Figure 5.
RAs are formed at FCLs. (A) U2Os-AP2-ITGB5-mScarlet cells plated on glass were treated with Cilengitide (10 µM) for 15 min, washed twice with fresh medium, and imaged live using TIRF microscopy at two frames per minute. Representative frames showing the growth of an RA from an FCL. (B) Analysis of AP2 and integrin αvβ5 (ITGB5) intensity over time. Left: FCL and αvβ5 clustering during RA assembly (n = 16 events). In this graph, time zero is defined as the arrival of the AP2 signal Right: ITGB5 clusters not stabilized by FCLs disassemble and are removed from the membrane by CME-mediated disassembly (n = 24 events). In this graph, time zero is defined as the disappearance of the ITGB5 signal. Events have been collected from four 1-h long time-lapse acquisitions. Mean ± SEM. (C) A schematic illustration of the results is shown in this figure. Scale bar, 5 µm.

RAs are formed at FCLs. (A) U2Os-AP2-ITGB5-mScarlet cells plated on glass were treated with Cilengitide (10 µM) for 15 min, washed twice with fresh medium, and imaged live using TIRF microscopy at two frames per minute. Representative frames showing the growth of an RA from an FCL. (B) Analysis of AP2 and integrin αvβ5 (ITGB5) intensity over time. Left: FCL and αvβ5 clustering during RA assembly (n = 16 events). In this graph, time zero is defined as the arrival of the AP2 signal Right: ITGB5 clusters not stabilized by FCLs disassemble and are removed from the membrane by CME-mediated disassembly (n = 24 events). In this graph, time zero is defined as the disappearance of the ITGB5 signal. Events have been collected from four 1-h long time-lapse acquisitions. Mean ± SEM. (C) A schematic illustration of the results is shown in this figure. Scale bar, 5 µm.

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