Cloning and localization of a conventional kinesin motor expressed exclusively in neurons

Niclas, Joshua; Navone, Francesca; Hom-Booker, Nora; Vale, Ronald D.

doi:10.1016/0896-6273(94)90314-x

Cited by 145 publications

(133 citation statements)

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“…After electrophoresis, the gels were either stained with Coomassie Brilliant Blue or blotted onto nitrocellulose (Towbin et al, 1979) at 0.4 A for 3 h. Immunolabeling of blots was performed essentially as described by Niclas et al (1994), with minor modifications (Vignali et al, 1996). Primary antibodies were the affinity-purified rabbit polyclonal antibody against nKHC and the affinity-purified rabbit polyclonal antibody against uKHC, raised, purified, and characterized as extensively described elsewhere (Niclas et al, 1994) and diluted 1:400 and 1:300, respectively. Both antibodies were a kind gift from Prof. Ron Vale and Dr. Joshua Niclas (Department of Pharmacology and Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA, U.S.A.).…”

Section: Sds-polyacrylamide Gel Electrophoresis (Page) and Immunoblotmentioning

confidence: 99%

“…Within neuronal cells, nKHC is present in the soma and in neuronal processes, both axons and dendrites, whereas it does not appear to be concentrated at synapses. Expression of nKHC appears to be neuron specific, because glial cells, at least in primary tissue culture, express uKHC but not nKHC (Niclas et al, 1994).…”

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confidence: 99%

“…Neuronal kinesin is an isoform of the plus end-directed motor protein kinesin that has been shown to be exclusively expressed in the nervous system (Niclas et al, 1994). Owing to its specific pattern of expression this conventional kinesin has been named "neuronal" to distinguish it from the ubiquitously distributed conventional isoform (Allan, 1995;Brady, 1995).…”

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confidence: 99%

“…Owing to its specific pattern of expression this conventional kinesin has been named "neuronal" to distinguish it from the ubiquitously distributed conventional isoform (Allan, 1995;Brady, 1995). Neuronal kinesin heavy chain (nKHC) is encoded by a gene distinct from the one specifying the ubiquitous kinesin heavy chain (uKHC), although the two proteins share a 65% amino acid sequence identity and a very similar domain organization (Niclas et al, 1994). Both their molecular structures show an N-terminal motor domain (Yang et al, 1989;Nakata and Hirokawa, 1995), an a-helical coiled coil rod (De Cuevas et al, 1992), and a small Cterminal globular domain that, despite its still unclear function, is thought to be involved in the interaction with intracellular cargo (Navone et al, 1992;Toyoshima et al, 1992;Andrews et al, 1993;Skoufias et al, 1994;Yu et al, 1995).…”

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confidence: 99%

“…Both their molecular structures show an N-terminal motor domain (Yang et al, 1989;Nakata and Hirokawa, 1995), an a-helical coiled coil rod (De Cuevas et al, 1992), and a small Cterminal globular domain that, despite its still unclear function, is thought to be involved in the interaction with intracellular cargo (Navone et al, 1992;Toyoshima et al, 1992;Andrews et al, 1993;Skoufias et al, 1994;Yu et al, 1995). The sequence of nKHC has the unique feature of a 70-amino-acid C-terminal stretch that is absent in the uKHC sequence (Niclas et al, 1994).…”

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confidence: 99%

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Expression of Neuronal Kinesin Heavy Chain Is Developmentally Regulated in the Central Nervous System of the Rat

