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ChIP-seq for TAZ (WWTR1) binding region in C2C12 myoblasts

ABSTRACT: ChIP-seq for TAZ (WWTR1) binding region in C2C12 myoblasts

PROVIDER: PRJEB26667 | ENA |

REPOSITORIES: ENA

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Similar Datasets

ChIP-seq for TAZ (WWTR1) binding region in C2C12 myoblasts

Project description:We demonstrated that TAZ positively regulates Irs1 gene transcription in muscle. Therefore we designed ChIP-seq experiment to reveal detailed mechanism of regulation. To capture TAZ in chromatin preparation, we made Flag-tagged TAZ expressing and control vector transduced C2C12 cells by retroviral infection. We used FLAG-conjugated beads to capture TAZ-chromatin complexes and ChIP-seq was perforemd. Among many TAZ binding sites, we focused Irs1 regulatory region because our primary purpose was to identify TAZ binding site for the regulation of Irs1 transcription.

2018-12-13 | E-MTAB-6764 | biostudies-arrayexpress

Human Cardiac Fibroblast BioID2 Interactome for SKI and TAZ(WWTR1)

Project description:We used adenoviral-mediated overexpression of MYC-BioID2, MYC-BioID2-SKI, MYC-BioID2-WWTR1 (TAZ) in human primary cardiac fibroblasts to elucidate the interaction between SKI and the Hippo signaling pathway. Original data is also available on the Global Proteome Machine (http://hs2.proteome.ca/tandem/thegpm_tandem.html). Datasets are identified as follows: GPM10000002938 and 2939 are untreated negative control cell lysates; GPM10000002941 and 2942 are "empty" MYC-BioID2 vector; GPM10000002943 and 2944 are MYC-BioID2-SKI; and GPM10000002944 and 2945 are MYC-BioID2-WWTR1(TAZ).

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Expression profile of RCC4 cells with TAZ (WWTR1) silencing

Project description:TAZ, also known as WWTR1, is the one of the effectors of Hippo pathway. With its paralog, YAP, TAZ promotes organ size growth as well as tumor metastasis. In human renal carcinoma cells, we found that TAZ-silencing induces resisntance toward erastin-induced ferroptosis. In this study, TAZ is silencing in clear cell carcinoma cell line RCC4 to elucidate the downstream targets that promotes the resistance toward erastin-induced ferroptosis.

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circRNA expression in C2C12 myoblasts and myotubes

Project description:To determine the circRNA expression profile in C2C12 myoblasts and myotubes, we used mouse circRNA microarray from Arraystar to examine the expression of circRNAs in C2C12 myoblasts and myotubes.

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lncRNA expression in C2C12 myoblasts and myotubes

Project description:To determine the lncRNA expression profile in C2C12 myoblasts and myotubes, we used mouse lncRNA microarray from Arraystar to examine the expression of lncRNAs in C2C12 myoblasts and myotubes.

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The lncRNA TAZ-AS202 promotes lung cancer progression through stabilization of the E2F1 transcription factor and activation of Ephrin signaling

Project description:Silencing of TAZ (WWTR1) and lncRNA TAZ-AS202 (WWTR1-AS1-202) by siRNA transfection on A549 cell line of lung cancer

2023-12-07 | E-MTAB-12507 | biostudies-arrayexpress

LaminB1 DamID in undifferentiated mouse C2C12 myoblasts (ATCC, Lot 59501261) and differentiated C2C12 myotubes

Project description:Maps of genomic regions in proximity to the nuclear lamina were determined in undifferentiated C2C12 myoblasts (MBs) and 6 day differentiated C2C12 myotubes (MTs) using DamID with a Dam-Lamin B1-encoding lentivirus.

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Project description:We show the application of 5mC antibody-based methylated DNA immunoprecipitation followed sequencing technology for high-through profiling of DNA methylation in mouse C2C12 myoblasts and myotubes. By analyzing the methylation status of immunoprecipitated DNA fragments, we generated genome-wide DNA methyaltion maps in mouse C2C12 myoblasts and myotubes. We find that DNA methylation levels in myoblasts at rDNA promter and coding regions are higher than that in myotubes but not changed in intergenic regions.

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Partial pluripotent reprogramming in C2C12 myoblasts

Project description:Partial pluripotent reprogramming in C2C12 myoblasts

| PRJNA810342 | ENA

Differentially expressed genes in c2c12 myoblasts

Project description:Proteosome inhibitors such as bortezomib (BTZ) have been used to treat muscle wasting in animal models. However, direct effect of BTZ on skeletal muscle cells has not been reported. In the present study, our data showed that C2C12 cells exhibited a dose-dependent decrease in cell viability in response to increasing concentrations of BTZ. We used microarrays to detail the differentially expressed genes in c2c12 myoblasts with different culture conditions.

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