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Systematic analysis of cis-elements in unstable mRNAs demonstrates that CUGBP1 is a key regulator of mRNA decay in muscle cells

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE21233: Expression data from C2C12 mouse myoblast with treatment actinomycin D GSE21235: mRNA immunoprecipitated with CUGBP1 in C2C12 Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Ju Youn Lee

PROVIDER: E-GEOD-21236 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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mRNA immunoprecipitated with CUGBP1 in C2C12

Project description:Dramatic changes in gene expression occur in response to extracellular stimuli and during differentiation. Although transcriptional effects are important, alterations in mRNA decay also play a major role in achieving rapid and massive changes in mRNA abundance. Moreover, just as transcription factor activity varies between different cell types, the factors influencing mRNA decay are also cell-type specific.GREs are recognized by CUGBP1, an RNA-binding protein and instability factor whose function is affected in several neuromuscular diseases. To dectect the mRNA associated with CUGBP1, we utilized RNA immunoprecipitation followed by microarray (RIP-Chip) to identify CUGBP1-associated transcripts. To identify the mRNA associated with CUGBP1, we performed the immunoprecipitation followed by microarray (RIP-Chip)

2010-07-08 | E-GEOD-21235 | biostudies-arrayexpress

Expression data from C2C12 mouse myoblast with treatment actinomycin D

Project description:Dramatic changes in gene expression occur in response to extracellular stimuli and during differentiation. Although transcriptional effects are important, alterations in mRNA decay also play a major role in achieving rapid and massive changes in mRNA abundance. Moreover, just as transcription factor activity varies between different cell types, the factors influencing mRNA decay are also cell-type specific. We have established the rates of decay for over 7000 transcripts expressed in mouse C2C12 myoblasts. To estimate mRNA decay rate in mouse muscle cells, we treated C2C12 mouse myoblasts with actinomycin D to inhibit transcription and collected samples at 0, 10, 50, 110 and 230 min.

2010-07-08 | E-GEOD-21233 | biostudies-arrayexpress

Exon array analysis in the mouse myoblast cell line, C2C12 cells treated with control-, Cugbp1- or Mbnl1-siRNA

Project description:CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs. To analyze more directly the role of CUGBP1/MBNL1 binding in alternative splicing, we performed exon array analysis in C2C12 cells using expression arrays. We analyzed total RNA of C2C12 cells treated with control-, Cugbp1- or Mbnl1-siRNA. RNA was harvested 48 hrs after transfection.

2012-01-03 | E-GEOD-29990 | biostudies-arrayexpress

The PARN deadenylase targets a discrete set of mRNAs for decay and regulates cell motility in mouse myoblasts

Project description:Almost all cellular mRNAs terminate in a 3M-bM-^@M-^Y poly(A) tail, the removal of which can induce both translational silencing and mRNA decay. Mammalian cells encode many poly(A)-specific exoribonucleases but their individual roles are poorly understood. Here, we undertook an analysis of the role of PARN deadenylase in mouse myoblasts using global measurements of mRNA decay rates. Our results reveal that a discrete set of mRNAs exhibit altered mRNA decay as a result of PARN depletion and that stabilization is associated with increased poly(A) tail length and translation. We determined that stabilization of mRNAs does not generally result in their increased abundance supporting the idea that mRNA decay is coupled to transcription. Importantly, PARN knockdown has wide ranging effects on gene expression that specifically impact the extracellular matrix and cell migration. Finally, although PARN has its own unique target transcripts it also influences some genes whose expression is modulated by other deadenylases. In order to investigate the role of PARN deadenyl on mRNA decay in mouse muscle cells , C2C12 cells were transfected by shRNA knockdown of PARN and treated with actinomycin D to inhibit transcription. Total RNA was isolated from three replicates at 0, 15, 30, 60, 120 and 240 minutes. The CTRL cell line stably transfected with LKO1 vector was described previously (GSE21233).

2012-08-31 | E-GEOD-35944 | biostudies-arrayexpress

Expression profiles of primary cortical neurons after knocking down Cugbp1

Project description:To clarify the functional properties of Cugbp1, we established the differentially expressed alternative exons in Cugbp1-silenced primary cortical neurons by using exon-sensitive microarray technology. We analyzed total RNA of primary motor neuron infected with lentivirus expressing shRNA against mouse Cugbp1 or control. RNA was harvested 11 days after transfection.

