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. 2016 Apr 1;2(4):e1501290. doi: 10.1126/sciadv.1501290

Fig. 3. Nuclear TIE2 regulates DNA repair through a NHEJ mechanism.

Fig. 3

(A) γH2AX persistence in U251.EV, U251.Tie2, and U251.Tie2SS/AA cells in response to IR. (B) Formation of TIE2/DNA complexes in U251.Tie2 in response to IR, analyzed after DNA/protein cross-linking and protein elution from precipitated DNA. (C) γH2AX/TIE2 colocalization in HUVECs after IR treatment, as assessed by immunofluorescence and confocal microscopy. (D) TIE2 complexes in HUVECs in response to ANG1, ANG2, and IR stimuli. IP, immunoprecipitation; WCL, whole-cell lysate. (E) Increased NHEJ efficiency in TIE2-expressing cells. GFP, green fluorescent protein. (F) Increased recovery of NHEJ reporter plasmids in TIE2-expressing cells. (G) TIE2 silencing results in decreased NHEJ efficiency. (H) Silencing endogenous TIE2 in U87 MG cells results in decreased NHEJ efficiency. (I) NHEJ efficiency is jeopardized in cytoplasmic-sequestered TIE2. Data represent means ± SD; **P ≤ 0.01, ***P ≤ 0.001.