ArticleBioMed research international2015
Loss of flfl Triggers JNK-Dependent Cell Death in Drosophila.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Protein Phosphatase 4 Negatively Regulates the Immune Deficiency-NF-κB Pathway during theJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- An RNAi Screen for Genes Required for Growth ofG3 (Bethesda, Md.) · 2019Article
- APLP2 Modulates JNK-Dependent Cell Migration inBioMed research international · 2018Article
- The protein phosphatase 4 complex promotes the Notch pathway andBiology open · 2017Article
- PLATINUM SENSITIVE 2 LIKE impacts growth, root morphology, seed set, and stress responses.PloS one · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
falafel (flfl) encodes a Drosophila homolog of human SMEK whose in vivo functions remain elusive. In this study, we performed gain-of-function and loss-of-function analysis in Drosophila and identified flfl as a negative regulator of JNK pathway-mediated cell death. While ectopic expression of flfl suppresses TNF-triggered JNK-dependent cell death, loss of flfl promotes JNK activation and cell death in the developing eye and wing. These data report for the first time an essential physiological function of flfl in maintaining tissue homeostasis and organ development. As the JNK signaling pathway has been evolutionary conserved from fly to human, a similar role of PP4R3 in JNK-mediated physiological process is speculated.
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