refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 91 results
Sort by

Filters

Technology

Platform

accession-icon GSE110429
ERK3 is essential for establishment of epithelial architecture
  • organism-icon Xenopus laevis
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The atypical mitogen-activated protein kinase ERK3 is essential for establishment of epithelial architecture.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE110427
ERK3 is essential for establishment of epithelial architecture [ERK3 KD]
  • organism-icon Xenopus laevis
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)

Description

Establishment and maintenance of epithelial architecture are essential for embryonic development and adult physiology. Here, we show that ERK3, a poorly characterized atypical MAPK, regulates epithelial architecture in vertebrates. In Xenopus embryonic epidermal epithelia, ERK3 knockdown impairs adherens and tight junction protein distribution, as well as tight junction barrier function, resulting in epidermal breakdown. Moreover, in human breast epithelial cancer cells, inhibition of ERK3 expression induces thickened epithelia with aberrant adherens and tight junctions. Microarray results suggest an involvement of TFAP2A, a transcription factor important for epithelial gene expression, in ERK3-dependent gene expression changes. TFAP2A knockdown phenocopies ERK3 knockdown in both Xenopus embryos and human cells, and ERK3 is required for full activation of TFAP2A-dependent transcription. Our findings thus reveal that ERK3 regulates epithelial architecture, possibly in cooperation with TFAP2A.

Publication Title

The atypical mitogen-activated protein kinase ERK3 is essential for establishment of epithelial architecture.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE110428
ERK3 is essential for establishment of epithelial architecture [ERK3 KD vs. TFAP2A KD]
  • organism-icon Xenopus laevis
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)

Description

Establishment and maintenance of epithelial architecture are essential for embryonic development and adult physiology. Here, we show that ERK3, a poorly characterized atypical MAPK, regulates epithelial architecture in vertebrates. In Xenopus embryonic epidermal epithelia, ERK3 knockdown impairs adherens and tight junction protein distribution, as well as tight junction barrier function, resulting in epidermal breakdown. Moreover, in human breast epithelial cancer cells, inhibition of ERK3 expression induces thickened epithelia with aberrant adherens and tight junctions. Microarray results suggest an involvement of TFAP2A, a transcription factor important for epithelial gene expression, in ERK3-dependent gene expression changes. TFAP2A knockdown phenocopies ERK3 knockdown in both Xenopus embryos and human cells, and ERK3 is required for full activation of TFAP2A-dependent transcription. Our findings thus reveal that ERK3 regulates epithelial architecture, possibly in cooperation with TFAP2A.

Publication Title

The atypical mitogen-activated protein kinase ERK3 is essential for establishment of epithelial architecture.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE33767
The protein kinase MLTK Is a key regulator for chondrogenesis.
  • organism-icon Xenopus laevis
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)

Description

Sox9 acts together with Sox5 or Sox6 as a master regulator for chondrocyte differentiation; however, how these transcription factors functionally interact and collaborate to regulate chondrogenesis remains unclear. Here we show that the protein kinase MLTK plays an essential role in the onset of chondrogenesis through triggering the induction of Sox6 by Sox9. Knockdown of MLTK in Xenopus embryos results in drastic loss of craniofacial cartilages without defects in neural crest formation. We also find that Sox6 is specifically induced during craniofacial chondrogenesis and this induction is inhibited by MLTK knockdown. Remarkably, Sox6-knockdown embryos display essentially the same phenotype as the MLTK-knockdown embryos; the drastic loss of cartilages and the marked down-regulation of genes involved in chondrogenesis. Microarray analysis reveals a remarkable similarity between Sox6-depleted and MLTK-depleted embryos in their gene expression pattern. Moreover, we find that ectopic expression of MLTK can induce Sox6 expression in a Sox9-dependent manner. These results identify a novel, key regulator for chondrogenesis.

Publication Title

The protein kinase MLTK regulates chondrogenesis by inducing the transcription factor Sox6.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE26381
The Kinase SGK1 in the Endoderm and Mesoderm Promotes Ectodermal Survival by Downregulating Components of the Death-Inducing Signaling Complex
  • organism-icon Xenopus laevis
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

A balance between cell survival and apoptosis is essential for animal development. Although proper development involves multiple interactions between germ layers, little is known about the intercellular and intertissue signaling pathways that promote cell survival in neighboring or distant germ layers . We show that serum- and glucocorticoid-inducible kinase 1 (SGK1) promoted ectodermal cell survival during early Xenopus embryogenesis through a non-cell-autonomous mechanism. Dorsal depletion of SGK1 in Xenopus embryos resulted in shortened axes and reduced head structures with defective eyes, and ventral depletion led to defective tail morphologies. Although the gene encoding SGK1 was mainly expressed in the endoderm and dorsal mesoderm, knockdown of SGK1 caused excessive apoptosis in the ectoderm. SGK1-depleted ectodermal explants showed little or no apoptosis, suggesting non-cell-autonomous effects of SGK1 on ectodermal cells. Microarray analysis revealed that SGK1 knockdown increased the expression of genes encoding FADD and caspase-10, components of the death-inducing signaling complex (DISC). Inhibition of DISC function suppressed excessive apoptosis in SGK1-knockdown embryos. SGK1 acted through the transcription factor nuclear factor kappaB to stimulate production of bone morphogenetic protein 7 (BMP7), and overexpression of BMP7 in SGK1-knockdown embryos reduced the abundance of DISC components. We show that phosphoinositide 3-kinase (PI3K) functioned upstream of SGK1, thus revealing an endodermal and mesodermal pathway from PI3K to SGK1 to NF-kappaB that produces BMP7, which provides a survival signal to the ectoderm by decreasing DISC function.

