14-3-3epsilon inhibits MK5-mediated cell migration by disrupting F-actin polymerization
Copyright policy )14-3-3epsilon inhibits MK5-mediated cell migration by disrupting F-actin polymerization
The signal pathway by which 14-3-3epsilon inhibits cell migration induced by MAPK-activated protein kinase 5 (MK5) was investigated in cultured HeLa cells. Both in vivo and in vitro analyses have revealed that 14-3-3epsilon interacts with MK5. 14-3-3epsilon bound to MK5 inhibits the phosphorylation of HSP27, a known substrate of MK5. Disturbance of actin cytoskeleton organization by 14-3-3epsilon was shown in transfected cells transiently expressing 14-3-3epsilon as well as established cells stably expressing 14-3-3epsilon. Moreover, overexpression of 14-3-3epsilon resulted in the inhibition of cell migration induced by MK5 overexpression or TNFalpha treatment. Our results suggest that 14-3-3epsilon bound to MK5 inhibits cell migration by inhibiting the phosphorylation of HSP27 whose phosphorylation regulates F-actin polymerization, actin cytoskeleton organization and subsequent actinfilament dynamics.
- Chonnam National University Korea (Republic of)
- Korean Association Of Science and Technology Studies Korea (Republic of)
- Korea Advanced Institute of Science and Technology Korea (Republic of)
- Chung-Ang University Korea (Republic of)
Tumor Necrosis Factor-alpha, HSP27 Heat-Shock Proteins, Intracellular Signaling Peptides and Proteins, Protein Serine-Threonine Kinases, Models, Biological, Actins, Neoplasm Proteins, 14-3-3 Proteins, Cell Movement, Humans, Phosphorylation, Cytoskeleton, Heat-Shock Proteins, HeLa Cells, Molecular Chaperones, Protein Binding
Tumor Necrosis Factor-alpha, HSP27 Heat-Shock Proteins, Intracellular Signaling Peptides and Proteins, Protein Serine-Threonine Kinases, Models, Biological, Actins, Neoplasm Proteins, 14-3-3 Proteins, Cell Movement, Humans, Phosphorylation, Cytoskeleton, Heat-Shock Proteins, HeLa Cells, Molecular Chaperones, Protein Binding
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).68 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Top 10% influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 10% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 10%
Citations provided by BIP!Popularity provided by BIP!