000157169 001__ 157169
000157169 005__ 20240229123131.0
000157169 0247_ $$2doi$$a10.1101/gad.338681.120
000157169 0247_ $$2pmid$$apmid:32675324
000157169 0247_ $$2ISSN$$a0890-9369
000157169 0247_ $$2ISSN$$a1549-5477
000157169 0247_ $$2altmetric$$aaltmetric:86036113
000157169 037__ $$aDKFZ-2020-01449
000157169 041__ $$aeng
000157169 082__ $$a570
000157169 1001_ $$00000-0001-5710-9590$$aSzulzewsky, Frank$$b0
000157169 245__ $$aComparison of tumor-associated YAP1 fusions identifies a recurrent set of functions critical for oncogenesis.
000157169 260__ $$aCold Spring Harbor, NY$$bLaboratory Press$$c2020
000157169 3367_ $$2DRIVER$$aarticle
000157169 3367_ $$2DataCite$$aOutput Types/Journal article
000157169 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1597321162_16052
000157169 3367_ $$2BibTeX$$aARTICLE
000157169 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000157169 3367_ $$00$$2EndNote$$aJournal Article
000157169 500__ $$aVolume 34, Issue 15-16, 1 August 2020, Pages 1051-1064
000157169 520__ $$aYAP1 is a transcriptional coactivator and the principal effector of the Hippo signaling pathway, which is causally implicated in human cancer. Several YAP1 gene fusions have been identified in various human cancers and identifying the essential components of this family of gene fusions has significant therapeutic value. Here, we show that the YAP1 gene fusions YAP1-MAMLD1, YAP1-FAM118B, YAP1-TFE3, and YAP1-SS18 are oncogenic in mice. Using reporter assays, RNA-seq, ChIP-seq, and loss-of-function mutations, we can show that all of these YAP1 fusion proteins exert TEAD-dependent YAP activity, while some also exert activity of the C'-terminal fusion partner. The YAP activity of the different YAP1 fusions is resistant to negative Hippo pathway regulation due to constitutive nuclear localization and resistance to degradation of the YAP1 fusion proteins. Genetic disruption of the TEAD-binding domain of these oncogenic YAP1 fusions is sufficient to inhibit tumor formation in vivo, while pharmacological inhibition of the YAP1-TEAD interaction inhibits the growth of YAP1 fusion-expressing cell lines in vitro. These results highlight TEAD-dependent YAP activity found in these gene fusions as critical for oncogenesis and implicate these YAP functions as potential therapeutic targets in YAP1 fusion-positive tumors.
000157169 536__ $$0G:(DE-HGF)POF3-312$$a312 - Functional and structural genomics (POF3-312)$$cPOF3-312$$fPOF III$$x0
000157169 588__ $$aDataset connected to CrossRef, PubMed,
000157169 7001_ $$00000-0002-6661-3024$$aArora, Sonali$$b1
000157169 7001_ $$00000-0003-3672-5575$$aHoellerbauer, Pia$$b2
000157169 7001_ $$aKing, Claire$$b3
000157169 7001_ $$aNathan, Erica$$b4
000157169 7001_ $$aChan, Marina$$b5
000157169 7001_ $$aCimino, Patrick J$$b6
000157169 7001_ $$aOzawa, Tatsuya$$b7
000157169 7001_ $$0P:(DE-He78)0ac2bd1a9fb1823a351ee4434d80808b$$aKawauchi, Daisuke$$b8$$udkfz
000157169 7001_ $$0P:(DE-He78)a7c1bbac024fa232d9c6b78443328d9d$$aPajtler, Kristian W$$b9$$udkfz
000157169 7001_ $$aGilbertson, Richard J$$b10
000157169 7001_ $$aPaddison, Patrick J$$b11
000157169 7001_ $$00000-0002-6730-0281$$aVasioukhin, Valeri$$b12
000157169 7001_ $$aGujral, Taranjit S$$b13
000157169 7001_ $$00000-0002-3792-7120$$aHolland, Eric C$$b14
000157169 773__ $$0PERI:(DE-600)1467414-2$$a10.1101/gad.338681.120$$gp. genesdev;gad.338681.120v1$$n15-16$$p 1051-1064$$tGenes & development$$v34$$x1549-5477$$y2020
000157169 909CO $$ooai:inrepo02.dkfz.de:157169$$pVDB
000157169 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)0ac2bd1a9fb1823a351ee4434d80808b$$aDeutsches Krebsforschungszentrum$$b8$$kDKFZ
000157169 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)a7c1bbac024fa232d9c6b78443328d9d$$aDeutsches Krebsforschungszentrum$$b9$$kDKFZ
000157169 9131_ $$0G:(DE-HGF)POF3-312$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vFunctional and structural genomics$$x0
000157169 9141_ $$y2020
000157169 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bGENE DEV : 2018$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2020-01-10
000157169 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bGENE DEV : 2018$$d2020-01-10
000157169 9201_ $$0I:(DE-He78)B062-20160331$$kB062$$lB062 Pädiatrische Neuroonkologie$$x0
000157169 980__ $$ajournal
000157169 980__ $$aVDB
000157169 980__ $$aI:(DE-He78)B062-20160331
000157169 980__ $$aUNRESTRICTED