Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global gene expression profiles of MT knockout and wild-type mice in the condition of doxorubicin-induced cardiomyopathy

ABSTRACT: The present study was designed using MT knockout mice in concert with genomic approaches to explore the possible molecular and cellular mechanisms involved in the protective effects of MT against DOX cardiotoxicity. MT-M-bM-^EM- /M-bM-^EM-! null (MT-/-) mice and corresponding wild-type mice (MT+/+) were administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of saline. Animals were sacrificed on the 4th day after DOX administration and samples were collected for further analyses. Global gene expression profiles of cardiac mRNA from two genotype mice revealed that 381 characteristically MT-responsive genes were identified between MT+/+ mice and MT-/- mice in response to DOX, including fos, ucp3, car3, atf3, map3k6, etc.. Functional analysis implied MAPK signaling pathway, p53 signaling pathway, Jak-STAT signaling pathway, PPAR signaling pathway, Wnt signaling pathway, etc. might be involved to mediate the protection of DOX cardiomyopathy by MT. Results from the present study not only validated the previously reported possible mechanisms of MT protection against DOX toxicity, but also provided new clues into the molecular mechanisms involved in this process. Male MT+/+ & MT-/- mice (6-8 weeks old) were randomly assigned to treatment or control groups and administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of normal saline solution (NS) respectively. Animals were sacrificed on the 4th day after DOX injection, and samples were collected for further microarray analyses.

ORGANISM(S): Mus musculus

SUBMITTER: Yi Shuai

PROVIDER: E-GEOD-23598 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Global gene expression profiles of MT knockout and wild-type mice in the condition of doxorubicin-induced cardiomyopathy

Project description:The present study was designed using MT knockout mice in concert with genomic approaches to explore the possible molecular and cellular mechanisms involved in the protective effects of MT against DOX cardiotoxicity. MT-Ⅰ/Ⅱ null (MT-/-) mice and corresponding wild-type mice (MT+/+) were administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of saline. Animals were sacrificed on the 4th day after DOX administration and samples were collected for further analyses. Global gene expression profiles of cardiac mRNA from two genotype mice revealed that 381 characteristically MT-responsive genes were identified between MT+/+ mice and MT-/- mice in response to DOX, including fos, ucp3, car3, atf3, map3k6, etc.. Functional analysis implied MAPK signaling pathway, p53 signaling pathway, Jak-STAT signaling pathway, PPAR signaling pathway, Wnt signaling pathway, etc. might be involved to mediate the protection of DOX cardiomyopathy by MT. Results from the present study not only validated the previously reported possible mechanisms of MT protection against DOX toxicity, but also provided new clues into the molecular mechanisms involved in this process.

2013-08-10 | GSE23598 | GEO

Impact of CDK4-deficiency on EM-BM-5-myc driven B-lymphoma

Project description:Impact of CDK4-deficiency on EM-BM-5-myc driven B-lymphoma By crossing mating CDK4 Knockout mice with EM-BM-5-myc mice,We found CDK4-deficiency enhances the EM-BM-5-myc induced B-lymphoma.We further to discover the molecular mechanism B-lymphoma cells form the cdk4+/+ EM-BM-5-myc and cdk4-/-EM-BM-5-myc mice and then culturing for RNA extraction and hybridization on Affymetrix microarrays.

2012-12-16 | E-GEOD-21683 | biostudies-arrayexpress

Crosslinking-Mass Spectrometry data for structural analysis of Doublecortin-Microtubule interaction

Project description:Doublecortin (DCX) is a microtubule (MT) associated protein that regulates MT structure and function during neuronal development and mutations in DCX lead to a spectrum of neurological disorders. The structural properties of MT-bound DCX remain poorly resolved. Here, we describe the molecular architecture of the DCX-MT complex through an integrative modeling approach that combines data from X-ray crystallography, cryo-EM and a high-fidelity chemical crosslinking method. We demonstrate that DCX interacts with MTs through its N-terminal domain and induces a lattice-dependent self-association involving both the C-terminal structured domain and the C-tails, in a conformation that favors an open, domain-swapped state. The networked state is shown to accommodate multiple different attachment points on the MT lattice, all of which orient the C-tails away from the lattice. As numerous disease mutations cluster in the C-terminus and regulatory phosphorylations cluster in the C-tail, our study shows that lattice-driven self-assembly is an important property of DCX.

