Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA140711 | ENA |
REPOSITORIES: ENA
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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
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
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.
2012-01-03 | GSE29990 | GEO
Project description:mRNA decay analysis in the mouse myoblast cell line, C2C12 cells treated with conrtol-, Cugbp1- or Mbnl1-siRNA
| PRJNA138367 | ENA
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.
2012-01-03 | GSE27583 | GEO
Project description: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
2010-07-08 | E-GEOD-21236 | biostudies-arrayexpress
Project description:CUG-binding protein 1 (CUGBP1) and muscleblind-like 1 (MBNL1) are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. We extensively determined RNA-binding sites of CUGBP1 and MBNL1 to investigate their roles in RNA processing. We also analyzed polypyrimidine tract-binding protein (PTB) as a control. CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, respectively, and regulate alternative splicing events. Moreover, CUGBP1 and MBNL1 are preferentially bound to the 3' untranslated regions (UTRs), in particular of genes for RNA-binding proteins, and facilitate decay of the bound mRNAs. In addition, CUGBP1 and MBNL1 mutually destabilize mRNA. Precise temporal regulation of CUGBP1 and MBNL1 are likely to be essential for accurate control of destabilization of a broad spectrum of genes as well as of alternative splicing events in cell differentiation and tissue development.
2012-01-04 | E-MTAB-414 | biostudies-arrayexpress
Project description:Myotonic dystrophy type 1 (DM1) is caused by the nuclear accumulation of mutant DMPK mRNA containing CUG-repeat expansions, resulting in a trans-dominant effect on RNA processing by sequestration of MBNL1 and activation of CELF1 splicing regulators. Here, we present a comprehensive study of the MBNL1 and CELF1-regulated splicing in the HeLa cell line that may participate in the complex phenotype of the DM1 disease. We have performed human GeneChip Exon array experiments with RNAs extracted from HeLa cells in which MBNL1 or CELF1 were silenced or over-expressed. MBNL1 or CELF1-silenced HeLa cells showed changes in the expression of 170 probe sets (150 genes) and 893 probe sets (613 genes), whereas MBNL1 or CELF1 over-expression on these cells had 812 probe sets (589 genes) and 684 probe sets (531 genes) altered, respectively. In MBNL1-silenced cells we have found and validated by RT-qPCR the exclusion of RASIP1 exon 4 and of KIF13A exon 26 and the inclusion of MBNL2 exon 5. Furthermore, we have found exclusion of LCOR exon 6 and PIP4K2C exon 1, and inclusion TCF12 exon 16, with dependence on the silencing degree of MBNL1, In MBNL1 over-expressed HeLa cells we have found and validated by RT-qPCR a potent inclusion of CD44 exon 8, CD44 exon 11 and the 3´UTR of TRAF2. We have then mimicked the misregulation of MBNL1 and CELF1 protein levels of DM1 in HeLa cells, finding new altered splicing events. These alterations were found in genes that encode proteins involved in myoblast differentiation and migration (CD44, RASIP1) and muscle development (TCF12 transcription factor), estrogen and thyroid receptor interactor (LCOR), as well as proteins involved in transduction signaling pathways (PIP4K2C, TRAF2) and intracellular trafficking (KIF13A). These results provide potential contributing genes that could help to explain the complex phenotype of the DM1 disease.
2016-12-21 | GSE41987 | GEO
Project description:We conducted RNASeq using mRNA extracted from C2C12 mouse myoblast cells transfected with non-targeting control (NTC) or RBM39 siRNA, to elucidate the effect of RBM39 on regulation of BMP4 pathway
2022-02-22 | GSE197107 | GEO
Project description:In urodele amphibians, limb regeneration involves the dedifferentiation of muscle myotubes into single cells that may acquire pluripotent potential. We have employed small molecules (myoseverin and BIO) to attempt to reproduce this behavior in mammalian muscle culture. C2C12 myotubes derived from the C2C12 myoblast cell line were induced to undergo cellularization by myoseverin treatment, which destabilizes tubulin filaments. The GSK-3 inhibitor, BIO, was then used to induce dedifferentiation. Induce neuron formation; the cells were incubated with 250 nM reversine for 48 h, and neural induction media (DMEM/F12 supplemented with N2 (Invitrogen)) and 1.5 uM all-trans retinoic acid for 7 days. C2C12 murine myoblast cell line and 48 h 10 uM BIO treated C2C12 cellulate (derived by 20 M myoseverin treatment for 48 h)
2011-12-08 | GSE34238 | GEO