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Article Addendum
Autophagy and Neurodegeneration
Masaaki Komatsu, Eiki Kominami and Keiji Tanaka
volume 2 | issue 4
October/November/December 2006Pages: 311 - 313
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The proteasome and lysosome are sophisticated apparatuses capable of shredding unnecessary proteins in eukaryotic cells. The proteasome and its partner ubiquitin (which functions as a destination signal for proteolysis) play crucial roles in selective breakdown of not only short-lived regulatory proteins but also abnormal proteins that need to be rapidly eliminated from the cells. It is generally accepted that deficits of the proteasome-ubiquitin system are associated with various neurodegenerative diseases, since ubiquitin-positive inclusions frequently appear in neurons of patients and mice models of neurodegenerative diseases. However, investigators working in the field of neuronal diseases have focused their attention in recent years on autophagy (Greek for “the eating of oneself”) following the recent discovery that ablation of autophagy leads to accumulation of ubiquitin-positive inclusions, which are the pathological hallmark of neurodegenerative diseases. Here we discuss the consequences of autophagy deficiency in neurons.
Addendum to:
Loss of Autophagy in the Central Nervous System Causes Neurodegeneration in Mice
Masaaki Komatsu, Satoshi Waguri, Tomoki Chiba, Shigeo Murata, Jun-ichi Iwata, Isei Tanida, Takashi Ueno, Masato Koike, Yasuo Uchiyama, Eiki Kominami and Keiji Tanaka
Nature 2006; In press (Published on line 19 April 2006)
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.