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Processed data to replicate findings in our study on the role of the TRPC6 ion channel in DMD.

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Genetic and Pharmacologic TRPC6 Inhibition Improves Muscle Function and Survival in Mice with Moderate and Severe Muscular Dystrophy

Introduction

We performed a bulk RNA-seq study to investigate the role of the TRPC6 in abnormal force and calcium stress-response in DMD-model mouse cardiomycytes. In this study, we looked at gene expression in mice with double knockout of dystrophin and eutrophin (DKO), and either knock out TRPC6 in this DMD model or pharmacologically inhibit the channel with the selective drug BI-749327. The manuscript can be found [here](add link when available). Here, we share the counts tables and metadata to enable downstream analysis. Unfortunately, because of a data transfer error, the raw reads are currently not available, though we will continue to work to make them available in the future. We have also attached the downstream differential gene expression analysis done by GeneWiz.

Data

The following files are available:

  • counts.csv and metadata.csv: Counts (mapped by STAR and counted with featureCounts) for this bulk RNA-seq experiment.

  • deseq2_bl.zip: Some of the differential gene expression analysis done by GeneWiz. This mostly just includes the actual output of DESeq2 (or whatever equivalent GeneWiz uses).

Please feel free to email or raise an issue if any other materials are desired!

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Processed data to replicate findings in our study on the role of the TRPC6 ion channel in DMD.

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