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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human 293 T cells infected with ASLV

ABSTRACT: Human 293T cells engineered to express the TVA receptor (see Mitchell et al., PLoS) infected with an ASLV vector. RNA isolated 48 hours later. ***PLEASE NOTE***; Series entries GSE1408 & GSE1409 no longer exist. All data discussed in the author's PLoS publication (PubMed ID 15314653) is available under GSE1407 & GSE1410. ***PLEASE NOTE***

ORGANISM(S): Homo sapiens

SUBMITTER: Richard Steven Mitchell

PROVIDER: E-GEOD-1410 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ASLV vector infected 293t-TVA cells

Project description:Human 293T cells engineered to express the TVA receptor (see Mitchell et al., PLoS) infected with an ASLV vector. RNA isolated 48 hours later. ***PLEASE NOTE*** Series entries GSE1408 & GSE1409 no longer exist. All data discussed in the author's PLoS publication (PubMed ID 15314653) is available under GSE1407 & GSE1410. ***PLEASE NOTE*** Keywords: repeat sample

2004-05-19 | GSE1410 | GEO

HIV-based vector infected cells

Project description:SupT1, PBMC, or IMR90 cells were infected with an HIV-based vector (see Schroder et al., Cell 110:521-9) and the RNA isolated 48 hours after infection. ***PLEASE NOTE*** Series entries GSE1408 & GSE1409 no longer exist. All data discussed in the author's PLoS publication (PubMed ID 15314653) is available under GSE1407 & GSE1410. ***PLEASE NOTE*** Keywords: repeat sample

2004-05-19 | GSE1407 | GEO

Transcription profiling of human SupT1, PBMC or IMR90 cells infected with an HIV-based vector

Project description:SupT1, PBMC, or IMR90 cells were infected with an HIV-based vector (see Schroder et al., Cell 110:521-9) and the RNA isolated 48 hours after infection. ***PLEASE NOTE***; Series entries GSE1408 & GSE1409 no longer exist. All data discussed in the author's PLoS publication (PubMed ID 15314653) is available under GSE1407 & GSE1410. ***PLEASE NOTE***

2007-08-04 | E-GEOD-1407 | biostudies-arrayexpress

Homo sapiens

Project description:ASLV vector infected 293t-TVA cells

| PRJNA90085 | ENA

Altered DNA Methylation in Leukocytes with Trisomy 21

Project description:The primary abnormality in Down syndrome (DS), trisomy 21, is well known, but how this chromosomal gain produces the complex DS phenotype, including immune system defects, is not well understood. We profiled DNA methylation in total peripheral blood leukocytes (PBL) and T-lymphocytes from adults with DS and normal controls and found gene-specific abnormalities of CpG methylation in DS, with many of the differentially methylated genes having known or predicted roles in lymphocyte development and function. NOTE 1: the analysis in Kerkel et al., PLOS Genet, 2010 was carried out after removing probes for genes on the X and Y chromosomes. NOTE 2: these GEO data have been analyzed with this latest version of BeadStudio; the data in the supplementary tables of Kerkel et al., PLOS Genetics, 2010, were from these same Bead chips, but extracted using an earlier version of this software. This re-extraction does not affect the conclusions in Kerkel et al., PLOS Genetics, 2010.

2010-11-18 | GSE25395 | GEO

Proteomic Response of Cupriavidus metallidurans CH34 to gold stress

Project description:Proteomic response of Cupriavidus metallidurans CH34 to gold stress as in comparison to copper stress and control. Please note that 25Au in gel file names is a typo and should read 50Au.

2016-10-26 | PXD005034 | Pride

Effects of daf-2 mutation, dietary restriction and age on C.elegans proteome

Project description:The overarching project goal was to describe proteome differences between long- and normal-living C.elegans worms. The associated publications are http://www.ncbi.nlm.nih.gov/pubmed/24555535 http://www.ncbi.nlm.nih.gov/pubmed/24002365

2015-05-13 | PXD002161 | Pride

Expression data from Xenopus anterior gut RFX6 knockdown

Project 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.

2011-01-24 | GSE23642 | GEO

Gene expression profiling of mouse tumors arising from Keratin 6-positive mammary cells

Project description:Conventional transgenic and knockout models do not allow selective introduction of oncogenic alterations into the progenitor population of mammary cells; thus, the role of progenitor cells in mammary tumorigenesis is yet unknown. By generating transgenic mice expressing tva – encoding the receptor for avian leukosis virus subgroup A (ALV/A) – from the Keratin 6a (K6) gene promoter, we found that K6+ mammary cells are bipotential progenitor cells, but not stem cells. These K6+ cells were readily induced to form tumors by intraductal injection of RCAS (an ALV/A-derived vector) carrying the gene encoding polyoma middle T antigen. Compared with tumors induced by the same oncogene-expressing virus in transgenic mice expressing tva from the commonly used MMTV LTR or other murine models of breast cancer, tumors in this K6-tva line were unique in that they resemble the normal breast-like subtype of human breast cancer. Consequently, these observations suggest that the cell of origin affects mammary tumor phenotypes. This K6-tva model may be useful for preclinical testing of targeted therapy for normal-like breast cancers in patients. Keywords: Three group comparison We carried out Affymetrix array analysis of five RCAS-PyMT-induced tumors each from K6-tva mice and MMTV-tva mice, as well as five mammary tumors from MMTV-PyMT transgenic mice.

2011-05-09 | E-GEOD-20614 | biostudies-arrayexpress

Iridovirus and Microsporidian Linked to Honey Bee Colony Decline

Project description:this is the raw data accompanying the following publication: Bromenshenk JJ, Henderson CB, Wick CH, Stanford MF, Zulich AW, Jabbour RE, Deshpande SV, McCubbin PE, Seccomb RA, Welch PM, Williams T, Firth DR, Skowronski E, Lehmann MM, Bilimoria SL, Gress J, Wanner KW, Cramer RA Jr. Iridovirus and microsporidian linked to honey bee colony decline. PLoS One. 2010 Oct 6;5(10):e13181. doi: 10.1371/journal.pone.0013181. PubMed PMID: 20949138; PubMed Central PMCID: PMC2950847.

2014-11-19 | MSV000078942 | MassIVE

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