression of PGC-1a evoked strong anti-apoptotic effects. Finally, we found that retinal levels of PGC-1 expression are reduced in different mouse models for retinitis pigmentosa. We demonstrate that PGC-1a is a central coordinator of energy production and, importantly, all of the major processes involved in retinal damage and subsequent repair. Together with the observed dysregulation of PGC-1a and PGC-1b in retinitis pigmentosa mouse models, these findings thus imply that PGC-1a might be an attractive target for therapeutic approaches aimed at retinal degeneration diseases.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE80522
The genomic context and co-recruitment of SP1 affect ERR co-activation by PGC-1 in muscle cells
  • organism-icon Mus musculus
  • sample-icon 9 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

The Genomic Context and Corecruitment of SP1 Affect ERRα Coactivation by PGC-1α in Muscle Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE51190
Transcriptional network analysis in muscle reveals AP-1 as a partner of PGC-1 in the regulation of the hypoxic gene program [microarray: kD_AP1]
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Illumina Genome Analyzer II

Description

Skeletal muscle tissue shows an extraordinary cellular plasticity, but the underlying molecular mechanisms are still poorly understood. Here we use a combination of experimental and computational approaches to unravel the complex transcriptional network of muscle cell plasticity centered on the peroxisome proliferator-activated receptor coactivator 1 (PGC-1), a regulatory nexus in endurance training adaptation. By integrating data on genome-wide binding of PGC-1 and gene expression upon PGC-1 over-expression with comprehensive computational prediction of transcription factor binding sites (TFBSs), we uncover a hitherto underestimated number of transcription factor partners involved in mediating PGC-1 action. In particular, principal component analysis of TFBSs at PGC-1 binding regions predicts that, besides the well-known role of the estrogen-related receptor (ERR), the activator protein-1 complex (AP-1) plays a major role in regulating the PGC-1-controlled gene program of hypoxia response. Our findings thus reveal the complex transcriptional network of muscle cell plasticity controlled by PGC-1.

Publication Title

Transcriptional network analysis in muscle reveals AP-1 as a partner of PGC-1α in the regulation of the hypoxic gene program.

Sample Metadata Fields

Treatment

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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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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