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Correction to: PRMT1-mediated H4R3me2a recruits SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling
Genome Medicine volume 13, Article number: 154 (2021)
Correction to: Genome Med 13, 58 (2021)
In this article  the incorrect figure was shown as Fig. 5 and the incorrect figure appeared in Additional File 1 as Fig. S7. The figures should have appeared as shown below. The original article has been updated.
Yao B, et al. PRMT1-mediated H4R3me2a recruits SMAR CA4 to promote colorectal cancer progression by enhancing EGFR signaling. Genome Med. 2021;13:58. https://doi.org/10.1186/s13073-021-00871-5.
Supplementary figures and related figure legends. Fig. S1. SMARCA4 binds specifically to histone H4R3me2a mark. Fig. S2. ITC assay to identify direct interactions between SMARCA4-F4 and H4, H4R3me2a, or H4R3me2s peptides. Fig. S3. Interation of SMARCA4 and PRMT1. Fig. S4. Identification of transcriptional targets for PRMT1 and SMARCA4 in HCT116 cells. Fig. S5. Characterization of ATAC-seq, along with ChIP-Seq of SMARCA4, H3K4me1, H3K4me3, H3K27ac in HCT116 cells. Fig. S6. PRMT1 and SMARCA4 cooperatively activate TNS4 and EGFR transcription in SW620 and HCT116 cells. Fig. S7. SMARCA4 couples with PRMT1 to promote CRC cell proliferation in SW620 and HCT116 cells. Fig. S8. AMI-1, a PRMT1 inhibitor, blocks HCT116 cell proliferation, and inhibits TNS4 and EGFR expression. Fig. S9. Combined treatment with AMI-1 and Cetuximab synergistically protects Apcmin/+ mice against DSS-induced CRC progression.
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Yao, B., Gui, T., Zeng, X. et al. Correction to: PRMT1-mediated H4R3me2a recruits SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling. Genome Med 13, 154 (2021). https://doi.org/10.1186/s13073-021-00966-z