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. 2021 May 7;11:9803. doi: 10.1038/s41598-021-89379-x

Figure 1.

Figure 1

ACE2 is targeted by γS after ectodomain shedding. (A) Schematic and scaled representation of γS targets JAGGED1 or NOTCH1, with ACE2, ACE2-C9 and ACE2-GFP. Domains and regions targeted by sheddases are depicted. Predicted molecular weight of ACE2ΔE after TMPRSS2/ADAM17-mediated cleavage is shown. (B) Western blots from 293 T cells transfected with ACE2-C9 with or without TMPRSS2, then treated with DBZ (dibenzazepine 100 nM) ( +), or DMSO (−). Mobility consistent with full length (FL) and ACE2 lacking its ectodomain (ACE2ΔE) indicated. ACE2ΔE generated in the absence of TMPRSS2 has a higher molecular weight, which corresponds to ADAM17-mediated shedding. (C) Western blots from 293 T cells transfected with ACE2-C9 with or without PMA (200 nM, 15 h) treatment. (D) Western blots from 293 T cells transfected with ACE-C9, with or without TMPRSS2, or treated with PMA, with or without two γS inhibitors [DBZ (dibenzazepine, 100 nM) or CmpE (compound E, 40 nM)]. (E) Western blots from 293 T cells transfected with ACE2-GFP, with or without TMPRSS2, then treated with DBZ and/or MG132 (1 µM, 15 h). (F) Western blots from 293 T cells transfected with ACE2-GFP, with or without PMA, DBZ and/or MG132. (G) Western blots from immunoprecipitates derived from 293 T cells transfected with ACE2-C9, with or without TMPRSS2, then treated with DBZ. Data is representative of 2–3 independent experiments.