Frank S Ong

TL;DR: Knowing the structural differences between the two ACE domains should allow clinicians to envision new therapies for diseases not currently treated with ACE inhibitors, and these reagents will undoubtedly be powerful tools for probing the physiologic actions of each ACE domain.

TL;DR: The current commonly used predictive pharmacogenetic biomarkers in clinical oncology molecular testing are discussed, including BRAF V600E for vemurafenib in melanoma and ERBB2 (HER2/neu) for trastuzumab in breast cancer.

TL;DR: Knowing the in vivo role of each ACE domain has great significance for developing ACE domain-specific inhibitors and for understanding the full effects of the anti-ACE pharmaceuticals in widespread clinical use.

TL;DR: It is shown that the inactivation of the N-terminal catalytic site of ACE significantly reduced bleomycin-induced lung fibrosis and implicates AcSDKP in the mechanism of protection, which could suggest a possible means to increase tolerance toBleomycin and to treat fibrosing lung diseases.

TL;DR: It is suggested that ACE2 metabolizes ANG II in the kidney at neutral and basic pH, while PCP catalyzes the same reaction at acidic pH, the first report demonstrating that renal ANG-(1-7) formation from ANG II is independent of ACE2.