Suppression of myopathic lamin mutations by muscle‐specific activation of AMPK and modulation of downstream signaling
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Summary
It is hypothesized that the cytoplasmic aggregates of NE proteins trigger signaling pathways that alter cellular homeostasis, causing muscle dysfunction and transcriptomics data from human muscle biopsy tissue revealed misregulation of the AMP‐activated protein kinase (AMPK), 4E‐binding protein 1 (4E‐BP1) andautophagy/proteostatic pathways.
- Type
- article
- Published
- 2018-09-18
- Cited by
- 20
- References
- 86
- Access
- Open access
- OpenAlex
- https://openalex.org/W2892305313
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:52310983
Keywords
LMNA, Lamin, Biology, Cell biology, AMPK
References
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Cited by
- Drosophila p38 MAPK Interacts with BAG-3/starvin to Regulate Age-dependent Protein Homeostasis
- The Neuronal Overexpression of Gclc in Drosophila melanogaster Induces Life Extension With Longevity-Associated Transcriptomic Changes in the Thorax
- Time-restricted feeding restores muscle function in Drosophila models of obesity and circadian-rhythm disruption
- Genetic Control of Muscle Diversification and Homeostasis: Insights from Drosophila
- Drosophila p38 MAPK interacts with BAG‐3/starvin to regulate age‐dependent protein homeostasis
- In Silico and In Vivo Analysis of Amino Acid Substitutions That Cause Laminopathies
- Modulation of muscle redox and protein aggregation rescues lethality caused by mutant lamins
- Combined Transcriptomic and Proteomic Profiling to Unravel Osimertinib, CARP-1 Functional Mimetic (CFM 4.17) Formulation and Telmisartan Combo Treatment in NSCLC Tumor Xenografts
- Time-restricted feeding promotes muscle function through purine cycle and AMPK signaling in Drosophila obesity models
- The D84G mutation in STIM1 causes nuclear envelope dysfunction and myopathy in mice
- The D84G mutation in STIM1 causes nuclear envelope dysfunction and myopathy in mice
- Cdk8/CDK19 promotes mitochondrial fission through Drp1 phosphorylation and can phenotypically suppress pink1 deficiency in Drosophila
- Global Proteomic Analysis Reveals Alterations in Differentially Expressed Proteins Between Cardiopathic LMNA Mutations
- Creatine and l-carnitine attenuate muscular laminopathy in the LMNA mutation transgenic zebrafish
- Genetic and Pathophysiological Basis of Cardiac and Skeletal Muscle Laminopathies
- Perinuclear organelle trauma at the nexus of cardiomyopathy pathogenesis arising from loss of function LMNA mutation
- Molecular mechanism on autophagy associated cardiovascular dysfunction in Drosophila melanogaster
- Advanced human iPSC-based modelling of LMNA-related congenital muscular dystrophy enables development of targeted genetic therapies for muscle laminopathies
- Drosophila as a Model for Studying the Roles of Lamins in Normal Tissues and Laminopathies
- Creatine and L-carnitine attenuate muscular laminopathy in the LMNA mutation transgenic zebrafish
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