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Impairment of Mitochondrial Calcium Buffering Links Mutations in C9ORF72 and TARDBP in iPS-Derived Motor Neurons from Patients with ALS/FTD
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What this work says
Outgoing claims: the papers this work cites, builds on, or argues with.
inferredcites →https://doi.org/10.1002/ana.410280106openalex-snapshot
Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis
inferredcites →https://doi.org/10.1002/humu.22244openalex-snapshot
A Pan‐ E uropean Study of the C9orf72 Repeat Associated with FTLD : Geographic Prevalence, Genomic Instability, and Intermediate Repeats
inferredcites →https://doi.org/10.1002/stem.2388openalex-snapshot
C9orf72 Hexanucleotide Expansions Are Associated with Altered Endoplasmic Reticulum Calcium Homeostasis and Stress Granule Formation in Induced Pluripotent Stem Cell-Derived Neurons from Patients with Amyotrophic Lateral Sclerosis and Frontotemporal Dementia
inferredcites →https://doi.org/10.1006/exnr.1997.6599openalex-snapshot
Visualization of NMDA Receptor-Induced Mitochondrial Calcium Accumulation in Striatal Neurons
inferredcites →https://doi.org/10.1007/s00401-019-01996-zopenalex-snapshot
An ALS case with 38 (G4C2)-repeats in the C9orf72 gene shows TDP-43 and sparse dipeptide repeat protein pathology
inferredcites →https://doi.org/10.1016/0140-6736(93)92615-zopenalex-snapshot
Cell culture evidence for neuronal degeneration in amyotrophic lateral sclerosis being linked to glutamate AMPA/kainate receptors
inferredcites →https://doi.org/10.1016/j.ceca.2014.02.008openalex-snapshot
The elusive importance of being a mitochondrial Ca2+ uniporter
inferredcites →https://doi.org/10.1016/j.ceca.2017.01.003openalex-snapshot
The endoplasmic reticulum-mitochondria coupling in health and disease: Molecules, functions and significance
inferredcites →https://doi.org/10.1016/j.cell.2012.10.011openalex-snapshot
MICU1 Is an Essential Gatekeeper for MCU-Mediated Mitochondrial Ca2+ Uptake that Regulates Cell Survival
inferredcites →https://doi.org/10.1016/j.celrep.2017.11.064openalex-snapshot
MICU2 Restricts Spatial Crosstalk between InsP3R and MCU Channels by Regulating Threshold and Gain of MICU1-Mediated Inhibition and Activation of MCU
inferredcites →https://doi.org/10.1016/j.molcel.2014.01.013openalex-snapshot
MICU1 and MICU2 Finely Tune the Mitochondrial Ca2+ Uniporter by Exerting Opposite Effects on MCU Activity
inferredcites →https://doi.org/10.1016/j.nbd.2014.12.010openalex-snapshot
TARDBP pathogenic mutations increase cytoplasmic translocation of TDP-43 and cause reduction of endoplasmic reticulum Ca2+ signaling in motor neurons
inferredcites →https://doi.org/10.1016/j.neuron.2011.09.010openalex-snapshot
A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD
inferredcites →https://doi.org/10.1016/j.neuron.2011.09.011openalex-snapshot
Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS
inferredcites →https://doi.org/10.1016/j.neuron.2013.10.015openalex-snapshot
RNA Toxicity from the ALS/FTD C9ORF72 Expansion Is Mitigated by Antisense Intervention
inferredcites →https://doi.org/10.1016/s0896-6273(00)80038-0openalex-snapshot
Dominant Role of Mitochondria in Clearance of Large Ca2+ Loads from Rat Adrenal Chromaffin Cells
inferredcites →https://doi.org/10.1016/s1474-4422(12)70043-1openalex-snapshot
Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study
inferredcites →https://doi.org/10.1038/35097565openalex-snapshot
From charcot to lou gehrig: deciphering selective motor neuron death in als
inferredcites →https://doi.org/10.1038/nbt.3049openalex-snapshot
Combinatorial analysis of developmental cues efficiently converts human pluripotent stem cells into multiple neuronal subtypes
inferredcites →https://doi.org/10.1038/ncomms4996openalex-snapshot
ER–mitochondria associations are regulated by the VAPB–PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43
inferredcites →https://doi.org/10.1038/ncomms6999openalex-snapshot
Human iPSC-derived motoneurons harbouring TARDBP or C9ORF72 ALS mutations are dysfunctional despite maintaining viability
inferredcites →https://doi.org/10.1038/nrn1971openalex-snapshot
Molecular biology of amyotrophic lateral sclerosis: insights from genetics
inferredcites →https://doi.org/10.1038/s41467-017-02729-0openalex-snapshot
C9ORF72 repeat expansion causes vulnerability of motor neurons to Ca2+-permeable AMPA receptor-mediated excitotoxicity
inferredcites →https://doi.org/10.1056/nejm199205283262204openalex-snapshot
Decreased Glutamate Transport by the Brain and Spinal Cord in Amyotrophic Lateral Sclerosis
inferredcites →https://doi.org/10.1093/hmg/ddz107openalex-snapshot
Altered calcium dynamics and glutamate receptor properties in iPSC-derived motor neurons from ALS patients with C9orf72, FUS, SOD1 or TDP43 mutations
inferredcites →https://doi.org/10.1126/scitranslmed.3007529openalex-snapshot
Targeting RNA Foci in iPSC-Derived Motor Neurons from ALS Patients with a C9ORF72 Repeat Expansion
inferredcites →https://doi.org/10.1371/journal.pone.0055785openalex-snapshot
MICU2, a Paralog of MICU1, Resides within the Mitochondrial Uniporter Complex to Regulate Calcium Handling
inferredcites →https://doi.org/10.1523/jneurosci.14-01-00348.1994openalex-snapshot
Mitochondria buffer physiological calcium loads in cultured rat dorsal root ganglion neurons
inferredcites →https://doi.org/10.15252/emmm.201809423openalex-snapshot
Repeat‐associated non‐AUG translation in C9orf72‐ALS/FTD is driven by neuronal excitation and stress
What points at this work
Incoming claims: where this work appears in other papers’ reference lists and arguments.
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Image-Based Quantitation of Kainic Acid-Induced Excitotoxicity as a Model of Neurodegeneration in Human iPSC-Derived Neurons
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PolyGA targets the ER stress-adaptive response by impairing GRP75 function at the MAM in C9ORF72-ALS/FTD
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Cell and gene therapy for amyotrophic lateral sclerosis
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inferred← citeshttps://doi.org/10.1016/j.celrep.2024.113681openalex-snapshot
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Homozygous ALS-linked mutations in TARDBP/TDP-43 lead to hypoactivity and synaptic abnormalities in human iPSC-derived motor neurons
inferred← citeshttps://doi.org/10.1016/j.mcn.2025.103992openalex-snapshot
Mitochondrial fission and fusion in neurodegenerative diseases:Ca2+ signalling
inferred← citeshttps://doi.org/10.1016/j.nbd.2020.105050openalex-snapshot
An ALS-linked mutation in TDP-43 disrupts normal protein interactions in the motor neuron response to oxidative stress
inferred← citeshttps://doi.org/10.1016/j.nbd.2024.106673openalex-snapshot
Expanded ATXN1 alters transcription and calcium signaling in SCA1 human motor neurons differentiated from induced pluripotent stem cells
inferred← citeshttps://doi.org/10.1016/j.neuron.2025.11.001openalex-snapshot
TDP-43 dysfunction compromises UPF1-dependent mRNA metabolism in ALS
inferred← citeshttps://doi.org/10.1016/j.neuron.2026.02.003openalex-snapshot
Targeting PGAM5-driven mitochondrial integrated stress response slows ALS progression across subtypes
inferred← citeshttps://doi.org/10.1016/j.pneurobio.2022.102297openalex-snapshot
Aberrant neural activity in prefrontal pyramidal neurons lacking TDP-43 precedes neuron loss
inferred← citeshttps://doi.org/10.1016/j.stem.2021.12.008openalex-snapshot
Human stem cell models of neurodegeneration: From basic science of amyotrophic lateral sclerosis to clinical translation
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Single-cell transcriptomics identifies master regulators of neurodegeneration in SOD1 ALS iPSC-derived motor neurons
inferred← citeshttps://doi.org/10.1016/j.stemcr.2024.05.008openalex-snapshot
Cellular and axonal transport phenotypes due to the C9ORF72 HRE in iPSC motor and sensory neurons
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inferred← citeshttps://doi.org/10.1038/s41467-023-37630-6openalex-snapshot
Integrated transcriptome landscape of ALS identifies genome instability linked to TDP-43 pathology
inferred← citeshttps://doi.org/10.1038/s41467-023-41603-0openalex-snapshot
C9orf72-ALS human iPSC microglia are pro-inflammatory and toxic to co-cultured motor neurons via MMP9
inferred← citeshttps://doi.org/10.1038/s41467-023-44215-wopenalex-snapshot
Mutant GGGGCC RNA prevents YY1 from binding to Fuzzy promoter which stimulates Wnt/β-catenin pathway in C9ALS/FTD
inferred← citeshttps://doi.org/10.1038/s41573-022-00612-2openalex-snapshot
