Mitochondrial translational defect extends lifespan in C. elegans by activating UPRmt
2022
- 119Usage
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Usage119
- Views84
- Downloads35
Dataset Description
To study the function of mitochondrial tars-1 (representing the ORF encoding CeThrRS-1), we used CRISPR–Cas9 to generate a mitochondrial tars-1 knockdown strain of C. elegans named tars-1(ora1) Ⅱ by mutating the start codon “ATG1” to “ACG1”, and the stain was confirmed by whole-exome sequencing.To study the mechanism of abnormal phenotypes in tars-1(ora1) Ⅱ, RNA-Seq was performed. We performed quantitative proteomics by LC–MS/MS to detect the protein abundance in N2 and tars-1(ora1) Ⅱ. Mitochondrial and cytosolic translation are dynamically regulated in a synchronized manner .
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