摘要
C31, consisting of 31 amino acid residues, is generated from the carboxyl terminal fragments (CTFs) of amyloid precursor protein (APP). It has been shown that C31 causes apoptosis in neurons and is present in brains of Alzheimer disease (AD) patients. Using whole-cell patch clamp techniques, we investigated effects of C31 on voltage-gated calcium channel (VGCC) currents and the protective effects of β-estradiol on PC12 cells. The results demonstrated that C31 induced a significant increase of the VGCC currents in PC12 cells, which was blocked by β-estradiol. These results suggest that modulation of intracellular calcium levels by VGCC may in part be involved in C31 induced neuronal death associated with AD.
| 源语言 | 英语 |
|---|---|
| 页(从-至) | 102-105 |
| 页数 | 4 |
| 期刊 | Neuroscience Letters |
| 卷 | 382 |
| 期 | 1-2 |
| DOI | |
| 出版状态 | 已出版 - 1 7月 2005 |
| 已对外发布 | 是 |
指纹图谱
探究 'C31 enhances voltage-gated calcium channel currents in undifferentiated PC12 cells' 的科研主题。它们共同构成独一无二的指纹。引用此
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