001     304085
005     20250831022504.0
024 7 _ |a 10.26508/lsa.202503295
|2 doi
024 7 _ |a pmid:40846632
|2 pmid
024 7 _ |a altmetric:180591984
|2 altmetric
037 _ _ |a DKFZ-2025-01753
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Haas, Alexander
|b 0
245 _ _ |a Wnt10b signaling regulates replication stress-induced chromosomal instability in human cancer.
260 _ _ |a Heidelberg
|c 2025
|b EMBO Press
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 1756290964_16146
|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 Wnt signaling pathways are involved in various developmental and tissue maintenance functions, whereas deregulated Wnt signaling is closely linked to human cancer. Recent work revealed that loss of Wnt signaling impairs mitosis and causes abnormal microtubule growth at the mitotic spindle resulting in chromosome missegregation and aneuploidy, both of which are hallmarks of cancer cells exhibiting chromosomal instability (CIN). Here, we show that upon DNA replication stress, a condition typically associated with CIN, Wnt10b acts to prevent increased microtubule dynamics from the S phase until mitosis, thereby ensuring faithful chromosome segregation. Interestingly, replication stress-induced chromosomal breaks are also efficiently suppressed by Wnt10b. Thus, our results show that Wnt10b signaling regulates replication stress-induced chromosome missegregation and breakage, and hence is a determinant for broad genome instability in cancer cells.
536 _ _ |a 312 - Funktionelle und strukturelle Genomforschung (POF4-312)
|0 G:(DE-HGF)POF4-312
|c POF4-312
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: inrepo02.dkfz.de
650 _ 7 |a Wnt Proteins
|2 NLM Chemicals
650 _ 7 |a WNT10B protein, human
|2 NLM Chemicals
650 _ 7 |a Proto-Oncogene Proteins
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Chromosomal Instability: genetics
|2 MeSH
650 _ 2 |a DNA Replication: genetics
|2 MeSH
650 _ 2 |a Neoplasms: genetics
|2 MeSH
650 _ 2 |a Neoplasms: metabolism
|2 MeSH
650 _ 2 |a Wnt Proteins: metabolism
|2 MeSH
650 _ 2 |a Wnt Proteins: genetics
|2 MeSH
650 _ 2 |a Mitosis: genetics
|2 MeSH
650 _ 2 |a Cell Line, Tumor
|2 MeSH
650 _ 2 |a Chromosome Segregation: genetics
|2 MeSH
650 _ 2 |a Wnt Signaling Pathway: genetics
|2 MeSH
650 _ 2 |a Microtubules: metabolism
|2 MeSH
650 _ 2 |a Genomic Instability
|2 MeSH
650 _ 2 |a Signal Transduction
|2 MeSH
650 _ 2 |a Proto-Oncogene Proteins
|2 MeSH
700 1 _ |a Wenz, Friederike
|0 0009-0003-0114-2772
|b 1
700 1 _ |a Hattemer, Janina
|b 2
700 1 _ |a Wesslowski, Janine
|0 0000-0003-3674-1372
|b 3
700 1 _ |a Davidson, Gary
|0 0000-0002-2264-5518
|b 4
700 1 _ |a Voloshanenko, Oksana
|0 P:(DE-He78)ad64f12d9ccfe830ecddc2fe9635c569
|b 5
|u dkfz
700 1 _ |a Boutros, Michael
|0 P:(DE-He78)3c0da8e3caa2aa50cad85152aa0465ad
|b 6
|u dkfz
700 1 _ |a Acebron, Sergio P
|b 7
700 1 _ |a Bastians, Holger
|0 0000-0001-7915-3648
|b 8
773 _ _ |a 10.26508/lsa.202503295
|g Vol. 8, no. 11, p. e202503295 -
|0 PERI:(DE-600)2948687-7
|n 11
|p e202503295
|t Life science alliance
|v 8
|y 2025
|x 2575-1077
909 C O |p VDB
|o oai:inrepo02.dkfz.de:304085
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 5
|6 P:(DE-He78)ad64f12d9ccfe830ecddc2fe9635c569
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 6
|6 P:(DE-He78)3c0da8e3caa2aa50cad85152aa0465ad
913 1 _ |a DE-HGF
|b Gesundheit
|l Krebsforschung
|1 G:(DE-HGF)POF4-310
|0 G:(DE-HGF)POF4-312
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Funktionelle und strukturelle Genomforschung
|x 0
914 1 _ |y 2025
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b LIFE SCI ALLIANCE : 2022
|d 2024-12-10
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2024-12-10
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2024-12-10
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2022-02-08T19:01:09Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2022-02-08T19:01:09Z
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b DOAJ : Anonymous peer review
|d 2022-02-08T19:01:09Z
915 _ _ |a Creative Commons Attribution CC BY (No Version)
|0 LIC:(DE-HGF)CCBYNV
|2 V:(DE-HGF)
|b DOAJ
|d 2022-02-08T19:01:09Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2024-12-10
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2024-12-10
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2024-12-10
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2024-12-10
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2024-12-10
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2024-12-10
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2024-12-10
915 _ _ |a IF < 5
|0 StatID:(DE-HGF)9900
|2 StatID
|d 2024-12-10
915 _ _ |a Article Processing Charges
|0 StatID:(DE-HGF)0561
|2 StatID
|d 2024-12-10
915 _ _ |a Fees
|0 StatID:(DE-HGF)0700
|2 StatID
|d 2024-12-10
920 1 _ |0 I:(DE-He78)B110-20160331
|k B110
|l B110 Signalwege funktionelle Genomik
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-He78)B110-20160331
980 _ _ |a UNRESTRICTED


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21