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. 2014 May 8;111(21):7723–7728. doi: 10.1073/pnas.1318761111

Fig. 4.

Fig. 4.

Adam17 polymorphic variants differentially regulate canonical TGFβ-SMAD signaling output. (A) Position of C57 amino acid substitutions within the ADAM17 protein. (B) Evolutionary conservation of ADAM17 amino acid residues 113 and 594/613 from chick to human. (C) TGFβ1/Smad2/3-mediated transcriptional responses of NIH 3T3 fibroblasts transfected with expression vectors encoding NIH.Adam17, Adam17Asp113Asn, Adam17Ileu613Val, or C57.Adam17 Asp113Asn,Ileu613Val. Cells were transfected with the indicated Adam17 expression constructs together with a Smad2/3-responsive pCAGA-luciferase construct. Note that exogenous ADAM17 expression was in vast excess to that of endogenous NIH 3T3 ADAM17 (Fig. S2). Activation of luciferase was assayed 24 h after addition, or not, of 1 ng/mL TGFβ. *P ≤ 0.05, **P ≤ 0.01. Each experiment was independently reproduced three times with three technical replicates within each experiment.