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Description

L., Chapman, J

Proteinase 3 activity in sputum from subjects with alpha-1-antitrypsin deficiency and COPD

The mechanism appears to involve Gq-PLC-PKC-mediated reduction of Smad2/3 pS465/467 downstream of autocrine TGF-1, partially through NRF2-HO-1 oxidative stress quenching that removes the ROS second signal required for maximal Smad transcriptional co-activator activity