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accession-icon GSE10086
Expression profiling of V600E BRAF and RTK-activated cells upon MEK inhibition
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This study used microarray expression analysis to identify global changes in transcript alteration in response to MEK inhibition. Genes under ERK control were identified in a panel of V600E BRAF and RTK-activated tumor cells and xenografts, using short-term inhibition of ERK activity using the MEK inhibitor PD0325901 (Pfizer).

Publication Title

(V600E)BRAF is associated with disabled feedback inhibition of RAF-MEK signaling and elevated transcriptional output of the pathway.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10087
Paired MEK inhibited and control
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This study used microarray expression analysis to identify global changes in transcript alteration in response to MEK inhibition. Genes under ERK control were identified in a panel of V600E BRAF and RTK-activated tumor cells and xenografts, using short-term inhibition of ERK activity using the MEK inhibitor PD0325901 (Pfizer).

Publication Title

(V600E)BRAF is associated with disabled feedback inhibition of RAF-MEK signaling and elevated transcriptional output of the pathway.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE10088
Time course of MEK inhibition
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This study used microarray expression analysis to identify global changes in transcript alteration in response to MEK inhibition. Genes under ERK control were identified in a representative V600E BRAF cell line as a function of time following exposure to a small molecule inhibitor of MEK.

Publication Title

(V600E)BRAF is associated with disabled feedback inhibition of RAF-MEK signaling and elevated transcriptional output of the pathway.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11766
Transcriptional repression of c-Myb and GATA-2 is involved in the effects of C/EBP in p210 BCR/ABL-expressing cells
  • organism-icon Mus musculus
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Levels of C/EBP are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis. To assess the mechanisms involved in these effects, C/EBP targets were identified by microarray analyses. Upon C/EBP activation, expression of c-Myb and GATA-2 was repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBP was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBP while c-Myb siRNA treatment enhanced C/EBP-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBP but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBP induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBP activation. In summary, the effects of C/EBP in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2. Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBP appear to involve different transcription-regulated targets.

Publication Title

Transcriptional repression of c-Myb and GATA-2 is involved in the biologic effects of C/EBPalpha in p210BCR/ABL-expressing cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12120
Transcriptional re-programming of primary human macrophages by IRF-3 and IRF-7
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina humanRef-8 v1.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional re-programming of primary macrophages reveals distinct apoptotic and anti-tumoral functions of IRF-3 and IRF-7.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12002
Transcriptional profiles of Ad-F7 transduced macrophages treated with anti-IFNAR2 antibody or control isotype (IgG)
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina humanRef-8 v1.0 expression beadchip

Description

Determine the role of interferons in the transcriptional profile of Ad-F7 transduced primary human macrophages using neutralizing antibody for the type I IFN receptor (IFNAR2).

Publication Title

Transcriptional re-programming of primary macrophages reveals distinct apoptotic and anti-tumoral functions of IRF-3 and IRF-7.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP050116
Suppression of Transcriptional Drift Extends C. elegans Lifespan by Postponing the Onset of Mortality
  • organism-icon Caenorhabditis elegans
  • sample-icon 43 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Longevity mechanisms increase lifespan by counteracting the effects of aging. However, whether longevity mechanisms counteract the effects of aging continually throughout life, or whether they act during specific periods of life, preventing changes that precede mortality is unclear. Here, we uncover transcriptional drift, a phenomenon that describes how aging causes genes within functional groups to change expression in opposing directions. These changes cause a transcriptome-wide loss in mRNA stoichiometry and loss of co-expression patterns in aging animals, as compared to young adults. Using Caenorhabditis elegans as a model, we show that extending lifespan by inhibiting serotonergic signals by the antidepressant mianserin attenuates transcriptional drift, allowing the preservation of a younger transcriptome into an older age. Our data are consistent with a model in which inhibition of serotonergic signals slows age-dependent physiological decline and the associated rise in mortality levels exclusively in young adults, thereby postponing the onset of major mortality. Overall design: In this study set out to measure aging in the transcriptome by determining drift-variance changes with age in C.elegans. We set up three different cohorts of water or mianserin treated animals. The title of each cohort indicates the treatment (e.g. h2o or mia), the concentration (mia2, mia10, mia50), the day when the treatment was started (e.g. d1= day 1 of adulthood) and the day when the sample was collected (e.g. d10= day 10 of adulthood). cohort #1: Celegans was treated with water or mianserin (50uM) on day 1 and RNA was harvested on day1 (water only), d3, d5 and day 10 (file titles: h2o d1/d1, h2o d1/d3, h2o d1/d5, h2o d1/d10, mia50 d1/d3, mia50 d1/d5, mia50 d1/d10) cohort #2: Celegans was treated with mianserin (50uM) starting on day 3, and day 5, RNA was harvested on day 5 or 10 (file titles: mia50 d3/d10, mia50 d5/d10, mia50 d3/d5) cohort #3: Celegans was treated with mianserin 2 uM and 10 uM Mianserin on day 1 and Rna harvested on day 5 (file titles: mia2 d1/d5, mia10 d1/d5)

Publication Title

Suppression of transcriptional drift extends C. elegans lifespan by postponing the onset of mortality.

Sample Metadata Fields

Subject

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accession-icon GSE17073
Differentially expressed genes among cells constituting an in vitro human lung carcinogenesis system
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Genes differentially expressed among cells constituting an in vitro human lung carcinogenesis model consisting of normal, immortalized, transformed and tumorigenic bronchial epithelial cells were identified. The differentially expressed genes were then analyzed to determine their relevance to the gene expression patterns of clinical non-small cell lung cancer (NSCLC) samples as well as the clinical outcome of patients with this disease.

Publication Title

Identification of gene signatures and molecular markers for human lung cancer prognosis using an in vitro lung carcinogenesis system.

Sample Metadata Fields

Cell line

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accession-icon GSE18517
Gene expression profiling in Al-tolerant and Al-sensitive soybean under aluminum stress
  • organism-icon Glycine max
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

Gene expression profiling in soybean under aluminum stress: genes differentially expressed between Al-tolerant and Al-sensitive genotypes.

Publication Title

Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE18518
Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity
  • organism-icon Glycine max
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level.

Publication Title

Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.

Sample Metadata Fields

Specimen part, Treatment

View Samples
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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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