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accession-icon GSE6518
Conjugated linoleic acid (CLA) and Caco-2 cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The effect of CLA on gene expression in Caco-2 cells

Publication Title

Conjugated linoleic acid alters global gene expression in human intestinal-like Caco-2 cells in an isomer-specific manner.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE3776
Comparison of Hematopoietic Stem Cell, Mast Cell Precursor and Mature Mast Cell Gene Expression
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

We are interested in comparing expression patterns of hematopoletic stem cells, mast cell precursors and mature mast cells. Our group recently reported that murine mast cells express CD34, Sca-1 and c-kit. Microarray analysis may uncover other novel surface antigens useful in separating mast cells from stem cells.

Publication Title

Prion protein expression and release by mast cells after activation.

Sample Metadata Fields

Sex

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accession-icon GSE23875
Stage-specific sensitivity to p53 restoration in lung cancer
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Stage-specific sensitivity to p53 restoration during lung cancer progression.

Sample Metadata Fields

Sex, Specimen part, Cell line

View Samples
accession-icon GSE23874
Stage-specific sensitivity to p53 restoration in lung cancer: tumor data
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Tumorigenesis is a multistep process that results from the sequential accumulation of mutations in key oncogene and tumor-suppressor pathways. The quest to personalize cancer medicine based on targeting these underlying genetic abnormalities presupposes that sustained inactivation of tumor suppressors and activation of oncogenes are required for tumor maintenance. Mutations in the p53 tumor-suppressor pathway are a hallmark of cancer and significant efforts toward pharmaceutical reactivation of mutant p53 pathways are underway1-3. Here we show that restoration of p53 in established murine lung tumors leads to significant but incomplete tumor cell loss specifically in malignant adenocarcinomas but not in adenomas. Also, we define amplification of MAPK signaling as a critical determinant of malignant progression. The differential response to p53 restoration depends on activation of the Arf tumor suppressor downstream of hyperactive MAPK signaling. We propose that p53 naturally limits malignant progression by responding to increased oncogenic signaling, but is unresponsive to low levels of oncogene activity that are sufficient for early stages of lung tumor development. These data suggest that restoration of pathways important in tumor progression, as opposed to initiation, may lead to incomplete tumor regression due to the stage-heterogeneity of tumor cell populations.

Publication Title

Stage-specific sensitivity to p53 restoration during lung cancer progression.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE23873
Stage-specific sensitivity to p53 restoration in lung cancer: cell line data
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Tumorigenesis is a multistep process that results from the sequential accumulation of mutations in key oncogene and tumor-suppressor pathways. The quest to personalize cancer medicine based on targeting these underlying genetic abnormalities presupposes that sustained inactivation of tumor suppressors and activation of oncogenes are required for tumor maintenance. Mutations in the p53 tumor-suppressor pathway are a hallmark of cancer and significant efforts toward pharmaceutical reactivation of mutant p53 pathways are underway1-3. Here we show that restoration of p53 in established murine lung tumors leads to significant but incomplete tumor cell loss specifically in malignant adenocarcinomas but not in adenomas. Also, we define amplification of MAPK signaling as a critical determinant of malignant progression. The differential response to p53 restoration depends on activation of the Arf tumor suppressor downstream of hyperactive MAPK signaling. We propose that p53 naturally limits malignant progression by responding to increased oncogenic signaling, but is unresponsive to low levels of oncogene activity that are sufficient for early stages of lung tumor development. These data suggest that restoration of pathways important in tumor progression, as opposed to initiation, may lead to incomplete tumor regression due to the stage-heterogeneity of tumor cell populations.

Publication Title

Stage-specific sensitivity to p53 restoration during lung cancer progression.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP156583
Transcriptome profiles of B cell subsets from healthy and SLE subjects
  • organism-icon Homo sapiens
  • sample-icon 266 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

SLE is characterized by the production of autoantibodies that arise from the B cell lineage. Therefore, we sought to assess the epigenetic and transcriptome profiles of distinct B cell subsets known to be expanded in SLE from healthy and SLE subjects. These data define the differentiation heirarchy of B cell subsets and the epigenetic and transcriptional consequences of SLE on human B cells. Overall design: Five distinct B cell subsets were FACS isolated from a cohort of SLE and HC subjects. For a subset of subjects, circulating Antibody Secreting Cells (ASC) were also isolated for comparisons. Cells were FACS sorted into lysis buffer and RNA purified and transcriptome profiles determined by RNA-seq.

Publication Title

Epigenetic programming underpins B cell dysfunction in human SLE.

Sample Metadata Fields

Specimen part, Disease stage, Subject

View Samples
accession-icon GSE28795
Expression data from E. coli cells overexpressing either GreA or GreB in ppGpp0 cells in the dksA+ or dksA- background
  • organism-icon Escherichia coli
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Strains devoid of ppGpp (relA spoT; called ppGpp0), and ppGpp0 dksA- exhibit several amino acid requirements for growth on minimal media. We found that overexpression of DksA can complement some of those requirements. Since DksA is a factor that binds to the RNA polymerase secondary channel, we wondered if other secondary channel proteins might also exert a similar role with respect to growth on minimal media. In our study we found that GreA and partially GreB can in fact complement these requirements under certain conditions. Here, we wished to investigate a broader effect of GreA and GreB on ppGpp0 and ppGpp0 dksA- strains. Since the parent strains are unable to grow in minimal media, we had to supplement the M9 glucose medium with a set of amino acids (DFHILQSTV). We found that both, GreA and GreB can affect a much larger set of genes in the absence of dksA, than in its presence. Also, GreA seems to affect more genes than GreB, under both conditions.

Publication Title

Effects on growth by changes of the balance between GreA, GreB, and DksA suggest mutual competition and functional redundancy in Escherichia coli.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15406
Expression data from E. coli cells overexpressing GraL for short and long periods of time
  • organism-icon Escherichia coli
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Imprecise transcription termination within Escherichia coli greA leader gives rise to an array of short transcripts, GraL.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE15404
Expression data from E. coli cells overexpressing GraL for short periods of time
  • organism-icon Escherichia coli
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

While studying greA expression, we noted presence of an intrinsic terminator in the leader region of greA mRNA transcript. We found this terminator to be quite efficient both in vivo and in vitro. This region seems to be conserved among many enteric bacteria. Judging from fitness experiments, the resulting short RNAs (50-59nt long) exert biological effects. This lead us to propose that greA leader region encodes a novel small non-coding RNA that we collectively call GraL.

Publication Title

Imprecise transcription termination within Escherichia coli greA leader gives rise to an array of short transcripts, GraL.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE15405
Expression data from E. coli cells overexpressing GraL for long periods of time
  • organism-icon Escherichia coli
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

While studying greA expression, we noted presence of an intrinsic terminator in the leader region of greA mRNA transcript. We found this terminator to be quite efficient both in vivo and in vitro. This region seems to be conserved among many enteric bacteria. Judging from fitness experiments, the resulting short RNAs (50-59nt long) exert biological effects. This lead us to propose that greA leader region encodes a novel small non-coding RNA that we collectively call GraL.

Publication Title

Imprecise transcription termination within Escherichia coli greA leader gives rise to an array of short transcripts, GraL.

Sample Metadata Fields

No sample metadata fields

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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