Amyotrophic lateral sclerosis: a neurodegenerative disorder poised for successful therapeutic translation
inferred← citeshttps://doi.org/10.1038/s41582-023-00845-8openalex-snapshot
Nutritional and metabolic factors in amyotrophic lateral sclerosis
inferred← citeshttps://doi.org/10.1038/s41582-024-01049-4openalex-snapshot
Targeting common disease pathomechanisms to treat amyotrophic lateral sclerosis
inferred← citeshttps://doi.org/10.1038/s41593-025-02049-3openalex-snapshot
TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes
inferred← citeshttps://doi.org/10.1038/s41598-022-09751-3openalex-snapshot
Hyperexcitability in young iPSC-derived C9ORF72 mutant motor neurons is associated with increased intracellular calcium release
inferred← citeshttps://doi.org/10.1038/s41598-022-16896-8openalex-snapshot
Human iPSC co-culture model to investigate the interaction between microglia and motor neurons
inferred← citeshttps://doi.org/10.1038/s44324-025-00049-2openalex-snapshot
Calcium-mediated regulation of mitophagy: implications in neurodegenerative diseases
inferred← citeshttps://doi.org/10.1042/bst20230190openalex-snapshot
CRISPRi: a way to integrate iPSC-derived neuronal models
inferred← citeshttps://doi.org/10.1080/01616412.2021.1893564openalex-snapshot
Overview of stem cells therapy in amyotrophic lateral sclerosis
inferred← citeshttps://doi.org/10.1080/02699052.2021.1909139openalex-snapshot
Minocycline improves cognition and molecular measures of inflammation and neurodegeneration following repetitive mTBI
inferred← citeshttps://doi.org/10.1080/21541248.2021.1892443openalex-snapshot
The progress inC9orf72research: ALS/FTD pathogenesis, functions and structure
inferred← citeshttps://doi.org/10.1080/21678421.2021.1985789openalex-snapshot
Theme 03 - IN VITRO EXPERIMENTAL MODELS
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Theme 05 - Human Cell Biology and Pathology (including iPSC studies)
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TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes
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Counter-regulation of RNA stability by UPF1 and TDP43
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Dynamic changes in chromosome and nuclear architecture during maturation of normal and ALS C9orf72 motor neurons
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inferred← citeshttps://doi.org/10.1186/s13041-025-01174-1openalex-snapshot
Alternative 3′ UTR polyadenylation is disrupted in the rNLS8 mouse model of ALS/FTLD
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Stimulating VAPB-PTPIP51 ER-mitochondria tethering corrects FTD/ALS mutant TDP43 linked Ca2+ and synaptic defects
inferred← citeshttps://doi.org/10.1186/s40478-024-01857-1openalex-snapshot
Molecular pathology, developmental changes and synaptic dysfunction in (pre-) symptomatic human C9ORF72-ALS/FTD cerebral organoids
inferred← citeshttps://doi.org/10.1186/s40478-025-01927-yopenalex-snapshot
Kaempferol enhances ER-mitochondria coupling and protects motor neurons from mitochondrial dysfunction and ER stress in C9ORF72-ALS
inferred← citeshttps://doi.org/10.1186/s40478-025-01964-7openalex-snapshot
Structural and functional studies of the VAPB-PTPIP51 ER-mitochondria tethering proteins in neurodegenerative diseases
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inferred← citeshttps://doi.org/10.21203/rs.3.rs-6782801/v1openalex-snapshot
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Disruption of the VAPB-PTPIP51 ER-mitochondria tethering proteins in post-mortem human amyotrophic lateral sclerosis
inferred← citeshttps://doi.org/10.3389/fcell.2023.1094356openalex-snapshot
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inferred← citeshttps://doi.org/10.3389/fncel.2021.660693openalex-snapshot
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inferred← citeshttps://doi.org/10.3389/fncel.2021.668500openalex-snapshot
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inferred← citeshttps://doi.org/10.3389/fphys.2023.1217815openalex-snapshot
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inferred← citeshttps://doi.org/10.3390/antiox12112008openalex-snapshot
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inferred← citeshttps://doi.org/10.3390/antiox13020240openalex-snapshot
Mitochondria Dysfunction and Neuroinflammation in Neurodegeneration: Who Comes First?
