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accession-icon GSE5999
Characterization of Gene Expression At the Human Maternal-Fetal Interface
  • organism-icon Homo sapiens
  • sample-icon 72 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Microarray analysis to globally assess gene expression at the maternal-fetal interface

Publication Title

Gene expression profiling of the human maternal-fetal interface reveals dramatic changes between midgestation and term.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE43806
Klf5 controls bone marrow homing of stem cells and progenitors through Rab5-mediated membrane Beta1/Beta2-integrin expression
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The Kruppel-like factor 5 (Klf5) regulates pluripotent stem cell self-renewal but its role in somatic stem cells is unknown. Klf5 deficient hematopoietic stem cells and progenitors (HSC/P) fail to engraft after transplantation. This HSC/P defect was associated with impaired bone marrow (BM) homing and lodging and decreased retention in BM. The Klf5/ HSC/P homing defect associated with decreased adhesion to fibronectin and expression of membrane-bound 1/2-integrins. In vivo inducible gain-of-function of Klf5 in HSC translated into increased HSC/P adhesion. The expression of Rab5 family members, mediators of 1/2-integrin recycling in the early endosome, was decreased in Klf5/ HSC/P. Klf5 binds directly to the promoter of Rab5a/b and overexpression of Rab5b rescued the expression of activated 1/2-integrins, adhesion and BM homing of Klf5/ HSC/P. Altogether, these data indicate that Klf5 is indispensable for adhesion, homing, lodging and retention of HSC/P in the BM through Rab5-dependent post-translational regulation of Beta1/Beta2 integrins.

Publication Title

Klf5 controls bone marrow homing of stem cells and progenitors through Rab5-mediated β1/β2-integrin trafficking.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE4066
Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiation.
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Exposure to ultraviolet (UV) irradiation is the major cause of nonmelanoma skin cancer, the most common form of cancer in the United States. UV irradiation has a variety of effects on the skin associated with carcinogenesis, including DNA damage and effects on signal transduction. The alterations in signaling caused by UV regulate inflammation, cell proliferation, and apoptosis. UV also activates the orphan receptor tyrosine kinase and proto-oncogene Erbb2 (HER2/neu). In this study, we demonstrate that the UV-induced activation of Erbb2 regulates the response of the skin to UV. Inhibition or knockdown of Erbb2 before UV irradiation suppressed cell proliferation, cell survival, and inflammation after UV. In addition, Erbb2 was necessary for the UV-induced expression of numerous proinflammatory genes that are regulated by the transcription factors nuclear factor-kappaB and Comp1, including interleukin-1beta, prostaglandin-endoperoxidase synthase 2 (Cyclooxygenase-2), and multiple chemokines. These results reveal the influence of Erbb2 on the UV response and suggest a role for Erbb2 in UV-induced pathologies such as skin cancer.

Publication Title

Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE38680
GAA deficiency (Pompe Disease) in infantile-onset patients
  • organism-icon Homo sapiens
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Pompe disease is a genetic disorder resulting from a deficiency of lysosomal acid alpha-glucosidase (GAA) that manifests as a clinical spectrum with regard to symptom severity and rate of progression. In this study, we used microarrays to examine gene expression from the muscle of two cohorts of infantile-onset Pompe patients to identify transcriptional differences that may contribute to the disease phenotype. We found strong similarities among the gene expression profiles generated from biceps and quadriceps, and identified a number of signaling pathways altered in both cohorts. We also found that infantile-onset Pompe patient muscle had a gene expression pattern characteristic of immature or regenerating muscle, and exhibited many transcriptional markers of inflammation, despite having few overt signs of inflammatory infiltrate. Further, we identified genes exhibiting correlation between expression at baseline and response to therapy. This combined dataset can serve as a foundation for biological discovery and biomarker development to improve the treatment of Pompe disease.

Publication Title

Transcriptional response to GAA deficiency (Pompe disease) in infantile-onset patients.

