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000163508 037__ $$aDZNE-2022-00268
000163508 041__ $$aEnglish
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000163508 245__ $$aDirect Interaction of ATP7B and LC3B Proteins Suggests a Cooperative Role of Copper Transportation and Autophagy.
000163508 260__ $$aBasel$$bMDPI$$c2021
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000163508 520__ $$aMacroautophagy/autophagy plays an important role in cellular copper clearance. The means by which the copper metabolism and autophagy pathways interact mechanistically is vastly unexplored. Dysfunctional ATP7B, a copper-transporting ATPase, is involved in the development of monogenic Wilson disease, a disorder characterized by disturbed copper transport. Using in silico prediction, we found that ATP7B contains a number of potential binding sites for LC3, a central protein in the autophagy pathway, the so-called LC3 interaction regions (LIRs). The conserved LIR3, located at the C-terminal end of ATP7B, was found to directly interact with LC3B in vitro. Replacing the two conserved hydrophobic residues W1452 and L1455 of LIR3 significantly reduced interaction. Furthermore, autophagy was induced in normal human hepatocellular carcinoma cells (HepG2) leading to enhanced colocalization of ATP7B and LC3B on the autophagosome membranes. By contrast, HepG2 cells deficient of ATP7B (HepG2 ATP7B-/-) showed autophagy deficiency at elevated copper condition. This phenotype was complemented by heterologous ATP7B expression. These findings suggest a cooperative role of ATP7B and LC3B in autophagy-mediated copper clearance.
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000163508 650_7 $$2Other$$aATPase copper transporting beta
000163508 650_7 $$2Other$$aHepG2
000163508 650_7 $$2Other$$aLC3 interaction region
000163508 650_7 $$2Other$$aWilson disease
000163508 650_7 $$2Other$$aautophagosome-lysosome fusion
000163508 650_7 $$2NLM Chemicals$$aMAP1LC3B protein, human
000163508 650_7 $$2NLM Chemicals$$aMicrotubule-Associated Proteins
000163508 650_7 $$0789U1901C5$$2NLM Chemicals$$aCopper
000163508 650_7 $$0EC 7.2.2.8$$2NLM Chemicals$$aATP7B protein, human
000163508 650_7 $$0EC 7.2.2.8$$2NLM Chemicals$$aCopper-Transporting ATPases
000163508 650_2 $$2MeSH$$aAmino Acid Sequence
000163508 650_2 $$2MeSH$$aBiological Transport: drug effects
000163508 650_2 $$2MeSH$$aCopper: metabolism
000163508 650_2 $$2MeSH$$aCopper: pharmacology
000163508 650_2 $$2MeSH$$aCopper-Transporting ATPases: chemistry
000163508 650_2 $$2MeSH$$aCopper-Transporting ATPases: metabolism
000163508 650_2 $$2MeSH$$aHep G2 Cells
000163508 650_2 $$2MeSH$$aHumans
000163508 650_2 $$2MeSH$$aMicrotubule-Associated Proteins: metabolism
000163508 650_2 $$2MeSH$$aProtein Binding: drug effects
000163508 650_2 $$2MeSH$$aProtein Transport: drug effects
000163508 7001_ $$00000-0002-0669-3421$$aPomorski, Adam$$b1
000163508 7001_ $$aHuth, Katharina$$b2
000163508 7001_ $$aHund, Christina$$b3
000163508 7001_ $$aPetters, Janine$$b4
000163508 7001_ $$00000-0001-9252-5784$$aKrężel, Artur$$b5
000163508 7001_ $$0P:(DE-2719)2811732$$aHermann, Andreas$$b6$$udzne
000163508 7001_ $$aLukas, Jan$$b7
000163508 770__ $$aThe Autophagic Process in Human Physiology and Pathogenesis
000163508 773__ $$0PERI:(DE-600)2661518-6$$a10.3390/cells10113118$$gVol. 10, no. 11, p. 3118 -$$n11$$p3118$$tCells$$v10$$x2073-4409$$y2021
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