Vignali

Lizier²,

Sprocati

et al. 1997

Journal of Neurochemistry

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Abstract:The kinesin family of motor proteins comprises at least two isoforms of conventional kinesin encoded by different genes: ubiquitous kinesin, expressed in all cells and tissues, and neuronal kinesin, expressed exclusively in neuronal cells. In the present study, we have analyzed the expression of the two kinesin isoforms by immunochemistry at different stages of development of the rat CNS. We have found that the level of expression of neuronal kinesin is five to eight times higher in developing than in adult rat brains, whereas that of ubiquitous kinesin is only~2.5 times higher in maturing versus adult brains. Moreover, we have studied the distribution of neuronal kinesin by light microscopic immunocytochemistry in the rat brain at different postnatal ages and have found this protein not only to be more highly expressed in juvenile than in adult rat brains but also to show a different pattern of distribution. In particular, tracts of axonal fibers were clearly stained at early postnatal stages of development but were markedly unlabeled in adult rat brains. Our results indicate that the expression of at least one isoform of conventional neuron-specific kinesin is up-regulated in the developing rat CNS and suggest that this protein might play an important role in microtubule-based transport during the maturation of neuronal cells in vivo. Key Words: Microtubule-based motors-Conventional kinesin isoforms-Quantitative protein expression-Immunocytochemical localization-Brain development.

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Section: Sds-polyacrylamide Gel Electrophoresis (Page) and Immunoblotmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Expression of Neuronal Kinesin Heavy Chain Is Developmentally Regulated in the Central Nervous System of the Rat

Vignali

Lizier²,

Sprocati

et al. 1997

Journal of Neurochemistry

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Kinesin Superfamily Proteins

Hirokawa

Takemura

2008

Protein Science Encyclopedia

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Originally published in: Molecular Motors. Edited by Manfred Schliwa. Copyright © 2003 Wiley‐VCH Verlag GmbH & Co. KGaA Weinheim. Print ISBN: 3‐527‐30594‐0 The sections in this article are Introduction The Kinesin Superfamily Proteins N‐Kinesins N ‐1 Kinesins N ‐2 Kinesins N ‐3 Kinesins The Unc 104/ KIF 1 family The KIF 13 family The KIF 16 family N‐4 Kinesins The KIF 3 family The Osm 3/ KIF 17 family N‐5 Kinesins N‐6 Kinesins The CHO 1/ KIF 23 family The KIF 20/ Rab 6 kinesin family N‐7 Kinesins N‐8 Kinesins The K id/ KIF 22 family The KIF 18 family N ‐9 Kinesins N ‐10 Kinesins N ‐11 Kinesins M‐Kinesins C ‐Kinesins C ‐1 Kinesins C ‐2 Kinesins Orphans Cargoes of KIFs; Specificity and Redundancy Recognition and Binding to Cargoes How to Determine the Direction of Transport

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Atlas stumbled: Kinesin light chain‐1 variant E triggers a vicious cycle of axonal transport disruption and amyloid‐β generation in Alzheimer's disease

2014

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Substantial evidence implicates fast axonal transport (FAT) defects in neurodegeneration. In Alzheimer's disease (AD), it is controversial whether transport defects cause or arise from amyloid-β (Aβ)-induced toxicity. Using a novel, unbiased genetic screen, Morihara et al. identified kinesin light chain-1 splice variant E (KLC1vE) as a modifier of Aβ accumulation. Here, we propose three mechanisms to explain this causal role. First, KLC1vE reduces APP transport, leading to Aβ accumulation. Second, reduced transport of APP by KLC1vE triggers an ER stress response that activates the amyloidogenic pathway. Third, KLC1vE impairs transport of other KLC1 cargos that regulate amyloidogenesis, promoting Aβ retention within the secretory pathway. Collectively, KLC1vE perpetuates a vicious cycle of Aβ generation, kinase dysregulation, and global FAT impairment that inevitably leads to cellular toxicity. These concepts implicate alternative splicing of KLC1 in AD and suggest that the reciprocal influence of transport mechanisms on disease states contributes to neurodegeneration.

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Cloning and localization of a conventional kinesin motor expressed exclusively in neurons

Cited by 145 publications

References 44 publications

Expression of Neuronal Kinesin Heavy Chain Is Developmentally Regulated in the Central Nervous System of the Rat

Expression of Neuronal Kinesin Heavy Chain Is Developmentally Regulated in the Central Nervous System of the Rat

Kinesin Superfamily Proteins

Atlas stumbled: Kinesin light chain‐1 variant E triggers a vicious cycle of axonal transport disruption and amyloid‐β generation in Alzheimer's disease

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