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. 2006 Jun 5;173(5):781–793. doi: 10.1083/jcb.200601059

Figure 7.

Figure 7.

V12Rac1 restores the lactation defect observed in β1 integrin–null acini. (A) MECs from Itgβ1fx/fx mice were left untreated or were infected in monolayer with Cre-expressing adenovirus (Ad-CreM1) for 24 h and examined for β1 integrin by immunoblotting. (B) Cells treated as in A were reinfected with Ad–β-galactosidase (lanes 3 and 6) or Ad-mycV12Rac1 (lanes 4 and 7) in suspension for 1 h and were replated onto BM matrix for 24 h. 3D acini were untreated or stimulated with Prl for 24 h and analyzed for β-casein synthesis by immunoblotting. (C) Rac activity in 3D acini on BM matrix either uninfected or infected with Ad–β-galactosidase or Ad-CreM1. Rac activity was almost abolished in β1 integrin–null acini.