ArticlePloS one2018
Phenotypic characterization of SETD3 knockout Drosophila.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
- Functional Analysis of the Histidine N-Methyltransferase SETD3 in Endometriosis.International journal of molecular sciences · 2026Article
- The role of post-translational modifications in driving abnormal cardiovascular complications at high altitude.Frontiers in cardiovascular medicine · 2022Review
- Genotype to Phenotype: CRISPR Gene Editing Reveals Genetic Compensation as a Mechanism for Phenotypic Disjunction of Morphants and Mutants.International journal of molecular sciences · 2021Review
- SETD3 protein is the actin-specific histidineeLife · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysine methylation is a reversible post-translational modification that affects protein function. Lysine methylation is involved in regulating the function of both histone and non-histone proteins, thereby influencing both cellular transcription and the activation of signaling pathways. To date, only a few lysine methyltransferases have been studied in depth. Here, we study the Drosophila homolog of the human lysine methyltransferase SETD3, CG32732/dSETD3. Since mammalian SETD3 is involved in cell proliferation, we tested the effect of dSETD3 on proliferation and growth of Drosophila S2 cells and whole flies. Knockdown of dSETD3 did not alter mTORC1 activity nor proliferation rate of S2 cells. Complete knock-out of dSETD3 in Drosophila flies did not affect their weight, growth rate or fertility. dSETD3 KO flies showed normal responses to starvation and hypoxia. In sum, we could not identify any clear phenotypes for SETD3 knockout animals, indicating that additional work will be required to elucidate the molecular and physiological function of this highly conserved enzyme.
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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.