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- Shimizu Shigeomi
- 東京医科歯科大学・難治疾患研究所・病態細胞生物
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- Arakawa Satoko
- 東京医科歯科大学・難治疾患研究所・病態細胞生物
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- Nishida Yuya
- 東京医科歯科大学・難治疾患研究所・病態細胞生物
Bibliographic Information
- Other Title
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- Atg5非依存性オートファジーの形態学と分子生物学
- Atg5 ヒイソンセイ オートファジー ノ ケイタイガク ト ブンシ セイブツガク
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Abstract
<p>Atg5 and Atg7 are considered as essential molecules for induction of macroautophagy. However, we found that cells lacking Atg5 or Atg7 can still form autophagosomes/autolysosomes and perform autophagy-mediated protein degradation when subjected to certain stresses. Although lipidation of LC3 is accepted to be a good indicator of macroautophagy, it did not occur during the Atg5/Atg7-independent alternative macroautophagy. Unlike conventional macroautophagy, autophagosomes seemed to be generated in a Rab9-dependent manner by the fusion of the phagophore with vesicles derived from the trans-Golgi and late endosomes. Mammalian macroautophagy can occur via at least two different pathways, which are an Atg5/Atg7-dependent conventional pathway and an Atg5/Atg7-independent alternative pathway.</p>
Journal
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- KENBIKYO
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KENBIKYO 45 (2), 94-96, 2010-06-30
The Japanese Society of Microscopy
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Keywords
Details 詳細情報について
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- CRID
- 1390002184865770240
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- NII Article ID
- 130007788943
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- NII Book ID
- AA11917781
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- ISSN
- 24342386
- 13490958
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- NDL BIB ID
- 10769427
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- Text Lang
- ja
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- Data Source
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- JaLC
- NDL
- CiNii Articles
- KAKEN
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- Abstract License Flag
- Disallowed