refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 400 results
Sort by

Filters

Technology

Platform

accession-icon GSE49658
Human inositol polyphosphate multikinase regulates transcript-selective nuclear mRNA export to preserve genome integrity
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Messenger (m)RNA export from the nucleus is essential for eukaryotic gene expression. Here, we identify a transcript-selective nuclear export mechanism affecting certain human transcripts, enriched for functions in genome duplication and repair, controlled by inositol polyphosphate multikinase (IPMK), an enzyme catalyzing inositol polyphosphate and phosphoinositide turnover. We studied transcripts encoding RAD51, a protein essential for DNA repair by homologous recombination (HR), to characterize the mechanism underlying IPMK-regulated mRNA export. IPMK depletion or catalytic inactivation selectively decreases the nuclear export of RAD51 mRNA, and RAD51 protein abundance, thereby impairing HR. Recognition of a sequence motif in the untranslated region of RAD51 transcripts by the mRNA export factor ALY requires IPMK. Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), an IPMK product, restores ALY recognition in IPMK-depleted cell extracts, suggesting a mechanism underlying transcript selection. Our findings implicate IPMK in a transcript-selective mRNA export pathway controlled by phosphoinositide turnover that preserves genome integrity in humans.

Publication Title

Human inositol polyphosphate multikinase regulates transcript-selective nuclear mRNA export to preserve genome integrity.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE12584
Microarray analysis of the interaction between Rhopalosiphum padi and partially resistant or susceptible barley lines
  • organism-icon Hordeum vulgare, Hordeum vulgare subsp. spontaneum
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Barley Genome Array (barley1)

Description

The bird cherry-oat aphid (Rhopalosiphum padi L.) (Homoptera: Aphididae) is an important pest on cereals causing plant growth reduction but no specific leaf symptoms. Breeding of barley (Hordeum vulgare L.) for R. padi resistance shows that there are several resistance genes involved, reducing aphid growth. In an attempt to identify candidate sequences for resistance-related genes, we performed a microarray analysis of gene expression after two days of aphid infestation in two susceptible barley lines and two genotypes with partial resistance. One of the four lines is a descendant of two of the other genotypes. The analysis revealed large differences in gene induction between the four lines, indicating substantial variation in response even between closely related genotypes. Genes induced in the aphid-infested tissue were mainly related to defence, primary metabolism and signalling. Only twenty-four genes were induced in all lines, none of them related to oxidative stress or secondary metabolism. Few genes were down-regulated and none of those was common to all four lines. There were differences in aphid-induced gene regulation between resistant and susceptible lines, and results from control plants without aphids also revealed differences in constitutive gene expression between the two types of lines. Candidate sequences for both induced and constitutive resistance factors have been identified, among them a proteinase inhibitor, a Ser/Thr kinase and several thionins.

Publication Title

Microarray analysis of the interaction between the aphid Rhopalosiphum padi and host plants reveals both differences and similarities between susceptible and partially resistant barley lines.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE48466
Expression data from well-differentiated human bronchial epithelial cells infected with H1N1 Influenza isolates
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to compare the gene expression profiles of different H1N1 isolates (seasonal and pandemic) in lung epithelial cells in vitro.

Publication Title

Early host responses of seasonal and pandemic influenza A viruses in primary well-differentiated human lung epithelial cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE36378
Mapping the Transcriptional Landscape of Autoimmune Targeted Tissues: Transient Alterations in the Extracellular Milieu Precede Innate and Delayed Adaptive Immune Responses in Spontaneous Experimental Autoimmunity.
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The C57BL/6.NOD-Aec1Aec2 mouse is a model for primary Sjgrens syndrome and was constructed by introducing two genetic intervals derived from the NOD mouse that confers Sjgrens syndrome (SjS)-like disease in SjS-non-susceptible C57BL/6 mice.

