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Autophagy regulates lipid metabolism
A previously unknown function for autophagy in regulating intracellular lipid stores (macrolipophagy) is identified that could have important implications for human diseases with lipid over-accumulation such as those that comprise the metabolic syndrome.
Autophagy: Renovation of Cells and Tissues
It is explored how recent mouse models in combination with advances in human genetics are providing key insights into how the impairment or activation of autophagy contributes to pathogenesis of diverse diseases, from neurodegenerative diseases such as Parkinson disease to inflammatory disorders such as Crohn disease.
Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production
It is shown that Atg16L1 (autophagy-related 16-like 1), which is implicated in Crohn's disease, regulates endotoxin-induced inflammasome activation in mice and is an essential component of the autophagic machinery responsible for control of the endot toxin-induced inflammatory immune response.
Homeostatic Levels of p62 Control Cytoplasmic Inclusion Body Formation in Autophagy-Deficient Mice
The findings highlight the unexpected role of homeostatic level of p62, which is regulated by autophagy, in controlling intracellular inclusion body formation, and indicate that the pathologic process associated with autophagic deficiency is cell-type specific.
Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice
Conditional knockout mice of Atg7 were generated and showed the important role of autophagy in starvation response and the quality control of proteins and organelles in quiescent cells.
Loss of autophagy in the central nervous system causes neurodegeneration in mice
It is found that mice lacking Atg7 specifically in the central nervous system showed behavioural defects, including abnormal limb-clasping reflexes and a reduction in coordinated movement, and died within 28 weeks of birth, and that impairment of autophagy is implicated in the pathogenesis of neurodegenerative disorders involving ubiquitin-containing inclusion bodies.
Toll-like receptor signalling in macrophages links the autophagy pathway to phagocytosis
It is shown that a particle that engages TLRs on a murine macrophage while it is phagocytosed triggers the autophagosome marker LC3 to be rapidly recruited to the phagosome in a manner that depends on theAutophagy pathway proteins ATG5 and ATG7; this process is preceded by recruitment of beclin 1 and phosphoinositide-3-OH kinase activity.
The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1
The findings indicate that the pathological process associated with p62 accumulation results in hyperactivation of Nrf2 and delineates unexpected roles of selective autophagy in controlling the transcription of cellular defence enzyme genes.
PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy
Defective mitochondrial quality control is shown to be a mechanism for neurodegeneration in some forms of Parkinson's disease.