Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice

By Taichi Hara, Kenji Nakamura, M. Matsui, A. Yamamoto, Yohko Nakahara, Rika Suzuki-Migishima, M. Yokoyama, K. Mishima, I. Saito, Hideyuki Okano and 1 more. Nature, 2006

4,005 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/8f5b2baf12715b74e495052df4ba973b5c94c792

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Citations in the corpus

The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress (2007, background): “In addition, a low level of constitutive autophagy is also important for controlling the quality of proteins and organelles, in order to maintain cell functio”
Eaten alive: a history of macroautophagy (2010, background): “In addition, two parallel mouse studies using neuronal-specific knockouts of Atg5 or Atg7 demonstrate that basal autophagy controls the constitutive turnover of soluble, cytosolic proteins to prevent the accumulation of abnormal neuroproteins that may cause symptoms of neurodegeneratio”
Oxidative stress induces autophagic cell death independent of apoptosis in transformed and cancer cells (2008, background): “In mice lacking autophagy, neural cell death is increased leading to neurological disorders.(25) On the other hand, autophagic cell death was shown to be induced by a short mitochondrial form of the ARF tumor suppressor protein p19 in HEK293T cells mediated by changes in the mitochondrial membrane p”
Macrophage Autophagy Plays a Protective Role in Advanced Atherosclerosis (2012, methodology): “In contrast, there were very few double membranes in untreated macrophages or in 7KC-treated macrophages from Atg5Lysmcre mice, which lack the key autophagy protein ATG5 (Hara et al., 2006).”
Autophagy is required to maintain muscle mass. (2009, methodology): “Detergent-soluble and -insoluble fractions were obtained according to (Hara et al., 2006).”
Principles and Current Strategies for Targeting Autophagy for Cancer Treatment (2011, background): “garbage disposal provokes degenerative and inflammatory diseases (38, 39) and may contribute to cancer.”
Tau fragmentation, aggregation and clearance: the dual role of lysosomal processing. (2009, background): “In agreement with this scenario, it has been reported that disruption of autophagy led to the accumulation of abnormal proteins in neurons (60,61).”
Essential regulation of cell bioenergetics by constitutive InsP3 receptor Ca2+ transfer to mitochondria. (2010, positive): “Atg5 lox/lox mice (Hara et al., 2006) were infected with AAV-TGB-Cre or AAV-TGB-GFP (amplified and purified by the U. Pennsylvania Vector Core) for hepatocyte-specific expression of either Cre or GFP. Cells then were isolated by the two step perfusion method.”
Serine 403 phosphorylation of p62/SQSTM1 regulates selective autophagic clearance of ubiquitinated proteins. (2011, methodology): “The atg5-deficient mice showed ubiquitin-positive inclusions in Molecular Cell 44, 27 neurons (Hara et al., 2006), and these inclusions were p62 positive as also reported in atg7-deficient mice (Komatsu et al., 2007).”
A role for ubiquitin in selective autophagy. (2009, background): “One explanation for the delayed onset of the apparent neuron-specific autophagy defects in p62 knockout mice (in comparison to those seen in the Atg7- and Atg5-deficient mice [Hara et al., 2006; Komatsu et al., 2006]) may be the existence of functional homologs of p62 in higher organisms.”
Distinct regulation of autophagic activity by Atg14L and Rubicon associated with Beclin 1- phosphatidylinositol 3-kinase complex (2009, positive): “S5c ), indicating that these are ubiquitylated protein inclusions, as previously shown in Atg5 - or Atg7 -deficient mouse-tissue”
Autophagy Suppresses Tumorigenesis Through Elimination of p62 (2009, neutral): “Upregulation of ubiquitinated proteins, although common in tissues of autophagy-defective mice (Hara et al., 2006; Komatsu et al., 2006), was not striking in atg5!/! tumors (Figure 3H).”