2022
DOI: 10.1096/fj.202101900rr
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Recruitment of dynein and kinesin to viral particles

Abstract: Dynein and kinesin are cytoskeletal motor proteins involved in transporting cellular cargos and viruses. Throughout viral infection, they actively participate in the virus life cycle in the cell during entry, genome replication, and departure. Through their retrograde and anterograde transport, dynein and kinesin assist in promoting viral infection as well as the cellular defense response. This review highlights the crucial roles kinesin and dynein play in facilitating viral proliferation and aims to exhibit t… Show more

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Cited by 4 publications
(1 citation statement)
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“…The dynein/dynactin complex and kinesin transport cytoplasmic cargo, such as mitochondria, viral particles, synaptic vesicles, lysosomes, signaling endosomes, autophagosomes, and microtubules, in a retrograde and anterograde manner, respectively [88, 89]. Disruption of cargo transportation by defects in these motor proteins could result in a range of neurodevelopmental and neurodegenerative diseases, dysfunction of lacrimal acinar cells, disturbed innate and acquired immune response to viral infection, as well as enhancing the activity of NF-κB; a well-known transcriptional factor involved in the pathogenesis of SjS [47, 9093]. Furthermore, the disruption of dynein and dynactin can impair autophagy and cause defects in the salivary glands, muscles, and nervous system in a motor-independent manner [94].…”
Section: Discussionmentioning
confidence: 99%
“…The dynein/dynactin complex and kinesin transport cytoplasmic cargo, such as mitochondria, viral particles, synaptic vesicles, lysosomes, signaling endosomes, autophagosomes, and microtubules, in a retrograde and anterograde manner, respectively [88, 89]. Disruption of cargo transportation by defects in these motor proteins could result in a range of neurodevelopmental and neurodegenerative diseases, dysfunction of lacrimal acinar cells, disturbed innate and acquired immune response to viral infection, as well as enhancing the activity of NF-κB; a well-known transcriptional factor involved in the pathogenesis of SjS [47, 9093]. Furthermore, the disruption of dynein and dynactin can impair autophagy and cause defects in the salivary glands, muscles, and nervous system in a motor-independent manner [94].…”
Section: Discussionmentioning
confidence: 99%