Ciliary kinesins beyond IFT: Cilium length, disassembly, cargo transport and signalling.
Autor: | Reilly ML; Laboratory of Hereditary Kidney Diseases, INSERM UMR 1163, Paris Descartes University, Imagine Institute, Paris, 75015, France.; Paris Diderot University, Paris, 75013, France., Benmerah A; Laboratory of Hereditary Kidney Diseases, INSERM UMR 1163, Paris Descartes University, Imagine Institute, Paris, 75015, France. |
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Jazyk: | angličtina |
Zdroj: | Biology of the cell [Biol Cell] 2019 Apr; Vol. 111 (4), pp. 79-94. Date of Electronic Publication: 2019 Feb 15. |
DOI: | 10.1111/boc.201800074 |
Abstrakt: | Cilia and flagella are microtubule-based antenna which are highly conserved among eukaryotes. In vertebrates, primary and motile cilia have evolved to exert several key functions during development and tissue homoeostasis. Ciliary dysfunction in humans causes a highly heterogeneous group of diseases called ciliopathies, a class of genetic multisystemic disorders primarily affecting kidney, skeleton, retina, lung and the central nervous system. Among key ciliary proteins, kinesin family members (KIF) are microtubule-interacting proteins involved in many diverse cellular functions, including transport of cargo (organelles, proteins and lipids) along microtubules and regulating the dynamics of cytoplasmic and spindle microtubules through their depolymerising activity. Many KIFs are also involved in diverse ciliary functions including assembly/disassembly, motility and signalling. We here review these ciliary kinesins in vertebrates and focus on their involvement in ciliopathy-related disorders. (© 2019 Société Française des Microscopies and Société de Biologie Cellulaire de France. Published by John Wiley & Sons Ltd.) |
Databáze: | MEDLINE |
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