Publication Title

The kinase SGK1 in the endoderm and mesoderm promotes ectodermal survival by down-regulating components of the death-inducing signaling complex.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE141650
Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

We demonstrated that, four weeks after the pulmonary artery banding (PAB) operation, rats could be divided into two groups: an F+ group in which the fibrotic area occupied more than 6.5% of the whole area of the heart tissues, and an F- group in which the fibrotic area occupied less than 6.5% of this area.

Publication Title

Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE6367
Gene profile of breast cancers with immunohistochemical phenotypes of ER+/- and/or HER2+/-
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

Hormones and growth factors accelerate cell proliferation of breast cancer cells, and these molecules are well investigated targets for drug development and application. The mechanisms of cell proliferation of breast cancers lacking estrogen receptor (ER) and HER2 have not been fully understood. The purpose of the present study is to find genes that are differentially expressed in breast cancers and that might significantly contribute to cell proliferation in these cancers. Forty tumor samples, consisting of ten each of immunohistochemically ER(+)/HER2(-), ER(+)/HER2(+), ER(-)/HER2(+), and ER(-)/HER2(-) cancer were analyzed using oligonucleotide microarrays. Both genes and tumor samples were subjected to hierarchical clustering. ER(+)/HER2(-) breast cancers and ER(-)/HER2(-) cancers tended to form a tumor cluster, but HER2 positive breast cancers were split into different tumor clusters.

Publication Title

Overexpression of E2F-5 correlates with a pathological basal phenotype and a worse clinical outcome.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE67896
Gene expression profiles of inoculated tumor cells in TNC-KO mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Tenascin-C (TNC), a cancer-associated extracellular matrix glycoprotein, plays a pivotal role in tumor growth. To identify the genes regulated by TNC during tumor growth, we performed a tumor growth assay, DNA microarray analysis, and quantitative real-time PCR (qRT-PCR). Mouse mammary tumor cells were subcutaneously inoculated into GRS/A (WT) and GRS/A-TgH(Tnc) (TNKO) mice. Tumors in WT mice significantly increased in volume with expressing TNC while tumors in TNKO mice showed hardly detectable levels of TNC. Tumor gene expression profiles between TNKO and WT mice were compared using DNA microarray analysis. We found that 447 genes were up-regulated (TNKO>WT) and 667 genes were down-regulated (TNKO<WT) in the TNKO group. We then classified these genes by Gene Ontology (GO) terms in order to elucidate their biological function. There were three GO terms found related to tumor growth, namely, acute inflammatory response, cell adhesion, and response to wounding. Eighty-three of the genes primarily involved in these GO terms were further validated by qRT-PCR. Eight genes: Tnc, Cxcl2, Cxcl1, Hbegf, Chl1, Cd44, Serpina3n, and F3 were significantly down-regulated relative to the WT. Eighteen genes: Saa3, P2rx7, Ptgs1, Ptger2, Comp, Steap4, Il1rn, Il1b, Ncf1, Mst1, Nfb1, Ctsb, Tnfrsf1a, Tnfrsf1b, Cd24a, Adam17, Mtpn, and Sox4 were significantly up-regulated relative to the WT. These results support our hypothesis that TNC has multi-faceted effects on both the tumor cells and their microenvironment. First, TNC acts on the tumor cells directly by up-regulating genes involved in cancer cell proliferation through the CXCL1/2 and CXCR2 pathway. Second, TNC controls the tumor microenvironment by promoting angiogenesis through the CXCL1/2 and CXCR2 pathway, and by suppressing inflammatory gene expression through a separate pathway.

Publication Title

Comprehensive DNA microarray expression profiles of tumors in tenascin-C-knockout mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE80985
Expresion data from primary retinal pigment epithelium (RPE) and immortalized RPE
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to detail the global gene expression of primary RPE and immortalized RPE.

Publication Title

Identification of a Gene Encoding Slow Skeletal Muscle Troponin T as a Novel Marker for Immortalization of Retinal Pigment Epithelial Cells.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE108566
Expression data from human induced pluripotent stem cells II
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to detail the global gene expression of human induced pluripotent stem cells

Publication Title

Tumorigenicity-associated characteristics of human iPS cell lines.

Sample Metadata Fields

Cell line

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact