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000125959 0247_ $$2doi$$a10.1007/s00018-015-2087-8
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000125959 0247_ $$2ISSN$$a1420-9071
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000125959 041__ $$aeng
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000125959 1001_ $$0P:(DE-He78)a8657988a6082d4d90605e15cd5d3302$$aBrady, Anne$$b0$$eFirst author$$udkfz
000125959 245__ $$aMitophagy programs: mechanisms and physiological implications of mitochondrial targeting by autophagy.
000125959 260__ $$aBasel$$bBirkhäuser$$c2016
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000125959 520__ $$aMitochondria are an essential source of ATP for cellular function, but when damaged, mitochondria generate a plethora of stress signals, which lead to cellular dysfunction and eventually programmed cell death. Thus, a major component of maintaining cellular homeostasis is the recognition and removal of dysfunctional mitochondria through autophagy-mediated degradation, i.e., mitophagy. Mitophagy further constitutes a developmental program, and undergoes a high degree of crosstalk with apoptosis. Reduced mitochondrial quality control is linked to disease pathogenesis, suggesting the importance of process elucidation as a clinical target. Recent work has revealed multiple mitophagy programs that operate independently or undergo crosstalk, and require modulated autophagy receptor activities at outer membranes of mitochondria. Here, we review these mitophagy programs, focusing on pathway mechanisms which recognize and target mitochondria for sequestration by autophagosomes, as well as mechanisms controlling pathway activities. Furthermore, we provide an introduction to the currently available methods for detecting mitophagy.
000125959 536__ $$0G:(DE-HGF)POF3-312$$a312 - Functional and structural genomics (POF3-312)$$cPOF3-312$$fPOF III$$x0
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000125959 650_7 $$2NLM Chemicals$$aBNIP3 protein, human
000125959 650_7 $$2NLM Chemicals$$aMembrane Proteins
000125959 650_7 $$2NLM Chemicals$$aMicrotubule-Associated Proteins
000125959 650_7 $$2NLM Chemicals$$aProto-Oncogene Proteins
000125959 650_7 $$2NLM Chemicals$$aUbiquitin
000125959 650_7 $$0EC 2.3.2.27$$2NLM Chemicals$$aUbiquitin-Protein Ligases
000125959 650_7 $$0EC 2.3.2.27$$2NLM Chemicals$$aparkin protein
000125959 7001_ $$0P:(DE-He78)5bf984e94f0a31773a103cd293e01f92$$aBrady, Nathan$$b1$$eLast author$$udkfz
000125959 773__ $$0PERI:(DE-600)1458497-9$$a10.1007/s00018-015-2087-8$$gVol. 73, no. 4, p. 775 - 795$$n4$$p775 - 795$$tCellular and molecular life sciences$$v73$$x1420-9071$$y2016
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000125959 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)5bf984e94f0a31773a103cd293e01f92$$aDeutsches Krebsforschungszentrum$$b1$$kDKFZ
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000125959 9141_ $$y2016
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