ArticleThe Journal of biological chemistry2019
Tricarboxylic acid cycle activity suppresses acetylation of mitochondrial proteins during early embryonic development in
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 27 citations in OpenAlex.
- A mitochondrial redox switch licenses the onset of morphogenesis in animals.bioRxiv : the preprint server for biology · 2024Article
- Acylspermidines are conserved mitochondrial sirtuin-dependent metabolites.Nature chemical biology · 2024Article
- Allantoic fluid metabolome reveals specific metabolic signatures in chicken lines different for their muscle glycogen content.Scientific reports · 2023Article
- Effects of FeMicrobial cell factories · 2023Article
- Mechanisms ofMetabolites · 2022Article
- Aberrant methylmalonylation underlies methylmalonic acidemia and is attenuated by an engineered sirtuin.Science translational medicine · 2022Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tricarboxylic acid (TCA) cycle (or citric acid cycle) is responsible for the complete oxidation of acetyl-CoA and formation of intermediates required for ATP production and other anabolic pathways, such as amino acid synthesis. Here, we uncovered an additional mechanism that may help explain the essential role of the TCA cycle in the early embryogenesis of
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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.