Fig. 2: SWI/SNF complex associates with chromatin architecture via BRG1-RAD21 axis.

A-C. Endogenous co-IP assay with anti-ARID1A, CTCF, and RAD21 antibodies was performed in ARID1A WT and KO AB17 A, MEF cells (193-4), B and human HCC MHCC-97H cells C, and then blotting assay detected with the indicated antibodies. D Validation for the interaction between ARID1A/BRG1 and architectural elements CTCF/RAD21 in human liver cancer cell lines MHCC-97H, SK-HEP-1 and HepG2. E HEK293T cells transfected with the indicated constructs were subjected to co-IP assay with anti-T7 and -HA antibodies to verify the interaction between ARID1A and CTCF (Top) or RAD21 (Bottom). F The same as E but for detecting the interaction between BRG1 and CTCF (Top) or RAD21 (Bottom) with anti-Flag and -HA antibodies. G Validation for the interaction between BRG1 and RAD21 by co-IP assay in Flag-tagged BRG1-transfected HEK293T cells. H Glutathione S-transferase (GST) pull-down experiments using GST-RAD21 protein and in vitro translated BRG1 protein. BRG1 protein binding to GST or GST-RAD21 was detected by the anti-BRG1 antibody. I Immunofluorescent staining showing the colocalization of both BRG1 (green) and RAD21 (red) in mouse AB17, MEF cells (193-4), as well as human liver cancer MHCC-97H and SK-HEP-1 cells (Scale bar, 5 µm). J The ChIP-seq peaks of Ctcf, Rad21, Arid1a, and Brg1 were extensively overlapped in the genome distribution.