ArticleTraffic (Copenhagen, Denmark)2009
Spastin couples microtubule severing to membrane traffic in completion of cytokinesis and secretion.
Article in Traffic (Copenhagen, Denmark), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.
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
144 citing papers in PubMed, 1 synthesis or guideline pooled it, 240 citations in OpenAlex.
- Pooled it
- Inhibition of TFG function causes hereditary axon degeneration by impairing endoplasmic reticulum structure.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Telomeres in mitosis: organization and dynamics.Nucleus (Austin, Tex.) · 2026Review
- Prognostic, diagnostic and therapeutic value of the cancer tubulin code.Cancer metastasis reviews · 2026Review
- TPGS1 regulates central spindle microtubule glutamylation and remodeling during telophase and abscission.EMBO reports · 2026Article
- ESCRT-III function in membrane fission and repair.Nature reviews. Molecular cell biology · 2026Review
- Tubular ER dysfunction in neurodegenerative diseases.Neurobiology of disease · 2025Review
- Divergent functions of late ESCRT components in Giardia lamblia: Insights from subcellular distributions and protein interactions.PLoS neglected tropical diseases · 2025Article
- The unique contributions of Rab11 and Rab35 to the completion of cell division.Biological research · 2025Article
- Targeting MDM2 affects spastin protein levels and functions: implications for HSP treatment.Cell death discovery · 2025Article
- Cul-4 inhibition rescues spastin levels and reduces defects in hereditary spastic paraplegia models.Brain : a journal of neurology · 2024Article
- Review
- Cytokinetic abscission requires actin-dependent microtubule severing.Nature communications · 2024Article
- Roles of ESCRT-III polymers in cell division across the tree of life.Current opinion in cell biology · 2023Review
- Unconventional roles of chromatin remodelers and long non-coding RNAs in cell division.Cellular and molecular life sciences : CMLS · 2023Review
- Vesicle-mediated transport of ALIX and ESCRT-III to the intercellular bridge during cytokinesis.Cellular and molecular life sciences : CMLS · 2023Article
- Spastin is required for human immunodeficiency virus-1 efficient replication through cooperation with the endosomal sorting complex required for transport (ESCRT) protein.Virologica Sinica · 2023Article
- Spastin is an essential regulator of male meiosis, acrosome formation, manchette structure and nuclear integrity.Development (Cambridge, England) · 2023Article
- Article
- Phosphorylation mutation impairs the promoting effect of spastin on neurite outgrowth without affecting its microtubule severing ability.European journal of histochemistry : EJH · 2023Article
84 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the gene encoding the microtubule (MT)-severing protein spastin are the most common cause of hereditary spastic paraplegia, a genetic condition in which axons of the corticospinal tracts degenerate. We show that not only does endogenous spastin colocalize with MTs, but that it is also located on the early secretory pathway, can be recruited to endosomes and is present in the cytokinetic midbody. Spastin has two main isoforms, a 68 kD full-length isoform and a 60 kD short form. These two isoforms preferentially localize to different membrane traffic pathways with 68 kD spastin being principally located at the early secretory pathway, where it regulates endoplasmic reticulum-to-Golgi traffic. Sixty kiloDalton spastin is the major form recruited to endosomes and is also present in the midbody, where its localization requires the endosomal sorting complex required for transport-III-interacting MIT domain. Loss of midbody MTs accompanies the abscission stage of cytokinesis. In cells lacking spastin, a MT disruption event that normally accompanies abscission does not occur and abscission fails. We suggest that this event represents spastin-mediated MT severing. Our results support a model in which membrane traffic and MT regulation are coupled through spastin. This model is relevant in the axon, where there also is co-ordinated MT regulation and membrane traffic.
Indexed as
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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.