These data reveal the significance of S2 and S3 interactions in substrate binding emphasizing the role for residue 67 in modulating both sites, providing a plausible explanation for the FheCL3 collagenolytic activity essential to host invasion. The unique specificity of FheCL3 could be exploited in the design of specific inhibitors selectively directed to specific infective stage parasite proteinases.
No takes yet. Share an insight, caveat, or question.
Corvo et al. (2013) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: