Key result
Treatment of mammalian cells with BDM for 1 minute rapidly de-localizes actin leading edge components including the Arp2/3 complex, WAVE, and VASP, blocking actin incorporation.
Population
Mammalian cell lines (Swiss3T3 and BS-C-1 cells), platelet nm-myosinII S1 fragment, and Listeria monocytogenes
Comparison
2,3-butanedione monoxime treatment vs Media control, cytochalasin D, blebbistatin, or…
Design
Preclinical
Authors
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BDM effects on motility should not be attributed to myosin II inhibition; challenges prior interpretations and leaves open actin-specific mechanisms in cell studies.
BDM treatment rapidly de-localizes actin leading edge components, explaining cellular effects previously misattributed to non-muscle myosin II inhibition.
Yarrow et al. (2003) studied this question. 2,3-Butanedione monoxime (BDM) vs. Media control or cytochalasin D was evaluated on Actin incorporation and localization of Arp3, VASP, and WAVE at the leading edge. Treatment of mammalian cells with BDM for 1 minute rapidly de-localizes actin leading edge components including the Arp2/3 complex, WAVE, and VASP, blocking actin incorporation.
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