ArticleGenetics2006
Loss-of-function mutations in a glutathione S-transferase suppress the prune-Killer of prune lethal interaction.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Altered Localization of Hybrid Incompatibility Proteins in Drosophila.Molecular biology and evolution · 2019Article
- Glutathione S-Transferase Regulates Mitochondrial Populations in Axons through Increased Glutathione Oxidation.Neuron · 2019Article
- GFZF, a GlutathioneMolecular and cellular biology · 2018Article
- Moving Speciation Genetics Forward: Modern Techniques Build on Foundational Studies inGenetics · 2017Review
- Article
- An essential cell cycle regulation gene causes hybrid inviability in Drosophila.Science (New York, N.Y.) · 2015Article
- Article
- Developmental function of Nm23/awd: a mediator of endocytosis.Molecular and cellular biochemistry · 2009Review
- The cystic fibrosis transmembrane recruiter the alter ego of CFTR as a multi-kinase anchor.Pflugers Archiv : European journal of physiology · 2007Review
- The Suppressor of Killer of prune, a unique glutathione S-transferase.Journal of bioenergetics and biomembranes · 2006Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prune gene of Drosophila melanogaster is predicted to encode a phosphodiesterase. Null alleles of prune are viable but cause an eye-color phenotype. The abnormal wing discs gene encodes a nucleoside diphosphate kinase. Killer of prune is a missense mutation in the abnormal wing discs gene. Although it has no phenotype by itself even when homozygous, Killer of prune when heterozygous causes lethality in the absence of prune gene function. A screen for suppressors of transgenic Killer of prune led to the recovery of three mutations, all of which are in the same gene. As heterozygotes these mutations are dominant suppressors of the prune-Killer of prune lethal interaction; as homozygotes these mutations cause early larval lethality and the absence of imaginal discs. These alleles are loss-of-function mutations in CG10065, a gene that is predicted to encode a protein with several zinc finger domains and glutathione S-transferase activity.
Indexed as
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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.