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accession-icon GSE35062
Phytochrome Interacting Factors 4 and 5
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Phytochrome interacting factors 4 and 5 control seedling growth in changing light conditions by directly controlling auxin signaling.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE35057
Phytochrome Interacting Factor 4 and 5 regulate different set of genes in high and low red/far-red light
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

As sessile organisms plants developed a veriety of adaptive responses to the ever changing environment. One of these responses is the shade avoidance syndrome which is composed of different responses like elongation growth, hyponastic leafs or early flowering to shade (low R/FR). Phytochrcome Interacting Factor 4 and 5 are bHLH transcription factors reported to activate gene expression upon perception of low R/FR. Using this miroarray experiment we identified new genes regulated by PIF4 and PIF5 in response to shade and investigated their genome wide role.

Publication Title

Phytochrome interacting factors 4 and 5 control seedling growth in changing light conditions by directly controlling auxin signaling.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE29353
Expression data for haploid Saccharomyces cerevisiae strains growing in a defined low glucose medium.
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

We used microarrays to assess differences in gene expression associated with single nucleotide polymorphisms occurred in three genes, PMA1, MDS3 and MKT1, as compared to a reference strain devoid of any mutations (Progenitor strain).

Publication Title

Cellular effects and epistasis among three determinants of adaptation in experimental populations of Saccharomyces cerevisiae.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7309
Requirement for ERK MAP kinase in mouse preimplantation development
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Preimplantation development is a crucial step for successful implantation and pregnancy. Although both compaction and blastocyst formation have been extensively studied, mechanisms regulating early cell division stages before compaction have remained unclear. Here, we show that ERK MAP kinase function is required for early embryonic cell division and normal cell-cell adhesion before compaction. Our analysis demonstrates that inhibition of ERK activation in the late 2-cell stage embryos leads to a reversible arrest in G2 phase in the 4-cell stage. The G2 arrested, 4-cell stage embryos show weakened cell-cell adhesion as compared to control embryos. Remarkably, microarray analyses show that most of the programmed changes of upregulated and downregulated gene expression during the 4- to 8-cell stages normally proceed in the 4-cell stage-arrested embryos, except for a portion of the genes whose expression profiles closely parallel the stages of embryonic development when arrested in G2 and released to resume development. These parallel genes include the genes encoding intercellular adhesion molecules, whose expression is found to be positively regulated by the ERK pathway. We also show that while ERK inactivation in the 8-cell stage embryos does not lead to cell division arrest, it does cause cell division arrest when cadherin-mediated cell-cell adhesion is disrupted. These results demonstrate an essential role of ERK function in the G2/M transition and the expression of adhesion molecules during the 2-cell to 8-cell stage embryos, and suggest a loose parallelism between the gene expression programs and the developmental stages before compaction.

Publication Title

Requirement for ERK MAP kinase in mouse preimplantation development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE35685
Lymphoid Priming in Human Bone Marrow Begins Prior to CD10 Expression with Up-Regulation of L-selectin
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Studies of adult human hematopoiesis have until now relied on the expression of CD10 to define lymphoid commitment. We report a novel lymphoid-primed population in human bone marrow that is generated from hematopoietic stem cells (HSC) prior to the onset of CD10 expression and B cell commitment, and is identified by high levels of the homing molecule L-selectin (CD62L). CD10-CD62Lhi progenitors have full lymphoid (B/T/NK) potential, and show reduced myeloid and absent erythroid potential. Genome-wide gene expression analysis demonstrates that the CD10-CD62Lhi population represents an intermediate stage of differentiation between CD34+CD38- HSC and CD34+lin-CD10+ progenitors marked by down-regulation of TAL1 and MPL, upregulation of E2A, CD3E and IL2RG expression, and absent B cell commitment or RAG1/2 expression. Immature CD34+CD1a- thymocytes are also CD62Lhi and L-selectin ligands are expressed at the cortico-medullary junction, suggesting a possible role for L-selectin in human thymic homing. These studies identify the earliest stage of lymphoid priming in human bone marrow.

Publication Title

Lymphoid priming in human bone marrow begins before expression of CD10 with upregulation of L-selectin.

Sample Metadata Fields

Specimen part

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accession-icon GSE150464
Role of PDK1 in Skeletal Muscle Hypertrophy Induced by Exercise Load
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Skeletal muscle mass is an important determinant of whole-body glucose disposal. We here show that mice (M-PDK1KO mice) with skeletal muscle–specific deficiency of 3'-phosphoinositide–dependent kinase 1 (PDK1), a key component of the phosphatidylinositol 3-kinase (PI3K) signaling pathway, manifest a reduced skeletal muscle mass under the static condition as well as impairment of exercise load–induced muscle hypertrophy.

Publication Title

Role of PDK1 in skeletal muscle hypertrophy induced by mechanical load.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP192834
Transcriptomic of MKD (MUC1 kidney disease) patient compares to normal derived kidney epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

bulk RNAseq of MUC1 kidney disease patient derived kidney epithelial cells compare to normal kidney cells. The goal of this study was to elucidate the biological mechanism underlying MUC1 kidney disease using MUC1 expressing cells derived from either a patient or a healthy individual kidney Overall design: Bulk RNAseq of immortalized patient compare to normal cell line

Publication Title

Small Molecule Targets TMED9 and Promotes Lysosomal Degradation to Reverse Proteinopathy.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP038970
small RNAseq analysis of the global retinal transcriptome of rod photoreceptor-specific Dicer1 conditional knockout mice and control littermates
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report RNAseq analysis of the transcriptome of retinas from mature rod-specific Dicer1 cKO mice and control littermates lacking Cre expression in order to better understand changes in gene regulation that could lead to retinal degeneration in cKO mice. Overall design: Examine retinal transcriptome of 3 biological replicates for each genotype from 4-week-old animals with tissue collected between 8:00 - 10:00AM

Publication Title

DICER1 is essential for survival of postmitotic rod photoreceptor cells in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP038971
RNAseq analysis of the global retinal transcriptome of rod photoreceptor-specific Dicer1 conditional knockout mice and control littermates
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiScanSQ

Description

We report RNAseq analysis of the transcriptome of retinas from mature rod-specific Dicer1 cKO mice and control littermates lacking Cre expression in order to better understand changes in gene regulation that could lead to retinal degeneration in cKO mice. Overall design: Examine retinal transcriptome of 3 biological replicates for each genotype from 4-week-old animals with tissue collected between 8:00 - 10:00AM

Publication Title

DICER1 is essential for survival of postmitotic rod photoreceptor cells in mice.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE30585
Gene expression changes induced by dimerization of intracellular c-Mpl in cord blood CD34+ progenitors
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Homodimerization of Mpl can also be accomplished in the absence of Tpo, by binding of a synthetic ligand (Chemical inducer of dimerization, CID) to a constitutively expressed fusion protein F36VMpl consisting of a ligand binding domain (F36V) and the intracellular signaling domain of Mpl. In contrast to Tpo stimulation, F36VMpl dimerization in human CD34+ progenitor cells generates robust erythropoiesis.

Publication Title

Novel pathways to erythropoiesis induced by dimerization of intracellular C-Mpl in human hematopoietic progenitors.

Sample Metadata Fields

Specimen part

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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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