Sample Metadata Fields

Sex, Specimen part, Disease, Treatment, Subject

View Samples
accession-icon SRP052872
Differential expression between Sh2b3 knockout and wild type mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To validate the predicted Sh2b3 derived gene regulatory subnetwork using integrative network approach in human population study, we examined the gene expression levels of whole blood in WT (wild-type) and Sh2b3-/- mice by RNA sequencing, and identified the differentially expressed genes. Overall design: RNA sequencing whole blood samples from 4 WT and 4 Sh2b3-/- mice.

Publication Title

Integrative network analysis reveals molecular mechanisms of blood pressure regulation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE68848
caArray_fine-00037: Rembrandt_GeneExpression
  • organism-icon Homo sapiens
  • sample-icon 577 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This is Rembrandt gene expression data (Affymetrix HG-U133Plus2).

Publication Title

Rembrandt: helping personalized medicine become a reality through integrative translational research.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE143998
Whole transcript analysis of amyloid beta 42 (Aβ42)-induced SH-SY5Y cells in control and treated groups
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

Whole transcript analysis of amyloid beta 42 (Aβ42)-induced SH-SY5Y cells in control and treated groups (curcumin, piperine and combination therapy) were assessed using microarray profiling. A number of up-regulated and down-regulated genes were altered in sample-specific group.

Publication Title

Explicating anti-amyloidogenic role of curcumin and piperine via amyloid beta (A<i>β</i>) explicit pathway: recovery and reversal paradigm effects.

Sample Metadata Fields

Sex, Specimen part, Cell line

View Samples
accession-icon GSE59422
Effect of Hypertension of Dendritic Cell Gene Expression
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Oxidative injury and inflammation have been implicated in the genesis of hypertension but the mechanisms involved are not fully understood. We describe a new pathway in which angiotensin II promotes dendritic cell (DC) activation of T cells and ultimately hypertension. NADPH oxidase-dependent superoxide production is increased 5-fold in DCs isolated from hypertensive mice as compared to sham-treated mice. This is associated with DC accumulation of protein-isoketal adducts and production of IL-6, IL-1 and IL-23. DCs from hypertensive mice but not sham mice promote survival and proliferation of CD8+ T cells in culture. Chemically diverse isoketal scavengers not only prevent activation and immunogenicity of DCs, but also attenuate angiotensin II-induced hypertension. Moreover, adaptive transfer of DCs from hypertensive mice prime development of hypertension in response to a subpressor dose of angiotensin II. Exposure of DCs to tert butyl hypdroperoxide promoted isoketal formation, DC stimulation of CD8+ T cell proliferation and primed hypertension in response to low dose angiotensin II. Serum isoprostanes, precursors to isoketals, were found to be elevated in humans with treated hypertension and were markedly elevated in patients with resistant hypertension. These studies show that angiotensin II-induced hypertension activates DCs, in large part by causing superoxide production and formation of isoketals. They define a new mechanism of hypertension and identify a potential new therapeutic approach for this disease.

Publication Title

DC isoketal-modified proteins activate T cells and promote hypertension.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE43437
Strength training with suppressed testosterone level
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human subjects were randomized for treatment with a GnRH-analogue, Goserelin, which suppresses endogenous testosterone or placebo for 12 weeks. Strength training was performed during the last 8 weeks. The suppression of testosterone resulted in an attenuation of the normal muscle adaptation to strength training (increased muscle mass and strength). To identify molecular signals involved in the response to testosterone levels, biopsies were obtained 4 hours after the last training session and gene expression compared with Affymetrix 3' microarrays. This timepoint should capture goserelin effect on both constitutive expression, training induced changes as well as acute exercise induced (4 hours) differences in mRNA levels.

Publication Title

The activity of satellite cells and myonuclei following 8 weeks of strength training in young men with suppressed testosterone levels.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

View Samples
accession-icon GSE55616
ARRB1 regulates prostate cancer cell metabolism
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Nuclear ARRB1 induces pseudohypoxia and cellular metabolism reprogramming in prostate 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)

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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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