Nicotinic Receptor Stimulation Blocks Neurotoxicity Induced by Amyloid-β via the Phosphatidylinositol-3-Kinase Cascade

Author(s):  
T. Kihara ◽  
S. Shimohama
2007 ◽  
Vol 58 ◽  
pp. S117
Author(s):  
Yuki Takada-Takatori ◽  
Toshiaki Kume ◽  
Yuta Ohgi ◽  
Tetsuhiro Niidome ◽  
Takeshi Fujii ◽  
...  

2002 ◽  
Vol 70 (3) ◽  
pp. 274-282 ◽  
Author(s):  
Takeshi Kihara ◽  
Shun Shimohama ◽  
Hideyuki Sawada ◽  
Kazuhiro Honda ◽  
Tomoki Nakamizo ◽  
...  

2010 ◽  
Vol 191 (4) ◽  
pp. 827-843 ◽  
Author(s):  
Zhixun Dou ◽  
Mohar Chattopadhyay ◽  
Ji-An Pan ◽  
Jennifer L. Guerriero ◽  
Ya-Ping Jiang ◽  
...  

Autophagy is an evolutionarily conserved cell renewal process that depends on phosphatidylinositol 3-phosphate (PtdIns(3)P). In metazoans, autophagy is inhibited by PtdIns(3,4,5)P3, the product of class IA PI3Ks, which mediates the activation of the Akt–TOR kinase cascade. However, the precise function of class IA PI3Ks in autophagy remains undetermined. Class IA PI3Ks are heterodimeric proteins consisting of an 85-kD regulatory subunit and a 110-kD catalytic subunit. Here we show that the class IA p110-β catalytic subunit is a positive regulator of autophagy. Genetic deletion of p110-β results in impaired autophagy in mouse embryonic fibroblasts, liver, and heart. p110-β does not promote autophagy by affecting the Akt–TOR pathway. Rather, it associates with the autophagy-promoting Vps34–Vps15–Beclin 1–Atg14L complex and facilitates the generation of cellular PtdIns(3)P. Our results unveil a previously unknown function for p110-β as a positive regulator of autophagy in multicellular organisms.


Toxicology ◽  
2008 ◽  
Vol 243 (1-2) ◽  
pp. 43-50 ◽  
Author(s):  
Kyu-Yong Lee ◽  
Seong-Ho Koh ◽  
Min Young Noh ◽  
Seung Hyun Kim ◽  
Young Joo Lee

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