Home > Publications Database > Direct Interaction of ATP7B and LC3B Proteins Suggests a Cooperative Role of Copper Transportation and Autophagy. > print

001     163508
005     20230915092422.0
024 7 _ |a 10.3390/cells10113118
|2 doi
024 7 _ |a pmid:34831341
|2 pmid
024 7 _ |a pmc:PMC8625360
|2 pmc
024 7 _ |a altmetric:117862002
|2 altmetric
037 _ _ |a DZNE-2022-00268
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Pantoom, Supansa
|b 0
245 _ _ |a Direct Interaction of ATP7B and LC3B Proteins Suggests a Cooperative Role of Copper Transportation and Autophagy.
260 _ _ |a Basel
|c 2021
|b MDPI
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1655461434_22301
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
500 _ _ |a (CC BY)
520 _ _ |a Macroautophagy/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.
536 _ _ |a 353 - Clinical and Health Care Research (POF4-353)
|0 G:(DE-HGF)POF4-353
|c POF4-353
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a ATPase copper transporting beta
|2 Other
650 _ 7 |a HepG2
|2 Other
650 _ 7 |a LC3 interaction region
|2 Other
650 _ 7 |a Wilson disease
|2 Other
650 _ 7 |a autophagosome-lysosome fusion
|2 Other
650 _ 7 |a MAP1LC3B protein, human
|2 NLM Chemicals
650 _ 7 |a Microtubule-Associated Proteins
|2 NLM Chemicals
650 _ 7 |a Copper
|0 789U1901C5
|2 NLM Chemicals
650 _ 7 |a ATP7B protein, human
|0 EC 7.2.2.8
|2 NLM Chemicals
650 _ 7 |a Copper-Transporting ATPases
|0 EC 7.2.2.8
|2 NLM Chemicals
650 _ 2 |a Amino Acid Sequence
|2 MeSH
650 _ 2 |a Biological Transport: drug effects
|2 MeSH
650 _ 2 |a Copper: metabolism
|2 MeSH
650 _ 2 |a Copper: pharmacology
|2 MeSH
650 _ 2 |a Copper-Transporting ATPases: chemistry
|2 MeSH
650 _ 2 |a Copper-Transporting ATPases: metabolism
|2 MeSH
650 _ 2 |a Hep G2 Cells
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Microtubule-Associated Proteins: metabolism
|2 MeSH
650 _ 2 |a Protein Binding: drug effects
|2 MeSH
650 _ 2 |a Protein Transport: drug effects
|2 MeSH
700 1 _ |a Pomorski, Adam
|0 0000-0002-0669-3421
|b 1
700 1 _ |a Huth, Katharina
|b 2
700 1 _ |a Hund, Christina
|b 3
700 1 _ |a Petters, Janine
|b 4
700 1 _ |a Krężel, Artur
|0 0000-0001-9252-5784
|b 5
700 1 _ |a Hermann, Andreas
|0 P:(DE-2719)2811732
|b 6
|u dzne
700 1 _ |a Lukas, Jan
|b 7
770 _ _ |a The Autophagic Process in Human Physiology and Pathogenesis
773 _ _ |a 10.3390/cells10113118
|g Vol. 10, no. 11, p. 3118 -
|0 PERI:(DE-600)2661518-6
|n 11
|p 3118
|t Cells
|v 10
|y 2021
|x 2073-4409
856 4 _ |y OpenAccess
|u https://pub.dzne.de/record/163508/files/DZNE-2022-00268.pdf
856 4 _ |y OpenAccess
|x pdfa
|u https://pub.dzne.de/record/163508/files/DZNE-2022-00268.pdf?subformat=pdfa
909 C O |o oai:pub.dzne.de:163508
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 6
|6 P:(DE-2719)2811732
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-353
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Clinical and Health Care Research
|x 0
914 1 _ |y 2021
915 _ _ |a Creative Commons Attribution CC BY (No Version)
|0 LIC:(DE-HGF)CCBYNV
|2 V:(DE-HGF)
|b DOAJ
|d 2021-05-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2021-05-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2021-05-04
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2021-05-04
915 _ _ |a Fees
|0 StatID:(DE-HGF)0700
|2 StatID
|d 2021-05-04
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a Article Processing Charges
|0 StatID:(DE-HGF)0561
|2 StatID
|d 2021-05-04
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b CELLS-BASEL : 2021
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2022-01-07T08:42:17Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2022-01-07T08:42:17Z
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b DOAJ : Blind peer review
|d 2022-01-07T08:42:17Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
|d 2022-11-30
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2022-11-30
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b CELLS-BASEL : 2021
|d 2022-11-30
920 1 _ |0 I:(DE-2719)1510100
|k AG Teipel
|l Clinical Dementia Research Rostock /Greifswald
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)1510100
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21