Essential role for autophagy protein Atg7 in the maintenance of axonal homeostasis and the prevention of axonal degeneration

By M. Komatsu, Q. Wang, G. Holstein, V. Friedrich, Jun-ichi Iwata, E. Kominami, Brian T. Chait, Keiji Tanaka, Zhenyu Yue. Proceedings of the National Academy of Sciences of the United States of America, 2007

635 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/73f846c97a911a634346c77e4884b8bc776a5451

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. M. Komatsu
2. N. Mizushima

In Epidemiology

1. N. Mizushima
2. M. Komatsu
3. D. Klionsky
4. Beth Levine
5. I. Slaninová
6. T. Ueno
7. Keiji Tanaka
8. E. Kominami

In Physiology

1. N. Mizushima
2. M. Komatsu
3. Masayuki Yamamoto
4. E. Kominami
5. T. Ueno
6. I. Slaninová
7. Beth Levine
8. D. Klionsky

Citations in the corpus

• Autophagy and Neurodegeneration: Pathogenic Mechanisms and Therapeutic Opportunities. (2017, neutral): “The earliest signs of homeostatic disruption in these mice are Purkinje axonal swellings, which are observed prior to progressive dystrophy and degeneration of the axon (Komatsu et al., 2007b; Nishiyama et al., 2007).”
• Hepatic Stellate Cells and Liver Fibrosis (2013, neutral): “Similar to stellate cells, autophagy contributes to the intracellular catabolism of lipids in hepatocytes, fibroblasts (274), and neurons (150, 151).”
• Autophagy: Renovation of Cells and Tissues (2011, background): “Simultaneous deletion of either p62 or Nrf2 dramatically attenuates the liver injury resulting from autophagy deficiency (Komatsu et al., 2007a, 2010).”
• Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice. (2007, background): “Why do autophagy-deficient mice develop neurodegeneration? Analyses of Purkinje cell-specific Atg7knockout mice demonstrated that Atg7-deficient Purkinje cells initially causes cell-autonomous, progressive dystrophy (manifested by axonal swelling) and degeneration of the axon terminals followed by c”
• Loss of mTOR-dependent macroautophagy causes autistic-like synaptic pruning deficits (2014, neutral): “…of autophagy genes ATG7 or ATG5 causes neurodegeneration associated with aberrant organelles and ubiquitin-rich inclusions in neuronal cell bodies (Hara et al., 2006; Komatsu et al., 2006), as well as disrupted membrane homeostasis in axon terminals (Komatsu et al., 2007b; Hernandez et al., 2012).”
• Autophagy gone awry in neurodegenerative diseases (2010, neutral): “More recent studies using similar genetic approaches have now confirmed an essential function of autophagy in neuronal development and remodelin”
• Distinct regulation of autophagic activity by Atg14L and Rubicon associated with Beclin 1- phosphatidylinositol 3-kinase complex (2009, neutral): “Statistical analyses were carried out as described previousl”