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accession-icon GSE33413
Functional Genomic Analysis Of Barley(Hordeum vulgare L.) Grain Protein Accumulation
  • organism-icon Hordeum vulgare
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Barley Genome Array (barley1)

Description

Effect of high grain protein locus on barley grain protein accumulation. Gene expression levels were analysed in Karl, a low grain protein variety with its near-isogenic line 10_11(has high grain protein locus, chromosome 6)using Barley1 22k affymetrix chip. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Aravind Jukanti. The equivalent experiment is BB53 at PLEXdb.]

Publication Title

Comparative transcriptome profiling of near-isogenic barley (Hordeum vulgare) lines differing in the allelic state of a major grain protein content locus identifies genes with possible roles in leaf senescence and nitrogen reallocation.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE45935
Exon level gene expression profile of the prefrontal cortex region of Df(16)A+/- mice, a mouse model of 22q11.2 microdeletion syndrome
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Df16(A)+/- mice line is a model of human 22q11 microdeletion syndrome. We conducted an unbiased evaluation of the transcriptional difference in the prefrontal cortex between mutant and wild type animals at exon level. These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1 The reasoning behind this expression profiling is that consistent alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. Df(16)A+/- mice line is a model of human 22q11 microdeletion syndrome.

Publication Title

The pattern of cortical dysfunction in a mouse model of a schizophrenia-related microdeletion.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE94314
Cadmium (Cd) induced expression changes in the Arabidopsis thaliana accessions Col-0 and Bur-0
  • organism-icon Arabidopsis thaliana
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Metal tolerance is often a result of metal storage or distribution. Thus, with the goal of advancing the molecular understanding of such metal homeostatic mechanisms, natural variation of metal tolerance in Arabidopsis thaliana was investigated. Substantial variation exists in tolerance of excess copper (Cu), zinc (Zn) and cadmium (Cd). Two accessions, Col-0 and Bur-0, and a recombinant inbred line (RIL) population derived from these parents were chosen for further analysis of Cd and Zn tolerance variation, which is evident at different plant ages in various experimental systems and appears to be genetically linked. Three QTLs, explaining in total nearly 50 % of the variation in Cd tolerance, were mapped. The one obvious candidate gene in the mapped intervals, HMA3, is unlikely to contribute to the variation. In order to identify additional candidate genes the Cd responses of Col-0 and Bur-0 were compared at the transcriptome level. The sustained common Cd response of the two accessions was dominated by processes implicated in plant pathogen defense. Accession-specific differences suggested a more efficient activation of acclimative responses as underlying the higher Cd tolerance of Bur-0. The second hypothesis derived from the physiological characterization of the accessions is a reduced Cd accumulation in Bur-0.

Publication Title

Natural variation in Arabidopsis thaliana Cd responses and the detection of quantitative trait loci affecting Cd tolerance.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP069968
mRNA-seq from Nutlin-3a, doxorubicin, and DMSO treated HCT116 p21-/- cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

We sequenced mRNA from HCT116 p21-/- cells treated with Nutlin-3a, doxorubicin, or DMSO for 24 h. Overall design: Examination of mRNA levels from HCT116 p21-/- cells treated with Nutlin-3a, doxorubicin, or DMSO for 24 h using four replicates each.

Publication Title

Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9408
Identification of putative Arabidopsis DEMETER target genes by GeneChip Analysis
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

We used Affymetrix Arabidopsis ATH1 GeneChip to profile RNAs active in wild type columbia (glabrous) and CaMV::DME pollen and stamens.

