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. 2022 Sep 18;9(31):2202855. doi: 10.1002/advs.202202855

Figure 7.

Figure 7

Gained LLPS of fusion oncoproteins drive oncogenes overactivation. The structural features of the two typical fusion oncoprotein EWS‐FLI1 and NUP98‐HOXA9 are shown on the left. Both oncoproteins are endowed with LLPS and transcription regulatory element binding ability. A) In Ewing sarcoma (EWS), EWS‐FLI1 establishes condensates at tumor‐specific GGAA repeat microsatellites and specifically recruit BRG1/BRM‐associated factor (BAF) complexes for oncogenes transcription. B) In leukemia, NUP98‐HOXA9 occupies chromatin and forms SEs‐like condensates which promotes leukemogenesis. EWSR1, EWS RNA binding protein 1; FLI1, friend leukemia virus integration site 1; NUP98, Nucleoporin 98 kDa; HOXA9, Homeobox A9; DHR, degenerate hexapeptide repeat; RBD, RNA binding domain; AD, activation domain; DBD, DNA‐binding domain.