Fig. 2 | Communications Biology

Fig. 2

From: Bone morphogenetic protein signaling is required for RAD51-mediated maintenance of genome integrity in vascular endothelial cells

Fig. 2

DNA damage leads to a depletion of BMPR2 and RAD51. a Pulmonary microvascular endothelial cells (PMVECs) were treated with DNA damaging agent mitomycin C (MMC) or vehicle (H2O, Con) for 14 h followed by qRT-PCR analysis of BMPR2, BRCA1, and RAD51 mRNA relative to GAPDH mRNA (n = 3). b PMVECs were treated with MMC or vehicle (H2O, Con) for 14 h or 24 h, followed by immunoblot analysis of RAD51, BMPR2, and GAPDH (loading control). Representative image and the quantitation of three independent experiments are shown (n = 3). c RAD51, BMPR2, and GAPDH (loading control) protein amount in PMVECs treated with vehicle (H2O, Con) or MMC with or without proteasome inhibitor MG-132 were analyzed by immunoblot. Representative image and the quantitation of three independent experiments are shown (n = 3). Bars represent mean ± SEM from three different experiments per conditions in (a–c). *P < 0.05, **P < 0.01, and ***P < 0.001 versus respective control. Unpaired two-tail t-test was used in (a, b). One-way ANOVA followed by Tukey’s multiple comparisons test was used in (c)

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