ArticleMolecular and cellular biology2014
In vivo interaction proteomics reveal a novel p38 mitogen-activated protein kinase/Rack1 pathway regulating proteostasis in Drosophila muscle.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Feeding a rich diet supplemented with the translation inhibitor cycloheximide decreases lifespan and ovary size in Drosophila.Biology open · 2024Article
- Feeding a rich diet supplemented with the translation inhibitor cycloheximide decreases lifespan and ovary size in Drosophila.bioRxiv : the preprint server for biology · 2024Article
- Early-adulthood spike in protein translation drives aging via juvenile hormone/germline signaling.Nature communications · 2023Article
- Protein translation paradox: Implications in translational regulation of aging.Frontiers in cell and developmental biology · 2023Review
- RACK1 is evolutionary conserved in satellite stem cell activation and adult skeletal muscle regeneration.Cell death discovery · 2022Article
- Drosophila p38 MAPK interacts with BAG-3/starvin to regulate age-dependent protein homeostasis.Aging cell · 2021Article
- RACK1 modulates polyglutamine-induced neurodegeneration by promoting ERK degradation in Drosophila.PLoS genetics · 2021Article
- Proteostasis-associated aging: lessons from a Drosophila model.Genes & genomics · 2021Review
- Evolutionarily conserved transcription factors drive the oxidative stress response inThe Journal of experimental biology · 2020Article
- Review
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- Phosphoregulation of the oncogenic protein regulator of cytokinesis 1 (PRC1) by the atypical CDK16/CCNY complex.Experimental & molecular medicine · 2019Article
- A Drosophila Model of Intellectual Disability Caused by Mutations in the Histone Demethylase KDM5.Cell reports · 2018Article
- Definition of a RACK1 Interaction Network inG3 (Bethesda, Md.) · 2017Article
- Asc1p/RACK1 Connects Ribosomes to Eukaryotic Phosphosignaling.Molecular and cellular biology · 2017Article
- GSK3α and GSK3β Phosphorylate Arc and Regulate its Degradation.Frontiers in molecular neuroscience · 2017Article
- Cardiomyocyte-Specific Human Bcl2-Associated Anthanogene 3 P209L Expression Induces Mitochondrial Fragmentation, Bcl2-Associated Anthanogene 3 Haploinsufficiency, and Activates p38 Signaling.The American journal of pathology · 2016Article
- AealRACK1 expression and localization in response to stress in C6/36 HT mosquito cells.Journal of proteomics · 2015Article
- RACK1, a versatile hub in cancer.Oncogene · 2015Review
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Several recent studies suggest that systemic aging in metazoans is differentially affected by functional decline in specific tissues, such as skeletal muscle. In Drosophila, longevity appears to be tightly linked to myoproteostasis, and the formation of misfolded protein aggregates is a hallmark of senescence in aging muscle. Similarly, defective myoproteostasis is described as an important contributor to the pathology of several age-related degenerative muscle diseases in humans, e.g., inclusion body myositis. p38 mitogen-activated protein kinase (MAPK) plays a central role in a conserved signaling pathway activated by a variety of stressful stimuli. Aging p38 MAPK mutant flies display accelerated motor function decline, concomitant with an enhanced accumulation of detergent-insoluble protein aggregates in thoracic muscles. Chemical genetic experiments suggest that p38-mediated regulation of myoproteostasis is not limited to the control of reactive oxygen species production or the protein degradation pathways but also involves upstream turnover pathways, e.g., translation. Using affinity purification and mass spectrometry, we identified Rack1 as a novel substrate of p38 MAPK in aging muscle and showed that the genetic interaction between p38b and Rack1 controls muscle aggregate formation, locomotor function, and longevity. Biochemical analyses of Rack1 in aging and stressed muscle suggest a model whereby p38 MAPK signaling causes a redistribution of Rack1 between a ribosome-bound pool and a putative translational repressor complex.
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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.