ArticleCell reports2016
Neuronal Nuclear Membrane Budding Occurs during a Developmental Window Modulated by Torsin Paralogs.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- Transcriptomic profiling of DYT-TOR1A patient-derived iPSC reveals dysregulation in extracellular matrix, lipid metabolism, and Chr22q11.23.BMC medical genomics · 2025Article
- Loss of nuclear envelope bud formation leads to mitophagy initiation inAutophagy reports · 2025Article
- TorsinA is essential for neuronal nuclear pore complex localization and maturation.Nature cell biology · 2024Article
- RANBP17 Overexpression Restores Nucleocytoplasmic Transport and Ameliorates Neurodevelopment in Induced DYT1 Dystonia Motor Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Manipulation of the nuclear envelope-associated protein SLAP during mammalian brain development affects cortical lamination and exploratory behavior.Biology open · 2024Article
- m6A-dependent circular RNA formation mediates tau-induced neurotoxicity.bioRxiv : the preprint server for biology · 2024Article
- Nuclear envelope budding and its cellular functions.Nucleus (Austin, Tex.) · 2023Article
- Pathophysiology of Dyt1-Science translational medicine · 2023Article
- TorsinA is essential for the timing and localization of neuronal nuclear pore complex biogenesis.bioRxiv : the preprint server for biology · 2023Article
- DYT-Frontiers in neuroscience · 2023Review
- Atypical nuclear envelope condensates linked to neurological disorders reveal nucleoporin-directed chaperone activities.Nature cell biology · 2022Article
- The chaperone DNAJB6 surveils FG-nucleoporins and is required for interphase nuclear pore complex biogenesis.Nature cell biology · 2022Article
- Impact of Nuclear Envelope Stress on Physiological and Pathological Processes in Central Nervous System.Neurochemical research · 2022Review
- Review
- Oligodendrocyte and Extracellular Matrix Contributions to Central Nervous System Motor Function: Implications for Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2022Review
- Genetic evidence of aberrant striatal synaptic maturation and secretory pathway alteration in a dystonia mouse model.Dystonia (Lausanne, Switzerland) · 2022Article
- Torsin and NEP1R1-CTDNEP1 phosphatase affect interphase nuclear pore complex insertion by lipid-dependent and lipid-independent mechanisms.The EMBO journal · 2021Article
- TorsinA restoration in a mouse model identifies a critical therapeutic window for DYT1 dystonia.The Journal of clinical investigation · 2021Article
- Disease Modeling with Human Neurons Reveals LMNB1 Dysregulation Underlying DYT1 Dystonia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
DYT1 dystonia is a neurodevelopmental disease that manifests during a discrete period of childhood. The disease is caused by impaired function of torsinA, a protein linked to nuclear membrane budding. The relationship of NE budding to neural development and CNS function is unclear, however, obscuring its potential role in dystonia pathogenesis. We find NE budding begins and resolves during a discrete neurodevelopmental window in torsinA null neurons in vivo. The developmental resolution of NE budding corresponds to increased torsinB protein, while ablating torsinB from torsinA null neurons prevents budding resolution and causes lethal neural dysfunction. Developmental changes in torsinB also correlate with NE bud formation in differentiating DYT1 embryonic stem cells, and overexpression of torsinA or torsinB rescues NE bud formation in this system. These findings identify a torsinA neurodevelopmental window that is essential for normal CNS function and have important implications for dystonia pathogenesis and therapeutics.
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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.