Key result
Cofilin relies on three distinct protein sites to sever actin and maintain cell viability.
Why the study?
The molecular mechanism underlying the filament-severing activity of cofilin and its essential role for cell viability were not fully understood.
Population
Deltacof1 yeast cells and mammalian cells
Comparison
Three mutants of porcine cofilin with differing severing activities
Design
Preclinical molecular and cellular study
Authors
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Cofilin accelerates subunit release over fragmentation in actin turnover; leaves open relevance to cardiac cytoskeletal dynamics.
The actin-severing activity of cofilin is essential for cell viability and is exerted by the co-operation of at least three distinct sites.
Moriyama et al. (2002) studied this question. Mutants of porcine cofilin was evaluated on Actin-severing activity and cell viability. The actin-severing activity of cofilin is essential for cell viability and is exerted by the co-operation of at least three distinct sites on the protein.
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