Skip to main content
Fig. 6 | Cell Communication and Signaling

Fig. 6

From: Golgi tethering factor golgin-97 suppresses breast cancer cell invasiveness by modulating NF-κB activity

Fig. 6

The interaction of golgin-97 with Arl1 is not necessary for its function in the modulation of NF-κB activity. a Golgin-97 WT, but not the YA mutant, interacts with Arl1. HeLa cells expressing WT EGFP-golgin-97 or the YA mutant were extracted and subsequently immunoprecipitated as described in the Materials and Methods. Input (30 μg) and IP products were analyzed by western blot with anti-golgin-97, anti-Arl1 or anti-actin antibodies. b Representative images of the subcellular localization of Arl1 (red) and golgin-97 WT, YA, del-GRIP and del-C mutants (green) in HeLa cells. Schematic diagram presents the golgin-97 truncations and mutations used in this study. Scale bars, 10 μm. Asterisks indicate golgin-97-overexpressing cells. c Western blot analysis of IκBα expression in the WT golgin-97 or the YA mutant-rescued golgin-97-knockdown HeLa or MDA-MB-231 cells. Actin was used as the internal control. Quantitative results are presented as the means±SEM from three independent experiments. *p < 0.05

Back to article page