Skip to main content
. 2017 Sep 18;8(65):108556–108570. doi: 10.18632/oncotarget.20998

Figure 4. PKCα phosphorylated Rab37 at T172 and inhibited GTP binging ability.

Figure 4

(A) PC-14 cells were transfected with various Rab37 phospho-mimetic D mutants followed by analysis of cell migration and invasion abilities (upper). The quantitative results were determined by two-tailed Student’s t-test (lower). Data represented mean ± SD. (n = 3). Original magnification: 100X. (B) Recombinant PKCα and purified WT or GST-tagged Rab37-T172A were used in an in vitro kinase assay in the presence or absence of Go6976. The phosphorylation signal of Rab37 was analyzed by immunoblotting. (C) PC-14 cells expressing HA-tagged WT or T172A mutant of Rab37 protein were treated with PMA. The lysates were collected for IP with anti-HA antibody and immunocomplexes were blotted for p-S/T proteins and HA-tagged Rab37. (D) Lysates from cell expressing various FLAG-tagged Rab37 mutants were subjected to GTP binding assay. (E). EV, WT or T172A mutant of HA-tagged Rab37 were transfected into PC-14 cells, the lysates were used for GTP binding assay following PMA treatment.