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신경돌기발생에 있어서 Reelin-Dab1의 역할
- Alternative Title
- Role of Reelin-Dab1 Signaling in the Neuritogenesis
- Author(s)
- Cho, Sung Kuk
- Alternative Author(s)
- Cho Sung Kuk
- Advisor
- 이영돈
- Department
- 일반대학원 의생명과학과
- Publisher
- The Graduate School, Ajou University
- Publication Year
- 2016-02
- Language
- eng
- Alternative Abstract
- Reelin is a secreted extracellular glycoprotein in the Cajal-Retzius cell that binds to the very low density lipoprotein receptor (VLDLR) and apolipoprotein E receptor 2 (ApoER2), inducing tyrosine phosphorylation of Dab1, a cytoplasmic adaptor protein of receptors. The Reelin-Dab1 signaling is regulatory key to migration and positioning of neuronal cell during brain development. It also reported that Reelin-deficient mice (reeler) showed a significant decrease in neurite formation and this depression was rescued by Reelin treatment. The neuritogenesis has been known to be promoted by the activation of Gαi/o signaling. Activated Gαi and Gαo were obviously localized in terminal portions of growing neuritis. Here, I study that a crosstalk between Reelin and Gαi/o signaling is involved in neurite formation. Reelin-induced neuritogenesis was suppressed by treatment of PTX and siRNA of Gαi and Gαο. Moreover, Reelin treatment induced activation of MAPK and JNK involved in the Gαi/o pathway. Also, in the precedent mechanism, the binding activity of Src to Dab1 and Gαo was prominently increased by Reelin. This result represents that neuritogenesis by Reelin facilitated through the activation of Gαi/o signaling. Also, expression of Reelin receptor, VLDLR is increased in the reeler mice than wild type mice at postnatal 3-14 days during the cerebellar development. But, ApoER2 is not changed. In addition, VLDL receptor in the cultured cerebellar cell is disappeared by Reelin treatment. This result represent clue about compensatory effect that is receptor gene expression through Reelin signal pathway
- Fulltext
- Appears in Collections:
- Graduate School of Ajou University > Department of Biomedical Sciences > 4. Theses(Ph.D)
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