2013-04-18 | E-GEOD-46147 | biostudies-arrayexpress

Expression profiles of primary cortical neurons after knocking down Tdp-43 and Cugbp1

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-18 | E-GEOD-46148 | biostudies-arrayexpress

mRNA decay analysis in the mouse myoblast cell line, C2C12 cells treated with conrtol-, Cugbp1- or Mbnl1-siRNA

Project description:CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs. To analyze more directly the role of CUGBP1/MBNL1 binding to the 3’ UTR, we performed global analysis of mRNA stability in C2C12 cells using expression arrays, and found that CUGBP1 and MBNL1 regulate decay of endogenous mRNAs. We analyzed total RNA of C2C12 cells treated with control-, Cugbp1- or Mbnl1-siRNA. We analyzed 3 time points after addition of actionmycin D (0, 2.5, 5 hours).

2012-01-03 | E-GEOD-27583 | biostudies-arrayexpress

Global characterization of miR-574-5p decoy to CUGBP1 in human lung cancer using a mass spectrometry proteomics approach

Project description:We aimed to characterize decoy to the RNA-binding protein CUG-RNA binding protein 1 (CUGBP1 mechanism in A549 lung cancer cells. We identified several new canonical targets of CUGBP1 but those were not regulated by miR-574-5p via the decoy mechanism. This can be explained by the localization of CUGBP1 and miR-574-5p in the nucleus, where CUGBP1 regulates alternative splicing. Next, we analyzed the 3’UTRs of potential targets and found that the decoy-dependent regulation of mPGES-1 splicing is unique. Therefore, we postulate that in A549 cells mPGES-1 is the only protein regulated by the decoy mechanism of CUGBP1 and miR-574-5p which suggests that the decoy mechanism allows the specific regulation of the expression of distinct targets.

2020-03-02 | PXD016803 | Pride

Expression Profiling on Human Cell Lines with Different Acetylation Levels

Project description:Expression Profiling on Human Cell Lines with Different Acetylation Levels Expression profiling of human cell lines with different acetylation levels.

2014-08-06 | E-GEOD-49640 | biostudies-arrayexpress

Sympathetic neuropathy of the bone marrow haematopoietic stem cell niche is essential for myeloproliferative neoplasms

Project description:Myeloproliferative neoplasms (MPNs) are diseases caused by mutations in the haematopoietic stem cell (HSC) compartment. Most MPN patients have a common acquired mutation of Janus kinase 2 (JAK2) gene in HSCs that renders this kinase constitutively active, leading to uncontrolled cell expansion. The bone marrow (BM) microenvironment might contribute to the clinical outcomes of this common event. We previously showed that BM nestin+ mesenchymal stem cells (MSCs) innervated by sympathetic nerve fibres regulate normal HSCs. Here we demonstrate that abrogation of this regulatory circuit is essential for MPN pathogenesis. Sympathetic nerve fibres, supporting Schwann cells and nestin+ MSCs are consistently reduced in the BM of MPN patients and mice expressing the human JAK2V617F mutation in HSCs. Unexpectedly, MSC reduction is not due to differentiation but is caused by BM neural damage and Schwann cell death triggered by interleukin-1b produced by mutant HSCs. In turn, in vivo depletion of nestin+ cells or their production of CXCL12 expanded mutant HSCs and accelerated MPN progression. In contrast, administration of neuroprotective or sympathomimetic drugs prevented mutant HSC expansion. Treatment with b3-adrenergic agonists that restored the sympathetic regulation of nestin+ MSCs prevented the loss of these cells and blocked MPN progression by indirectly reducing leukaemic stem cells. Our results demonstrate that mutant HSC-driven niche damage critically contributes to disease manifestation in MPN and identify niche-forming MSCs and their neural regulation as promising therapeutic targets. Total RNA was isolated from BM CD45- CD31- Ter119- Nes-GFP+ cells obtained from Nes-gfp mice 10 weeks after transplantation with Mx1-cre;JAK2-V617F (n=3) or control cells (n=1). RNA was amplified using the NuGen Ovation system and hybridized to the Affymetrix MoGene 1.0 ST array.

2014-03-12 | E-GEOD-55801 | biostudies-arrayexpress

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