Publication Title

Transcriptional landscapes of emerging autoimmunity: transient aberrations in the targeted tissue's extracellular milieu precede immune responses in Sjögren's syndrome.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE71977
Genome-wide profiling of inflammatory cistrome reveals AP-1/c-Jun as a key regulator of TNFalpha-mediated triple-negative breast cancer progression.
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer, Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE71915
Genome-wide profiling of inflammatory cistrome reveals AP-1/c-Jun as a key regulator of TNFalpha-mediated triple-negative breast cancer progression [microarray]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st), Illumina Genome Analyzer

Description

Triple-negative breast cancer (TNBC) represents a highly aggressive form of breast cancer with limited treatment options. Proinflammatory cytokines such as TNFalpha can facilitate tumor progression and metastasis. However, our knowledge of the molecular mechanisms underlying TNBC progression mediated by inflammation is still limited. Here, we define the AP-1 transcription factor c-Jun cistrome, which is comprised of 13800 binding sites responsive to TNFalpha-induced signaling in TNBC cells. In addition, we show that c-Jun regulates nearly a third of the TNFalpha-elicited transcriptome. Expression of the c-Jun-regulated pro-invasion gene program is strongly associated with clinical outcomes in TNBCs. Mechanistically, we demonstrate that c-Jun drives TNFalpha-mediated TNBC tumorigenicity by transcriptional regulation of Ninj1. As exemplified by the c-Jun bound CXC chemokine genes clustered on chromosome 4, we demonstrate that NF-kB might be a pioneer factor and is required for the regulation of TNFalpha-inducible inflammatory genes, whereas c-Jun has little effect. Together, our results uncover AP-1 as an important determinant for inflammation-induced cancer progression, rather than inflammatory response.

Publication Title

AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE42806
Gene expression profiling in tibial muscular dystrophy and control skeletal muscle
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Tibial muscular dystrophy (TMD) is a late onset, autosomal dominant distal myopathy that results from mutations in the two last domains of titin. The cascade of molecular events leading from the causative Titin mutations to the preterm death of muscle cells in TMD is largely unknown. To identify these components, we used gene expression profiling of muscle biopsies from TMD patients and healthy controls.

Publication Title

Gene expression profiling in tibial muscular dystrophy reveals unfolded protein response and altered autophagy.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Subject

View Samples
accession-icon GSE6979
Gene expression analysis of Kidneys from FGF23 TG and WT mice
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Fibroblast growth factor-23 (FGF23), a circulating protein produced in bone, causes renal inorganic phosphate (Pi) wasting by down-regulation of sodium phosphate co-transporter 2a (Npt2a). The mechanism behind this action is unknown. We have previously generated transgenic mice (TG) expressing human wild-type FGF23 under the control of the 1 (I) collagen promoter. In this study we performed a large scale gene expression study of kidneys from TG mice and wild-type littermates. Several genes that play a role in Pi regulation had decreased expression levels, such as Npt2a, but also Pdzk1 which is a scaffolding protein known to interact with NPT2a. Importantly, the Klotho gene, a suggested crucial co-factor for FGF23 receptor binding and activation, was the most affected decreased gene. However, other genes proposed to regulate Pi levels, such as secreted Frizzled Related Protein 4 (sFRP4), Na+/H+ exchanger regulatory factor 1 (NHERF1) and the FGF-receptors 1-4, revealed no changes. Interestingly, expression levels of inflammatory response genes were increased and histological analysis revealed tubular nephropathy in the TG mice kidneys. In conclusion, FGF23 TG mice have altered kidney gene expression levels of several genes thought to be part of Pi homeostasis and an increase in inflammatory response genes, data supported by histological analysis. These findings may lead to further understanding of how FGF23 mediates its actions on renal Pi regulation.

Publication Title

Gene expression analysis of kidneys from transgenic mice expressing fibroblast growth factor-23.

Sample Metadata Fields

Age

View Samples
accession-icon GSE13725
Peripheral WBC from Brahman and Holstein-Friesian cattle infested with the cattle tick Rhipicephalus microplus
  • organism-icon Bos indicus, Bos taurus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

This trial was undertaken to examine the perhipheral cellular and antibody response of cattle following infestation with the cattle tick, Rhipicephalus microplus. The information from the Affymetrix gene expression data is used to complement other measurements of immune function such as cellular subset composition and antibody response in cattle of high (Brahman) and low (Holstein-Friesian) resistance to the cattle tick.

Publication Title

Immunological profiles of Bos taurus and Bos indicus cattle infested with the cattle tick, Rhipicephalus (Boophilus) microplus.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE46441
Insights into the invasiveness of triple negative breast cancer from genome-wide profiling of transcription factor AP-1
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st), Illumina Genome Analyzer

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide profiling of AP-1-regulated transcription provides insights into the invasiveness of triple-negative breast cancer.

Sample Metadata Fields

Specimen part, 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