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accession-icon SRP117360
The Arabidopsis transcription factor TCP5 during petal and inflorescence development
  • organism-icon Arabidopsis thaliana
  • sample-icon 31 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-sequencing performed on petals and inflorescence of Arabidopsis plants. The study provides insight into the role of the TCP5 transcription factor and its molecular mechanism underlying petal growth, using knock-out, overexpression and induction lines on which RNA-sequencing was performed. Overall design: Analysis of differential gene expression using petals from TCP5 overexpression and knockout lines, as well as inflorescences of an inducible TCP5 mutant.

Publication Title

Novel functions of the Arabidopsis transcription factor TCP5 in petal development and ethylene biosynthesis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon E-MEXP-1138
Transcription profiling of mature pollen grains from wild type and AtMIKC* MADS-box gene knock-out Arabidopsis plants
  • organism-icon Arabidopsis thaliana
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Effects of loss-of-function of AtMIKC* MADS-box genes on the mature Arabidopsis pollen transcriptome.

Publication Title

MADS-complexes regulate transcriptome dynamics during pollen maturation.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE54312
HDG1 transcription factor targets
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

The AIL transcription factor BABY BOOM (BBM) is required together with the related PLETHORA proteins for embryo and root meristem development and its expression is sufficient to confer pluripotency and totipotency to somatic tissues. We show that BBM and other AIL proteins interact with multiple members of the L1/epidermal-expressed HD-ZIP class IV / HOMEODOMAIN GLABROUS (HDG) transcription factor family. Ectopic overexpression of HDG1, HDG11 and HDG12 genes induces a reduced growth phenotype, and analysis of HDG1 overexpression lines shows that this growth reduction is due to both root and shoot meristem arrest. To understand how HDG1 controls cell proliferation, as well as its functional relationship with BBM, we performed microarray experiments to identify candidate genes that are directly regulated by HDG1, and compared these to the set of genes that are directly regulated by BBM expression.

Publication Title

AIL and HDG proteins act antagonistically to control cell proliferation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP154301
NuRD-interacting protein ZFP296 regulates genome-wide NuRD localization and differentiation of mouse embryonic stem cells (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The Nucleosome Remodeling and Deacetylase (NuRD) complex plays an important role in gene expression regulation, stem cell self-renewal, and lineage commitment. Yet little is known about the dynamics of NuRD during cellular differentiation. Here, we study these dynamics using genome-wide profiling and quantitative interaction proteomics in mouse embryonic stem cells (ESCs) and neural progenitor cells (NPCs). The genomic targets of NuRD are highly dynamic during differentiation, with most binding occurring at cell-type specific promoters and enhancers. We identify ZFP296 as a novel, ESC-specific NuRD interactor that also interacts with the SIN3A complex. ChIP-sequencing in Zfp296 knockout (KO) ESCs reveals decreased NuRD binding both genome-wide and at ZFP296 binding sites, although this has little effect on the transcriptome. Nevertheless, Zfp296 KO ESCs exhibit delayed induction of lineage-specific markers upon differentiation to embryoid bodies. In summary, we identify an ESC-specific NuRD interacting protein which regulates genome-wide NuRD binding and cellular differentiation. Overall design: RNA-seq samples of wildtype R1 ESCs and Zfp296 CRISPR KO clone 2 R1 ESCs

Publication Title

NuRD-interacting protein ZFP296 regulates genome-wide NuRD localization and differentiation of mouse embryonic stem cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE108036
Comparative analysis of cartilage tissue from ANP32A knockout mice and wildtype C57/Bl6 mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

A genetic association between the ANP32A gene and osteoarthritis has been suggested. We compared transcriptome profiles of the articular cartilage and subchondral bone from mice deficient in ANP32A with wild-type mice to get insights into the role of ANP32A in the pathogenesis of ostearthritis.

Publication Title

ANP32A regulates ATM expression and prevents oxidative stress in cartilage, brain, and bone.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP106954
N6-methyladenosine (m6A) recruits and repels proteins to regulate mRNA homeostasis
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon

Description

RNA modifications are integral to regulation of RNA metabolism. One such abundant mRNA modification is m6A, which impacts various aspects of RNA metabolism including splicing, transport and degradation. Current knowledge about proteins recruited to m6A to carry out these molecular processes is still limited. Here we describe a comprehensive and systematic mass spectrometry-based screening of m6A interactors in various cell types and species. Amongst the main findings, we identified G3BP1 as a protein, which is repelled by m6A and which positively regulates mRNA stability in an m6A regulated manner. Furthermore, we identified FMR1 as a novel, RNA sequence context dependent m6A reader, thus revealing a connection between an mRNA modification and an autism spectrum disorder. Collectively, our data represents a rich resource for the community and sheds further light on the complex interplay between m6A, m6A interactors and mRNA homeostasis. Overall design: Transcriptome wide profiling of G3BP1 and G3BP2 binding sites and mRNA half-live measurement after G3BP1 overexpression or knockdown.

