學術產出-Periodical Articles

題名 Knockdown of protein kinase CK2 blocked gene expression mediated by brain-derived neurotrophic factor-induced serum response element
作者 趙知章
Chao, Chih-Chang
SP, Yang
CY, Lo
HM, Tseng
貢獻者 神科所
關鍵詞 Antiapoptosis ; brain-derived neurotrophic factor ; Mcl-1 ; protein kinase CK2 ; serum response element-mediated transcription
日期 2019-04
上傳時間 20-Feb-2020 11:56:22 (UTC+8)
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.
關聯 Chinese Journal of Physiology, Vol.62, pp.63-69
資料類型 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.
dc.format.extent 1393130 bytes-
dc.format.extent 73 bytes-
dc.format.extent 73 bytes-
dc.format.extent 71 bytes-
dc.format.extent 72 bytes-
dc.format.extent 72 bytes-
dc.format.extent 75 bytes-
dc.format.mimetype application/pdf-
dc.format.mimetype text/html-
dc.format.mimetype text/html-
dc.format.mimetype text/html-
dc.format.mimetype text/html-
dc.format.mimetype text/html-
dc.format.mimetype text/html-
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