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. 2017 May 18;8(26):43201–43217. doi: 10.18632/oncotarget.17970

Figure 5. RIP1 clusteres to SGs during NDV infection.

Figure 5

Figure 5

(A) Subcellular distribution of RIP1. HeLa cells were mock-infected or infected with NDV for 16 h. The subcellular distribution of RIP1 and NP were analyzed with immunostaining using anti-RIP1-N or anti-RIP1-C (green), and anti-NP (red). Nuclei were stained with DAPI (blue). Images were acquired by a META 510 confocal laser-scanning microscope (Zeiss). Merged images illustrate RIP1/NP/DAPI fluorescence. (B) RIP1 is not co-localized well with RIP3 either during NDV infection or by the treatment of necroptosis stimulators. HeLa cells were mock-infected, infected with NDV for 16 h, or treated with necroptosis stimulators TNF-α, Z-VAD-FMK, and AT406 (T+Z+A) for 10 h. The subcellular distribution of RIP1 and RIP3 were analyzed with immunostaining using anti-RIP1-N or anti-RIP1-C (green), and anti-RIP3 (red). Nuclei were stained with DAPI (blue). Merged images illustrate RIP1/RIP3/DAPI fluorescence. (C) RIP1 is co-localized with SG marker G3BP1 during NDV infection. HeLa cells were mock-infected or NDV-infected for 16 h. The subcellular distribution of RIP1 and G3BP1 were analyzed with immunostaining using anti-RIP1-N or anti-RIP1-C (green), and anti-G3BP1 (red). Nuclei were stained with DAPI (blue). Merged images illustrate RIP1/G3BP1/DAPI fluorescence.

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