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首页> 外文期刊>Journal of Cellular Physiology >Apoptosis induced clustering of IP(3)R1 in nuclei of non-differentiated PC12 cells.
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Apoptosis induced clustering of IP(3)R1 in nuclei of non-differentiated PC12 cells.

机译：细胞凋亡诱导集群IP (3) R1的细胞核的non-differentiated PC12细胞。

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摘要

Inositol 1,4,5-trisphosphate (IP(3)) receptors are emerging as key sites for regulation by pro- and anti-apoptotic factors. Induction of apoptosis for 3 h increased mRNA and protein levels of type 1 IP(3) receptors in non-differentiated (ND), but not in differentiated (D) PC12 cells. Inhibitors of the IP(3) R's calcium release-2-aminoethoxydiphenyl borate (2-APB) and xestospongin-completely prevented Bax and caspase-3 mRNA increase after treatment with the apoptosis inducer set (AIK), and this reinforces the importance of IP(3) R1 in the apoptosis of ND PC12 cells. Apoptosis induction not only increases the IP(3) R1 protein, but it also causes formation of IP(3) R1 clusters in the nucleus which most likely result from fusion of the nucleoplasmic reticulum and/or IP(3) R1 translocation to the nucleus. This is quite similar to the observations noted after overexpression of IP(3) R1 in PC12 cells. The amount of IP(3) induced calcium release was higher in control than in AIK-treated cells. From our results we propose that after the apoptosis induction the amount of intranuclear calcium decreased dramatically due to the increase of calcium permeability of the nuclear calcium store vesicles. Therefore, increase of the calcium permeability may result from IP(3) receptors translocation to nuclei that can boost the calcium transport through IP(3) receptors.
机译：肌醇1 4 5-trisphosphate (IP(3)受体成为关键的网站支持和监管抗凋亡的因素。3 h增加信使rna和蛋白质水平的类型1 IP(3)受体non-differentiated (ND),但是不是在分化PC12细胞(D)。IP (3) R的钙release-2-aminoethoxydiphenyl硼酸(2-APB)和xestospongin-completely阻止伯灵顿和caspase-3 mRNA在治疗后继续增加细胞凋亡诱导物集()AIK队效力,这加强了知识产权的重要性(3)R1 ND的细胞凋亡PC12细胞。增加了IP (3) R1蛋白质,但它也原因形成的IP (3) R1集群核,最有可能的融合结果核质网和/或IP (3) R1核易位。类似于观察后指出过度的IP (3) R1 PC12细胞。数量的IP(3)诱导钙释放控制高于AIK-treated细胞。我们的结果,我们建议后细胞凋亡感应的数量在细胞核内的钙由于的增加急剧减少核钙的钙渗透率商店囊泡。渗透率可能导致从IP(3)受体核,可以提高易位钙运输通过IP(3)受体。

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