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accession-icon GSE115247
Interrupted reprogramming of Alveolar Type II cells induces progenitor-like cells that ameliorate pulmonary fibrosis
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

We describe here an interrupted reprogramming strategy to generate "induced Progenitor-Like (iPL) cells" from Alveolar Epithelial Type II (AEC-II) cells. A carefully defined period of transient expression of reprogramming factors (Oct4, Sox2, Klf4 and c-Myc; OSKM) is able to rescue the limited in vitro clonogenic capacity of AEC-II cells, potentially by activation of a bipotential progenitor-like state.

Publication Title

Interrupted reprogramming of alveolar type II cells induces progenitor-like cells that ameliorate pulmonary fibrosis.

Sample Metadata Fields

Specimen part

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accession-icon SRP001995
Comparison of small RNA levels in Dicer helicase mutants
  • organism-icon Caenorhabditis elegans
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Years after the discovery that Dicer is a key enzyme in gene-silencing, the role of its helicase domain remains enigmatic. Here we show that this domain is critical for accumulation of certain endogenous small interfering RNAs (endo-siRNAs) in C. elegans. The domain is required for the production of the direct products of Dicer, or primary endo-siRNAs, and consequently, affects levels of downstream intermediates, the secondary endo-siRNAs. Consistent with the role of endo-siRNAs in silencing, their loss correlates with an increase in cognate mRNA levels. We find that the helicase domain of Dicer is not required for microRNA (miRNA) processing, or RNA interference following exposure to exogenous double-stranded RNA. Comparisons of wildtype and helicase-defective strains using deep-sequencing analyses show that the helicase domain is required by a subset of annotated endo-siRNAs, in particular, those associated with the slightly longer 26 nucleotide small RNA species containing a 5' guanosine. Overall design: We reintroduced either wildtype Dicer, or Dicer harboring a mutation (K39A) in it''s helicase domain, into dcr-1(ok247) mutant worms via transgene rescue. We then used high-throughput sequencing to compare levels of small RNAs present in each of these strains.

Publication Title

Dicer's helicase domain is required for accumulation of some, but not all, C. elegans endogenous siRNAs.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE10775
Expression profiling of mammalian Schwann cells in response to treatment with NRG and/or IGF
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Comparison of the changes in mitochondrial gene expression of cells in which extracellular growth factors and/or mitogens have been added.

Publication Title

Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE117438
SigX ECF sigma factor deletion mutant expression profile in Pseudomonas aeruginosa H103 in LB medium
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

Analysis of a SigX knockout mutant of Pseudomonas aeruginosa H103 strain in LB.

Publication Title

The absence of SigX results in impaired carbon metabolism and membrane fluidity in Pseudomonas aeruginosa.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16028
Longitudinal study of gene expression in healthy individuals
  • organism-icon Homo sapiens
  • sample-icon 108 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The gene expression profile of blood drawn from healthy individuals was studied over a period of six months, at five time points. The gene expression profiles appeared to be constant over one month and to slightly vary over three months. A small proportion of genes were found to be differentially regulated according to gender. Differential gene regulation by age (in subjects 2555 years of age versus subjects > 55 years of age) was not observed.

Publication Title

A longitudinal study of gene expression in healthy individuals.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE136952
Autophagy maintains intestinal stem cell integrity
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The intestinal epithelium is continuously renewed by a pool of intestinal stem cells expressing Lgr5. We show that deletion of the key autophagy gene Atg7 affects the survival of Lgr5+ intestinal stem cells. Mechanistically, this involves defective DNA repair, oxidative stress, and altered interactions with the microbiota. This study highlights the importance of autophagy in maintaining the integrity of intestinal stem cells.

Publication Title

Essential role for autophagy protein ATG7 in the maintenance of intestinal stem cell integrity.

Sample Metadata Fields

Specimen part

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accession-icon E-MTAB-991
Transcription profiling by array of human colon cancer xenografted in immunodeficient mice and rats to investigate clinical heterogeneity
  • organism-icon Homo sapiens
  • sample-icon 115 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

Patient-derived xenograft models are considered to represent the heterogeneity of human cancers and might be more relevant preclinical models to evaluate effective therapeutic agents. Our consortium joins efforts to extensively develop and characterize a new collection of patient-derived colorectal cancer models. From 86 unsupervised surgical colon sample collection, 54 tumors were successfully xenografted in immunodeficient mice and rats, representing 35 primary tumors, 5 peritoneal carcinosis and 14 metastases. Our histological and molecular characterization of patient tumors, first passage on mice and later passages includes the sequence of key genes involved in CRC (ie APC, KRAS, TP53), CGH array and transcriptomic analysis. This comprehensive characterization demonstrates that our collection recapitulates the clinical situation regarding the histopathological and molecular diversity of colorectal cancers. Moreover, patient tumors and corresponding models are clustering together which gives the opportunity to look for relevant signatures and comparison studies between clinical and preclinical data. Hence, we performed pharmacological monotherapy studies with standard of care for colon cancer (5-FU, oxaliplatin, irinotecan, cetuximab). Through this extensive in vivo analysis, we have compared the molecular profile with the drug sensitivity of each tumor models, and run an equivalent of a cetuximab phase II clinical trial in a preclinical setting. Our results confirm the key role of KRAS mutation in the cetuximab resistance and demonstrate that such collection could bring benefit to evaluate novel targeted therapeutic strategies and potentially help the stratification strategy for cancer patients according to molecular marker. This set correspond to 82 CGH profiles, with 7 samples from patient tumor and 75 samples from mouse xenograft at different passages P0 to P9. All hybridizations are performed with Human CGH 244K Agilent arrays (amadid 014693) in dual color with Human DNA Promega (sex matched) as reference. ID for biosources without an -Px suffix correspond to tumor patients. ID with a suffix correspond to xenograft with 0 for the first passage.

Publication Title

Characterization of a large panel of patient-derived tumor xenografts representing the clinical heterogeneity of human colorectal cancer.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Time

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accession-icon SRP068648
The miR-17~92 microRNA cluster is a global regulator of tumor metabolism
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

mRNA expression in Eµ-Myc lymphoma cells expressing or lacking miR-17~92 Overall design: Eµ-Myc B-cell lymphomas harboring conditional alleles of miR-17~92 were cultured with or without 4-OHT to generate isogenic tumour cells with homozygous deletion of miR-17~92. Wild type (fl) and miR-17~92-deleted (del) Eµ-Myc cells were cultured for 48 hours under regular growth conditions, and RNA isolated for sequencing analysis.

Publication Title

The miR-17∼92 microRNA Cluster Is a Global Regulator of Tumor Metabolism.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP068927
Transcriptome comparison of LUBEL catalytic dead mutants to their parental line
  • organism-icon Drosophila melanogaster
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Effect of LUBEL catalytic dead mutation in immune response Overall design: Mutation was introduced in the LUBEL catalytic region by CRISPR/Cas9 techonology in Drosophila melanogaster and their transcriptome was compared in control (sample 23930 to 23941) and e.coli pricked samples (sample 28984 to 28995).

Publication Title

Linear ubiquitination by LUBEL has a role in Drosophila heat stress response.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon SRP077570
Transcriptome comparison of LUBEL catalytic dead mutant to its parental line
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Effect of LUBEL catalytic dead mutation upon Heastshock Overall design: Mutation was introduced in CG11321 catalytic region by CRISPR/Cas9 techonology in Drosophila melanogaster and transcriptome was compared in untreated and heatshocked samples

Publication Title

Linear ubiquitination by LUBEL has a role in Drosophila heat stress response.

Sample Metadata Fields

Treatment, Subject

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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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