ArticleFrontiers in molecular biosciences2017
Torsin ATPases: Harnessing Dynamic Instability for Function.
Article in Frontiers in molecular biosciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- On the origin of the nucleus: a hypothesis.Microbiology and molecular biology reviews : MMBR · 2023Review
- Molecular mechanism of hyperactivation conferred by a truncation of TRPA1.Nature communications · 2023Article
- Motor deficit and lack of overt dystonia in Dlx conditional Dyt1 knockout mice.Behavioural brain research · 2023Article
- Identification of resistance gene analogs of the NBS-LRR family through transcriptome probing andFrontiers in genetics · 2022Article
- TorsinA folding and N-linked glycosylation are sensitive to redox homeostasis.Biochimica et biophysica acta. Molecular cell research · 2021Article
- Alteration of the cholinergic system and motor deficits in cholinergic neuron-specific Dyt1 knockout mice.Neurobiology of disease · 2021Article
- Investigating the role of striatal dopamine receptor 2 in motor coordination and balance: Insights into the pathogenesis of DYT1 dystonia.Behavioural brain research · 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
- The abnormal firing of Purkinje cells in the knockin mouse model of DYT1 dystonia.Brain research bulletin · 2020Article
- Lipid and protein dynamics that shape nuclear envelope identity.Molecular biology of the cell · 2020Review
- Torsin ATPase deficiency leads to defects in nuclear pore biogenesis and sequestration of MLF2.The Journal of cell biology · 2020Article
- The Role of Torsin AAA+ Proteins in Preserving Nuclear Envelope Integrity and Safeguarding Against Disease.Biomolecules · 2020Review
- Resolving the TorsinA Oligomerization Conundrum: The Glycan Hypothesis.Frontiers in molecular biosciences · 2020Article
- Molecular switch-like regulation in motor proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
- Mutant torsinA in the heterozygous DYT1 state compromises HSV propagation in infected neurons and fibroblasts.Scientific reports · 2018Article
- Dynamic functional assembly of the Torsin AAA+ ATPase and its modulation by LAP1.Molecular biology of the cell · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Torsins are essential, disease-relevant AAA+ (ATPases associated with various cellular activities) proteins residing in the endoplasmic reticulum and perinuclear space, where they are implicated in a variety of cellular functions. Recently, new structural and functional details about Torsins have emerged that will have a profound influence on unraveling the precise mechanistic details of their yet-unknown mode of action in the cell. While Torsins are phylogenetically related to Clp/HSP100 proteins, they exhibit comparatively weak ATPase activities, which are tightly controlled by virtue of an active site complementation through accessory cofactors. This control mechanism is offset by a TorsinA mutation implicated in the severe movement disorder DYT1 dystonia, suggesting a critical role for the functional Torsin-cofactor interplay
Indexed as
Identifiers
What OpenQuestion holds
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.