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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA profiling of skeletal muscle in RP58 knockout mice

ABSTRACT: To predict RP58-regulated genes involved in skeletal myogenesis, RNA profiling experiments were performed, comparing RNA derived from skeletal muscle tissue of a RP58+/+ mouse to that from a RP58 knockout (KO) mouse at E18.5. Importantly, well-known dominant-negative inhibitors of muscle differentiation, the Id family of genes (Id1/Id2/Id3), were upregulated in the RP58 KO muscle. On the contrary, a number of muscle differentiation-related genes, such as Ckm, troponin and Myosin, were downregulated in the same sample. These results indicate that the repressor protein RP58 is important for muscle terminal differentiation, possibly suppressing the gene expression of muscle differentiation genes such as the Ids. Keywords: Knockout tissue Skeletal muscles of WT and RP58 KO mice (E18.5 diaphragm) were dissected under a microscope and RNA was extracted using ISOGEN (Nippongene). After EtOH precipitation, RNA was dissolved into DEPC-DW and its concentration was determined. Microarray analysis - cRNA was synthesized. 10 ug of cRNA were hybridized to Affymetrix mouse 430A 2.0 arrays. Signal intensities were calculated using the RMA method. MAPPFinder (www.genmapp.org) was used to integrate expression data with known pathways.

ORGANISM(S): Mus musculus

SUBMITTER: Hiroshi Asahara

PROVIDER: E-GEOD-16595 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RNA profiling of skeletal muscle in RP58 knockout mice

Project description:To predict RP58-regulated genes involved in skeletal myogenesis, RNA profiling experiments were performed, comparing RNA derived from skeletal muscle tissue of a RP58+/+ mouse to that from a RP58 knockout (KO) mouse at E18.5. Importantly, well-known dominant-negative inhibitors of muscle differentiation, the Id family of genes (Id1/Id2/Id3), were upregulated in the RP58 KO muscle. On the contrary, a number of muscle differentiation-related genes, such as Ckm, troponin and Myosin, were downregulated in the same sample. These results indicate that the repressor protein RP58 is important for muscle terminal differentiation, possibly suppressing the gene expression of muscle differentiation genes such as the Ids. Keywords: Knockout tissue

2009-07-31 | GSE16595 | GEO

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Project description:To predict Rp58-regulated gene involved in myogenesis, RNA profiling experiments were performed, comparing RNA derived from C2C12 with or without expressing shRNA for Rp58. As a result, 271 genes were upregulated in C2C12 stably expressing shRNA-Rp58 cells compared with control C2C12 cells. As Rp58 is repressor in C2C12, we hypothesized that Rp58 regulates gene cluster which expression is downregulated in accordance with Rp58 expression and myogenesis progression. In this regard, we also characterized dynamic gene expression patterns during myogenesis by microarray at 4 different stage (GM, day 0, 2, 4) of C2C12 myogenesis assays and found that 399 genes expression is characterized as downregulation pattern during myogenesis. Importantly, this down regulation gene set and upregulated genes by shRNA for Rp58 were highly overlapped. Experiment Overall Design: C2C12 murine skeletal muscle cells were purchased from American Type Experiment Overall Design: culture Collection (ATCC). These cells were mainteined in GM (DMEM Experiment Overall Design: supplemented with 10% FBS). Cells were grown in GM and after reaching Experiment Overall Design: counfluence, the medium was switched to DM (DMEM supplemented with 2% hourse serum) and further incubated. The medium was changed every 2 days. Culture was performed by using within five passages cells. For the experiment of shRNA for Rp58, transfection was performed by using Lipofectamin 2000 (Invitrogen). Stable transfectants were obtained by selection of the transfected C2C12 cells for two weeks. Experiment Overall Design: Microarray analysis - RNA was isolated as described from C2C12, and cRNA was synthesized. 10 ug of cRNA were hybridized to Affymetrix mouse 430 2.0 arrays. Intensity values were quantified using RMA algorithm. Experiment Overall Design: MAPPFinder (www.genmapp.org) was used to integrate expression data with known pathways.

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Misregulation of alternative splicing of BIN1 leads to T-tubule alterations and muscle weakness in myotonic dystrophy

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