Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

46 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression analysis of the effect of overexpression of Cebpb shRNA in mouse 4T1 mammary tumor cells

ABSTRACT: Investigation of whole genome gene expression level changes in mouse 4T1 mammary tumors expressing Cebpb shRNA, compared to 4T1 tumors expressing control shRNA. Analysis of mouse 4T1 mammary tumors expressing Cebpb shRNA compared to control shRNA are further described in Johansson & Berg et al 2012. A 10 chip study using total RNA recovered from five separate 4T1 tumors expressing Cebpb shRNA and five separate 4T1 tumors expressing control shRNA. All tumors were surgically removed after subcutaneous implantation in syngeneic BALB/c mice two weeks earlier. Each chip measures the expression level of 44,170 genes from Mus Musculus with fourteen 24-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.

ORGANISM(S): Mus musculus

SUBMITTER: Jonas Fuxe

PROVIDER: E-GEOD-40825 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression analysis of the effect of overexpression of Cebpb shRNA in mouse 4T1 mammary tumor cells

Project description:Investigation of whole genome gene expression level changes in mouse 4T1 mammary tumors expressing Cebpb shRNA, compared to 4T1 tumors expressing control shRNA. Analysis of mouse 4T1 mammary tumors expressing Cebpb shRNA compared to control shRNA are further described in Johansson & Berg et al 2012.

2012-09-28 | GSE40825 | GEO

Alterations in the gene expression profile in patients treated with cyclophosphamide

Project description:Investigation of whole genome gene expression level changes in patients treated with cyclophosphamide We have studied the gene expression profile for 11 patients with different types of hematological malignancies but all of them have been treated with CP i.v. Eleven patients were enrolled in this study. All of them were treated by i.v. infusion of CP 60 mg/kg/day once for 2 days followed by TBI. Blood samples were collected from each patient before the start of CP infusion, 6 h after CP first dose, before CP second dose (24 h after first dose) and 6 h after it.

2013-11-15 | E-GEOD-51907 | biostudies-arrayexpress

Mutations in BCKD-kinase lead to a potentially treatable form of autism with epilepsy

Project description:Autism is present in 1% of the population, yet treatments are extremely limited. We identified homozygous inactivating mutations in the BCKDK gene in families presenting with autism and epilepsy. The encoded branched chain ketoacid dehydrogenase kinase protein is responsible for phosphorylation-mediated inactivation of the E1-alpha subunit of branched chain ketoacid dehydrogenase, itself mutated in Maple Syrup Urine Disease (MSUD). Patients with homozygous BCKDK mutations display reductions in BCKDK mRNA and protein, E1-alpha phosphorylation and serum branched chain amino acids (BCAAs). Bckdk knockout mice show abnormal brain amino acids profiles and neurobehavioral defects, which are largely corrected by dietary BCAA supplementation. Thus autism presenting with epilepsy due to BCKDK mutations represent a new and potentially treatable disease. A 51 chip study that includes both human and mouse samples to investigate the expression changes that result in a mutation or knockout of the BCKDK gene. Starting with human fibroblasts from three affecteds and two controls, cells were converted into IPSs, then NPCs, and finally Neurons. Each of these cell types were used to view the expression changes between a cells with a BCKDK mutation versus controls. Finally, a mouse knockout was performed to verify consistency of the expression pattern differences between the BCKCK knockout and wild-type. Samples are labeled as Affected if the sample came from a patient with a BCKDK mutation and WildType otherwise. Samples were usually replicated once.

2012-07-17 | E-GEOD-39447 | biostudies-arrayexpress

Geographical and host plant influences on transcriptional variation in Drosophila mojavensis: mapping gene expression differences in both sexes

Project description:Geographical and host plant influences on transcriptional variation in Drosophila mojavensis: mapping gene expression differences in both sexes. (1. Punta Onah:PO07; 2. Organ Pipe National Monument:OPNM08; 3. Punta Prieta:PP08; & 4. San Quintin:SQ08). The experiment was designed to investigate effects of host plant (diet), mating status (mated:M or nonmated:V) and sex (male:male or Female:F) on transcriptome. A total of 128 hybridizations were performed in this entire experiment (127 in the final analysis). We used 135K 12-plex NimbleGen arrays. Total RNA was recovered from each sample listed below. The experimental design consisted a total of four populations (1. Punta Onah:PO; 2. Organ Pipe National Monument:OPNM; 3. Punta Prieta:PP; & 4. San Quintin:SQ), two mating status (mated:M or nonmated:V), both the sexes (male:male or Female:F) fed on two different diet regimes (Agria and Organ pipe). Each chip measures the expression level of 15528 transcripts. Four to 5 replicates were used for each type (R-1, R-2, R-3 etc.)

