Home > Publications Database > TRAF6 Phosphorylation Prevents Its Autophagic Degradation and Re-Shapes LPS-Triggered Signaling Networks. > print

001     155695
005     20240403115639.0
024 7 _ |a 10.3390/cancers13143618
|2 doi
024 7 _ |a pmid:34298830
|2 pmid
024 7 _ |a pmc:PMC8303406
|2 pmc
037 _ _ |a DZNE-2021-00863
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Busch, Julia
|b 0
245 _ _ |a TRAF6 Phosphorylation Prevents Its Autophagic Degradation and Re-Shapes LPS-Triggered Signaling Networks.
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 1712136068_27005
|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
520 _ _ |a The ubiquitin E3 ligase TNF Receptor Associated Factor 6 (TRAF6) participates in a large number of different biological processes including innate immunity, differentiation and cell survival, raising the need to specify and shape the signaling output. Here, we identify a lipopolysaccharide (LPS)-dependent increase in TRAF6 association with the kinase IKKε (inhibitor of NF-κB kinase subunit ε) and IKKε-mediated TRAF6 phosphorylation at five residues. The reconstitution of TRAF6-deficient cells, with TRAF6 mutants representing phosphorylation-defective or phospho-mimetic TRAF6 variants, showed that the phospho-mimetic TRAF6 variant was largely protected from basal ubiquitin/proteasome-mediated degradation, and also from autophagy-mediated decay in autolysosomes induced by metabolic perturbation. In addition, phosphorylation of TRAF6 and its E3 ligase function differentially shape basal and LPS-triggered signaling networks, as revealed by phosphoproteome analysis. Changes in LPS-triggered phosphorylation networks of cells that had experienced autophagy are partially dependent on TRAF6 and its phosphorylation status, suggesting an involvement of this E3 ligase in the interplay between metabolic and inflammatory circuits.
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a IKKε
|2 Other
650 _ 7 |a LPS
|2 Other
650 _ 7 |a NF-κB
|2 Other
650 _ 7 |a TRAF6
|2 Other
650 _ 7 |a autophagy
|2 Other
650 _ 7 |a kinase activation
|2 Other
650 _ 7 |a phosphorylation
|2 Other
650 _ 7 |a signaling
|2 Other
700 1 _ |a Moreno, Rita
|b 1
700 1 _ |a de la Vega, Laureano
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Saul, Vera Vivian
|b 3
700 1 _ |a Bacher, Susanne
|b 4
700 1 _ |a Zweydorf, Felix
|0 P:(DE-2719)2811552
|b 5
|u dzne
700 1 _ |a Ueffing, Marius
|0 P:(DE-HGF)0
|b 6
700 1 _ |a Weber, Axel
|0 P:(DE-HGF)0
|b 7
700 1 _ |a Gloeckner, Christian Johannes
|0 P:(DE-2719)2811291
|b 8
|u dzne
700 1 _ |a Linne, Uwe
|0 P:(DE-HGF)0
|b 9
700 1 _ |a Kracht, Michael
|0 P:(DE-HGF)0
|b 10
700 1 _ |a Schmitz, Michael Lienhard
|0 P:(DE-HGF)0
|b 11
770 _ _ |a NF-kB Signaling in Cellular Responses to Threats, Cancer Development and Therapy
773 _ _ |a 10.3390/cancers13143618
|g Vol. 13, no. 14, p. 3618 -
|0 PERI:(DE-600)2527080-1
|n 14
|p 3618
|t Cancers
|v 13
|y 2021
|x 2072-6694
856 4 _ |y OpenAccess
|u https://pub.dzne.de/record/155695/files/DZNE-2021-00863.pdf
856 4 _ |y OpenAccess
|x pdfa
|u https://pub.dzne.de/record/155695/files/DZNE-2021-00863.pdf?subformat=pdfa
909 C O |o oai:pub.dzne.de:155695
|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 5
|6 P:(DE-2719)2811552
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 8
|6 P:(DE-2719)2811291
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 0
913 0 _ |a DE-HGF
|b Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-342
|3 G:(DE-HGF)POF3
|2 G:(DE-HGF)POF3-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms and Model Systems
|x 0
914 1 _ |y 2021
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2022-11-30
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)1050
|2 StatID
|b BIOSIS Previews
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2021-05-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
|d 2022-11-30
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b CANCERS : 2021
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2022-01-24T07:56:58Z
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2021-05-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2022-01-24T07:56:58Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|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 OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
|d 2022-11-30
915 _ _ |a Article Processing Charges
|0 StatID:(DE-HGF)0561
|2 StatID
|d 2021-05-04
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b CANCERS : 2021
|d 2022-11-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2021-05-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2022-11-30
915 _ _ |a Fees
|0 StatID:(DE-HGF)0700
|2 StatID
|d 2021-05-04
920 1 _ |0 I:(DE-2719)1210007
|k AG Gloeckner
|l Functional Neuroproteomics and Translational Biomarkers in Neurodegenerative Diseases
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)1210007
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21