ArticleThe EMBO journal2014
Ret rescues mitochondrial morphology and muscle degeneration of Drosophila Pink1 mutants.
Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Rethinking 'rare'Journal of Parkinson's disease · 2025Pooled it
- FETCH enables fluorescent labeling of membrane proteins in vivo with spatiotemporal control inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Creatine Kinase-MM/Proto-oncogene Tyrosine-Protein Kinase Receptor as a Sensitive Indicator for Duchenne Muscular Dystrophy Carriers.Molecular neurobiology · 2024Article
- Effects of glial-derived neurotrophic factor on remodeling and mitochondrial function in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Enhancer-activated RET confers protection against oxidative stress to KMT2A-rearranged acute myeloid leukemia.Cancer science · 2024Article
- Selpercatinib combination with the mitochondria-targeted antioxidant MitoQ effectively suppresses RET-mutant thyroid cancer.NPJ precision oncology · 2024Article
- Synaptic defects in a drosophila model of muscular dystrophy.Frontiers in cellular neuroscience · 2024Article
- Extracellular freezing induces a permeability transition in the inner membrane of muscle mitochondria of freeze-sensitive but not freeze-tolerantFrontiers in physiology · 2024Article
- Article
- Neuroprotective Effects of Lycium Barbarum Fruit Extract on Pink1Plant foods for human nutrition (Dordrecht, Netherlands) · 2023Article
- Ubiquitination at the lysine 27 residue of the Parkin ubiquitin-like domain is suggestive of a new mechanism of Parkin activation.Human molecular genetics · 2022Article
- Glutamate metabolism directs energetic trade-offs to shape host-pathogen susceptibility in Drosophila.Cell metabolism · 2021Article
- Glial-derived neurotrophic factor in human airway smooth muscle.Journal of cellular physiology · 2021Article
- A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila.PLoS genetics · 2021Article
- Oxidative-Signaling in Neural Stem Cell-Mediated Plasticity: Implications for Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Optogenetic delivery of trophic signals in a genetic model of Parkinson's disease.PLoS genetics · 2021Article
- Article
- Ral function in muscle is required for flight maintenance inSmall GTPases · 2020Article
- PARIS induced defects in mitochondrial biogenesis drive dopamine neuron loss under conditions of parkin or PINK1 deficiency.Molecular neurodegeneration · 2020Article
- Long-term in vivo imaging of Drosophila larvae.Nature protocols · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD)-associated Pink1 and Parkin proteins are believed to function in a common pathway controlling mitochondrial clearance and trafficking. Glial cell line-derived neurotrophic factor (GDNF) and its signaling receptor Ret are neuroprotective in toxin-based animal models of PD. However, the mechanism by which GDNF/Ret protects cells from degenerating remains unclear. We investigated whether the Drosophila homolog of Ret can rescue Pink1 and park mutant phenotypes. We report that a signaling active version of Ret (Ret(MEN₂B) rescues muscle degeneration, disintegration of mitochondria and ATP content of Pink1 mutants. Interestingly, corresponding phenotypes of park mutants were not rescued, suggesting that the phenotypes of Pink1 and park mutants have partially different origins. In human neuroblastoma cells, GDNF treatment rescues morphological defects of PINK1 knockdown, without inducing mitophagy or Parkin recruitment. GDNF also rescues bioenergetic deficits of PINK knockdown cells. Furthermore, overexpression of Ret(MEN₂B) significantly improves electron transport chain complex I function in Pink1 mutant Drosophila. These results provide a novel mechanism underlying Ret-mediated cell protection in a situation relevant for human PD.
Indexed as
Identifiers
What OpenQuestion holds
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.