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Publication : Dysbindin engages in c-Jun N-terminal kinase activity and cytoskeletal organization.

First Author  Kubota K Year  2009
Journal  Biochem Biophys Res Commun Volume  379
Issue  2 Pages  191-5
PubMed ID  19094965 Mgi Jnum  J:144529
Mgi Id  MGI:3831072 Doi  10.1016/j.bbrc.2008.12.017
Citation  Kubota K, et al. (2009) Dysbindin engages in c-Jun N-terminal kinase activity and cytoskeletal organization. Biochem Biophys Res Commun 379(2):191-5
abstractText  A number of reports have provided genetic evidence for an association between the DTNBP1 gene (coding dysbindin) and schizophrenia. In addition, sandy mice, which harbor a deletion in the DTNBP1 gene and lack dysbindin, display behavioral abnormalities suggestive of an association with schizophrenia. However, the mechanism by which the loss of dysbindin induces schizophrenia-like behaviors remains unclear. Here, we report that small interfering RNA-mediated knockdown of dysbindin resulted in the aberrant organization of actin cytoskeleton in SH-SY5Y cells. Furthermore, we show that morphological abnormalities of the actin cytoskeleton were similarly observed in growth cones of cultured hippocampal neurons derived from sandy mice. Moreover, we report a significant correlation between dysbindin expression level and the phosphorylation level of c-Jun N-terminal kinase (JNK), which is implicated in the regulation of cytoskeletal organization. These findings suggest that dysbindin plays a key role in coordinating JNK signaling and actin cytoskeleton required for neural development.
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