Publication Title

N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) recruits and repels proteins to regulate mRNA homeostasis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP107747
Specific labeling of stem cell activity in human colorectal organoids using an ASCL2-responsive minigene
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Organoid technology provides the possibility to culture human colon tissue and patient-derived colorectal cancers (CRC) while maintaining all functional and phenotypic characteristics. Labeling of human colon stem cells (CoSCs), especially in normal and benign tumor organoids, is challenging and therefore limits usability of multi-patient organoid libraries for CoSC research. Here, we developed STAR (STem cell Ascl2 Reporter), a minimal enhancer/promoter element that reports transcriptional activity of ASCL2, a master regulator of LGR5+ CoSC fate. Among others via lentiviral infection, STAR minigene labels stem cells in normal as well as in multiple engineered and patient-derived CRC organoids of different stage and genetic make-up. STAR revealed that stem cell driven differentiation hierarchies and the capacity of cell fate plasticity (de-differentiation) are present at all stages of human CRC development. The flexible and user-friendly nature of STAR applications in combination with organoid technology will facilitate basic research on human adult stem cell biology. Overall design: Cells from different colon organoid types were FACS sorted for stem STemness Ascl2 Reporter activity for transcriptome profiling by RNA-seq.

Publication Title

Specific Labeling of Stem Cell Activity in Human Colorectal Organoids Using an ASCL2-Responsive Minigene.

Sample Metadata Fields

Subject

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accession-icon GSE19301
Gene Expression Patterns in Peripheral Blood Mononuclear Cells Associated with Asthma Exacerbation Attack
  • organism-icon Homo sapiens
  • sample-icon 220 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

A large, prospective, non-interventional study was designed to study gene expression changes in peripheral blood mononuclear cells (PBMCs) associated with asthma exacerbations over the course of a year. PBMC samples were collected from subjects at the time of the study visits defined as 1) Quiet: during stable disease at 3 month intervals, 2) Exacerbation: during a 14 day period of deteriorating asthma and 3) Follow-up: within 14 days after cessation of an exacerbation. Gene expression levels during stable asthma, exacerbation, and two weeks after an exacerbation were compared.

Publication Title

Pathways activated during human asthma exacerbation as revealed by gene expression patterns in blood.

Sample Metadata Fields

Specimen part, Race

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accession-icon GSE15907
Immunological Genome Project data Phase 1
  • organism-icon Mus musculus
  • sample-icon 638 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Gene-expression microarray datasets generated as part of the Immunological Genome Project (ImmGen). Primary cells from multiple immune lineages are isolated ex-vivo, primarily from young adult B6 male mice, and double-sorted to >99% purity. RNA is extracted from cells in a centralized manner, amplified and hybridized to Affymetrix 1.0 ST MuGene arrays. Protocols are rigorously standardized for all sorting and RNA preparation. Data is released monthly in batches of cell populations.

Publication Title

Transcriptomes of the B and T lineages compared by multiplatform microarray profiling.

Sample Metadata Fields

Sex, Age

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accession-icon GSE85333
Transcriptional effects of anti-inflammatory or anti-depressant drugs on primary human macrophages inflammatory response
  • organism-icon Homo sapiens
  • sample-icon 182 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

The direct communication between our central nervous and inflammatory signalling systems is a well-recognised, yet poorly understood relationship. To increase our understanding of this relationship, we examined the metabolism of serotonin and its precursor tryptophan in macrophages under inflammatory settings. Both are involved in inflammatory signalling and known to play a major role in mood regulation. Tryptophan depletion by macrophages during inflammation can consequently result in a reduction of serotonin systemically and has been suggested to cause depression. Increased understanding of this system could help overcome the problem of treatment resistant depressed patients. To this end, we treated primary human monocyte derived macrophages with a range of anti-depressant/anti-inflammatory drugs and analysed their transcriptional profile under various inflammatory conditions. In addition to the classic endotoxic driver of inflammation, LPS, we also used IFN which is a constitutive cytokine shown to directly induce depression when administered in high doses. The anti-depressant drugs were not found to have any significant effects on macrophage inflammatory signalling. However, the anti-inflammatories drugs were found to alter components of the serotonin/tryptophan metabolism pathways. This study increases our understanding of the intricacies of immune/mood cross-talk and offers into developing anti-inflammatories as co-treatment for depression.

Publication Title

Effects of anti-inflammatory drugs on the expression of tryptophan-metabolism genes by human macrophages.

Sample Metadata Fields

Sex, Specimen part, 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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