Matches in Nanopublications for { ?s ?p "To explore the role of caspase 3 on CSE-induced DNA damage, immunoblotting for caspase 3 and functional evaluation of caspase 3 activity was performed. Under control conditions, BEAS-2B cells produced the 32-kD caspase 3 precursor, and cigarette smoke significantly increased its steady state level in the cell (Figure 6A). In accord with the apoptosis data, cigarette smoke did not convert the precursor form of caspase 3 (32 kD) into the active form (18 kD or smaller fragments), whereas CPT did (Figure 6A)." ?g. }
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- _4 value "To explore the role of caspase 3 on CSE-induced DNA damage, immunoblotting for caspase 3 and functional evaluation of caspase 3 activity was performed. Under control conditions, BEAS-2B cells produced the 32-kD caspase 3 precursor, and cigarette smoke significantly increased its steady state level in the cell (Figure 6A). In accord with the apoptosis data, cigarette smoke did not convert the precursor form of caspase 3 (32 kD) into the active form (18 kD or smaller fragments), whereas CPT did (Figure 6A)." provenance.
- _3 value "To explore the role of caspase 3 on CSE-induced DNA damage, immunoblotting for caspase 3 and functional evaluation of caspase 3 activity was performed. Under control conditions, BEAS-2B cells produced the 32-kD caspase 3 precursor, and cigarette smoke significantly increased its steady state level in the cell (Figure 6A). In accord with the apoptosis data, cigarette smoke did not convert the precursor form of caspase 3 (32 kD) into the active form (18 kD or smaller fragments), whereas CPT did (Figure 6A)." provenance.