ArticleThe Journal of cell biology2012
Microtubule stability, Golgi organization, and transport flux require dystonin-a2-MAP1B interaction.
Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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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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.
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Who cites it
38 citing papers in PubMed, 62 citations in OpenAlex.
- Roles of dystonin isoforms in the maintenance of neural, muscle, and cutaneous tissues.Anatomical science international · 2024Review
- Role of tubulin post-translational modifications in peripheral neuropathy.Experimental neurology · 2023Review
- TREX1 Deficiency Induces ER Stress-Mediated Neuronal Cell Death by Disrupting CaMolecular neurobiology · 2022Article
- Article
- Motor Skills: Recruitment of Kinesins, Myosins and Dynein during Assembly and Egress of Alphaherpesviruses.Viruses · 2021Review
- HSV-1 Cytoplasmic Envelopment and Egress.International journal of molecular sciences · 2020Review
- The molecular chaperone Hsp90 maintains Golgi organization and vesicular trafficking by regulating microtubule stability.Journal of molecular cell biology · 2020Article
- The molecular chaperone Hsp90α deficiency causes retinal degeneration by disrupting Golgi organization and vesicle transportation in photoreceptors.Journal of molecular cell biology · 2020Article
- HSAN-VI: A spectrum disorder based on dystonin isoform expression.Neurology. Genetics · 2020Article
- Paxillin family of focal adhesion adaptor proteins and regulation of cancer cell invasion.International review of cell and molecular biology · 2020Article
- Microtubule-Dependent Trafficking of Alphaherpesviruses in the Nervous System: The Ins and Outs.Viruses · 2019Review
- RASSF1A, puppeteer of cellular homeostasis, fights tumorigenesis, and metastasis-an updated review.Cell death & disease · 2019Review
- Infection and Transport of Herpes Simplex Virus Type 1 in Neurons: Role of the Cytoskeleton.Viruses · 2018Review
- Structure of the Golgi apparatus is not influenced by a GAG deletion mutation in the dystonia-associated gene Tor1a.PloS one · 2018Article
- Prognostic value of molecular events from negative surgical margin of non-small-cell lung cancer.Oncotarget · 2017Article
- Spectraplakin family proteins - cytoskeletal crosslinkers with versatile roles.Journal of cell science · 2017Review
- ORF7 of Varicella-Zoster Virus Is Required for Viral Cytoplasmic Envelopment in Differentiated Neuronal Cells.Journal of virology · 2017Article
- Epithelial-to-mesenchymal transition drives a pro-metastatic Golgi compaction process through scaffolding protein PAQR11.The Journal of clinical investigation · 2017Article
- Identification of novel MYO18A interaction partners required for myoblast adhesion and muscle integrity.Scientific reports · 2016Article
- Microtubule plus-end tracking proteins in neuronal development.Cellular and molecular life sciences : CMLS · 2016Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Loss of function of dystonin cytoskeletal linker proteins causes neurodegeneration in dystonia musculorum (dt) mutant mice. Although much investigation has focused on understanding dt pathology, the diverse cellular functions of dystonin isoforms remain poorly characterized. In this paper, we highlight novel functions of the dystonin-a2 isoform in mediating microtubule (MT) stability, Golgi organization, and flux through the secretory pathway. Using dystonin mutant mice combined with isoform-specific loss-of-function analysis, we found dystonin-a2 bound to MT-associated protein 1B (MAP1B) in the centrosomal region, where it maintained MT acetylation. In dt neurons, absence of the MAP1B-dystonin-a2 interaction resulted in altered MAP1B perikaryal localization, leading to MT deacetylation and instability. Deacetylated MT accumulation resulted in Golgi fragmentation and prevented anterograde trafficking via motor proteins. Maintenance of MT acetylation through trichostatin A administration or MAP1B overexpression mitigated the observed defect. These cellular aberrations are apparent in prephenotype dorsal root ganglia and primary sensory neurons from dt mice, suggesting they are causal in the disorder.
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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.