Skip to main content
. 2007 Feb 22;26(5):1199–1210. doi: 10.1038/sj.emboj.7601576

Figure 2.

Figure 2

The C-terminal proline-rich region of Hip1R interacts with cortactin. (A) His-tagged Hip1R 1–1068; 346–1068 and 1–655 (400 nM) pull-down assays using GST and GST-cortactin (800 nM). Bound and unbound fractions were analyzed by Coomassie blue staining (upper panel), and by Western blotting using an anti-Hip1R antibody (lower panel). (B) His-tagged cortactin (400 nM) pull-down assays using GST and GST-Hip1R 1–312; 346–655; 766–1068 (10 μM). Bound and unbound fractions were analyzed by Coomassie blue staining (upper panel), and by Western blotting using an anti-cortactin antibody (lower panel). (C) His-tagged Hip1R 1–1017 (400 nM) pull-down assays using GST, GST-cortactin (1–546) and GST-SH3-cortactin (491–546) (800 nM). Bound and unbound fractions were analyzed by Western blotting using an anti-His tag antibody (upper panel) and by Coomassie blue staining (middle panel). The same experiment was carried out in parallel with His-tagged Hip1R 1–1068 (full length) as a positive control, bound and unbound fractions were analyzed by Western blotting using an anti-His tag antibody (lower panel). (D) Summary of the binding assay results. All experiments were performed three times with similar results.

HHS Vulnerability Disclosure