Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 박신영 | - |
dc.date.accessioned | 2021-10-25T01:21:43Z | - |
dc.date.available | 2021-10-25T01:21:43Z | - |
dc.date.issued | 2020-01 | - |
dc.identifier.citation | CELLULAR AND MOLECULAR NEUROBIOLOGY, v. 40, no. 1, page. 153-166 | en_US |
dc.identifier.issn | 0272-4340 | - |
dc.identifier.issn | 1573-6830 | - |
dc.identifier.uri | https://link.springer.com/article/10.1007%2Fs10571-019-00732-1 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/165677 | - |
dc.description.abstract | Bcl-2 is overexpressed in the nervous system during neural development and plays an important role in modulating cell survival. In addition to its anti-apoptotic function, it has been suggested previously that Bcl-2 might act as a mediator of neuronal differentiation. However, the mechanism by which Bcl-2 might influence neurogenesis is not sufficiently understood. In this study, we aimed to determine the non-apoptotic functions of Bcl-2 during neuronal differentiation. First, we used microarrays to analyze the whole-genome expression patterns of rat neural stem cells overexpressing Bcl-2 and found that Bcl-2 overexpression induced the expression of various neurogenic genes. Moreover, Bcl-2 overexpression increased the neurite length as well as expression of Bmp4, Tbx3, and proneural basic helix–loop–helix genes, such as NeuroD1, NeuroD2, and Mash1, in H19-7 rat hippocampal precursor cells. To determine the hierarchy of these molecules, we selectively depleted Bmp4, Tbx3, and NeuroD1 in Bcl-2-overexpressing cells. Bmp4 depletion suppressed the upregulation of Tbx3 and NeuroD1 as well as neurite outgrowth, which was induced by Bcl-2 overexpression. Although Tbx3 knockdown repressed Bcl-2-mediated neurite elaboration and downregulated NeuroD1 expression, it did not affect Bcl-2-induced Bmp4 expression. While the depletion of NeuroD1 had no effect on the expression of Bcl-2, Bmp4, or Tbx3, Bcl-2-mediated neurite outgrowth was suppressed. Taken together, these results demonstrate that Bcl-2 regulates neurite outgrowth through the Bmp4/Tbx3/NeuroD1 cascade in H19-7 cells, indicating that Bcl-2 may have a direct role in neuronal development in addition to its well-known anti-apoptotic function in response to environmental insults. | en_US |
dc.description.sponsorship | This work was supported by a National Research Foundation of Korea (NRF) Grant funded by the Korean government (MSIP) (NRF-2016R1A2B4015358) and partly supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2013R1A1A2061420). In addition, this research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant Number: HI19C0611), and supported by the research fund of Hanyang University (HY-2019). | en_US |
dc.language.iso | en | en_US |
dc.publisher | SPRINGER/PLENUM PUBLISHERS | en_US |
dc.subject | Bcl-2 | en_US |
dc.subject | Neurite outgrowth | en_US |
dc.subject | Bmp4 | en_US |
dc.subject | Tbx3 | en_US |
dc.subject | NeuroD1 | en_US |
dc.title | Bcl-2 Overexpression Induces Neurite Outgrowth via the Bmp4/Tbx3/NeuroD1 Cascade in H19-7 Cells | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 40 | - |
dc.identifier.doi | 10.1007/s10571-019-00732-1 | - |
dc.relation.page | 153-166 | - |
dc.relation.journal | CELLULAR AND MOLECULAR NEUROBIOLOGY | - |
dc.contributor.googleauthor | Lee, Yun Young | - |
dc.contributor.googleauthor | Choi, Hye-jin | - |
dc.contributor.googleauthor | Lee, So Young | - |
dc.contributor.googleauthor | Park, Shin-Young | - |
dc.contributor.googleauthor | Kang, Min-Jeong | - |
dc.contributor.googleauthor | Han, Jinil | - |
dc.contributor.googleauthor | Han, Joong-Soo | - |
dc.relation.code | 2020054153 | - |
dc.sector.campus | S | - |
dc.sector.daehak | RESEARCH INSTITUTE[S] | - |
dc.sector.department | HBRI | - |
dc.identifier.pid | ttokttoki | - |
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