Filters
Technology
Platform
GSE23642
Xenopus laevis
18 Downloadable Samples
Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)
Description
Recently a new neonatal diabetes syndrome, Mitchell-Riley syndrome, was discovered. To identify the genetic cause of the syndrome homozygosity mapping was used, several chromosomal regions were linked to Mitchell-Riley syndrome. In situ hybridization of genes from one such region using model organism Xenopus laevis identified RFX6 as a potential candidate gene; mutant forms of RFX6 were subsequently found in Mitchell-Riley patients. Analysis of the expression pattern of RFX6 in Xenopus development shows it is expressed broadly in the endoderm early in development, and later RFX6 becomes restricted to the endocrine cells of the gut and pancreas. Morpholino knockdown of RFX6 in Xenopus caused a loss of pancreas marker gene expression. Injection of exogenous wild type RFX6 rescued the morpholino phenotype in Xenopus tadpoles. Attempts to rescue the loss-of-function phenotype using mutant forms of RFX6 found in Mitchell-Riley patients were unsuccessful suggesting the changes lead to loss-of-function and could be the cause of Mitchell-Riley syndrome. Microarray analysis of gene expression in knockdown tissue suggested a downregulation in marker genes for lung, stomach and heart, ambiguous results for the liver, and an upregulation in kidney marker gene expression. RT-PCR and in situ hybridization confirms a loss of lung, stomach and heart gene expression, no change in liver marker hex and an upregulation in kidney marker KcnJ1. The fact that the morpholino phenotype affects multiple organs suggests that RFX6 has a broad role early in endoderm development.
Publication Title
Functional analysis of Rfx6 and mutant variants associated with neonatal diabetes.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MerTK Is a Functional Regulator of Myelin Phagocytosis by Human Myeloid Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Myeloid cells are prominent cellular constituents of the CNS. Under physiologic conditions, these include microglia within the parenchyma and systemic compartment derived macrophages localized to the perivascular spaces. Defining the relative distribution and functions of microglia versus blood-derived macrophages in the CNS parenchyma under pathologic conditions remains a challenge due to limitations in being able to distinguish these cell types. Approaches to distinguishing microglia and macrophages in experimental models include use of chimeric and parabiotic animals and molecular genetic techniques to selectively differentially label or delete a specific cell type. The current report will compare gene expression of human microglia and macrophages under distinct states of activation or polarization and relate these to their roles in tissue injury and protection /repair in the central nervous system (CNS).
Publication Title
MerTK Is a Functional Regulator of Myelin Phagocytosis by Human Myeloid Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Myeloid cells are prominent cellular constituents of the CNS. Under physiologic conditions, these include microglia within the parenchyma and systemic compartment derived macrophages localized to the perivascular spaces. Defining the relative distribution and functions of microglia versus blood-derived macrophages in the CNS parenchyma under pathologic conditions remains a challenge due to limitations in being able to distinguish these cell types. Approaches to distinguishing microglia and macrophages in experimental models include use of chimeric and parabiotic animals and molecular genetic techniques to selectively differentially label or delete a specific cell type. The current report will compare gene expression of human microglia and macrophages under distinct states of activation or polarization and relate these to their roles in tissue injury and protection /repair in the central nervous system (CNS).
Publication Title
MerTK Is a Functional Regulator of Myelin Phagocytosis by Human Myeloid Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 17 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
TGFbi (transforming growth factor-beta-induced) is a secreted protein and is capable of binding to both extracellular matrix (ECM) and cells. It thus acts as a bifunctional molecule enhancing ECM and cell interactions, a lack of which results in dysfunction of many cell types. In this study, we investigated the role of TGFbi in the function and survival of islets. Based on DNA microarray analysis followed by qPCR confirmation, the TGFbi gene showed drastic increases in expression in islets after culture. We demonstrated that recombinant TGFbi could preserve the integrity and enhance the function of cultured islets. Such a beneficial effect was mediated via signalling through FAK. Exogenous TGFbi was capable of sustaining high-level FAK phosphorylation in isolated islets, and FAK knockdown by siRNA in islets resulted in compromised islet function. TGFbi Tg islets showed better integrity and insulin release after in vitro culture. In vivo, b-cell proliferation was detectable in Tg but not wild type pancreata. At age above 12 months, Tg pancreata contained giant islets. Tg mice displayed better glucose tolerance than the controls. Tg islets were more potent in lowering blood glucose when transplanted into syngeneic mice with streptozotocin-induced diabetes, and these transplanted islets also underwent regeneration. Our results indicate that TGFbi is a vital trophic factor promoting islet survival, function and regeneration. At least some of its beneficial effect was mediated by signalling through FAK.
Publication Title
TGF-beta i promotes islet beta-cell function and regeneration.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
Gene expression profiles of CD3e-proficient and CD3e-deficient were analysed using Affymetrix cDNA arrays (MOAE430)
Publication Title
Genetic interactions involved in TAL1- induced acute lymphoblastic leukemia
Sample Metadata Fields
Age, Specimen part, Disease, Disease stage, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The methyltransferase G9a was found to play a role in the disease progression of a murine model of AML.
Publication Title
The methyltransferase G9a regulates HoxA9-dependent transcription in AML.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
let-7 Modulates Chromatin Configuration and Target Gene Repression through Regulation of the ARID3B Complex.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Expression of let-7i results in transcriptome alteractions in head and neck cancer cell line, OECM1.
Publication Title
let-7 Modulates Chromatin Configuration and Target Gene Repression through Regulation of the ARID3B Complex.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Previous studies in our laboratory have shown that low folate diet (control diet with 2mg folate/kg, low folate diet with 0.3mg folate/kg) can induce intestinal tumors in BALB/c mice. In addition, we reported that C57Bl/6J mice did not form tumors under the same conditions.
Publication Title
Differential gene expression and methylation in the retinoid/PPARA pathway and of tumor suppressors may modify intestinal tumorigenesis induced by low folate in mice.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples