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  1. Analyzed Page
  2. Matching Content Categories
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  5. How Does Doi.org Make Money
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We began analyzing https://www.molbiolcell.org/doi/10.1091/mbc.e08-03-0309, but it redirected us to https://www.molbiolcell.org/doi/10.1091/mbc.e08-03-0309. The analysis below is for the second page.

Title[redir]:
The Atg8 Conjugation System Is Indispensable for Proper Development of Autophagic Isolation Membranes in Mice | Molecular Biology of the Cell
Description:
Autophagy is an evolutionarily conserved bulk-protein degradation pathway in which isolation membranes engulf the cytoplasmic constituents, and the resulting autophagosomes transport them to lysosomes. Two ubiquitin-like conjugation systems, termed Atg12 and Atg8 systems, are essential for autophagosomal formation. In addition to the pathophysiological roles of autophagy in mammals, recent mouse genetic studies have shown that the Atg8 system is predominantly under the control of the Atg12 system. To clarify the roles of the Atg8 system in mammalian autophagosome formation, we generated mice deficient in Atg3 gene encoding specific E2 enzyme for Atg8. Atg3-deficient mice were born but died within 1 d after birth. Conjugate formation of mammalian Atg8 homologues was completely defective in the mutant mice. Intriguingly, Atg12–Atg5 conjugation was markedly decreased in Atg3-deficient mice, and its dissociation from isolation membranes was significantly delayed. Furthermore, loss of Atg3 was associated with defective process of autophagosome formation, including the elongation and complete closure of the isolation membranes, resulting in malformation of the autophagosomes. The results indicate the essential role of the Atg8 system in the proper development of autophagic isolation membranes in mice.

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Custom-built

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Keywords {🔍}

atg, mefs, atgdeficient, figure, mice, structures, autophagy, wildtype, isolation, google, scholar, cells, formation, medline, membranes, atgatg, crossref, mizushima, conjugation, system, conjugate, mutant, cell, protein, membrane, komatsu, ohsumi, autophagosomes, autophagosome, gfpatg, hepatocytes, atgl, autophagosomelike, analysis, dots, conditions, observed, essential, results, starvation, tanida, biol, form, analyses, nutrient, degradation, enzyme, nutrientrich, detected, mouse,

Topics {✒️}

nanogold-conjugated anti-rabbit fab' de novo gfpatg5-dots time-lapse recordings proceeded hsatg4b/hsapg4b/autophagin-1 cleaves gfpatg5-introduced atg7-deficient mefs neomycin-resistant gene cassette time-lapse imaging analysis neo-resistant gene cassette silver-enhanced gold particles human apg3p/aut1p homologue pmxs-puro retrovirus vectors sds-polyacrylamide gel electrophoresis approximately 350-kda apg12-apg5 high electron-dense material starvation-induced atg16l-positive structures retrovirus vector pmxs-puro time-lapse video microscopy specific-pathogen free facilities crescent-shaped isolation membranes long-lived protein degradation short-lived regulatory proteins pre-embedding immunoelectron microscopy introduced gfp-tagged atg5 atg7-deficient adult hepatocytes atg3-deficient mouse tissues retrovirus-mediated gene transfer ag12–atg5–atg16l complex pre-autophagosomal structure organized form atg8/lc3-pe conjugate gfpatg5-introduced immortalized mefs double-membrane structure called cup-shaped isolation membranes generating atg3 null-mice atg5/atg16l-positive dots atg16l/gfpatg5-positive dots gfpatg5/atg16l-positive dots atg3-deficient mice displayed atg5-null purkinje cells wild-type mef consists atg5-deficient es cells atg12–atg5–atg16l complex atg12-atg5-atg16l complex anti-lc3 antibody revealed atg7-deficient purkinje cells atg12–atg5 conjugation reaction starvation-induced gfpatg5 dots atg3-deficient immortalized mefs atg12–atg5 conjugate interacts reduced atg12–atg5 conjugate starvation-induced protein degradation

Questions {❓}

  • Why is Atg12–Atg5 conjugation suppressed by loss of Atg3?

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External Links {🔗}(301)

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3.9s.