Ｇα１２

A team of a Negoro (moderate price) guest professors (internal medicine) of U.S. Harvard University discovered it and announced the protein about onset of acute renal failure to a U.S. science academy bulletin. The death rate of acute renal failure is high with approximately 50%, but there are only symptomatic treatments such as the artificial dialysis. I can expect it if I develop medicine holding a function of this protein in check when I lead to new treatment.
Clots are a chance, and, as for acute renal failure, the combination between the cells in the organization "renal tubule" of kidney reabsorbing water or glucose from the urinary cost that I filtered is broken and is known to develop. But it was unknown and disturbed the new medicine development what let you take a cell to pieces.
The team pays its attention to protein "Gα12" of the part of switch conveying a signal from the cell outside inside in cell surface. When this protein acted, I discovered that the combination between cells failed. In addition, I make the mouse that functions of this protein are always active artificially. Cells broke up more, and the function of the kidney came off.
I tell, Negoro "wants to aim at the innovative drug development I suppress the function of this protein, and to prevent acute renal failure". Because you hear that the number of people having acute renal failure is considerably high, you should be connected for innovative drug development.


急性腎不全の発症にかかわるたんぱく質を、米ハーバード大の根来（ねごろ）客員教授（内科学）らのチームが発見し、米科学アカデミー紀要に発 表した。急性腎不全の死亡率は約５割と高いが、人工透析などの対症療法しかない。このたんぱく質の働きを抑える薬を開発すれば、新たな治療につながると期 待できる。
　急性腎不全は、ろ過した尿の元から水分やブドウ糖などを再吸収する腎臓の組織「尿細管」にある細胞同士の結合が血栓などがきっかけとなって壊され、発症することが知られている。だが、何が細胞をばらばらにさせているのかが不明で、新薬開発の妨げとなっていた。
　チームは、細胞表面にあって、細胞外からの信号を内部に伝えるスイッチ役のたんぱく質「Ｇα１２」に着目。このたんぱく質が働くと、細胞同士の結合が壊れることを突き止めた。また、このたんぱく質の働きがいつも活発なマウスを人工的に作成。より細胞同士が ばらばらになって、腎臓の機能が落ちていた。
　根来さんは「このたんぱく質の働きを抑え、急性腎不全を防ぐ創薬を目指したい」と話す。急性腎不全を発病する方の数も相当高いと聞きますから創薬につながっていくといいですね。