监管的Na (+) - k (+) 2 cl(-)转运蛋白cGMP / cGMP-dependent蛋白激酶呋喃苯胺酸后我管理。

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娼妓F, Schinner E, Castrop H, Vitzthum H,霍夫曼F, Schlossmann J

监管的Na (+) - k (+) 2 cl(-)转运蛋白cGMP / cGMP-dependent蛋白激酶呋喃苯胺酸后我管理。

2月j . 2015年10月,282 (19):3786 - 98。doi: 10.1111 / febs.13376。Epub 2015年7月30日。

PubMed ID

26183401 (在PubMed

]

文摘

氯化钠再吸收的厚提升肢体亨利循环是由钠(+)- k (+) 2 cl(-)转运蛋白(NKCC2)。循环利尿剂速尿灵NKCC2的有效抑制剂。然而,调节电解质转运机制所知甚少。beplayapp考虑完善一氧化氮NKCC2活动的影响,cGMP可能参与了这一规定。cGMP-dependent蛋白激酶I (cGKI;PKGI)是一个cGMP靶蛋白磷酸化不同基质后通过cGMP激活。我们调查了潜在相关性cGMP / cGKI通路和NKCC2监管。我们对野生型小鼠(wt)和cGKIalpha-rescue呋喃苯胺酸。cGKIalpha-rescue老鼠表达cGKIalpha只有在光滑的控制阳性transgelin (SM22)启动子在cGKI缺乏背景。呋喃苯胺酸治疗增加了钠和氯化物的尿液排泄cGKIalpha-rescue老鼠相比,在wt老鼠。 We analyzed the phosphorylation of NKCC2 by western blotting and immunostaining using the phosphospecific antibody R5. The administration of furosemide significantly increased the phosphorylated NKCC2 signal in wt but not in cGKIalpha-rescue mice. NKCC2 activation led to its phosphorylation and membrane translocation. To examine whether cGKI was involved in this process, we analyzed vasodilator-stimulated phosphoprotein, which is phosphorylated by cGKI. Furosemide injection resulted in increased vasodilator-stimulated phosphoprotein phosphorylation in wt mice. We hypothesize that furosemide administration activated cGKI, leading to NKCC2 phosphorylation and membrane translocation. This cGKI-mediated pathway could be a mechanism to compensate for the inhibitory effect of furosemide on NKCC2.

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药物靶点

药物	目标	类	生物	药理作用	行动
呋喃苯胺酸	溶质载体家庭12成员1	蛋白质	人类	是的	抑制剂	细节