Basal Autophagy Is Required for the Efficient Catabolism of Sialyloligosaccharides

Seino, Junichi; Wang, Li; Harada, Yoichiro; Huang, Chengcheng; Ishii, Kumiko; Mizushima, Noboru; Suzuki, Tadashi

doi:10.1074/jbc.m113.464503

Cited by 41 publications

(37 citation statements)

References 40 publications

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“…Autophagy is a conserved catabolic mechanism that protects cells by delivering potentially toxic macromolecular aggregates (e.g. proteins, lipids, and glycans) and damaged or superfluous organelles to lysosomes for degradation (1)(2)(3)(4)(5)(6). Various stimuli, such as starvation, endoplasmic reticular stress, DNA damage, and reactive oxygen species, may trigger autophagy.…”

Section: Hematopoietic Stem Cells (Hsc)mentioning

confidence: 99%

Hierarchal Autophagic Divergence of Hematopoietic System

Cao

Zhang

Yuan

et al. 2015

Journal of Biological Chemistry

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Background: Autophagy is required in hematopoiesis and protects against leukemogenesis. Results: When ATG7-dependent canonical autophagy is impaired, ATG7-independent alternative autophagy engages in myeloid cells but not in hematopoietic stem cells. Conclusion:The integrity of hematopoietic stem cells is jeopardized by a lack of alternative autophagy. Significance: Learning autophagy organization in hematopoietic system is crucial for understanding hematopoietic stem cell transformation.

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Section: Hematopoietic Stem Cells (Hsc)mentioning

confidence: 99%

Hierarchal Autophagic Divergence of Hematopoietic System

Cao

Zhang

Yuan

et al. 2015

Journal of Biological Chemistry

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“…A putative POS-phosphatase activity was reported in the microsome fraction from human liver (14), but the molecular nature of this phosphatase is currently unknown. Moreover, we previously found that the induction of bulk autophagy by amino acid starvation reduces the levels of FNGs in the cytosol (34). Further studies will be needed to elucidate the molecular mechanism involved in the catabolism of small POSs.…”

Section: Discussionmentioning

confidence: 99%

Non-lysosomal Degradation of Singly Phosphorylated Oligosaccharides Initiated by the Action of a Cytosolic Endo-β-N-acetylglucosaminidase

Harada

Huang

Yamaki

et al. 2016

Journal of Biological Chemistry

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Dolichol-linked oligosaccharides (DLOs)3 are glycan donor substrates for asparagine (N)-linked glycosylation in mammals (1, 2). The biosynthesis of DLOs starts on the cytosolic side of the endoplasmic reticulum (ER) membrane with the assembly of Man 5 GlcNAc 2 -PP-Dol (1). This biosynthetic intermediate is flipped into the ER lumen and is converted to Glc 3 Man 9 GlcNAc 2 -PP-Dol. The fully assembled DLO is then transferred onto nascent polypeptides by the oligosaccharyltransferase (3).In mammalian cells, the biosynthesis of DLOs is regulated by the supply of glucose. When cells are deprived of glucose, incompletely assembled DLOs are produced (4 -9), which are rapidly degraded by a currently unclarified degradation system (2, 10, 11). The enzyme involved in the degradation has long been believed to hydrolyze the pyrophosphate bond of DLOs, releasing phosphorylated oligosaccharides (POSs) into the cytosol (Fig.

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“…Targets of autophagy can be specific proteins, nonspecific protein aggregates, or whole organelles, such as dysfunctional mitochondria. Basal autophagy is constitutive in most cell types (1)(2)(3), and it is estimated that basal autophagy is responsible for the catabolism of 1 to 1.5% of cellular proteins per hour even under nutrientrich conditions (4). However, because cell survival is constantly threatened by variations in both internal and external conditions, autophagy programs must be able to respond appropriately to stress.…”

Section: Introductionmentioning

confidence: 99%

Retrograde signaling from autophagy modulates stress responses

et al. 2017

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Macroautophagy is a process in which cytoplasmic components, including whole organelles, are degraded within lysosomes. Basally, this process is essential for homeostasis and is constitutively functional in most cells, but it can also be implemented as part of stress responses. We discuss findings showing that autophagy proteins can modulate and amplify the activities of transcription factors involved in stress responses, such as those in the p53, FOXO, MiT/TFE, Nrf2, and NFkB/Rel families. Thus, transcription factors not only amplify stress responses and autophagy but are also subject to retrograde regulation by autophagy-related proteins. Physical interactions with autophagy-related proteins, competition for activating intermediates, and "signalphagy," which is the role autophagy plays in the degradation of specific signaling proteins, together provide powerful tools for implementing negative feedback or positive feed-forward loops on the transcription factors that regulate autophagy. We present examples illustrating how this network interacts to regulate metabolic and physiologic responses.

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Basal Autophagy Is Required for the Efficient Catabolism of Sialyloligosaccharides

Abstract: Background:The role of autophagy in glycan catabolism remains to be clarified. Results: In Atg5Ϫ/Ϫ cells, defective in autophagosome formation, sialyloligosaccharides accumulate specifically in the cytosol.

Cited by 41 publications

References 40 publications

Hierarchal Autophagic Divergence of Hematopoietic System

Hierarchal Autophagic Divergence of Hematopoietic System

Non-lysosomal Degradation of Singly Phosphorylated Oligosaccharides Initiated by the Action of a Cytosolic Endo-β-N-acetylglucosaminidase

Retrograde signaling from autophagy modulates stress responses

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