Enables actin filament binding activity; phosphatidylinositol bisphosphate binding activity; and protein phosphatase binding activity. Involved in several processes, including cellular response to cytokine stimulus; negative regulation of cellular component organization; and positive regulation of cellular component organization. Acts upstream of or within cell projection organization and negative regulation of cell size. Located in several cellular components, including cofilin-actin rod; dendritic spine; and lamellipodium. Is active in glutamatergic synapse. Used to study myocardial infarction. Biomarker of several diseases, including epilepsy (multiple); impotence; muscular atrophy; ureteral obstruction; and vitamin B12 deficiency. Orthologous to human CFL1 (cofilin 1); PARTICIPATES IN insulin responsive facilitative sugar transporter mediated glucose transport pathway; Rab family mediated signaling pathway; Fc gamma receptor mediated signaling pathway; INTERACTS WITH 17beta-estradiol; 2,2',4,4'-Tetrabromodiphenyl ether; 2,3,7,8-tetrachlorodibenzodioxine.
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of CFL1 mRNA
[azoxystrobin co-treated with 2-chloro-N-(4-chlorobiphenyl-2-yl)nicotinamide co-treated with Chlorpyrifos co-treated with glyphosate co-treated with imidacloprid co-treated with Thiabendazole] results in decreased expression of CFL1 mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of CFL1 mRNA
[Capsaicin results in decreased phosphorylation of and results in increased activity of CFL1 protein] which results in increased import of Calcium more ...
[azoxystrobin co-treated with 2-chloro-N-(4-chlorobiphenyl-2-yl)nicotinamide co-treated with Chlorpyrifos co-treated with glyphosate co-treated with imidacloprid co-treated with Thiabendazole] results in decreased expression of CFL1 mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of CFL1 mRNA
Egtazic Acid inhibits the reaction [Capsaicin results in decreased phosphorylation of and results in increased activity of CFL1 protein] and Egtazic Acid inhibits the reaction [Ionomycin results in decreased phosphorylation of and results in increased activity of CFL1 protein]
[azoxystrobin co-treated with 2-chloro-N-(4-chlorobiphenyl-2-yl)nicotinamide co-treated with Chlorpyrifos co-treated with glyphosate co-treated with imidacloprid co-treated with Thiabendazole] results in decreased expression of CFL1 mRNA
[azoxystrobin co-treated with 2-chloro-N-(4-chlorobiphenyl-2-yl)nicotinamide co-treated with Chlorpyrifos co-treated with glyphosate co-treated with imidacloprid co-treated with Thiabendazole] results in decreased expression of CFL1 mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of CFL1 mRNA
Egtazic Acid inhibits the reaction [Ionomycin results in decreased phosphorylation of and results in increased activity of CFL1 protein] and Ionomycin results in decreased phosphorylation of and results in increased activity of CFL1 protein
methylmercury II affects the localization of and results in decreased phosphorylation of CFL1 protein and Probucol inhibits the reaction [methylmercury II affects the localization of and results in decreased phosphorylation of CFL1 protein]
[azoxystrobin co-treated with 2-chloro-N-(4-chlorobiphenyl-2-yl)nicotinamide co-treated with Chlorpyrifos co-treated with glyphosate co-treated with imidacloprid co-treated with Thiabendazole] results in decreased expression of CFL1 mRNA
Restoration of erectile function by suppression of corporal apoptosis, fibrosis and corporal veno-occlusive dysfunction with rho-kinase inhibitors in a rat model of cavernous nerve injury.
Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway.
Amyloid-beta and proinflammatory cytokines utilize a prion protein-dependent pathway to activate NADPH oxidase and induce cofilin-actin rods in hippocampal neurons.
