ArticleThe Journal of cell biology1998
Light chain-dependent regulation of Kinesin's interaction with microtubules.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
What it found
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Who cites it
126 citing papers in PubMed, 264 citations in OpenAlex.
- Structural basis of kinesin-1 autoinhibition and its control of microtubule-based motility.Science advances · 2026Article
- The Long Haul: Microtubule Motors as the Essential Supply Line for Neuronal Longevity.Journal of neurochemistry · 2026Review
- Expression of Axonal Transport Proteins in Dopaminergic Neurons of the Substantia Nigra in Mouse Models of Preclinical and Clinical Stages of Parkinson's Disease.International journal of molecular sciences · 2026Article
- Article
- Kinesin-1 is highly flexible and adopts an open conformation in the absence of cargo.iScience · 2026Article
- Rules of the road: how to turn off kinesin motors.The Biochemical journal · 2026Review
- The KASH protein UNC-83 differentially regulates kinesin-1 activity to control developmental stage-specific nuclear migration.Current biology : CB · 2025Article
- Impact of physiological ionic strength and crowding on kinesin-1 motility.Cell structure and function · 2025Article
- Mechanism and regulation of kinesin motors.Nature reviews. Molecular cell biology · 2025Review
- Involvement of kinesins in skeletal dysplasia: a review.American journal of physiology. Cell physiology · 2024Review
- Tropomyosin 1-I/C coordinates kinesin-1 and dynein motors during oskar mRNA transport.Nature structural & molecular biology · 2024Article
- Unraveling the interplay of kinesin-1, tau, and microtubules in neurodegeneration associated with Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- Modification of the neck-linker of KIF18A alters Microtubule subpopulation preference.Molecular biology of the cell · 2024Article
- Article
- A humanized Caenorhabditis elegans model of hereditary spastic paraplegia-associated variants in KLC4.Disease models & mechanisms · 2023Article
- Tubulin polyglutamylation differentially regulates microtubule-interacting proteins.The EMBO journal · 2023Article
- A humanizedbioRxiv : the preprint server for biology · 2023Article
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Glycogen synthase kinase 3β (GSK3β) and presenilin (PS) are key regulators of kinesin-1-mediated cargo motility within axons.Frontiers in cell and developmental biology · 2023Review
- KAP is the neuronal organelle adaptor for Kinesin-2 KIF3AB and KIF3AC.Molecular biology of the cell · 2022Article
66 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
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the mechanism by which conventional kinesin is prevented from binding to microtubules (MTs) when not transporting cargo. Kinesin heavy chain (HC) was expressed in COS cells either alone or with kinesin light chain (LC). Immunofluorescence microscopy and MT cosedimentation experiments demonstrate that the binding of HC to MTs is inhibited by coexpression of LC. Association between the chains involves the LC NH2-terminal domain, including the heptad repeats, and requires a region of HC that includes the conserved region of the stalk domain and the NH2 terminus of the tail domain. Inhibition of MT binding requires in addition the COOH-terminal 64 amino acids of HC. Interaction between the tail and the motor domains of HC is supported by sedimentation experiments that indicate that kinesin is in a folded conformation. A pH shift from 7.2 to 6.8 releases inhibition of kinesin without changing its sedimentation behavior. Endogenous kinesin in COS cells also shows pH-sensitive inhibition of MT binding. Taken together, our results provide evidence that a function of LC is to keep kinesin in an inactive ground state by inducing an interaction between the tail and motor domains of HC; activation for cargo transport may be triggered by a small conformational change that releases the inhibition of the motor domain for MT binding.
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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.