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| Title | Knockdown of protein kinase CK2 blocked gene expression mediated by brain-derived neurotrophic factor-induced serum response element |
| Creator | 趙知章 Chao, Chih-Chang SP, Yang CY, Lo HM, Tseng |
| Contributor | 神科所 |
| Key Words | Antiapoptosis ; brain-derived neurotrophic factor ; Mcl-1 ; protein kinase CK2 ; serum response element-mediated transcription |
| Date | 2019-04 |
| Date Issued | 20-Feb-2020 11:56:22 (UTC+8) |
| Summary | One of the principal signaling pathway outcomes from brain-derived neurotrophic factor (BDNF) is the activation of antiapoptotic pathways. In addition to the role of extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3 kinase, BDNF activates protein kinase CK2 to mediate its neuroprotective effect. The inhibition of CK2 activity has been shown to induce apoptosis. Although serum response element (SRE)-mediated transcription has been reported to be activated by BDNF and that the phosphorylation of serum response factor (SRF) by CK2 has been shown to enhance its DNA binding activity, the biological relevance of these interactions remains largely unclear. In the present study, we found that SRE-mediated transcription, CK2 activity, and SRF phosphorylation increased in PC12 cells under BDNF treatment. The transfection of CK2α siRNA blocked the enhancing effect of BDNF on SRE-mediated transcription, SRF phosphorylation, and Mcl-1 gene expression. Moreover, the blockade of CK2 diminished the antiapoptotic effects of BDNF on SRE-mediated transcription, Mcl-1 gene expression, and cell viability under rotenone-induced cytotoxicity. Our data may assist in the development of therapeutic strategies for inhibiting apoptosis during neurodegeneration. |
| Relation | Chinese Journal of Physiology, Vol.62, pp.63-69 |
| Type | article |
| DOI | https://doi.org/10.4103/CJP.CJP_1_19 |
| dc.contributor | 神科所 | |
| dc.creator (作者) | 趙知章 | |
| dc.creator (作者) | Chao, Chih-Chang | |
| dc.creator (作者) | SP, Yang | |
| dc.creator (作者) | CY, Lo | |
| dc.creator (作者) | HM, Tseng | |
| dc.date (日期) | 2019-04 | |
| dc.date.accessioned | 20-Feb-2020 11:56:22 (UTC+8) | - |
| dc.date.available | 20-Feb-2020 11:56:22 (UTC+8) | - |
| dc.date.issued (上傳時間) | 20-Feb-2020 11:56:22 (UTC+8) | - |
| dc.identifier.uri (URI) | http://nccur.lib.nccu.edu.tw/handle/140.119/128687 | - |
| dc.description.abstract (摘要) | One of the principal signaling pathway outcomes from brain-derived neurotrophic factor (BDNF) is the activation of antiapoptotic pathways. In addition to the role of extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3 kinase, BDNF activates protein kinase CK2 to mediate its neuroprotective effect. The inhibition of CK2 activity has been shown to induce apoptosis. Although serum response element (SRE)-mediated transcription has been reported to be activated by BDNF and that the phosphorylation of serum response factor (SRF) by CK2 has been shown to enhance its DNA binding activity, the biological relevance of these interactions remains largely unclear. In the present study, we found that SRE-mediated transcription, CK2 activity, and SRF phosphorylation increased in PC12 cells under BDNF treatment. The transfection of CK2α siRNA blocked the enhancing effect of BDNF on SRE-mediated transcription, SRF phosphorylation, and Mcl-1 gene expression. Moreover, the blockade of CK2 diminished the antiapoptotic effects of BDNF on SRE-mediated transcription, Mcl-1 gene expression, and cell viability under rotenone-induced cytotoxicity. Our data may assist in the development of therapeutic strategies for inhibiting apoptosis during neurodegeneration. | |
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| dc.relation (關聯) | Chinese Journal of Physiology, Vol.62, pp.63-69 | |
| dc.subject (關鍵詞) | Antiapoptosis ; brain-derived neurotrophic factor ; Mcl-1 ; protein kinase CK2 ; serum response element-mediated transcription | |
| dc.title (題名) | Knockdown of protein kinase CK2 blocked gene expression mediated by brain-derived neurotrophic factor-induced serum response element | |
| dc.type (資料類型) | article | |
| dc.identifier.doi (DOI) | 10.4103/CJP.CJP_1_19 | |
| dc.doi.uri (DOI) | https://doi.org/10.4103/CJP.CJP_1_19 |