Journal: Aging Cell
Article Title: Clearance of Senescent Cells by BCL XL ‐ PROTAC : A Novel Approach to Treat COPD ?
doi: 10.1111/acel.70487
Figure Lengend Snippet: BCL XL ‐PROTAC induces potent proteasomal degradation of BCL XL protein in human SAECs and shows high selectivity over BCL 2 degradation. Healthy small airway epithelial cells were treated with 10 −12 to 10 −4 M of BCL XL ‐PROTAC for 24 h. (a) BCL XL degradation by BCL XL ‐PROTAC via CRBN binder and MG132. (b) Protein levels of BCL XL and BCL 2 were measured in the cell lysates and the percentage of degradation, and the half maximal degradation concentration (DC 50 ) were calculated. (c) Cells were treated with BCL XL ‐PROTAC and 3 μM of the proteasome inhibitor MG132 or with a CRBN binder to compete with the E3 ligase binding. BCL XL degradation was measured in cell lysates and expressed as percentage of degradation and DC 50 . Plotted data are represented as mean +/− standard deviation of 3 independent experiments, each with 2 technical duplicates. 0% degradation indicate levels detected in vehicle/DMSO‐treated cells, and 100% degradation indicate no detectable BCL XL protein (= medium control).
Article Snippet: Primary small airway epithelial cells (SAEC) were cultured as monolayers in Small Airway Epithelial Cell Growth Medium (Promocell, Germany) on collagen (1% w/v) coated plates (Devulder et al. ).
Techniques: Concentration Assay, Binding Assay, Standard Deviation, Control