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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: A missense mutant of ocrl1 promotes apoptosis of tubular epithelial cells and disrupts endocytosis and the cell cycle of podocytes in Dent-2 Disease

Fig. 2

Knockdown of ocrl1 and overexpression of the ocrl1 mutant induced reactive oxygen species (ROS) production and apoptosis in HK-2 cells. A, HK-2 cells were transfected as indicated. The protein level of ocrl1 was determined by Western blot analysis (n = 3). B, Confocal microscopy demonstrated that the ocrl1 protein is primarily localized in the cytoplasm of HK-2 cells. C, Confocal microscopy showed that knockdown of ocrl1 and overexpression of ocrl1 mutant did not affect the cytoskeleton. D–G, Flow cytometry was conducted to assess ROS levels (D, E) and cell apoptosis (F, G) in HK-2 cells. Data were expressed as the mean ± standard error of the mean (SEM). *P < 0.05, †P < 0.01 vs. control; n = 3. si-ocrl1, siRNA targeting ocrl1; H318, adenoviral vectors overexpressing ocrl1 mutant

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