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. 2024 Nov 15;221(12):e20240959. doi: 10.1084/jem.20240959

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© 2024 Li et al.

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Figure 5. — MCRS1 upregulates MHC-I by interacting with YY1. (A) Identification of MCRS1-interacting proteins in mouse pancreatic cancer cells by IP-MS, with top hits shown (n = 1 for both groups). (B) STRING analysis of MCRS1-interacting proteins, with interaction detected between MCRS1 and YY1 and KAT8. (C) Expression of ISGs and MHC-I genes in Mcrs1^OX cells that were deficient in Yy1 or Kat8 by CRISPR-mediated gene knockout (n = 4, 3, 4, 4 for control, Mcrs1^OX, Mcrs1^OX;sgYy1, and Mcrs1^OX;sgKat8, respectively; presented as means ± SEM; ns, not significant, P ≥ 0.05; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; one-way ANOVA with Tukey’s multiple comparisons test; N = 2 independent experiments). (D) Increased MCRS1–YY1 interaction in Mcrs1^OX cells assessed by immunoprecipitation (N > 3 independent experiments). (E) De novo motif discovery of MCRS1-bound genomic regions, with the YY1 binding motif among the top enriched motifs. (F) Expression of ISGs and MHC-I genes in Yy1^OX cells (n = 3 for both groups; presented as means ± SEM; *, P < 0.05; **, P < 0.01; ****, P < 0.0001; two-tailed unpaired t test; N = 2 independent experiments). Source data are available for this figure: SourceData F5.