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. 2006 Dec 1;103(50):19004–19009. doi: 10.1073/pnas.0605170103

Fig. 2.

Fig. 2.

Direct interaction of SOX9 and RUNX2 through their DNA binding domains. (a) COS7 cells were transfected with 6xOSE2-luc reporter and expression plasmids for SOX9 and various RUNX2 deletion mutants. (b) COS7 cells were transfected with 6xOSE2-luc reporter and expression plasmids for SOX9 and a chimera construct RUNT-NFκB, which has the runt domain fused in framed with the NF-κB transactivation domain. (c) GST pull-down assays with 35S-labeled various SOX9 mutants as shown in Upper and purified GST-RUNT fusion protein. (d) EMSA were performed with a labeled Col10a1 probe containing a functional RUNX2 binding site previously described (15) and in vitro translated proteins as listed. The upper arrows indicate the RUNX2/DNA probe complex, and the lower arrow depicts the free unbound probe. Lane 1, empty pcDNA3.1 vector; lane 2, RUNX2 and empty pcDNA3.1 vector; lane 3, RUNX2 and control β-galactosidase; lane 4, RUNX2 and full-length SOX9; lane 5, full-length SOX9 and empty pcDNA vector; lane 6, RUNX2 and empty pcDNA3.1 vector; lane 7, RUNX2 and SOX9-N; lane 8, RUNX2 and SOX9-C.