ArticleScientific reports2016
Glutathione-conjugating and membrane-remodeling activity of GDAP1 relies on amphipathic C-terminal domain.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Unraveling GDAP1: Bridging Mitochondrial Biology and Peripheral Neuropathy.Biomolecules · 2026Review
- Peroxisome dynamics and inter-organelle interactions in neuronal health and disease.Frontiers in molecular neuroscience · 2025Review
- Abnormal redox balance at membrane contact sites causes axonopathy inResearch square · 2024Article
- Expanding the genetic spectrum of hereditary motor sensory neuropathies in Pakistan.BMC neurology · 2024Article
- Lysosomal membrane contact sites: Integrative hubs for cellular communication and homeostasis.Current topics in membranes · 2024Review
- Hidden Glutathione Transferases in the Human Genome.Biomolecules · 2023Article
- Differential effects of Mendelian GDAP1 clinical variants on mitochondria-lysosome membrane contacts sites.Biology open · 2023Article
- Structural insights into Charcot-Marie-Tooth disease-linked mutations in human GDAP1.FEBS open bio · 2022Article
- GDAP1 loss of function inhibits the mitochondrial pyruvate dehydrogenase complex by altering the actin cytoskeleton.Communications biology · 2022Article
- Review
- Case report: exome sequencing achieved a definite diagnosis in a Chinese family with muscle atrophy.BMC neurology · 2021Article
- Mitochondria-lysosome membrane contacts are defective in GDAP1-related Charcot-Marie-Tooth disease.Human molecular genetics · 2021Article
- Identification and functional characterization of novel GDAP1 variants in Chinese patients with Charcot-Marie-Tooth disease.Annals of clinical and translational neurology · 2020Article
- Structural and functional divergence of GDAP1 from the glutathione S-transferase superfamily.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Review
- Structure of the Complete Dimeric Human GDAP1 Core Domain Provides Insights into Ligand Binding and Clustering of Disease Mutations.Frontiers in molecular biosciences · 2020Article
- Calcium Deregulation and Mitochondrial Bioenergetics in GDAP1-Related CMT Disease.International journal of molecular sciences · 2019Review
- Protein Amphipathic Helix Insertion: A Mechanism to Induce Membrane Fission.Frontiers in cell and developmental biology · 2019Review
- NovelBioMed research international · 2019Article
- AMPK activation negatively regulates GDAP1, which influences metabolic processes and circadian gene expression in skeletal muscle.Molecular metabolism · 2018Article
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Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the ganglioside-induced differentiation associated protein 1 (GDAP1) cause severe peripheral motor and sensory neuropathies called Charcot-Marie-Tooth disease. GDAP1 expression induces fission of mitochondria and peroxisomes by a currently elusive mechanism, while disease causing mutations in GDAP1 impede the protein's role in mitochondrial dynamics. In silico analysis reveals sequence similarities of GDAP1 to glutathione S-transferases (GSTs). However, a proof of GST activity and its possible impact on membrane dynamics are lacking to date. Using recombinant protein, we demonstrate for the first time theta-class-like GST activity for GDAP1, and it's activity being regulated by the C-terminal hydrophobic domain 1 (HD1) of GDAP1 in an autoinhibitory manner. Moreover, we show that the HD1 amphipathic pattern is required to induce membrane dynamics by GDAP1. As both, fission and GST activities of GDAP1, are critically dependent on HD1, we propose that GDAP1 undergoes a molecular switch, turning from a pro-fission active to an auto-inhibited inactive conformation.
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