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accession-icon GSE53985
Myocilin regulates cell proliferation and survival by activating the ERK pathway
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Myocilin, a causative gene for open-angle glaucoma, encodes a secreted glycoprotein of unknown function. To elucidate its function(s), we produced a stably transfected HEK293 cell line expressing myocilin and compared the expression profiles between the myocilin-expressing cell line and a vector control cell line using Affymetrix GeneChip U133 plus 2.0 array. A significant portion of differentially-expressed genes in the myocilin-expressing cells was associated with cell growth and cell death, suggesting that myocilin may have an important role regulating cell growth/survival..

Publication Title

Myocilin regulates cell proliferation and survival.

Sample Metadata Fields

Cell line

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accession-icon SRP043463
Genome-wide identification of rat long non-coding RNAs
  • organism-icon Rattus norvegicus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

In the current study, we have focused on a distinct group of non-coding elements, lncRNA, and profiled renal tissues from three different inbred rat strains. We chose the three strains S, SHR and R for the main purpose of cataloging lncRNA annotations from the most widely used rat models of cardiovascular and renal disease. Overall design: Identification of lncRNAs on the rat genome by next generation RNA sequencing (NGS)

Publication Title

Genome-wide identification of long noncoding RNAs in rat models of cardiovascular and renal disease.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE61676
24h-response to bevacizumab erlortinib in non-small cell lung cancer from blood-based exon array profiling
  • organism-icon Homo sapiens
  • sample-icon 86 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

The mechanisms of action of the combined targeted therapy bevacizumab erlotinib in late stage non-squamous non-small cell lung cancer was investigated by means of whole genome exon arrays.

Publication Title

24h-gene variation effect of combined bevacizumab/erlotinib in advanced non-squamous non-small cell lung cancer using exon array blood profiling.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon GSE82247
Expression data from SHP specific siRNA or nonspecefic siRNA transfected rat astrocytes [extended study]
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

To clarify the effect of SHP in LXRs-mediated signaling pathway, we performed global gene expression analysis of SHP siRNA transfected- or control siRNA transfected- astrocytes after IFN- and LXRs agonist. Microarray analysis revealed that expression of several genes encoding inflammatory mediators were reversed in SHP siRNA transfected-astrocytes, when compared with control siRNA transfected-astrocytes.

Publication Title

Small heterodimer partner SHP mediates liver X receptor (LXR)-dependent suppression of inflammatory signaling by promoting LXR SUMOylation specifically in astrocytes.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE71764
Expression data from Arabidopsis during de-etiolation
  • organism-icon Arabidopsis thaliana
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Arabidopsis fc2-1 mutants fail to properly de-etiolate after a prolonged period in the dark. Our goal was to monitor whole genome expression during the first 2 hours of de-etiolation to determine the cuase of this growth arrest.

Publication Title

Ubiquitin facilitates a quality-control pathway that removes damaged chloroplasts.

Sample Metadata Fields

Specimen part

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accession-icon SRP070753
Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt
  • organism-icon Caenorhabditis elegans
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Organisms respond to mitochondrial stress through the upregulation of an array of protective genes, often perpetuating an early response to metabolic dysfunction across a lifetime. We find that mitochondrial stress causes widespread changes in chromatin structure through histone H3K9 di-methylation marks traditionally associated with gene silencing. Mitochondrial stress response activation requires the di-methylation of histone H3K9 through the activity of the histone methyltransferase met-2 and the nuclear co-factor lin-65. While globally the chromatin becomes silenced by these marks, remaining portions of the chromatin open up, at which point the binding of canonical stress responsive factors such as DVE-1 occurs. Thus, a metabolic stress response is established and propagated into adulthood of animals through specific epigenetic modifications that allow for selective gene expression and lifespan extension. Overall design: comparison of gene expression changes in response to cco-1 RNAi treatment in N2, lin-65(n3441) and met-2(ok2307) populations of C. elegans L4 animals

Publication Title

Mitochondrial Stress Induces Chromatin Reorganization to Promote Longevity and UPR(mt).

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE23643
Cardiac transcriptome profiles of S.LEW congenic strain compared with the hypertensive Dahl S rat
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Despite inheritance of hypertension in families, identifying genetic mechanisms predisposing individuals to hypertension has remained challenging. The effects of single genes contributing to the development of hypertension may not be readily detected in individuals whose genomes also contain other genetic factors that resist hypertension. By using a highly permissive rat genome for inherited hypertension, we demonstrate that increased expression of one such gene, Rififylin (Rffl), is a novel inherited risk factor for hypertension and increased mortality. Animals overexpressing Rffl demonstrated delayed endocytic recycling, accumulated polyubiquitinated proteins, increased beats/min of neonatal cardiomyocytes, had shorter QT-intervals and developed salt-insensitive hypertension very early in their life (50-52 days). Thus, the discovery of a physiological link between overexpression of rififylin and the development of hypertension constitutes a novel mechanism that could be targeted for rectifying normal QT-interval and preventing hypertension.

Publication Title

Augmented rififylin is a risk factor linked to aberrant cardiomyocyte function, short-QT interval and hypertension.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE22515
DEFINING A RAT BLOOD PRESSURE QUANTITATIVE TRAIT LOCUS TO A <81.8KB CONGENIC SEGMENT: COMPREHENSIVE SEQUENCING AND RENAL TRANSCRIPTOME ANALYSIS.
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Evidence from multiple linkage and genome-wide association studies suggest that human chromosome 2 (HSA2) contains alleles that influence blood pressure (BP). Homologous to a large segment of HSA2 is rat chromosome 9 (RNO9), to which a BP quantitative trait locus (QTL) was previously mapped. The objective of the current study was to further resolve this BP QTL. Eleven congenic strains with introgressed segments spanning <81.8kb to <1.33Mb were developed by introgressing genomic segments of RNO9 from the Dahl salt-resistant (R) rat onto the genome of the Dahl salt-sensitive (S) rat and tested for BP. The congenic strain with the shortest introgressed segment spanning <81.8kb significantly lowered BP of the hypertensive S rat by 25 mm Hg and significantly increased its mean survival by 45 days. In contrast, two other congenic strains had increased BP compared with the S. We focused on the <81.8kb congenic strain which represents the shortest genomic segment to which a BP QTL has been definitively mapped to date in any species. Sequencing of this entire region in both S and R rats detected 563 variants. The region did not contain any known or predicted rat protein coding genes. Further, a whole genome renal transcriptome analysis between S and the <81.8kb S.R congenic strain revealed alterations in several critical genes implicated in renal homeostasis. Taken together, our results provide the basis for future studies to examine the relationship between the candidate variants within the QTL region and the renal differentially expressed genes as potential causal mechanisms for BP regulation.

Publication Title

Defining a rat blood pressure quantitative trait locus to a &amp;lt;81.8 kb congenic segment: comprehensive sequencing and renal transcriptome analysis.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE60818
Expression and function of NAT12/NAA30 in glioblastoma
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE60706
Knockdown of NAT12/NAA30 decreases glioblastoma stem cell growth and tumorigenicity by regulating hypoxia response, p-MTOR (Ser2448) and p53 pathway
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Gene knockdown of NAT12/NAA30 led to decreased proliferation, sphere forming ability and mitochondrial hypoxia tolerance in the GSC T65 culture. Intracranial transplantation of these cells into SCID mice showed that the decreased NAT12/NAA30 expression correlated with the prolonged animal survival and reduced tumor size

Publication Title

Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.

Sample Metadata Fields

Specimen part, 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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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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