Skip to main content
. 2022 Apr 27;1(3):100028. doi: 10.1016/j.cellin.2022.100028

Fig. 5.

Fig. 5

Activation of α7 nAChR increases binding betweenThr180/Tyr182p-p38 MAPK and LMNB1. (A) ACH2 cells were treated with or without GTS-21 (40 μM) for 48 h, anti-p-p38 MAPK was used to capture the interaction proteins of p-p38 MAPK. (B) Liquid chromatography-tandem mass spectrometry (LC-MS/MS) analyze potential proteins interacting with p-p38 MAPK. The values in the table represent the number of non-specific peptides enriched. (C-E) The interaction between p-p38 MAPK and LMNB1 were confirmed in ACH2 and A549 cells. (C) Untreated or GTS-21 (40 μM) treated ACH2 cells were collected and pulled down interaction proteins by anti-p-p38 MAPK and anti- LMNB1 antibodies. The p-p38 MAPK and anti-LMNB1 were detected by western blotting. HIV-Luc/VSV-G pseudovirus infected A549 cells were untreated or treated with GTS-21 (40 μM) for 48 h, (D) cells were lysed and pulled down interaction proteins by anti-p-p38 MAPK8 and anti-LMNB1 antibodies, the p-p38 MAPK and anti-LMNB1 were detected by western blotting. (E) Cells were fixed and analyzed the intracellular co-localization of p-p38 MAPK and LMNB1 by immunofluorescence. Arrow heads indicate co-localization of p-p38 MAPK and LMNB1.