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@ARTICLE{Kobayashi:126886,
      author       = {H. Kobayashi and S. Saragai and A. Naito and K. Ichio and
                      D. Kawauchi$^*$ and F. Murakami},
      title        = {{C}alm1 signaling pathway is essential for the migration of
                      mouse precerebellar neurons.},
      journal      = {Development},
      volume       = {142},
      number       = {2},
      issn         = {1477-9129},
      address      = {Cambridge},
      publisher    = {The Company of Biologists},
      reportid     = {DKFZ-2017-02914},
      pages        = {375 - 384},
      year         = {2015},
      abstract     = {The 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.},
      keywords     = {Calm1 protein, mouse (NLM Chemicals) / Calmodulin (NLM
                      Chemicals) / DNA Primers (NLM Chemicals) / Calcium (NLM
                      Chemicals)},
      cin          = {B062},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25519244},
      doi          = {10.1242/dev.112680},
      url          = {https://inrepo02.dkfz.de/record/126886},
}