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Figure 1

From: LAP degradation product reflects plasma kallikrein-dependent TGF-β activation in patients with hepatic fibrosis

Figure 1

Determination of the LAP cleavage site produced during PLK-dependent TGF-β activation. (a) Schematic depiction of latent TGF-β1 activation by PLK. PLK cleaves LAP between R58 and L59 residues, which may destroy the interaction between LAP and active TGF-β1 molecule, releasing active TGF-β1 from the latent complex. LLC; large latent complex, SLC; small latent complex, LTBP; latent TGF-β binding protein. (b) The PLK cleavage site was determined by amino acid sequencing of LAP-DP isolated after SDS-PAGE. The amino acid sequences around the PLK cleavage site are illustrated. Antibodies (Ab), which specifically recognize cutting edges of LAP-DPs, were produced. White “Y” represents R58 antibody recognizing the N-terminal side R58 LAP-DP, whereas black “Y” represents L59 antibody recognizing the C-terminal side L59 LAP-DP.

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