Extracellular potassium deprivation reversibly dephosphorylates cofilin

Cofilin is essential for actin filament remodeling in various cell types. We previously reported that ouabain leads to dephosphorylation of cofilin, resulting in cytoskeletal reorganization and cell volume change. We report here that the extracellular [K +] e deprivation causes dephosphorylation of...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2006-07, Vol.345 (4), p.1393-1397
Main Authors: Jung, Jaehoon, Park, Heejin, Kim, Moonhee, Kim, Min-Jeong, Choi, Eung Chil, Lee, Kyunglim
Format: Article
Language:English
Subjects:
[K +] e (extracellular potassium concentration)
Actin Depolymerizing Factors - metabolism
Animals
Cell Size - drug effects
Cell volume
Cofilin
Cytoskeleton
Cytoskeleton - drug effects
Cytoskeleton - metabolism
Dose-Response Relationship, Drug
Mice
NIH 3T3 Cells
Phosphorylation
Phosphorylation - drug effects
Potassium - pharmacology
Time Factors
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Summary:Cofilin is essential for actin filament remodeling in various cell types. We previously reported that ouabain leads to dephosphorylation of cofilin, resulting in cytoskeletal reorganization and cell volume change. We report here that the extracellular [K +] e deprivation causes dephosphorylation of cofilin with disruption of cytoskeletal structures and cell shrinkage. These changes can be reversed by time-dependent restoration of [K +] e. Thus, these results suggest that the acute shift of [K +] e triggers a reversible change of cofilin phosphorylation which may be an essential event in the regulation of cytoskeletal architecture and cell volume.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2006.05.028