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神经生长因子通过增加bcl-2的量来拯救PC12细胞免于凋亡。

Nerve growth factor rescues PC12 cells from apoptosis by increasing amount of bcl-2.

作者信息

Katoh S, Mitsui Y, Kitani K, Suzuki T

机构信息

Radioisotope Research Institute, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Biochem Biophys Res Commun. 1996 Dec 13;229(2):653-7. doi: 10.1006/bbrc.1996.1859.

Abstract

Nerve growth factor (NGF) suppressed the decrease in number of viable PC12 cells after serum withdrawal from culture medium. Accordingly, the amount of bcl-2, a suppressive effector of apoptosis, increased in these cells. Bcl-2 antisense oligonucleotide suppressed not only the NGF-induced increase in bcl-2 but also NGF-induced neuronal differentiation. Results of fluorescent DNA staining indicated that NGF inhibited the chromatin condensation of PC12 cells resulting from serum withdrawal and further that the bcl-2 antisense oligonucleotide canceled this effect of NGF. The present results suggest that NGF rescues PC12 cells from apoptosis induced by serum withdrawal via up-regulation of bcl-2.

摘要

神经生长因子(NGF)抑制了从培养基中撤除血清后存活PC12细胞数量的减少。相应地,这些细胞中凋亡抑制因子bcl-2的量增加。bcl-2反义寡核苷酸不仅抑制了NGF诱导的bcl-2增加,还抑制了NGF诱导的神经元分化。荧光DNA染色结果表明,NGF抑制了因撤除血清导致的PC12细胞染色质凝聚,并且bcl-2反义寡核苷酸消除了NGF的这一作用。目前的结果表明,NGF通过上调bcl-2使PC12细胞从血清撤除诱导的凋亡中获救。

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