Molecular basis of canonical and bactericidal autophagy

Autophagy is a catabolic process by which cells degrade their own cytoplasmic constituents. Cells respond to the stress response of nutrient deficiency by degrading a portion of their cellular components to produce amino acids and energy. Recently, it became evident that the autophagic machinery is...

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Bibliographic Details
Published in:International immunology 2009-11, Vol.21 (11), p.1199-1204
Main Authors: Noda, Takeshi, Yoshimori, Tamotsu
Format: Article
Language:English
Subjects:
Amino acids
Animals
Atg14
Atg16L
Autophagy - immunology
Autophagy-Related Proteins
Bacteria
Bacteria - immunology
Carrier Proteins - metabolism
Energy
Humans
Immune system
Immunity, Innate - immunology
LC3
Mammalian cells
Membrane structure
Microtubule-Associated Proteins - metabolism
Nutrient deficiency
Phagocytosis
Phagosomes
Phagosomes - immunology
Phagosomes - metabolism
phosphatidylinositol 3-phosphate
Phosphatidylinositol Phosphates - metabolism
PI3P
Stress
Ubiquitin - immunology
Ubiquitin - metabolism
Ubiquitination - immunology
xenophagy
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Summary:Autophagy is a catabolic process by which cells degrade their own cytoplasmic constituents. Cells respond to the stress response of nutrient deficiency by degrading a portion of their cellular components to produce amino acids and energy. Recently, it became evident that the autophagic machinery is also involved in a kind of innate immune system. Some bacteria that invade mammalian cells are eventually entrapped in an autophagic membrane structure. In this review, we describe the current understanding of three of the basic components of the canonical autophagy machinery—LC3, the Atg16L complex and phosphatidylinositol 3-phosphate (PI3P)—which are dynamically associated with the autophagic structure. LC3 is proposed to function in autophagosome closure, whereas the Atg16L complex functions as an E3-like protein in ubiquitination-like reactions in the LC3 lipidation system. PI3P is a key determinant of the autophagic membrane. Further, their relation to bactericidal autophagy (i.e. xenophagy) will be introduced.
ISSN:0953-8178
1460-2377
DOI:10.1093/intimm/dxp088