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New links between protein N-terminal acetylation, dauer diapause, and the insulin/IGF-1 signaling pathway in Caenorhabditis elegans.
Article in Worm. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Forward genetic screening identifies novel roles for N-terminal acetyltransferase C and histone deacetylase in C. elegans development.Scientific reports · 2022Article
- Human NAA30 can rescue yeast mak3∆ mutant growth phenotypes.Bioscience reports · 2021Article
- Potential genetic damage to nematode offspring following exposure to triclosan during pregnancy.Molecular medicine reports · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Protein N-terminal acetylation is a widespread posttranslational modification in eukaryotes that is catalyzed by N-terminal acetyltransferases (NATs). The biochemical activity of NATs has been characterized extensively, whereas the biological function of NATs is only beginning to be defined. Here we comment on recent progress in understanding the function of NAT activity in C. elegans based on the characterization of natc-1 by Warnhoff et al. (2014) and daf-31 by Chen et al. (2014).(1,2) natc-1 encodes an auxiliary subunit of the NatC complex and modulates stress tolerance, dauer entry, and adult lifespan. daf-31 encodes the catalytic subunit of the NatA complex and affects dauer entry, dauer formation, and adult lifespan. The analysis of these genes and genetic studies of NATs in other organisms suggests protein N-terminal acetylation plays an evolutionarily conserved role in promoting growth and development and inhibiting stress resistance. Furthermore, we propose that NATs may regulate growth and development in response to external cues such as nutrient deprivation and other physiologic stresses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.