...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Urocortin stimulates tyrosine hydroxylase activity via the cAMP/protein kinase a pathway in rat Pheochromocytoma PC12 cells.
【24h】

Urocortin stimulates tyrosine hydroxylase activity via the cAMP/protein kinase a pathway in rat Pheochromocytoma PC12 cells.

机译：Urocortin通过cAMP /蛋白激酶刺激大鼠嗜铬细胞瘤PC12细胞中的酪氨酸羟化酶活性。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Urocortin is a novel mammalian member of the corticotrophin releasing factor (CRF)-related peptides. We have investigated the expression, mechanism of action and second messenger for urocortin in rat pheochromocytoma PC12 cells. We initially confirmed the expression of urocortin and CRF-R2beta, which is thought to be an endogenous receptor for urocortin, in PC12 cells. We also demonstrate that urocortin (> or = 1 nM) significantly elevates the level of cAMP in these cells. Moreover, alpha-helical CRF-(9-41), a more specific antagonist of CRF-R2 than CRF-R1 and the adenylate cyclase inhibitor SQ22536, inhibited the urocortin-induced increase in the level of cAMP. Thus, urocortin may exert its physiological role in chromaffin cells via CRF-R2beta coupling to adenylate cyclase. Urocortin (> or = 1 nM) significantly increased the mRNA level and activity of tyrosine hydroxylase (TH), a rate-limiting enzyme in the biosynthesis of catecholamine. Furthermore, urocortin-induced changes in TH-mRNA and activity were inhibited by H89 (a PKA inhibitor) and SQ22536 as well as alpha-helical CRF-(9-41). However, urocortin did not affect DNA synthesis or catecholamine secretion in these cells. In conclusion, we have demonstrated that urocortin stimulates catecholamine biosynthesis via the cAMP/protein kinase A pathway in PC12 cells, where both urocortin and its receptor, CRF-R2, are expressed.
机译：Urocortin是促肾上腺皮质激素释放因子（CRF）相关肽的新型哺乳动物成员。我们研究了尿嗜铬细胞瘤PC12细胞中尿皮质素的表达，作用机制和第二信使。我们最初确认了PC12细胞中尿皮质素和CRF-R2beta（被认为是尿皮质素的内源性受体）的表达。我们还证明了尿皮质素（>或= 1 nM）显着提高了这些细胞中的cAMP水平。此外，α-螺旋CRF-（9-41）是一种比CRF-R1和腺苷酸环化酶抑制剂SQ22536更特异性的CRF-R2拮抗剂，抑制了尿皮质素诱导的cAMP水平升高。因此，尿皮质素可能通过CRF-R2beta与腺苷酸环化酶偶联在嗜铬细胞中发挥其生理作用。 Urocortin（>或= 1 nM）显着提高了酪氨酸羟化酶（TH）的mRNA水平和活性，酪氨酸羟化酶是儿茶酚胺生物合成中的限速酶。此外，H89（一种PKA抑制剂）和SQ22536以及α-螺旋CRF-（9-41）抑制了尿皮质素诱导的TH-mRNA和活性的变化。但是，urocortin不会影响这些细胞中的DNA合成或儿茶酚胺分泌。总之，我们证明了尿皮质素通过PC12细胞中的cAMP /蛋白激酶A途径刺激了儿茶酚胺的生物合成，其中尿皮质素及其受体CRF-R2均在其中表达。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号