Publication Title

Identification of putative Arabidopsis DEMETER target genes by GeneChip analysis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE50058
A common rejection module for acute rejection in multiple organs identifies novel therapeutics.
  • organism-icon Homo sapiens
  • sample-icon 101 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Using meta-analysis of eight independent transplant datasets (236 graft biopsy samples) from four organs, we identified a common rejection module (CRM) consisting of 11 genes that were significantly overexpressed in acute rejection (AR) across all transplanted organs. The CRM genes could diagnose AR with high specificity and sensitivity in three additional independent cohorts (794 samples). In another two independent cohorts (151 renal transplant biopsies), the CRM genes correlated with the extent of graft injury and predicted future injury to a graft using protocol biopsies. Inferred drug mechanisms from the literature suggested that two FDA-approved drugs (atorvastatin and dasatinib), approved for non-transplant indications, could regulate specific CRM genes and reduce the number of graft infiltrating cells during acute rejection. We treated mice with HLA-mismatched murine cardiac transplant with atorvastatin and dasatinib and showed reduction of the CRM genes, significant reduction of graft infiltrating cells, and extended graft survival. We further validated the beneficial effect of atorvastatina on graft survival by retrospective analysis of electronic medical records of a single-center cohort of 2,515 renal transplant patients. In conclusion, we identified a CRM in transplantation that provides new opportunities for diagnosis, drug repositioning and rational drug design.

Publication Title

A common rejection module (CRM) for acute rejection across multiple organs identifies novel therapeutics for organ transplantation.

Sample Metadata Fields

Specimen part

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accession-icon GSE21689
MozAtlas: A comprehensive gene expression atlas of sex- and tissue-specificity in the malaria vector, Anopheles gambiae.
  • organism-icon Anopheles gambiae
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)

Description

Background.

Publication Title

A comprehensive gene expression atlas of sex- and tissue-specificity in the malaria vector, Anopheles gambiae.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP072566
RNA-Seq analysis of NKX2.2 knockdown in human pancreatic islets
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Aim:Transcriptional analysis of NKX2.2 knockdown versus control in human pancreatic islets Methods:Pancreatic islets from 3 human donors were transduced with an adenovirus encoding an shRNA directed against human NKX2.2 or a scrambled shRNA control. Total RNA was extracted.Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the human genome (Human: NCBI/build37.2)) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq. Results: Among the dysregulated genes with a p-value=0.05 are important genes for the maintenance of beta cell function and idenity. Conclusion: Nkx2.2 is a critical regulator of beta cell function and identity Overall design: mRNA profiles of the pancreatic islets from 3 human donors transduced with Ad.sh-NKX2.2 or scramble sh-RNA control vector were generated by deep sequencing , using Illumina HiSeq2000.

Publication Title

Genetic evidence that Nkx2.2 acts primarily downstream of Neurog3 in pancreatic endocrine lineage development.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP072565
RNA-Seq analysis of the pancreatic islets of beta cell specific adult Nkx2.2 mutant mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Aim:Transcriptional analysis of the pancreatic islets of adult Nkx2.2 flox/flox; RipCre mice versus control Methods:Pancreatic islets from 4week old Nkx2.2 mutant mice and controls were isolated and total RNA was extracted.Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq. Results: Among the downregulated genes with a p-value=0.05 are important genes for beta cell function and idenity.Among the upregulated genes with a p-value=0.05 are non beta endocrine hormones. Conclusion: Nkx2.2 activates important beta cell genes and actively represses non beta cell genes Overall design: mRNA profiles of the pancreatic islets of 4 week old control and Nkx2.2 mutant mice were generated by deep sequencing , in triplicate, using Illumina HiSeq2000.

Publication Title

Genetic evidence that Nkx2.2 acts primarily downstream of Neurog3 in pancreatic endocrine lineage development.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP033357
Analysis of transgene siRNAs and ARL-8-dependent siRNAs in Caenorhabditis elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We analyzed the C. elegans small RNA response to high copy transgene sequences expressed in the soma in a wild type and an eri-6/7 mutant background. We also analyzed small RNA defects in the arl-8(tm2472) mutant. Transgene siRNAs are 22 nt long, mostly antisense, and correspond to the promoter, coding regions, the 3''UTR and plamsid sequences present on the transgene. Transgene siRNAs are decreased in the eri-6/7 mutant. In the arl-8 mutant, 26G siRNAs in the ALG-3/4 dependent endogenous RNAi pathway are decreased. Overall design: Sequencing small RNAs from C. elegans transgenic strains and mutants.

Publication Title

Multiple small RNA pathways regulate the silencing of repeated and foreign genes in C. elegans.

Sample Metadata Fields

Specimen part, Cell line, 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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