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accession-icon GSE41177
Region-specific gene expression profiles in left atria of patients with valvular atrial fibrillation
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Of 54,675 expressed sequence tags, microarray analysis revealed that 391 genes were differently expressed (>1.5-fold difference) between LA-PV junction and LAA, including genes related to arrhythmia, cell death, fibrosis, hypertrophy, and inflammation. Microarray and q-PCR produced parallel results in analyzing the expression of particular genes. The expression of paired like homeodomain-2 (PITX2) and its target protein (short stature homeobox-2 [SHOX2]) was greater in LA-PV junction than in LAA, which may contribute to arrhythmogenesis. Five genes related to thrombogenesis were up-regulated in LAA, which may implicate for the preferential thrombus formation in LAA. Genes related to fibrosis were highly expressed in LAA, which was reflected by intense ultrastructural changes in this region

Publication Title

Region-specific gene expression profiles in the left atria of patients with valvular atrial fibrillation.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE79768
Atrial fibrillation is associated with altered left-to-right atria gene expression ratio: implications for arrhythmogenesis and thrombogenesis
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Atrial fibrillation (AF) causes atrial remodeling, and the left atrium (LA) is the favored substrate for maintaining AF. However, it remains unclear if AF remodels both atria differently and contributes to LA arrhythmogenesis and thrombogenesis.

Publication Title

Differential left-to-right atria gene expression ratio in human sinus rhythm and atrial fibrillation: Implications for arrhythmogenesis and thrombogenesis.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE86569
Different expression of inflammation-related proteins in human heart failure
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Background: Heart failure (HF) causes various inflammatory responses. It remains unclear whether the inflammation the cause or effect of HF. Therefore, we wished to characterize the transcript profiles in the left ventricle (LV) of preserved and failed hearts respectively.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE97044
Dynamic Changes in the Expressions of Elastogenesis- and Elastinolysis-Associated Genes and Remodeling of the Elastin Network in Volume-Overloaded Heart
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Background: In the remodeling process of the volume-overloaded heart, the extracellular matrix (ECM) may be dynamically modified to adapt to hemodynamic stress. We investigated the expression of ECM-related genes and modification of the elastin network in the remodeling process of the left ventricles (LVs) of rats with aortocaval fistulae. Methods and Findings: Gene array analysis identified 36 upregulated and 11 downregulated ECM-related genes during evolution from the compensated to the late decompensated phase. Ingenuity Pathway Analysis identified the formation of elastic fibers as an important biological function. Real-time PCR confirmed persistent upregulation of elastogenesis-associated genes, including elastin, lysyl oxidase, lysyl oxidase like-1, fibrillin 1, fibulin 2, versican and latent transforming growth factor beta binding protein 2 at various intervals. The expression levels and enzymatic activities of potent elastases, cathepsin S and cathepsin K increased during the early phase. Immunofluorescence confocal microscopy showed that the microstructure of the elastin network was preserved during the early phase, degraded during the compensated phase, partially repaired during the early decompensated phase, and reinforced during the late decompensated phase. Assessment of elastin concentrations in the LVs showed a consistent temporal pattern throughout the course.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE150661
The gene expression profiles associated with worsening left ventricle function after mitral valve repair
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Background:To assess left ventricular (LV) transcriptome determinants of worsening LV function after mitral valve (MV) repair.

Publication Title

Ubiquitin Pathway Is Associated with Worsening Left Ventricle Function after Mitral Valve Repair: A Global Gene Expression Study.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE81804
Bioenergetic Alterations in Colorectal Polyp and Cancer
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Background: The change of cellular energy metabolism in colorectal carcinogenesis is poorly understood. It is widely accepted tht most, if not all, colorectal cancers (CRCs) arise from adenomatous polyps (APs). Our aim was to characterize the mitochondrial and bioenergetic alternations in the adenoma-carcinoma sequence.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE74996
KLHL23 Regulates a Novel Positive-Feedback Signaling Loop of EMT Maintaining the Mesenchymal State of Cancer Cells during Metastasis
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Epithelial-mesenchymal transition (EMT) is initiated and regulated by a transcriptional reprogramming in response to microenvironmental cues. How cancer cells overcome the lack of such cues during the metastatic journey remains unclear. Here we report a novel positive-feedback loop of EMT that maintains the mesenchymal traits of cancer cells during metastasis. Using subgenome-wide screening, we identified KLHL23 as a tumor invasion suppressor, which binds to actin and suppresses actin-filament formation. Silencing or ectopic expression of KLHL23 induces EMT or MET (mesenchymal-epithelial transition), respectively, through its action on actin dynamics. Increased actin-dynamics by silencing KLHL23 or treatment with F-actin disruptors or inducers enhances the EMT transcriptional reprogramming via the induction of ROS, HIF-1a, HIF-2a and NOTCH signalling pathways in cancer cells under stress or ongoing EMT. Downregulation of KLHL23 is found in human liver and pancreatic cancers and associated with tumor metastasis and poor prognosis.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE90934
Differential gene expression and genomic methylation profile of U937 cells transduced with WT/mutant-DNMT3A
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE70512
Negative-Pressure Induces p120-Catenin Dependent Adherens Junction Disassembly
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Negative-pressure wound therapy has become widely available in modern chronic wound cares. Accelerated keratinocyte (HaCaT cell) movements and decreased E-cadherin expressions induced by the applied negative pressure gradient of 125 mmHg (NP) have been reported in previous studies. However, the molecular mechanism for E-cadherin regulations under NP remains unexplored. We highlighted the signal transduction involved in NP-induced E-cadherin regulation for keratinocytes in the study.

Publication Title

Negative pressure induces p120-catenin-dependent adherens junction disassembly in keratinocytes during wound healing.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE105251
Histidine-dependent protein methylation is required for compartmentalization of CTP synthase
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

CTP synthase (CTPS) forms compartmentalized filaments in response to substrate availability and environmental nutrient status. However, the physiological role of filaments and mechanisms for filament assembly are not well understood. Here, we provide evidence that CTPS forms filaments in response to histidine influx during glutamine starvation. CTPS protein levels remained stable in the presence of histidine during nutrient deprivation, followed by rapid cell growth following nutrient replenishment. Tetramer conformation-based filament formation restricted CTPS enzyme activity duringnutrient deprivation.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

View Samples
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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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