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000144769 1001_ $$0P:(DE-He78)a7c1bbac024fa232d9c6b78443328d9d$$aPajtler, Kristian$$b0$$eFirst author
000144769 245__ $$aYAP1 subgroup supratentorial ependymoma requires TEAD and nuclear factor I-mediated transcriptional programmes for tumorigenesis.
000144769 260__ $$a[London]$$bNature Publishing Group UK$$c2019
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000144769 520__ $$aYAP1 fusion-positive supratentorial ependymomas predominantly occur in infants, but the molecular mechanisms of oncogenesis are unknown. Here we show YAP1-MAMLD1 fusions are sufficient to drive malignant transformation in mice, and the resulting tumors share histo-molecular characteristics of human ependymomas. Nuclear localization of YAP1-MAMLD1 protein is mediated by MAMLD1 and independent of YAP1-Ser127 phosphorylation. Chromatin immunoprecipitation-sequencing analyses of human YAP1-MAMLD1-positive ependymoma reveal enrichment of NFI and TEAD transcription factor binding site motifs in YAP1-bound regulatory elements, suggesting a role for these transcription factors in YAP1-MAMLD1-driven tumorigenesis. Mutation of the TEAD binding site in the YAP1 fusion or repression of NFI targets prevents tumor induction in mice. Together, these results demonstrate that the YAP1-MAMLD1 fusion functions as an oncogenic driver of ependymoma through recruitment of TEADs and NFIs, indicating a rationale for preclinical studies to block the interaction between YAP1 fusions and NFI and TEAD transcription factors.
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000144769 7001_ $$aWei, Yiju$$b1
000144769 7001_ $$0P:(DE-He78)34b3639de467b2c700920d7cbc3d2110$$aOkonechnikov, Konstantin$$b2$$eFirst author
000144769 7001_ $$0P:(DE-HGF)0$$aSilva, Patricia B G$$b3$$eFirst author
000144769 7001_ $$0P:(DE-He78)7a849fbc18c1307faf2b3a4f84a62500$$aVouri, Mikaella$$b4
000144769 7001_ $$aZhang, Lei$$b5
000144769 7001_ $$0P:(DE-He78)b0b3740107f746e09dc23fdf25eb0629$$aBrabetz, Sebastian$$b6
000144769 7001_ $$0P:(DE-He78)a4101d4d75f0b7d1f24f67ccbe63164b$$aSieber, Laura$$b7
000144769 7001_ $$aGulley, Melissa$$b8
000144769 7001_ $$0P:(DE-He78)c865b84c0142dfa1def7dfeb70302918$$aMauermann, Monika$$b9
000144769 7001_ $$0P:(DE-He78)73c8cbd36c9b5a386838ad737a401dac$$aWedig, Tatjana$$b10
000144769 7001_ $$0P:(DE-He78)e73a0a4fab40344d89d693cbe1df3109$$aMack, Norman$$b11
000144769 7001_ $$aImamura Kawasawa, Yuka$$b12
000144769 7001_ $$0P:(DE-He78)36e1ec4777d5b7887344177dca41eae9$$aSharma, Tanvi$$b13
000144769 7001_ $$0P:(DE-He78)2a8fbc2efe7e5e468472d57f724fe39b$$aZuckermann, Marc$$b14
000144769 7001_ $$aAndreiuolo, Felipe$$b15
000144769 7001_ $$00000-0002-3792-7120$$aHolland, Eric$$b16
000144769 7001_ $$0P:(DE-He78)5100059e746b377e2e0a37c0e24f6bf7$$aMaass, Kendra$$b17
000144769 7001_ $$0P:(DE-He78)0e2afbe79bacc08410665f049d5208fa$$aKörkel-Qu, Huiqin$$b18
000144769 7001_ $$0P:(DE-He78)76aeb2431f7458c9261e69c5420390c6$$aLiu, Hai-Kun$$b19
000144769 7001_ $$0P:(DE-He78)a1f4b408b9155beb2a8f7cba4d04fe88$$aSahm, Felix$$b20
000144769 7001_ $$0P:(DE-He78)51bf9ae9cb5771b30c483e5597ef606c$$aCapper, David$$b21
000144769 7001_ $$00000-0003-0397-2019$$aBunt, Jens$$b22
000144769 7001_ $$00000-0002-7590-7390$$aRichards, Linda J$$b23
000144769 7001_ $$0P:(DE-He78)551bb92841f634070997aa168d818492$$aJones, David T W$$b24
000144769 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b25
000144769 7001_ $$0P:(DE-He78)082dd3179733e3e716a58eb90f418a78$$aChavez, Lukas$$b26
000144769 7001_ $$0P:(DE-He78)e13b4363c5fe858044ef8a39c02c870c$$aLichter, Peter$$b27
000144769 7001_ $$aHoshino, Mikio$$b28
000144769 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b29
000144769 7001_ $$0P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aKool, Marcel$$b30
000144769 7001_ $$aLi, Wei$$b31
000144769 7001_ $$0P:(DE-He78)0ac2bd1a9fb1823a351ee4434d80808b$$aKawauchi, Daisuke$$b32$$eLast author
000144769 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/s41467-019-11884-5$$gVol. 10, no. 1, p. 3914$$n1$$p3914$$tNature Communications$$v10$$x2041-1723$$y2019
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