001     148843
005     20240229123036.0
024 7 _ |a 10.1016/j.kint.2019.09.031
|2 doi
024 7 _ |a pmid:31882173
|2 pmid
024 7 _ |a 0085-2538
|2 ISSN
024 7 _ |a 1523-1755
|2 ISSN
024 7 _ |a 2157-1716
|2 ISSN
024 7 _ |a 2157-1724
|2 ISSN
024 7 _ |a altmetric:73381071
|2 altmetric
037 _ _ |a DKFZ-2020-00035
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Breitkopf, Daniel M
|b 0
245 _ _ |a The YB-1:Notch-3 axis modulates immune cell responses and organ damage in systemic lupus erythematosus.
260 _ _ |a New York, NY
|c 2020
|b Elsevier
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 1580992494_23279
|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 2020 Feb;97(2):289-303
520 _ _ |a Systemic lupus erythematosus (SLE) is an autoimmune disease and lupus nephritis is a major risk factor for morbidity and mortality. Notch-3 signaling induced by membrane-bound or soluble ligands such as YB-1 constitutes an evolutionarily conserved pathway that determines major decisions in cell fate. Mass spectrometry of extracellular YB-1 in sera from patients with SLE and lupus-prone mice revealed specific post-translational guanidinylation of two lysine residues within the highly conserved cold-shock domain of YB-1 (YB-1-G). These modifications highly correlated with SLE disease activity, especially in patients with lupus nephritis and resulted in enhanced activation of Notch-3 signaling in T lymphocytes. The importance of YB-1:Notch-3 interaction in T cells was further evidenced by increased interleukin (Il)10 expression following YB-1-G stimulation and detection of both, YB-1-G and Notch-3, in kidneys of MRL.lpr mice by mass spectrometry imaging. Notch-3 expression and activation was significantly up-regulated in kidneys of 20-week-old MRL.lpr mice. Notably, lupus-prone mice with constitutional Notch-3 depletion (B6.Faslpr/lprNotch3-/-) exhibited an aggravated lupus phenotype with significantly increased mortality, enlarged lymphoid organs and aggravated nephritis. Additionally, these mice displayed fewer regulatory T cells and reduced amounts of anti-inflammatory IL-10. Thus, our results indicate that the YB-1:Notch-3 axis exerts protective effects in SLE and that Notch-3 deficiency exacerbates the SLE phenotype.
536 _ _ |a 317 - Translational cancer research (POF3-317)
|0 G:(DE-HGF)POF3-317
|c POF3-317
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
700 1 _ |a Jankowski, Vera
|b 1
700 1 _ |a Ohl, Kim
|b 2
700 1 _ |a Hermann, Juliane
|b 3
700 1 _ |a Hermert, Daniela
|b 4
700 1 _ |a Tenbrock, Klaus
|b 5
700 1 _ |a Liu, Xiyang
|b 6
700 1 _ |a Martin, Ina V
|b 7
700 1 _ |a Wang, Jialin
|b 8
700 1 _ |a Groll, Fabian
|b 9
700 1 _ |a Gröne, Elisabeth
|0 P:(DE-He78)b72c4ee15f75cf6944080c339a34475b
|b 10
|u dkfz
700 1 _ |a Floege, Jürgen
|b 11
700 1 _ |a Ostendorf, Tammo
|b 12
700 1 _ |a Rauen, Thomas
|b 13
700 1 _ |a Raffetseder, Ute
|b 14
773 _ _ |a 10.1016/j.kint.2019.09.031
|g p. S0085253819310397
|0 PERI:(DE-600)2007940-0
|n 2
|p 289-303
|t Kidney international
|v 97
|y 2020
|x 0085-2538
909 C O |o oai:inrepo02.dkfz.de:148843
|p VDB
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 10
|6 P:(DE-He78)b72c4ee15f75cf6944080c339a34475b
913 1 _ |a DE-HGF
|l Krebsforschung
|1 G:(DE-HGF)POF3-310
|0 G:(DE-HGF)POF3-317
|2 G:(DE-HGF)POF3-300
|v Translational cancer research
|x 0
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF3
|b Gesundheit
914 1 _ |y 2020
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0310
|2 StatID
|b NCBI Molecular Biology Database
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
915 _ _ |a WoS
|0 StatID:(DE-HGF)0111
|2 StatID
|b Science Citation Index Expanded
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b KIDNEY INT SUPPL : 2017
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
915 _ _ |a WoS
|0 StatID:(DE-HGF)0110
|2 StatID
|b Science Citation Index
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1110
|2 StatID
|b Current Contents - Clinical Medicine
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b KIDNEY INT : 2017
915 _ _ |a IF < 5
|0 StatID:(DE-HGF)9900
|2 StatID
920 1 _ |0 I:(DE-He78)G130-20160331
|k G130
|l Zelluläre und Molekulare Pathologie
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-He78)G130-20160331
980 _ _ |a UNRESTRICTED


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21