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蛋白激酶C不参与小细胞肺癌细胞中蛙皮素反应的同源脱敏。

Protein kinase C is not involved in the homologous desensitization of bombesin responses in small cell lung cancer cells.

作者信息

Frankel A, Viallet J

机构信息

Department of Medicine, Montreal General Hospital, PQ, Canada.

出版信息

Exp Cell Res. 1993 Dec;209(2):398-401. doi: 10.1006/excr.1993.1327.

Abstract

Homologous desensitization of responses to bombesin in small cell lung cancer cells can be mimicked by protein kinase C-activating phorbol esters. We show that phorbol ester-induced desensitization can be blocked by prior treatment with the protein kinase C inhibitor staurosporine or prolonged pretreatment with phorbol esters. However, under these conditions, homologous desensitization to bombesin persists. These data indicate that phorbol ester-induced desensitization is distinguishable from bombesin-induced homologous desensitization. Protein kinase C is not a dominant component in the homologous desensitization to bombesin in small cell lung cancer cells.

摘要

在小细胞肺癌细胞中,对蛙皮素反应的同源脱敏可被激活蛋白激酶C的佛波酯模拟。我们发现,蛋白激酶C抑制剂星形孢菌素的预先处理或佛波酯的长时间预处理可阻断佛波酯诱导的脱敏。然而,在这些条件下,对蛙皮素的同源脱敏仍然存在。这些数据表明,佛波酯诱导的脱敏与蛙皮素诱导的同源脱敏是有区别的。蛋白激酶C不是小细胞肺癌细胞中对蛙皮素同源脱敏的主要成分。

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