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ID 47009
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Thumnail 65_5_279.pdf 5.06 MB
Author
Kasahara, Kyosuke
Abstract
Almost all mammalian cells carry one primary cilium that functions as a biosensor for chemical and mechanical stimuli. Genetic damages that compromise cilia formation or function cause a spectrum of disorders referred to as ciliapathies. Recent studies have demonstrated that some pharmacological agents and extracellular environmental changes can alter primary cilium length. Renal injury is a well-known example of an environmental insult that triggers cilia length modification. Lithium treatment causes primary cilia to extend in several cell types including neuronal cells;this phenomenon is likely independent of glycogen synthase kinase-3β inhibition. In renal epithelial cell lines, deflection of the primary cilia by fluid shear shortens them by reducing the intracellular cyclic AMP level, leading to a subsequent decrease in mechanosensitivity to fluid shear. Primary cilium length is also influenced by the dynamics of actin filaments and microtubules through the levels of soluble tubulin in the cytosol available for primary cilia extension. Thus, mammalian cells can adapt to the extracellular environment by modulating the primary cilium length, and this feedback system utilizing primary cilia might exist throughout the mammalian body. Further investigation is required concerning the precise molecular mechanisms underlying the control of primary cilium length in response to environmental factors.
Keywords
primary cilium length
lithium
cyclic AMP
soluble tubulin
intraflagellar transport
Amo Type
Review
Published Date
2011-10
Publication Title
Acta Medica Okayama
Volume
volume65
Issue
issue5
Publisher
Okayama University Medical School
Start Page
279
End Page
285
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
英語
Copyright Holders
CopyrightⒸ 2011 by Okayama University Medical School
File Version
publisher
Refereed
True
PubMed ID
Web of Sience KeyUT