Mitophagy controls beige adipocyte maintenance through a Parkin-dependent and UCP1-independent mechanism

Parkin is recruited selectively to impaired mitochondria and promotes their autophagy

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Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization

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Brown and Beige Fat: Physiological Roles beyond Heat Generation

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Mitochondrial Dysfunction and Oxidative Damage in parkin-deficient Mice

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Parkin-deficient Mice Exhibit Nigrostriatal Deficits but Not Loss of Dopaminergic Neurons

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The PINK1-PARKIN Mitochondrial Ubiquitylation Pathway Drives a Program of OPTN/NDP52 Recruitment and TBK1 Activation to Promote Mitophagy

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Bi-directional interconversion of brite and white adipocytes

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PPARγ agonists Induce a White-to-Brown Fat Conversion through Stabilization of PRDM16 Protein

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Autophagy regulates adipose mass and differentiation in mice

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Measuring In Vivo Mitophagy

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UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis

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Parkin-deficient mice are not a robust model of parkinsonism

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p62 in Cancer: Signaling Adaptor Beyond Autophagy

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Brown adipose tissue in the parametrial fat pad of the mouse

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Beige adipocyte maintenance is regulated by autophagy-induced mitochondrial clearance

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PKA Regulates PINK1 Stability and Parkin Recruitment to Damaged Mitochondria through Phosphorylation of MIC60

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