cJun is a transcription factor activated by phosphorylation by SAPK/JNK MAP kinase pathway that has been linked to atherosclerosis. Adenovirus mediated gene transfer of a dominant negative form of cJun in C57BL/6 mice increased greatly the apolipoprotein E (ApoE) mRNA and plasma apoE levels and induced dyslipidmia, characterized by increased plasma cholesterol, triglyceride and VLDL levels and accumulation of discoidal HDL particles. Unexpectedly, infection of ApoE-/- mice with adenovirus expressing dn-cJun reduced by 50% plasma cholesterol, suggesting that the dn-cJun affected other genes that control plamsa cholesterol. To determine the molecular pathways implicated in this process we performed whole genome expression profiling using total RNA from the liver of infected ApoE-/- mice.
A dominant negative form of the transcription factor c-Jun affects genes that have opposing effects on lipid homeostasis in mice.
No sample metadata fields
View SamplesTranscriptome profile of highly purified multipotential (P), erythroid (E), and myeloid (M) bone marrow progenitors from three RPS19 mutated Diamond-Blackfan anemia and six control human subjects.
Defective ribosomal protein gene expression alters transcription, translation, apoptosis, and oncogenic pathways in Diamond-Blackfan anemia.
Sex, Age, Specimen part, Disease, Subject
View Samplesmolecular profiles (HG-U95B,C,D,E) of biopsy skeletal muscle samples obtained from 10 normal individuals and 10 DMD patients
Gene expression profiling of Duchenne muscular dystrophy skeletal muscle.
No sample metadata fields
View SamplesThe aim of this study was to investigate the molecular mechanisms implicated in this mouse model of nemaline myopathy, and to further compare the molecular disease response in different skeletal muscles. For this purpose, snap frozen skeletla muscle specimens from wild type and transgenic for alpha tropomyosin slow mice were studied. Five different muscle types were used (diaphragm, plantaris, extensor digitorum longus, tibialis anterior, gastrocnemus). Mice were sacrificed between 7 and 10 months. RNA pools from 3-5 animals were created and each pool was hybridized to a U74Av2 Affymetrix GeneChip. Datasets from 36 GeneChips were included in this study.
Skeletal muscle repair in a mouse model of nemaline myopathy.
No sample metadata fields
View SamplesMolecular profiles of dystophin-deficient patients and normal human skeletal muscles on Affymetrix HG-U95A arrays
Gene expression comparison of biopsies from Duchenne muscular dystrophy (DMD) and normal skeletal muscle.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Reprogramming of the microRNA transcriptome mediates resistance to rapamycin.
Specimen part, Cell line
View SamplesThis study identified gene expression of Side Population (SP) and Main Population (MP) cells, isolated from adult murine skeletal muscle and Bone Marrow. Five different preparations of muscle SP, muscle MP, Bone marrw SP and Bone marrow MP cells were used as replicates.
Side population cells isolated from different tissues share transcriptome signatures and express tissue-specific markers.
No sample metadata fields
View SamplesThe Mesio-Temporal Lobe Epilepsy (MTLE) syndrome is the most common form of intractable epilepsies. It is characterized by the recurrence of focal seizures occurring in mesio-temporal limbic structures and is often associated with hippocampal sclerosis and drug resistance.
Glial responses during epileptogenesis in Mus musculus point to potential therapeutic targets.
Sex, Specimen part
View SamplesThe mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation. Inhibitors of mTOR are being evaluated as anti-tumor agents. Given the emerging role of microRNAs (miRNAs) in tumorgenesis we hypothesized that miRNAs could play important roles in the response of tumors to mTOR inhibitors. Rapamycin resistant myogenic cells developed by long-term rapamycin treatment showed extensive reprogramming of miRNAs expression, characterized by up-regulation of the mir-17~92 and related clusters and down-regulation of tumor-suppressor miRNAs. Antagonists of oncogenic miRNA families and mimics of tumor suppressor miRNAs (let-7) restored rapamycin sensitivity in resistant tumor cells. This study identified miRNAs as new downstream components of the mTOR-signaling pathway, which may determine the response of tumors to mTOR inhibitors.
Reprogramming of the microRNA transcriptome mediates resistance to rapamycin.
Specimen part, Cell line
View SamplesDuring development of the mammalian central nervous system (CNS), neurons and glial cells (astrocytes and oligodendrocytes) are generated from common neural precursor cells (NPCs). However, neurogenesis precedes gliogenesis, which normally commences at later stages of fetal telencephalic development. Astrocyte differentiation of mouse NPCs at embryonic day (E) 14.5 (relatively late gestation) is induced by activation of the transcription factor STAT3, whereas at E11.5 (mid-gestation) NPCs do not differentiate into astrocytes even when stimulated by STAT3-activating cytokines such as leukemia inhibitory factor (LIF). This can be explained in part by the fact that astrocyte-specific gene promoters are highly methylated in NPCs at E11.5, but other mechanisms are also likely to play a role. We therefore sought to identify genes involved in the inhibition of astrocyte differentiation of NPCs at midgestation. We first examined gene expression profiles in E11.5 and E14.5 NPCs, using Affymetrix GeneChip analysis, applying the Percellome method to normalize gene expression level. We then conducted in situ hybridization analysis for selected genes found to be highly expressed in NPCs at midgestation. Among these genes, we found that N-myc and high mobility group AT-hook 2 (Hmga2) were highly expressed in the E11.5 but not the E14.5 ventricular zone of mouse brain, where NPCs reside. Transduction of N-myc and Hmga2 by retroviruses into E14.5 NPCs, which normally differentiate into astrocytes in response to LIF, resulted in suppression of astrocyte differentiation. However, sustained expression of N-myc and Hmga2 in E11.5 NPCs failed to maintain the hypermethylated status of an astrocyte-specific gene promoter. Taken together, our data suggest that astrocyte differentiation of NPCs is regulated not only by DNA methylation but also by genes whose expression is controlled spatio-temporally during brain development.
Identification of genes that restrict astrocyte differentiation of midgestational neural precursor cells.
No sample metadata fields
View Samples