start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=5 article-no= start-page=279 end-page=285 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Factors That Influence Primary Cilium Length en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=MiyoshiKo en-aut-sei=Miyoshi en-aut-mei=Ko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KasaharaKyosuke en-aut-sei=Kasahara en-aut-mei=Kyosuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MiyazakiIkuko en-aut-sei=Miyazaki en-aut-mei=Ikuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=AsanumaMasato en-aut-sei=Asanuma en-aut-mei=Masato kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=primary cilium length kn-keyword=primary cilium length en-keyword=lithium kn-keyword=lithium en-keyword=cyclic AMP kn-keyword=cyclic AMP en-keyword=soluble tubulin kn-keyword=soluble tubulin en-keyword=intraflagellar transport kn-keyword=intraflagellar transport END start-ver=1.4 cd-journal=joma no-vol=122 cd-vols= no-issue=3 article-no= start-page=199 end-page=202 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=20101201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Neuronal cilia in pericentrin mutant mice kn-title=Pericentrin変異マウスにおける神経系繊毛 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Pericentrin遺伝子にホモで変異を持つマウス(ホモ変異マウス)では中枢神経系1次繊毛および嗅覚神経細胞の嗅繊毛の低形成が観察された.自発運動量,不安関連行動および海馬歯状回顆粒細胞下層での神経新生は,ホモ変異マウスと野生型マウスの間で有意な差異を認めなかった.一方,ホモ変異マウスは嗅覚機能の低下に加えて抗うつ行動を示したことから,中枢神経系1次繊毛の低形成は抗うつ効果を持つと考えられた. en-copyright= kn-copyright= en-aut-name=MiyoshiKo en-aut-sei=Miyoshi en-aut-mei=Ko kn-aut-name=三好耕 kn-aut-sei=三好 kn-aut-mei=耕 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学 en-keyword=神経系繊毛 kn-keyword=神経系繊毛 en-keyword=pericentrin kn-keyword=pericentrin en-keyword=嗅覚 kn-keyword=嗅覚 en-keyword=抗うつ kn-keyword=抗うつ END start-ver=1.4 cd-journal=joma no-vol=119 cd-vols= no-issue=3 article-no= start-page=235 end-page=239 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20080104 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Quinone formation as a common neurotoxic factor in dopaminergic neurotoxicity induced by an excess amount of cytosolic dopamine kn-title=小胞外過剰ドパミンによるドパミン神経障害における共通因子としてのキノン体生成 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MiyazakiIkuko en-aut-sei=Miyazaki en-aut-mei=Ikuko kn-aut-name=宮崎育子 kn-aut-sei=宮崎 kn-aut-mei=育子 aut-affil-num=1 ORCID= en-aut-name=AsanumaMasato en-aut-sei=Asanuma en-aut-mei=Masato kn-aut-name=浅沼幹人 kn-aut-sei=浅沼 kn-aut-mei=幹人 aut-affil-num=2 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=Francisco J.Diaz-Corrales kn-aut-sei=Francisco J. kn-aut-mei=Diaz-Corrales aut-affil-num=3 ORCID= en-aut-name=MiyoshiKo en-aut-sei=Miyoshi en-aut-mei=Ko kn-aut-name=三好耕 kn-aut-sei=三好 kn-aut-mei=耕 aut-affil-num=4 ORCID= en-aut-name=OgawaNorio en-aut-sei=Ogawa en-aut-mei=Norio kn-aut-name=小川紀雄 kn-aut-sei=小川 kn-aut-mei=紀雄 aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学 en-keyword=ドパミンキノン kn-keyword=ドパミンキノン en-keyword=パーキンソン病 kn-keyword=パーキンソン病 en-keyword=メタンフェタミン kn-keyword=メタンフェタミン en-keyword=キノン還元酵素 kn-keyword=キノン還元酵素 en-keyword=チロシナーゼ kn-keyword=チロシナーゼ END