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Fig. 7 | Cellular & Molecular Biology Letters

Fig. 7

From: The low-complexity domains of the KMT2D protein regulate histone monomethylation transcription to facilitate pancreatic cancer progression

Fig. 7

a Nude mice bearing established PANC1 xenograft tumors, including the vehicle group and sgRNA A1 × B2 group. After 2 weeks, tumor formation was monitored for a further 3 weeks. Interestingly, we could not detect tumor formation for PANC1 cells modified with LCD1 knockout, while the vehicle group could form tumors (red circle). b The proposed mechanistic model of for KMT2D LCDs in gene transcription. The knockout of KMT2D LCDs results in a loss of ability to form a stable LLPS microenvironment. The stability of WDR5 protein significantly decreased, and the protein–protein interactions between the components involved in the KMT2D–enzyme complex were attenuated. Some transcription factors, such as LIFR and KLF4, were markedly downregulated, attributed to the decrease in the H3K4me1 level. The left panel indicates the mechanism for full-length KMT2D, while the right panel indicates the mechanism for knocked out KMT2D LCDs

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