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accession-icon SRP098628
Genome-wide maps of chromatin state in pluripotent and lineage-committed cells.
  • organism-icon Anopheles gambiae
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Malaria infection renders humans more attractive to Anopheles gambiae sensu lato mosquitoes than uninfected people. The mechanisms remain unknown. Here, we show that an isoprenoid precursor produced by Plasmodium falciparum, (E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate (HMBPP), affects A. gambiae s.l. blood meal seeking and feeding behaviors, as well as susceptibility to infection. HMBPP acts indirectly by triggering human red blood cells to increase the release of CO2, aldehydes, and monoterpenes, which together enhance vector attraction, and stimulate vector feeding. When offered in a blood meal, HMBPP modulates neural, antimalarial, and oogenic gene transcription without affecting mosquito survival or fecundity, while in a P. falciparum infected blood meal, sporogony is increased. Overall design: Differential expression was quantified from whole body of mosquitoes in biological triplicates at 1, 3, 6 and 24 hours post treatment with either RBCs or hmbRBCs.

Publication Title

A key malaria metabolite modulates vector blood seeking, feeding, and susceptibility to infection.

Sample Metadata Fields

Subject, Time

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accession-icon GSE6547
Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35
  • organism-icon Caenorhabditis elegans
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process.

Publication Title

Transcriptome profiling of the C. elegans Rb ortholog reveals diverse developmental roles.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9246
Transcriptome profiling of slr-2, C.elegans C2H2 Zn-finger
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

Our slr-2 dataset showed strong overrepresentation of genes previously identified in a serial analysis of gene expression (SAGE) intestinal library (McGhee et al., 2006) (p << 0.01); 812 genes were common to both data sets. Consistent with the deregulation of intestinal genes, we observed repression of several important metabolic pathways, including the TOR and insulin signaling networks, suggesting that slr-2(ku297) mutants experience metabolic stress. We also compared differentially regulated genes in slr-2 and lin-35 single mutants. Again, we saw a statistically significant overlap (p-value < 0.01); 261 genes were present in both data sets. Strikingly, > 75% of genes common both datasets showed expression changes in the same direction, although the common dataset contained an approximately equal mixture of up and downregulated genes. Furthermore, more than fifty genes common to the lin-35 and slr-2 datasets are known to have intestinal-associated functions. That some of these common intestinal genes were absent from the gut SAGE library could be due to differences in the developmental stage of the animals assayed (adults versus L1s) as well as experimental approaches (SAGE versus microarrays)

Publication Title

Coordinated regulation of intestinal functions in C. elegans by LIN-35/Rb and SLR-2.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE54590
HEXIM knockdown triggers apoptosis-induced proliferation and deregulates Hedgehog signaling
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

We address the function of HEXIM, an inhibitor of the general transcriptional elongation regulator P-TEFb which regulates the transcriptional status of many developmental genes, during Drosophila development. We showed that HEXIM knockdown mutants display organs development failure. In the wing disc, it induces apoptosis and affects Hh signaling. The continuous death of proliferative cells is compensated by apoptosis-induced cell proliferation, in a manner similar to that of differentiated cells, together with high levels of Hh and Ci. We completed this analysis with microarrays to characterize the molecular phenotype of HEXIM knockdown during eye differentiation.

Publication Title

Functional Interaction between HEXIM and Hedgehog Signaling during Drosophila Wing Development.

Sample Metadata Fields

Specimen part

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accession-icon GSE7875
Deletion of PKBalpha/Akt1 affects thymic development
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The thymus constitutes the primary lymphoid organ for the majority of T cells. The phosphatidyl-inositol 3 kinase (PI3K) signaling pathway is involved in lymphoid development. Defects in single components of this pathway prevent thymocytes from progressing beyond early T cell developmental stages. Protein kinase B (PKB) is the main effector of the PI3K pathway. To determine whether PKB mediates PI3K signaling in early T cell development, we characterized PKB knockout thymi. Our results reveal a significant thymic hypocellularity in PKBalpha-/- neonates and an accumulation of early thymocyte subsets in PKBalpha-/- adult mice. The latter finding is specifically attributed to the lack of PKBalpha within the lymphoid component of the thymus. Microarray analyses show that the absence of PKBalpha in early thymocyte subsets modifies the expression of genes known to be involved in pre-TCR signaling, in T cell activation, and in the transduction of interferon-mediated signals. This report highlights the specific requirements of PKBalpha for thymic development.

Publication Title

Deletion of PKBalpha/Akt1 affects thymic development.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE13124
Natural compound screening
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Transcriptional expression data for bioactive small molecules for mechanism identification.

Publication Title

Identification of a novel topoisomerase inhibitor effective in cells overexpressing drug efflux transporters.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP137804
Influenza virus replication intensity and round of infection dictates the cellular response in vivo
  • organism-icon Mus musculus
  • sample-icon 39 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Influenza A virus has a broad cellular tropism in the respiratory tract. Infected epithelial cells sense the infection and initiate an antiviral response. To define the antiviral response at the earliest stages of infection we used two different single cycle replication reporter viruses. These tools demonstrated heterogeneity in virus replication levels in vivo. Transcriptional profiling demonstrated tiers of interferon stimulated gene responses that were dependent on the magnitude of virus replication. Uninfected cells and cells with blunted replication expressed a distinct and potentially protective ISG signature. Finally, we used these single cycle reporter viruses to determine the antiviral landscape during virus spread, which unveiled disparate protection mediated by IFN. Together these results highlight the complexity of virus-host interactions within the infected lung and suggest that magnitude and round of replication tune the antiviral response. Overall design: Mice were infected with 10^5 pfu of the indicated virus. Lungs from infefected C57BL/6 were taken at 24 hours post infection. Single cell suspensions were sorted for live CD45-CD31- and the indicated virus-driven fluorophore. Cells were FACS sorted directly into cell lysis buffer for RNA extraction. cDNA libraries were prepared using the SMARTer Universal Low Input RNA Kit (Takara Bio). SAmples were then profiled by illumina sequencing

Publication Title

Distinct antiviral signatures revealed by the magnitude and round of influenza virus replication in vivo.

Sample Metadata Fields

Specimen part, Cell line, Subject

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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

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accession-icon GSE60705
Gene expression in glioblastoma (GBM) tissues, glioblastoma stem-like cell (GSC) cultures and neural foetal cell line (NFC)
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This microarray contains expression data for two GBM tissue samples, four GSC cultures grown as spheres and one NFC culture grown as spheres

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)

fund-icon Fund the CCDL

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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