Disease relevance of CFL1

• Identification of cofilin, coronin, Rac and capZ in actin tails using a Listeria affinity approach [1].

High impact information on CFL1

• A core set of proteins including actin, Arp2/3 complex, profilin, capping protein, and ADF/cofilin can reconstitute the process in vitro, and mathematical models of the constituent reactions predict the rate of motion [2].
• After filaments have aged by hydrolysis of their bound ATP and dissociation of the gamma phosphate, ADF/cofilin proteins promote debranching and depolymerization [2].
• We investigated actin filament turnover rates, length, number, barbed end exposure, and binding of cofilin in bovine arterial endothelial cells moving at different speeds depending on their position in a confluent monolayer [3].
• Pretreatment of cultures with tautomycin, a protein phosphatase type 1 inhibitor, blocked the effect of cAMP on 1) the dephosphorylation of cofilin, 2) the decrease in RLC phosphorylation, and 3) the decrease in isometric tension [4].
• Activated cofilin correlates with increased F-actin severing activity in cell extracts from monolayers treated with forskolin/3-isobutyl-1-methylxanthine [4].

Biological context of CFL1

• This is consistent with cofilin activation being required for actin reorganization during exocytosis [5].
• Cofilin is one of the major actin depolymerizing proteins in eukaryotic cells and involved in many membrane modulating activities, such as cell growth and motility [5].

Anatomical context of CFL1

• Myosin phosphatase and cofilin mediate cAMP/cAMP-dependent protein kinase-induced decline in endothelial cell isometric tension and myosin II regulatory light chain phosphorylation [4].
• Cell components known to play a role in the actin-based motility of Listeria are VASP (vasodilatator-stimulated phosphoprotein), the multiprotein Arp2/3 complex and cofilin [1].
• Cofilin activation during Ca(2+)-triggered secretion from adrenal chromaffin cells [5].

Associations of CFL1 with chemical compounds

• Here we examined whether cofilin is activated upon Ca(2+) regulated noradrenalin secretion from bovine adrenal chromaffin cells [5].
• We found that triggering exocytosis by nicotine causes a dephosphorylation and thereby activation of cofilin [5].

References