論文修改價錢：監管TASK1的活動

論文修改價錢：監管TASK1的活動
這些結果指向一個獨特的機制,監管TASK1的活動。第三項目兩個孔隙域鉀通道TASK1受低氧誘導蛋白激酶C信號與缺血性心臟保護的作用。結果指向TASK1是預防的關鍵在缺氧細胞死亡。這是觀察到有抑制TASK1渠道在缺氧是通過PKC激活並可能導致一個新的目標在保護心肌細胞缺氧損傷時。的一個重要決定了在這個研究是TASK1發揮了不可或缺的作用,預防細胞死亡在hyopxia和發揮了重要作用在TASK1通道的抑制登的第四個項目有分析GLUT12函數及其在基底作用和胰島素依賴葡萄糖轉運蛋白。這部小說的監管機制GLUT12胰島素被探測。

論文修改價錢：監管TASK1的活動
這是預測,GLIT4胰島素調控過剩12易位到細胞表面,是受損而提出糖尿病狀態。從這些決定重要的見解了,讓我對研究更為敏感。從這些努力和研究3個已得到增強的理解電生理學和在體內動物模型建立。在未來我想參與,獲得更多的經驗在臨床前試驗開發可行的解決方案不同的心臟並發症。假設的膜蛋白LRRC8a鏈接內皮轉導vasorexalation和血壓調節通過PI3K-AKT-eNOS p66shc信號。本研究的主要目的是了解和識別小說離子通道在內皮細胞生物學。

論文修改價錢：監管TASK1的活動

These results pointed towards a unique mechanism that regulated the activities of TASK1. In the third project the two pore domain potassium channel TASK1 was regulated by hypoxia-induced protein kinase C signaling that implicated the role of ischemic cardioprotection. The results pointed towards the fact that TASK1 was crucial for prevention of cell death during hypoxia. It was observed that there was suppression of TASK1 channels during hypoxia was activated through PKC and could lead to a new target in protecting the Cardiac cells from damage during times of hypoxia. One of the important determinations made in this research was that the TASK1 played an integral role in prevention of the cell death during hyopxia and played an important role in the suppression of TASK1 channels during theIn the fourth project there was analysis of the GLUT12 functions and its role in basal and insulin-independent glucose transporters. The novel mechanism in the regulation of GLUT12 by insulin was probed.

論文修改價錢：監管TASK1的活動
It was predicted from this, GLIT4 insulin regulated GLUT 12 translocation to the cell surface and is impaired while presenting diabetes condition. From these determinations important insights were gained and have made me more attuned towards research studies. From these endeavors and research thre has been enhanced understanding of the electrophysiology and in in- vivo animal model building. In the future I want to participate and gain more experience in the preclinical trials to develop viable solutions for the different kinds of heart complications.Hypothesis of the membrane protein LRRC8a links endothelial mechanotransduction with vasorexalation and blood pressure regulation via PI3K-AKT-eNOS and in p66shc signaling. The primary purpose of this research is to understand and identify the novel ion channels in endothelial cell biology.