HTT regulates muscle differentiation in vitro.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA906531 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our study identified HTT as a key regulator of skeletal muscle differentiation in vitro.
2023-03-31 | GSE218996 | GEO
Project description:4 Treatment groups: A) Uninfected B) Infected 6 weeks prior with GFP-expressing recombinant lentivirus C) Infected 6 weeks prior with Htt-N171-19Q-expressing recombinant lentivirus D)Infected 6 weeks prior with Htt-N171-82Q-expressing recombinant lentivirus Keywords = huntington Keywords: parallel sample
2008-08-14 | GSE1918 | GEO
Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Keywords: gene expression study
2008-09-01 | GSE12481 | GEO
Project description:Mutation in the huntingtin (HTT) gene causes Huntington’s disease. Wild type Htt is essential for development as Htt knockout mice die at day E7.5. Increasing evidence suggests mutant Htt may alter neurogenesis and development of striatal neurons resulting in neuronal loss. Using mouse embryonic stem cells (mESCs), we examined the role of Htt in neural differentiation. We found Htt-null (HN) mESCs inefficient in generating neural stem cells. In contrast differentiation into progenitors of mesoderm and endoderm lineages was not affected. To investigate the basis for the lack of neural differentiation, we carried out gene expression profiling by RNA-seq to examine if genes involved in neural differentiation were dysregulated in HN mESCs.
2017-01-03 | GSE92905 | GEO
Project description:Gene expression profiling of human and murine in vitro muscle differentiation
| PRJNA288500 | ENA
Project description:mt-Ty 5´tiRNA regulates skeletal muscle cell proliferation and differentiation
| PRJNA899504 | ENA
Project description:The aim of the study was to characterize the molecular mechanism involved in TGF-M-CM-^_ mediated smooth muscle formation in vitro. We employed rat bone marrow derived Oct4 expressing clones of multipotent adult progenitor cells (rMAPC). We subjected these cells to differentiation towards smooth muscle cell as previously reported using TGF-M-CM-^_1. The differentiation process reuires 6 days with media change every 2 days followed by RNA harvest. RNA was isolated using commercially available kits (Qiagen RNA easy micro kit). RNA integrity and quality was assessed prior to labeling and hybridization. As a control RNA from rat aortic smooth muscle cells was commercially obtained. Two biological replicate clones of rMAPC cells were used for the differentiation to smooth muscle like cells. The RNA was harvested at days 0, 2, 4 and 6 in triplicates. The RNA from primary smooth muscle cells was commercially obtained and was used in duplicates as control.
2012-10-09 | E-GEOD-32990 | biostudies-arrayexpress
Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Experiment Overall Design: Primary neurons samples infected with TRE-Htt-N853-18Q or -82Q.
2008-10-25 | E-GEOD-12481 | biostudies-arrayexpress
Project description:Myogenesis 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.
2018-04-06 | GSE69455 | GEO
Project description:Myogenesis 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.
2018-04-06 | GSE69451 | GEO