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accession-icon GSE44265
HIV-1 Tat protein promotes neuronal dysfunction through disruption of microRNAs.
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Over the last decade, small noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators in the expression and function of eukaryotic genomes. It has been suggested that viral infections and neurological disease outcome may also be shaped by the influence of small RNAs. This has prompted us to suggest that HIV infection alters the endogenous miRNA expression patterns, thereby contributing to neuronal deregulation and AIDS dementia. Therefore, using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs due to its characteristic features such as release from the infected cells and taken up by noninfected cells. Using microRNA array assay, we demonstrated that Tat deregulates the levels of several miRNAs. Interestingly, miR-34a was among the most highly induced miRNAs in Tat-treated neurons. Tat also decreases the levels of miR-34a target genes such as CREB protein as shown by real time PCR. The effect of Tat was neutralized in the presence of anti-miR-34a. Using in situ hybridization assay, we found that the levels of miR-34a increase in Tat transgenic mice when compared with the parental mice. Therefore, we conclude that deregulation of neuronal functions by HIV-1 Tat protein is miRNA-dependent.

Publication Title

HIV-1 Tat protein promotes neuronal dysfunction through disruption of microRNAs.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE44266
Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders.
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders.

Publication Title

Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP010940
Radicicol treatment of Drosophila cells
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Drosophila S2 cells were treated with Heat-shock protein 90 (Hsp90) inhibitor radicicol for 15min, 30min and 1h. Poly(A) RNA was isolated and sequenced. Overall design: Kinetics of transcriptional response to Hsp90 inhibition

Publication Title

Hsp90 globally targets paused RNA polymerase to regulate gene expression in response to environmental stimuli.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE66583
Expression profiles in Zbtb20-overexpressed neural precursor cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Neural precursor cells (NPCs) are multipotent cells that can generate neurons, astrocytes, and oligodendrocytes in the mammalian central nervous system. Although Zbtb20 was expressed in NPCs, its functions in neural development are not fully understood. We performed microarray analysis to examine changes in gene expression between control and Zbtb20-overexpressed NPCs.

Publication Title

Zbtb20 promotes astrocytogenesis during neocortical development.

Sample Metadata Fields

Specimen part

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accession-icon GSE18361
Temporal gene expression analyisis from rice root (cv. Nipponbare) infected with Magnaporthe oryzae strain Guy11
  • organism-icon Oryza sativa
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Magnaporthe oryzae causes rice blast, the most devastating foliar fungal disease of cultivated rice. During disease development the fungus simultaneously maintains both biotrophic and necrotrophic growth corresponding to a hemi-biotrophic life style. The ability of M. oryzae to also colonize roots and subsequently develop blast symptoms on aerial tissue has been recognized. The fungal root infection strategy and the respective host responses are currently unknown. Global temporal expression analysis suggested a purely biotrophic infection process reflected by the rapid induction of defense response-associated genes at the early stage of root invasion and subsequent repression coinciding with the onset of intracellular fungal growth. The same group of down-regulated defense genes was increasingly induced upon leaf infection by M. oryzae where symptom development occurs shortly post tissue penetration. Our molecular analysis therefore demonstrates the existence of fundamentally different tissue-specific fungal infection strategies and provides the basis for enhancing our understanding of the pathogen life style.

Publication Title

Tissue-adapted invasion strategies of the rice blast fungus Magnaporthe oryzae.

Sample Metadata Fields

Specimen part

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accession-icon SRP012463
Mixture models and wavelet transforms reveal high confidence RNA-protein interaction sites in MOV10 PAR-CLIP data
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina Genome Analyzer IIx

Description

The Photo-Activatable Ribonucleoside-enhanced CrossLinking and ImmunoPrecipitation (PAR-CLIP) method was recently developed for global identification of RNAs interacting with proteins. The strength of this versatile method results from induction of specific T to C transitions at sites of interaction. However, current analytical tools do not distinguish between non-experimentally and experimentally induced transitions. Furthermore, geometric properties at potential binding sites are not taken into account. To surmount these shortcomings, we developed a two-step algorithm consisting of a non-parametric two-component mixture model and a wavelet-based peak calling procedure. Our algorithm can reduce the number of false positives up to 24% thereby identifying high confidence interaction sites. We successfully employed this approach in conjunction with a modified PAR-CLIP protocol to study the functional role of nuclear MOV10, a putative RNA helicase interacting with Argonaute2 and Polycomb. Our method, available as the R package wavClusteR, is generally applicable to any substitution-based inference problem in genomics. Overall design: The data comprises one MOV10 PAR-CLIP data file and one nuclear RNA-seq file

Publication Title

Mixture models and wavelet transforms reveal high confidence RNA-protein interaction sites in MOV10 PAR-CLIP data.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP090169
The evolutionary capacitor HSP90 buffers the regulatory effects of mammalian endogenous retroviruses.
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The molecular chaperone heat shock protein 90 (HSP90) is thought to buffer genetic variation uncoupling phenotypic outcome from individual genotypes. HSP90 thus acts as an evolutionary capacitor by facilitating an accumulation of natural genetic variation. The molecular mechanism underlying the buffering ability is unclear, and HSP90-contingent genetic variation maps both to coding and non-coding parts of the genome. Our genome-wide data indicate that a compromised chaperoning activity of HSP90 causes derepression of endogenous retroviruses (ERVs) in mouse somatic cells. This results in an upregulation of host genes located in the neighborhood of pre-existing ERVs insertion sites. We provide genetic and biochemical evidence that HSP90 cooperates with KAP1/ SETDB1 histone methyltranferase pathway to repress ERVs. Individual mouse strains have unique integration sites of ERVs in their genomes. Consequently distinct genes are responsive to HSP90 inhibitor in different mouse strains depending on the position of the genes vis-à-vis strain-specific ERV insertion sites. Since ERVs have been exapted to drive novel transcriptional networks during mammalian evolution, HSP90 may have acted as a capacitor by buffering variation caused by ERV in non-coding regions of the genome. Our studies provide the first molecular framework by which HSP90 can mitigate genetic variation in gene-regulatory regions affecting gene expression and phenotypes. Overall design: We have performed RNA-seq in mouse embryonic stem cells, neuronal progenitor cells and bone-marrow-derived macrophages treated with NVP-AUY922 in triplicates.

Publication Title

The evolutionary capacitor HSP90 buffers the regulatory effects of mammalian endogenous retroviruses.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE11119
SOL2 mutation affect gene expresstion at root apex
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Analysis of sol2 mutant. SOL2 protein is a receptor-like kinase

Publication Title

The receptor-like kinase SOL2 mediates CLE signaling in Arabidopsis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP069235
Gene expression in human glioblastoma specimens
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq3000

Description

We assessed global gene expression changes in 32 human glioblastoma specimens Overall design: Human mRNA profiles of 32 glioblastoma specimens, were obtained by sequencing on Illumina HiSeq 3000

Publication Title

Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP101840
Differential gene expression in MZudu v. WT zebrafish gastrulae
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

We report RNA-sequencing data from zebrafish embryos lacking both maternal and zygotic expression of udu (which encodes Gon4l) (MZudu) at tailbud (TB) stage. Transcripts were compared to stage-matched wild-type (WT) embryos to identify differentially expressed genes. Overall design: Sequencing of polyadenylated mRNAs from MZudu mutant and control WT embryos with 2 biological and 2 technical replicates per genotype - each with 3 lanes per sample.

Publication Title

Gon4l regulates notochord boundary formation and cell polarity underlying axis extension by repressing adhesion genes.

Sample Metadata Fields

No sample metadata fields

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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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