Fig. 6: GIT1-regulated Beclin1 phosphorylation at the Thr119 residue. | Cell Death & Disease

Fig. 6: GIT1-regulated Beclin1 phosphorylation at the Thr119 residue.

From: GIT1 contributes to autophagy in osteoclast through disruption of the binding of Beclin1 and Bcl2 under starvation condition

Fig. 6

a Representative immunoblot images showing the effect of GIT1 knockdown on the expression of p-mTOR/mTOR, p-ULK1/ULK1, p-Beclin1-S15/Beclin1, and p-Beclin1-T119/Beclin1 in the OCs under basal and starvation conditions. b Representative immunoblot images showing the effect of GIT1 overexpression on the expression of p-mTOR/mTOR, p-ULK1/ULK1, p-Beclin1-S15/Beclin1, and p-Beclin1-T119/Beclin1 in HEK293T cells under basal and starvation conditions. c-f Densitometric analysis showed the relative amounts of p-mTOR/mTOR (c), p-ULK1/ULK1 (d), p-Beclin1-S15/Beclin1 (e), and p-Beclin1-T119/Beclin1 (f) in GIT1 knockdown or GIT1-overexpressing cells compared with the relative controls under basal and starvation conditions (**p < 0.01, ns indicates no significance, Kruskal–Wallis test)

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