inferred← citeshttps://doi.org/10.3390/brainsci11080969openalex-snapshot
Differential NPY-Y1 Receptor Density in the Motor Cortex of ALS Patients and Familial Model of ALS
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Parkin beyond Parkinson’s Disease—A Functional Meaning of Parkin Downregulation in TDP-43 Proteinopathies
inferred← citeshttps://doi.org/10.3390/cells11040706openalex-snapshot
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inferred← citeshttps://doi.org/10.3390/cells11132049openalex-snapshot
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inferred← citeshttps://doi.org/10.3390/cells12060971openalex-snapshot
Induced Pluripotent Stem Cells and Their Applications in Amyotrophic Lateral Sclerosis
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Roles of Aging, Circular RNAs, and RNA Editing in the Pathogenesis of Amyotrophic Lateral Sclerosis: Potential Biomarkers and Therapeutic Targets
inferred← citeshttps://doi.org/10.3390/cells14050347openalex-snapshot
Age-Related Neurodegenerative Diseases: A Stem Cell’s Perspective
inferred← citeshttps://doi.org/10.3390/cells15040322openalex-snapshot
The Calcium Connection: Explaining Motor Neuron Vulnerability in ALS
inferred← citeshttps://doi.org/10.3390/cells15171536openalex-snapshot
Sigma-1 Receptor Stimulation Rescues FTD/ALS Mutant TDP43-Induced Disruption of the VAPB-PTPIP51 ER–Mitochondria Tethering Proteins via Inhibition of GSK3β
inferred← citeshttps://doi.org/10.3390/ijms22094705openalex-snapshot
Molecular Mechanisms Underlying TDP-43 Pathology in Cellular and Animal Models of ALS and FTLD
inferred← citeshttps://doi.org/10.3390/ijms22158196openalex-snapshot
Emerging hiPSC Models for Drug Discovery in Neurodegenerative Diseases
inferred← citeshttps://doi.org/10.3390/ijms22189832openalex-snapshot
Current Concepts on Genetic Aspects of Mitochondrial Dysfunction in Amyotrophic Lateral Sclerosis
inferred← citeshttps://doi.org/10.3390/ijms222010958openalex-snapshot
RNA Editing: A New Therapeutic Target in Amyotrophic Lateral Sclerosis and Other Neurological Diseases
inferred← citeshttps://doi.org/10.3390/ijms222111847openalex-snapshot
Insights into the Pathogenesis of Neurodegenerative Diseases: Focus on Mitochondrial Dysfunction and Oxidative Stress
inferred← citeshttps://doi.org/10.3390/ijms23020624openalex-snapshot
Patient-Specific iPSCs-Based Models of Neurodegenerative Diseases: Focus on Aberrant Calcium Signaling
inferred← citeshttps://doi.org/10.3390/ijms25137457openalex-snapshot
Unveiling New Genetic Variants Associated with Age at Onset in Alzheimer’s Disease and Frontotemporal Lobar Degeneration Due to C9orf72 Repeat Expansions
inferred← citeshttps://doi.org/10.3390/ijms26125671openalex-snapshot
Perspectives in Amyotrophic Lateral Sclerosis: Biomarkers, Omics, and Gene Therapy Informing Disease and Treatment
inferred← citeshttps://doi.org/10.3390/metabo12030233openalex-snapshot
Mechanistic Insights of Mitochondrial Dysfunction in Amyotrophic Lateral Sclerosis: An Update on a Lasting Relationship
inferred← citeshttps://doi.org/10.3390/pharmaceutics15020572openalex-snapshot
Delivery Systems for Mitochondrial Gene Therapy: A Review
inferred← citeshttps://doi.org/10.4103/nrr.nrr-d-25-00857openalex-snapshot
Mitochondria-associated endoplasmic reticulum membranes and calcium ion exchange: A novel direction for aging and neurodegenerative diseases
inferred← citeshttps://doi.org/10.4103/nrr.nrr-d-25-01790openalex-snapshot
Mesenchymal stem cell–derived extracellular vesicle treatment of induced pluripotent stem cell–derived motor neurons with different amyotrophic lateral sclerosis genetic backgrounds
inferred← citeshttps://doi.org/10.70389/pjs.100068openalex-snapshot
Mitochondrial Therapies for Neurodegenerative Diseases: Emerging Approaches and Challenges
inferred← citeshttps://doi.org/10.70675/164dc935z4a7ez4257z84e0zdc1cb89f94c1openalex-snapshot
Rôle de la protéine NEDL1, candidate dans la physiopathologie de la Sclérose Latérale Amyotrophique
inferred← citeshttps://doi.org/10.70675/381af2e4zf397z4e20z8f8dz5b80b0f86450openalex-snapshot
Could the overexpression of neuroglobin, via an intravenous administration of an AAV2/9 vector, durably attenuate cerebellar ataxia in Harlequin mice by preserving mitochondrial homeostasis?
inferred← citeshttps://doi.org/10.70675/9a7778aaz88c7z40b1z92d3zaf5699b86a09openalex-snapshot
Comprendre et modéliser la Sclérose Latérale Amyotrophique à début précoce
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