ArticleThe Journal of cell biology1995
Point mutation of adenosine triphosphate-binding motif generated rigor kinesin that selectively blocks anterograde lysosome membrane transport.
Article in The Journal of cell biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.
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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
118 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.
- Stay in touch with the endoplasmic reticulum.Science China. Life sciences · 2024Pooled it
- Dynein upsizes under load.Nature cell biology · 2026Article
- Adaptor-mediated recruitment of three dyneins to dynactin enhances force generation.Nature cell biology · 2026Article
- Article
- One gene, many phenotypes: the role of KIF5A in neurodegenerative and neurodevelopmental diseases.Cell communication and signaling : CCS · 2025Review
- Class II kinesin-12 facilitates cell plate formation by transporting cell plate materials in the phragmoplast.Nature plants · 2025Article
- An Arabidopsis Kinesin-14D motor is associated with midzone microtubules for spindle morphogenesis.Current biology : CB · 2024Article
- Spinning Disk Confocal Microscopy for Optimized and Quantified Live Imaging of 3D Mitochondrial Network.International journal of molecular sciences · 2024Article
- Review
- ZebrafishFrontiers in molecular neuroscience · 2024Article
- Characterization of the disease-causing mechanism of KIF3B mutations from ciliopathy patients.Frontiers in molecular biosciences · 2024Article
- Dominant negative variants in KIF5B cause osteogenesis imperfecta via down regulation of mTOR signaling.PLoS genetics · 2023Article
- Inhibition of endolysosome fusion increases exosome secretion.The Journal of cell biology · 2023Article
- Armadillo repeat-containing kinesin represents the versatile plus-end-directed transporter in Physcomitrella.Nature plants · 2023Article
- Dominantly acting KIF5B variants with pleiotropic cellular consequences cause variable clinical phenotypes.Human molecular genetics · 2023Article
- Short-Term and Long-Term Sensitization Differentially Alters the Composition of an Anterograde Transport Complex ineNeuro · 2023Article
- H-ABC- and dystonia-causingScience advances · 2022Article
- The motor domain of testis-enriched kinesin KIF9 is essential for its localization in the mouse flagellum.Experimental animals · 2022Article
- Lysate-based pipeline to characterize microtubule-associated proteins uncovers unique microtubule behaviours.Nature cell biology · 2022Article
- Hedgehog-induced ciliary trafficking of kinesin-4 motor KIF7 requires intraflagellar transport but not KIF7's microtubule binding.Molecular biology of the cell · 2022Article
58 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the study of motor proteins, the molecular mechanism of mechanochemical coupling, as well as the cellular role of these proteins, is an important issue. To assess these questions we introduced cDNA of wild-type and site-directed mutant kinesin heavy chains into fibroblasts, and analyzed the behavior of the recombinant proteins and the mechanisms involved in organelle transports. Overexpression of wild-type kinesin significantly promoted elongation of cellular processes. Wild-type kinesin accumulated at the tips of the long processes, whereas the kinesin mutants, which contained either a T93N- or T93I mutation in the ATP-binding motif, tightly bound to microtubules in the center of the cells. These mutant kinesins could bind to microtubules in vitro, but could not dissociate from them even in the presence of ATP, and did not support microtubule motility in vitro, thereby indicating rigor-type mutations. Retrograde transport from the Golgi apparatus to the endoplasmic reticulum, as well as lysosome dispersion, was shown to be a microtubule-dependent, plus-end-directed movement. The latter was selectively blocked in the rigor-mutant cells, although the microtubule minus-end-directed motion of lysosomes was not affected. We found the point mutations that make kinesin motor in strong binding state with microtubules in vitro and showed that this mutant causes a dominant effect that selectively blocks anterograde lysosome membrane transports in vivo.
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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.