This SuperSeries is composed of the SubSeries listed below.
A novel long non-coding RNA Myolinc regulates myogenesis through TDP-43 and Filip1.
Cell line, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
<i>Airn</i> Regulates Igf2bp2 Translation in Cardiomyocytes.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Screening and validation of lncRNAs and circRNAs as miRNA sponges.
Cell line
View SamplesMyogenesis is a complex process required for skeletal muscle formation during embryonic development and for regeneration and growth of myofibers in adults. Accumulating evidence suggests that long non-coding RNAs (lncRNAs) play key roles in regulating cell fate decision and function in various tissues. However, the role of lncRNAs in the regulation of myogenesis remains poorly understood. In this study, we identified a novel muscle-enriched lncRNA called "Myolinc (AK142388)", which we functionally characterized in the C2C12 myoblast cell line. Myolinc is predominately localized in the nucleus, and its levels increase upon induction of the differentiation. Knockdown of Myolinc impairs the expression of myogenic regulatory factors and formation of multinucleated myotubes in cultured myoblasts. Myolinc also regulates the expression of Filip1 in a cis-manner. Similar to Myolinc, knockdown of Filip1 inhibits myogenic differentiation. Furthermore, Myolinc binds to TAR DNA-binding protein 43 (TDP-43), a DNA/RNA-binding protein that regulates the expression of muscle genes (e.g. Acta1 and MyoD). Knockdown of TDP-43 inhibits myogenic differentiation. We also show that Myolinc-TDP-43 interaction is essential for the binding of TDP-43 to the promoter regions of muscle marker genes. Finally, we show that silencing of Myolinc inhibits skeletal muscle regeneration in adult mice. Altogether, our study identifies a novel lncRNA that controls key regulatory networks of myogenesis.
A novel long non-coding RNA Myolinc regulates myogenesis through TDP-43 and Filip1.
Cell line, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A systems immunology approach identifies the collective impact of 5 miRs in Th2 inflammation.
No sample metadata fields
View SamplesTo elucidate the function of Airn isoforms in the heart, we conducted RNA immunoprecipitation experiment followed by microarray (RIP-chip) in murine cardiomoycyte cell line HL-1.
<i>Airn</i> Regulates Igf2bp2 Translation in Cardiomyocytes.
Specimen part
View SamplesTo elucidate the function of Airn isoforms in the heart, we conducted loss-of-function experiments in murine cardiomoycyte cell line HL-1.
<i>Airn</i> Regulates Igf2bp2 Translation in Cardiomyocytes.
Specimen part
View SamplesIn order to provide functional data of kidney-specific long intergenic non-coding RNAs (lincRNA), loss-of-function study was conducted.
Logic programming to infer complex RNA expression patterns from RNA-seq data.
Cell line
View SamplesIntensive research in past two decades has uncovered the presence and importance of noncoding RNAs (ncRNAs), which includes microRNAs (miRs) and long ncRNAs (lncRNAs). These two classes of ncRNAs interact to a certain extent, as some lncRNAs bind to miRs to sequester them. Such lncRNAs are collectively called 'competing endogenous RNAs' or 'miRNA sponges'. In this study, we screened for lncRNAs that may act as miRNA sponges using the publicly available data sets and databases. To uncover the roles of miRNA sponges, loss-of-function experiments were conducted, which revealed the biological roles as miRNA sponges. LINC00324 is important for the cell survival by binding to miR-615-5p leading to the de-repression of its target BTG2 LOC400043 controls several biological functions via sequestering miR-28-3p and miR-96-5p, thereby changing the expressions of transcriptional regulators. Finally, we also screened for circular RNAs (circRNAs) that may function as miRNA sponges. The results were negative at least for the selected circRNAs in this study. In conclusion, miRNA sponges can be identified by applying a series of bioinformatics techniques and validated with biological experiments.
Screening and validation of lncRNAs and circRNAs as miRNA sponges.
Cell line
View SamplesAllergic asthma is a chronic inflammatory disease dominated by a CD4+ T helper 2 (Th2) cell signature. The immune response amplifies in self-enforcing loops, promoting Th2-driven cellular immunity and leaving the host unable to terminate inflammation. Posttranscriptional mechanisms, including miRNAs, are pivotal in maintaining immune-homeostasis. Since an altered expression of various miRNAs has been associated with T cell-driven diseases, including asthma, we hypothesized that miRNAs control mechanisms ensuring Th2 stability and maintenance in the lung. We isolated murine CD4+ Th2 cells from allergic inflamed lungs and profiled gene and microRNA expression.
A systems immunology approach identifies the collective impact of 5 miRs in Th2 inflammation.
No sample metadata fields
View Samples