Fig 4. Deletion of the N-terminal domain of MYSM1 upregulates H2AK119ub, promoting the inflammatory response.

(A) Schematic representation of the LPS-induced secondary infection cell model of sepsis usingPMsderived from WT and MYSM1ex2-Δ/Δ mice; Fig 4A: Citation to Use: Created in BioRender. An, Q. (2026) https://BioRender.com/lq1wp3y. (B, C, D) In the LPS-induced secondary infection model of sepsis usingPMsderived from WT and MYSM1ex2-Δ/Δ mice, IL-6 protein levels in the cell supernatant were detected by ELISA, and IL-6 and IL-1β mRNA expression levels in cell extracts were measured by RT-PCR. (E, F) Before inducing the secondary infection model of sepsis usingPMsderived from WT and MYSM1ex2-Δ/Δ mice with LPS,PMswere pretreated with 10 μM PRT4165 for 4 hours. The expression of IL-6 mRNA in the cell pellet was detected by RT-PCR, and the level of IL-6 protein in the cell supernatant was measured by ELISA. All experiments were repeated at least 3 times with similar results. The data are expressed as means ± SDs. Statistical analysis was performed using two-way ANOVA followed by Tukey’s multiple comparisons test (B, C, D, E, F). Data were considered statistically significant when *p ≤ 0.05, **p ≤ 0.01,***p ≤ 0.001, and ****p ≤ 0.0001. https://doi.org/10.6084/m9.figshare.30581501.