ArticleScientific reports2017
CMT-linked loss-of-function mutations in GDAP1 impair store-operated Ca
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
The trial behind it
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Who cites it
30 citing papers in PubMed.
- Research progress on the role and mechanism of STIM and Orai protein-mediated store-operated calcium entry in cardiovascular diseases.Channels (Austin, Tex.) · 2026Review
- Deletion of mitochondrial calcium uniporter enhances calcium signals by slowing calcium clearance and triggers adaptive transcriptomic remodeling.The Journal of biological chemistry · 2026Article
- Unraveling GDAP1: Bridging Mitochondrial Biology and Peripheral Neuropathy.Biomolecules · 2026Review
- Molecular characterization of recessively inherited ataxic and neuropathic disorders in consanguineous Pakistani families.Scientific reports · 2026Article
- Mitochondria-Associated Membranes: A Key Point of Neurodegenerative Diseases.CNS neuroscience & therapeutics · 2025Review
- Charcot Marie Tooth disease pathology is associated with mitochondrial dysfunction and lower glutathione production.Cellular and molecular life sciences : CMLS · 2025Article
- Abnormal redox balance at membrane contact sites causes axonopathy inResearch square · 2024Article
- Epigenetic regulation of the humanBiochemistry and biophysics reports · 2024Article
- Organ chips with integrated multifunctional sensors enable continuous metabolic monitoring at controlled oxygen levels.Biosensors & bioelectronics · 2024Article
- Differential effects of Mendelian GDAP1 clinical variants on mitochondria-lysosome membrane contacts sites.Biology open · 2023Article
- Chronic inhibition of the mitochondrial ATP synthase in skeletal muscle triggers sarcoplasmic reticulum distress and tubular aggregates.Cell death & disease · 2022Article
- GDAP1 loss of function inhibits the mitochondrial pyruvate dehydrogenase complex by altering the actin cytoskeleton.Communications biology · 2022Article
- Threshold of heteroplasmic truncating MT-ATP6 mutation in reprogramming, Notch hyperactivation and motor neuron metabolism.Human molecular genetics · 2022Article
- Effective therapeutic strategies in a preclinical mouse model of Charcot-Marie-Tooth disease.Human molecular genetics · 2021Article
- GDAP1 Involvement in Mitochondrial Function and Oxidative Stress, Investigated in a Charcot-Marie-Tooth Model of hiPSCs-Derived Motor Neurons.Biomedicines · 2021Article
- Mitochondria-lysosome membrane contacts are defective in GDAP1-related Charcot-Marie-Tooth disease.Human molecular genetics · 2021Article
- Mutations inInternational journal of molecular sciences · 2021Article
- Selective Neuron Vulnerability in Common and Rare Diseases-Mitochondria in the Focus.Frontiers in molecular biosciences · 2021Review
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GDAP1 is an outer mitochondrial membrane protein involved in Charcot-Marie-Tooth (CMT) disease. Lack of GDAP1 gives rise to altered mitochondrial networks and endoplasmic reticulum (ER)-mitochondrial interactions resulting in a decreased ER-Ca
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Registered trials
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