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accession-icon GSE31033
Differential expression between frb1 mutant Arabidopsis and wild-type
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Cell adhesion in plants is mediated predominantly by pectins, a group of complex cell wall associated polysaccharides. An Arabidopsis mutant, friable1 (frb1), was identified through a screen of T-DNA insertion lines that exhibited defective cell adhesion. Interestingly, the frb1 plants displayed both cell and organ dissociations and also ectopic organ fusions. The FRB1 gene encodes a Golgi-localized, plant specific protein with only weak sequence similarities to known proteins (DUF246). Unlike other cell adhesion deficient mutants, frb1 mutants do not have reduced levels of adhesion related cell wall polymers, such as pectins. Instead, FRB1 affects the abundance of galactose- and arabinose-containing oligosaccharides in the Golgi. Furthermore, frb1 mutants displayed alteration in pectin methylesterification, cell wall associated extensins and xyloglucan microstructure. We propose that abnormal FRB1 action has pleiotropic consequences on wall architecture, affecting both the extensin and pectin matrices, with consequent changes to the biomechanical properties of the wall and middle lamella, thereby influencing cell-cell adhesion.

Publication Title

The FRIABLE1 gene product affects cell adhesion in Arabidopsis.

Sample Metadata Fields

Specimen part

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accession-icon GSE55917
miR-126 Governs Human Leukemia Stem Cell Quiescence and Therapeutic Resistance
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

miR-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem Cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE55814
miR-126 governs human leukemia stem cell quiescence and therapeutic resistance [Illumina]
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

In acute myeloid leukemia (AML), leukemia stem cells (LSCs) play a central role in disease progression and recurrence due to their intrinsic capacity for self-renewal and chemotherapy resistance. Whereas epigenetic regulation balances normal blood stem cell self-renewal and fate decisions, mutation and dysregulation of epigenetic modifiers are now considered fundamental to leukemia initiation and progression. Alterations in miRNA function represent a non-canonical epigenetic mechanism influencing malignant hematopoiesis; however, the function of miRNA in LSC remains undetermined. Here we show that miRNA profiling of fractionated AML populations defines an LSC-specific signature that is highly predictive of patient survival. Gain-of-function genetic analysis demonstrated that miR-126 restrained cell cycle progression, prevented LSC differentiation, and increased LSC self-renewal. miR-126 promoted chemo-resistance, preserving LSC quiescence in part through suppression of the G0-to-G1 gatekeeper, CDK3. Thus, in AML, miRNAs influence patient outcome through post-transcriptional regulation of stemness programs in LSC.

Publication Title

miR-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem Cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE60451
Sternal cartilage microarray (WT vs. TIMPless)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Timps are natural metalloproteinase inhibitors that direct the cell microenvironment in health and disease, yet the essential requirement of this gene family in mammals is unknown. We generated quadruple Timp deficient mice lacking Timp1, Timp2, Timp3 and Timp4 (TIMPless) and found that Timp function is essential for postnatal lifespan, lung form and function and skeletogenesis. TIMPless mice survive embryogenesis but develop pervasive skeletal aberrations characterized by axial cartilage overgrowth and growth plate closure in long bones. We performed microarray analysis to identify signaling pathways affected by the loss of the entire Timp family in sternal cartilage.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE23445
Effect of JMJD2B depletion on the ER signaling pathway
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

JMJD2B is expressed in a high proportion of human breast tumors, and the expression levels significantly correlate with estrogen receptor (ER) positivity. To assess the effect of JMJD2B depletion on the ER signaling pathway, we performed genome-wide gene expression analysis using the Affymetrix Human Gene 1.0 ST array.

Publication Title

Histone demethylase JMJD2B functions as a co-factor of estrogen receptor in breast cancer proliferation and mammary gland development.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment

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accession-icon GSE7454
Modulation of gene expression by decitabine in U-2OS cells in vitro and in vivo
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background: Epigenetic modifications such as methylation silencing of genes with CpG-island-associated promoters is frequently observed in cancer. Studies regarding the implications of epigenetic modifications in osteosarcoma (OS) have been limited. The epigenetic drug decitabine is a potential re-activator of silenced genes through de-methylation, and is currently undergoing clinical trials for cancer treatment. No study to date has utilized decitabine to modify gene expression in OS-derived cells to identify gene-specific methylation targets that may have therapeutic importance. The objective of this study was to measure the response of the OS cell line, U-2OS, to decitabine treatment both in vitro and in vivo.

