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GSE13171
Homo sapiens
4 Downloadable Samples
Affymetrix Human Genome U95A Array (hgu95a)
Description
The gene coding for RNA binding motif protein 35A (RBM35A) is inactivated by frameshift mutations in an LS180 colon carcinoma cell line and in approximately in 50% of colon tumors with microsatellite instability. To get insight into the mechanism of action of these putative tumor suppressor gene we expressed functional copy of the RBM35A cDNA in the LS180 cells. We analyzed alterations in mRNA profiles in total and in polysomal fraction of mRNA in LS180 cells in response to expressing RBM35A gene under Tet off tetracycline inducible promoter.
Publication Title
RNA-binding motif protein 35A is a novel tumor suppressor for colorectal cancer.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Human infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.
Publication Title
Macrophage mitochondrial and stress response to ingestion of Cryptococcus neoformans.
Sample Metadata Fields
Specimen part, Cell line, Time
View Samples- Danio rerio
- 48 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Danio rerio
- 24 Downloadable Samples
Affymetrix Zebrafish Genome Array (zebrafish)
Description
Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.
Publication Title
Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Danio rerio
- 24 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.
Publication Title
Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 101 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Canonical and atypical E2Fs regulate the mammalian endocycle.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 35 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To understand the underlying cause and mechanisms of changes in hepatocyte ploidy upon Albumin-Cre mediated deletion of E2f7&8 and Mx1-Cre mediated deletion of E2f1,2&3, we analysed global gene expression of 6 weeks and 2 months liver tissues.
Publication Title
Canonical and atypical E2Fs regulate the mammalian endocycle.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 34 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Atopic dermatitis (AD) is a common pruritic dermatitis with macroscopically nonlesional skin that is often abnormal. Therefore, we used high-density oligonucleotide arrays to identify cutaneous gene transcription changes associated with early AD inflammation as potential disease control targets. Skin biopsy specimens analyzed included normal skin from five healthy nonatopic adults and both minimally lesional skin and nearby or contralateral nonlesional skin from six adult AD patients.
Publication Title
Early cutaneous gene transcription changes in adult atopic dermatitis and potential clinical implications.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To understand the underlying cause for the observed apoptosis in E2f1-3 deficient myeloid cells. We compared gene expression profiles of Cd11b+ sorted myeloid cells isolated from bone marrow of control (E2F1-/- ) and experimental (Mxcre;E2F1-/-2-/-3f/f ) mice.
Publication Title
E2f1-3 are critical for myeloid development.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 29 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Epigenetic mechanisms contribute to deregulated gene expression of hematopoietic progenitors in Myelodysplastic Syndromes (MDS). Hypomethylating agents are able to improve peripheral cytopenias in MDS patients. To identify critical gene expression changes induced by hypomethylating agents, we analyzed gene expression profiling (GEP) of myelodysplastic and normal CD34+ hematopoietic stem cells treated in vitro with or without decitabine. Four MDS and two untreated early stage Hodgkins lymphomas were analyzed for GEP. Mock treated CD34+ stem cells segregate according to diagnosis and karyotype. After decitabine treatment, gene expression changes were more consistent on MDS CD34+ cells with abnormal kayotype. Comparing decitabine-induced genes with those found down-regulated in mock-treated MDS cells, we identified a list of candidate tumor suppressor genes in MDS. By real-time RT-PCR we confirmed expression changes for three selected genes CD9, CXCR4 and GATA2 in 12 MDS patients and 4 controls. CD9 was widely repressed in most MDS CD34+ cell samples, although similar levels of methylation were found in both normal and MDS total bone marrows. CXCR4 promoter methylation was absent in total bone marrows from 36 MDS patients. In conclusion, changes in gene expression changes induced by hypomethylating treatment are more pronounced in CD34+ cells from abnormal karyotype.
Publication Title
Gene expression profiling of myelodysplastic CD34+ hematopoietic stem cells treated in vitro with decitabine.
Sample Metadata Fields
Sex, Age, Specimen part, Disease
View Samples