2022-05-04 | PXD033167 | Pride

Combinatory microarray and SuperSAGE analyses identify pairing-dependently transcribed genes in Schistosoma mansoni males, including follistatin [SuperSAGE]

Project description:Comparing the transcriptomes of pairing-experienced (EM) and pairing-unexperienced (UM) male Schistosoma mansoni (in biological triplicates) we detected 253 genes to be significantly differeantially (p < 1-10; log2ratios < -0.585 or > +0.585) transcribed. pairing-experienced (EM) and pairing-unexperienced (UM) male Schistosoma mansoni were compared by SuperSAGE (Matsumura et al., 2003; with minor changes: Molina et al., 2008), sequencing Illumina (Solexa)

2013-09-09 | E-GEOD-45628 | biostudies-arrayexpress

NFKB1 and NFKB2 differently modulate transcriptional profile of MT-2 cells

Project description:To investigate the effects of NFKB signaling, RNA-seq analysis was performed on both Jurkat and MT-2 cells. It was observed that either NFKB1 or NFKB2 knockout could alter the gene expression profile in MT-2 cells compared to Jurkat cells. Gene expression profiles of NFKB1/NFKB2 knockout Jurkat cells were compared to the mock edited Jurkat cells. On the other hand, it was hypothesized that the gene expression profile of MT-2 cells can be more drastically altered by NFKB1 or NFKB2 knockout. NFKB2 knockout MT-2 cells exhibited a unique gene expression profile compared to those of NFKB1 knockout MT-2 cells and mock edited MT-2 cells.

2023-11-01 | E-MTAB-13408 | biostudies-arrayexpress

Effect of Lead on Genome-Wide Expression in Developing Mouse Brain during Synaptogenesis

Project description:Lead exposure causes a variety of health effects, especially in children, that may include cognitive and behavioural problems. This study explores the mechanisms associated with this relationship by assessing alterations in gene expression of C57BL/6J pups treated with 50mg/kg lead compared to controls. In addition this study also analyzed brain gene expression differences in Metallothionein I and II (Mt-I and Mt-II) knockout mice treated with lead. Pups of three genotypes (C57BL/6J, Mt-KO with a C57BL/6J background and Heterozygote Mt-KO) were injected with lead acetate during synaptogenesis and weight-matched controls were injected with saline at the same time points. Whole brains were harvested and RNA extracted and pooled from 5 pups and hybridized to Mouse Genome 430 2.0 Arrays. In total 6 arrays were used, one for each genotype and treatment.

2014-01-20 | E-GEOD-26894 | biostudies-arrayexpress

RELA and RELC differently modulate transcriptional profile of MT-2 cells

Project description:To investigate the effects of NFKB signaling, RNA-seq analysis was performed on both Jurkat and MT-2 cells. It was observed that either RELA or RELC knockout could alter the gene expression profile in MT-2 cells compared to Jurkat cells.Gene expression profiles of RELA-C knockout Jurkat cells were compared to the mock edited Jurkat cells. On the other hand, it was hypothesized that the gene expression profile of MT-2 cells can be more drastically altered by RELA or RELC knockout compared to RELB knockout.

2024-08-01 | E-MTAB-14212 | biostudies-arrayexpress

PKM2 aggregation drives metabolism reprograming during aging process

Project description:Mice was administrated with doxorubicin (DOX) to induce premature aging. Also these mice were administered intragastrically with vehicle or K35 or K27 compounds. After 20 days, these mice were sacrificed for liver tissue which were subjected to RNA sequencing to find the differentially expressed genes between control and treated groups.

2024-06-24 | GSE268773 | GEO

Combinatory microarray and SuperSAGE analyses identify pairing-dependently transcribed genes in Schistosoma mansoni males, such as follistatin [Microarray]

Project description:Transcriptional profiling of S. mansoni pairing-experienced males (EM) vs. pairing unexperienced males (UM) Two conditions (EM vs. UM) with three biological samples of EM and in parallel other three biological samples of UM. For each sample (three EM and three UM) were performed four technical replicas.

2013-09-09 | E-GEOD-44193 | biostudies-arrayexpress

Differentially methylated genes in human IL-7Ra high and low EM CD8+ T cells

Project description:Genome wide DNA methylation profiling of IL-7Ra high and low EM CD8+ T cells. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,578 CpGs. Samples included 2 IL-7Ra high EM CD8+ T cells and 2 IL-7Ra high EM CD8+ T cells. Bisulphite converted DNA from the 4 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

2015-08-06 | E-GEOD-67816 | 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