Publication Title

Modulation by decitabine of gene expression and growth of osteosarcoma U2OS cells in vitro and in xenografts: identification of apoptotic genes as targets for demethylation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE55096
Molecular Adaptations of Striatal Spiny Projection Neurons During Levodopa-Induced Dyskinesia
  • organism-icon Mus musculus
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

L-3,4-dihydroxyphenylalanine (levodopa) treatment is the major pharmacotherapy for Parkinson's disease. However, almost all patients receiving levodopa eventually develop debilitating involuntary movements (dyskinesia). While it is known that striatal spiny projection neurons (SPNs) are involved in the genesis of this movement disorder, the molecular basis of dyskinesia is not understood. In this study, we identify distinct cell-type-specific gene expression changes that occur in sub-classes of SPNs upon induction of a parkinsonian lesion followed by chronic levodopa treatment. We identify several hundred genes whose expression is correlated with levodopa dose, many of which are under the control of AP-1 and ERK signaling. In spite of homeostatic adaptations involving several signaling modulators, AP-1-dependent gene expression remains highly dysregulated in direct pathway SPNs (dSPNs) upon chronic levodopa treatment. We also discuss which molecular pathways are most likely to dampen abnormal dopaminoceptive signaling in spiny projection neurons, hence providing potential targets for antidyskinetic treatments in Parkinson's disease.

Publication Title

Molecular adaptations of striatal spiny projection neurons during levodopa-induced dyskinesia.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE41233
Using Blood-Informative Transcripts in Geographical Genomics: Impact of Lifestyle on Gene Expression in Fijians
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This study explores the impact of lifestyle and environment on gene expression through whole transcriptome profiling of peripheral blood samples in Fijian population (native Melanesians and Indians) living in the rural and urban areas.

Publication Title

Using blood informative transcripts in geographical genomics: impact of lifestyle on gene expression in fijians.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE10023
Maize gene expression during infection with Ustilago maydis
  • organism-icon Zea mays
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

The fungal pathogen Ustilago maydis establishes a biotrophic relationship with its host plant maize. Hallmarks of the disease are large plant tumors in which fungal proliferation occurs. Plants have developed various defense pathways to cope with pathogens. We used microarrays to detail the global programme of gene expression during the infection process of Ustilago maydis in its host plant to get insights into the defense programs and the metabolic reprogramming needed to supply the fungus with nutrients.

Publication Title

Ustilago maydis infection strongly alters organic nitrogen allocation in maize and stimulates productivity of systemic source leaves.

Sample Metadata Fields

Specimen part

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accession-icon GSE67415
Ebf1 heterozygosity results in increased DNA damage in pro-B cells and their synergistic transformation by Pax5 haploinsufficiency
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Ebf1 is a transcription factor with documented, and dose dependent, functions in both normal and malignant B-lymphocyte development. In order to understand more about the role of Ebf1 in malignant transformation, we have investigated the impact of reduced functional Ebf1 dose on early B-cell progenitors. Gene expression analysis in loss and gain of function analysis suggested that Ebf1 was involved in the regulation of genes of importance for DNA repair as well as cell survival. Investigation of the level of DNA damage in steady state as well as after induction of DNA damage by UV light supported that pro-B cells lacking one functional allele of Ebf1 display a reduced ability to repair DNA damage. This was correlated to a reduction in expression of Rad51 and combined analysis of published 4C and chromatin Immuno precipitation data suggested that this gene is a direct target for Ebf1. Even though the lack of one allele of Ebf1 did not result in any dramatic increase of tumor formation, we noted a dramatic increase in the formation of pro-B cell leukemia in mice carrying a combined heterozygote mutation in the Ebf1 and Pax5 genes. Even though the tumors were phenotypically similar and stable, we noted a large degree of molecular heterogeneity well in line with a mechanism involving impaired DNA repair. Our data support the idea that Ebf1 controls homologous DNA repair in a dose dependent manner and that this may explain the frequent involvement of Ebf1 in human leukemia

Publication Title

Ebf1 heterozygosity results in increased DNA damage in pro-B cells and their synergistic transformation by Pax5 haploinsufficiency.

Sample Metadata Fields

Specimen part, Cell line, Time

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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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