2016-04-01 | E-GEOD-78852 | biostudies-arrayexpress

Expression analysis of Kasumi-1 cells treated with or without FTY720

Project description:The clinical outcomes of M2 subtype Acute Myeloid Leukemia (AML-M2) with t(8;21) are poor. Here we report that FTY720 (Fingolimod), a sphingosine analogue and an FDA approved drug for treatment of multiple sclerosis, showed great antitumorigenic activity against Kasumi-1 cell line, xenograft mouse model and leukemic blasts isolated from AML-M2 with t(8;21) patients. Primary investigation indicated that FTY720 caused cell apoptosis through caspase and protein phosphatase 2A (PP2A) activation. Transcriptomic profiling further revealed that FTY720 treatment could upregulate AML1 target genes and interfere with genes involved in ceramide synthesis. FTY720 treatment led to the elimination of AML1-ETO oncoprotein and caused cell cycle arrest. More importantly, FTY720 treatment resulted in rapid and significant increment of pro-apoptotic ceramide levels, determined by HPLC-ESI-MS/MS (high-performance liquid chromatography-electrospray ionization tandem mass spectrometry) based lipidomic approaches. Additionally, structural simulation model indicated that the directly binding of ceramide to inhibitor 2 of PP2A (I2PP2A) could reactivate PP2A and cause cell death. This study demonstrates, for the first time, that accumulation of ceramide plays a central role in FTY720 induced cell death of AML-M2 with t(8;21). Targeting sphingolipid metabolism by using FTY720 may provide novel insight into drug development for AML-M2 treatment. A six chip study using total RNA recovered from three separate cultures of DMSO-treated Kasumi-1 cells and three separate cultures of FTY720-treated Kasumi-1 cells.Each chip measures the expression level of genes from DMSO-/FTY720-treated Kasumi-1 cells.

2014-04-30 | E-GEOD-55772 | biostudies-arrayexpress

Expression analysis of neural progenitor cells derived from iPS cells generated from skin fibroblasts and umbilical cord mesenchymal cells

Project description:Investigation of whole genome gene expression level changes in neural progenitor cells derived from iPS cells generated from umbilical cord mesenchymal cells, compared to neural progenitor cells derived from iPS cells generated fromskin fibroblasts. Analyze the difference between neural progenitor cells derived from iPS cells generated from different origins. The method to induce reprogramming of somatic cells and human iPS cells for neural differentiation is described in Cai J, Li W, Su H, Qin D, Yang J, et al. (2010) Generation of human induced pluripotent stem cells from umbilical cord matrix and amniotic membrane mesenchymal cells. J Biol Chem 285: 11227-11234. and Kim DS, Lee JS, Leem JW, Huh YJ, Kim JY, et al. (2010) Robust enhancement of neural differentiation from human ES and iPS cells regardless of their innate difference in differentiation propensity. Stem Cell Rev 6: 270-281. A two-chip study using total RNA recovered from one neural progenitor cell line derived from iPS cells generated from skin fibroblasts (GZF1C7NSCP3) and one neural progenitor cell line derived from iPS cells generated from umbilical cord mesenchymal cells (VMC2C7NSCP3). No replicates were made. Each chip measures the expression level of 45,033 genes from the two samples with fourteen 60-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.

2013-05-06 | E-GEOD-46647 | biostudies-arrayexpress

AMPD2 Regulates GTP Synthesis and is Mutated in a Potentially-Treatable Neurodegenerative Brainstem Disorder

Project description:Purine biosynthesis and metabolism, conserved in all living organisms, is essential for cellular energy homeostasis and nucleic acids synthesis. The de novo synthesis of purine precursors is under tight negative feedback regulation mediated by adenine and guanine nucleotides. We describe a new early-onset distinct neurodegenerative condition resulting from mutations in the adenosine monophosphate deaminase 2 gene (AMPD2). Patients have characteristic brain imaging features of pontocerebellar hypoplasia (PCH), due to loss of brainstem and cerebellar parenchyma. We found that AMPD2 plays an evolutionary conserved role in the maintenance of cellular guanine nucleotide pools by regulating the feedback inhibition of adenosine derivatives on de novo purine synthesis. AMPD2 deficiency results in defective GTP-dependent initiation of protein translation, which can be rescued by administration of purine precursors. These data suggest AMPD2-related PCH as a new potentially treatable early-onset neurodegenerative disease. An 18 chip study, that compares iPSC derived neural progenitor cells from two individuals: a patient with pontocerebellar hypoplasia and an unaffected parent. Samples are run as either non-treated, treated with Adenosine, or treated with Adenosine and AICAr. Three replicates are included for every individuals in every treatment condition.

2013-12-01 | E-GEOD-46615 | biostudies-arrayexpress

Expression analysis of LncRNA in Tongue Squamous Cell Carcinoma (TSCC) and matched nonmalignant tissues (NC)

Project description:Investigation of LncRNA expression level changes in 9 paired of Tongue Squamous Cell Carcinoma specimens LncRNA profiling: TSCC vs NC

2013-10-30 | E-GEOD-51700 | biostudies-arrayexpress

Influence of NaCl on gene expression in Dickeya dadantii

Project description:Growth in 0.3 M NaCl M63 minimal medium affects the transcriptome of Dickeya dadantii 3937.in comparison to that of cells grown in M63 medium. NimbleGen design name 2005-05-31_Ogg_Erwinia_24mer, NimbleGen design ID 2181 A 1:2 expression design for 4597 genes from Dickeya dadantii 3937 with 20 24-mer probe pairs (PM/MM) per gene. Each probe is replicated 2 times. The design includes random GC and other control probes. Protocol: High-density DNA array prepared with Maskless Array Synthesizer (MAS) technology. See manufacturer's website at http://www.nimblegen.com/.

2015-11-01 | E-GEOD-64739 | biostudies-arrayexpress

Expression analysis of Xylella fastidiosa PD Temecula strain grown in different media

Project description:Investigation of whole genome gene expression level changes in Xylella fastidiosa grown in minimal media XFM and XFM supplied with pectin or glucan (Host polysaccharides) , compared to cell grown in the complex media PWG. The cells grown in the minimal medium XFM supplied with host polysaccharides specially pectin are transmissible by the insect vector when delivered to the vector through artificial diet system. This does not happen with cells grown in the complex media. 4 (4 plex chips) study using total RNA recovered from 4 independents replicates for Xylella fastidiosa grown on PWG, XFM, XFM-glucan and XFM-pectin.

2009-10-03 | E-GEOD-18369 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data