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000126886 0247_ $$2doi$$a10.1242/dev.112680
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000126886 0247_ $$2ISSN$$a0022-0752
000126886 0247_ $$2ISSN$$a0950-1991
000126886 0247_ $$2ISSN$$a1477-9129
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000126886 037__ $$aDKFZ-2017-02914
000126886 041__ $$aeng
000126886 082__ $$a570
000126886 1001_ $$aKobayashi, Hiroaki$$b0
000126886 245__ $$aCalm1 signaling pathway is essential for the migration of mouse precerebellar neurons.
000126886 260__ $$aCambridge$$bThe Company of Biologists$$c2015
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000126886 520__ $$aThe calcium ion regulates many aspects of neuronal migration, which is an indispensable process in the development of the nervous system. Calmodulin (CaM) is a multifunctional calcium ion sensor that transduces much of the signal. To better understand the role of Ca(2+)-CaM in neuronal migration, we investigated mouse precerebellar neurons (PCNs), which undergo stereotyped, long-distance migration to reach their final position in the developing hindbrain. In mammals, CaM is encoded by three non-allelic CaM (Calm) genes (Calm1, Calm2 and Calm3), which produce an identical protein with no amino acid substitutions. We found that these CaM genes are expressed in migrating PCNs. When the expression of CaM from this multigene family was inhibited by RNAi-mediated acute knockdown, inhibition of Calm1 but not the other two genes caused defective PCN migration. Many PCNs treated with Calm1 shRNA failed to complete their circumferential tangential migration and thus failed to reach their prospective target position. Those that did reach the target position failed to invade the depth of the hindbrain through the required radial migration. Overall, our results suggest the participation of CaM in both the tangential and radial migration of PCNs.
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000126886 650_7 $$2NLM Chemicals$$aCalm1 protein, mouse
000126886 650_7 $$2NLM Chemicals$$aCalmodulin
000126886 650_7 $$2NLM Chemicals$$aDNA Primers
000126886 650_7 $$0SY7Q814VUP$$2NLM Chemicals$$aCalcium
000126886 7001_ $$aSaragai, Shunsuke$$b1
000126886 7001_ $$aNaito, Atsushi$$b2
000126886 7001_ $$aIchio, Koji$$b3
000126886 7001_ $$0P:(DE-He78)0ac2bd1a9fb1823a351ee4434d80808b$$aKawauchi, Daisuke$$b4$$udkfz
000126886 7001_ $$aMurakami, Fujio$$b5
000126886 773__ $$0PERI:(DE-600)2007916-3$$a10.1242/dev.112680$$gVol. 142, no. 2, p. 375 - 384$$n2$$p375 - 384$$tDevelopment <Cambridge>$$v142$$x1477-9129$$y2015
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000126886 9141_ $$y2015
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