Genomes and Genes
Summary: A member of the cofilin family of proteins that is expressed in MUSCLE CELLS. It has ACTIN depolymerization activity that is dependent on HYDROGEN-ION CONCENTRATION.
- Wang Y, Kuramitsu Y, Ueno T, Suzuki N, Yoshino S, Iizuka N, et al. Differential expression of up-regulated cofilin-1 and down-regulated cofilin-2 characteristic of pancreatic cancer tissues. Oncol Rep. 2011;26:1595-9 pubmed publisher..Therefore, cofilin isoforms may serve as candidates for clinically useful biomarkers or therapeutic targets for PC. ..
- Clarke N. Skeletal muscle disease due to mutations in tropomyosin, troponin and cofilin. Adv Exp Med Biol. 2008;642:40-54 pubmed
- Larsson P, Henriksson Larsén K. Body composition and performance in cross-country skiing. Int J Sports Med. 2008;29:971-5 pubmed publisher..636 to 0.867; p < 0.05 to p < 0.01). We suggest that large amounts of lean body mass, especially in the arms, seem to be of great importance for cross-country skiing performance. ..
- Yamaguchi H, Condeelis J. Regulation of the actin cytoskeleton in cancer cell migration and invasion. Biochim Biophys Acta. 2007;1773:642-52 pubmed
- Marcoux N, Vuori K. EGF receptor activity is essential for adhesion-induced stress fiber formation and cofilin phosphorylation. Cell Signal. 2005;17:1449-55 pubmed..These studies demonstrate adhesion-dependent regulation of cofilin phosphorylation, and identify a novel role for EGFR in integrin signaling. ..
- Pipp F, Boehm S, Cai W, Adili F, Ziegler B, Karanovic G, et al. Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler Thromb Vasc Biol. 2004;24:1664-8 pubmed..This increased number and size of collateral vessels to a hitherto unknown degree. Fluid shear stress is the primary and strongest arteriogenic stimulus. ..
- Ockeloen C, Gilhuis H, Pfundt R, Kamsteeg E, Agrawal P, Beggs A, et al. Congenital myopathy caused by a novel missense mutation in the CFL2 gene. Neuromuscul Disord. 2012;22:632-9 pubmed publisher..Given the clinical variability and the multitude of histological features of congenital myopathies, CFL2 sequence analysis should be considered in patients presenting with an autosomal recessive form of congenital myopathy. ..
- Kawauchi K, Tan W, Araki K, Abu Bakar F, Kim M, Fujita H, et al. p130Cas-dependent actin remodelling regulates myogenic differentiation. Biochem J. 2012;445:323-32 pubmed publisher..The results of the present study suggest that p130Cas phosphorylation, mediated by integrin ?3, facilitates cofilin inactivation and promotes myogenic differentiation through modulating actin cytoskeleton remodelling. ..
- Moey M, Rajapurohitam V, Zeidan A, Karmazyn M. Ginseng (Panax quinquefolius) attenuates leptin-induced cardiac hypertrophy through inhibition of p115Rho guanine nucleotide exchange factor-RhoA/Rho-associated, coiled-coil containing protein kinase-dependent mitogen-activated protein kinase pathway. J Pharmacol Exp Ther. 2011;339:746-56 pubmed publisher..These results demonstrate a potent inhibitory effect of ginseng against leptin-induced cardiac hypertrophy, an effect associated with prevention of p115RhoGEF-RhoA/ROCK-dependent p38 MAPK activation. ..
- Hunter J, Zeidan A, Javadov S, Kilic A, Rajapurohitam V, Karmazyn M. Nitric oxide inhibits endothelin-1-induced neonatal cardiomyocyte hypertrophy via a RhoA-ROCK-dependent pathway. J Mol Cell Cardiol. 2009;47:810-8 pubmed publisher..These findings may be important in understanding the mechanisms of anti-ET-1 and anti-hypertrophic effects of NO as well as in the development of novel RhoA-targeted therapeutic interventions for treating cardiac hypertrophy. ..
- Erkutlu I, Cigiloglu A, Kalender M, Alptekin M, Demiryurek A, Suner A, et al. Correlation between Rho-kinase pathway gene expressions and development and progression of glioblastoma multiforme. Tumour Biol. 2013;34:1139-44 pubmed publisher..The expression of these genes may be related to response of multimodal therapy or these parameters could be used to determine possible unresponsive patients before treatment. ..
- Lee M, San Martin A, Mehta P, Dikalova A, Garrido A, Datla S, et al. Mechanisms of vascular smooth muscle NADPH oxidase 1 (Nox1) contribution to injury-induced neointimal formation. Arterioscler Thromb Vasc Biol. 2009;29:480-7 pubmed publisher..Inhibition of Nox1 may be an efficient strategy to suppress neointimal formation. ..
- Zhao W, Su Y, Su R, Ba C, Zeng R, Song H. The full length cloning of a novel porcine gene CFL2b and its influence on the MyHC expression. Mol Biol Rep. 2009;36:2191-9 pubmed publisher..1% identity with the CFL2b in human and mouse, respectively. Taken together, our research revealed that porcine CFL2b may be involved in the regulation muscle fiber trait by affecting the expression of MyHC. ..
- Agrawal P, Greenleaf R, Tomczak K, Lehtokari V, Wallgren Pettersson C, Wallefeld W, et al. Nemaline myopathy with minicores caused by mutation of the CFL2 gene encoding the skeletal muscle actin-binding protein, cofilin-2. Am J Hum Genet. 2007;80:162-7 pubmed
- Lee C, Park H, So H, Kim H, Lee K, Choi W, et al. Proteomic profiling and identification of cofilin responding to oxidative stress in vascular smooth muscle. Proteomics. 2006;6:6455-75 pubmed..These results suggest that cofilin is one of the proteins regulated by H2O2 treatment in vascular smooth muscle, and has an important role in the induction of vascular apoptosis through PTP-dependent mechanisms. ..
- Chhabra D, Dos Remedios C. Cofilin, actin and their complex observed in vivo using fluorescence resonance energy transfer. Biophys J. 2005;89:1902-8 pubmed..Our data suggest there is significantly more cofilin-G-actin complex and less free cofilin in the nucleus than in the cytoplasm. ..
- Xiang S, Ouyang K, Yung B, Miyamoto S, Smrcka A, Chen J, et al. PLCÎµ, PKD1, and SSH1L transduce RhoA signaling to protect mitochondria from oxidative stress in the heart. Sci Signal. 2013;6:ra108 pubmed publisher..b>Cofilin 2 translocates to mitochondria in response to oxidative stress or ischemia/reperfusion injury, and both S1P ..
- Vartiainen M, Mustonen T, Mattila P, Ojala P, Thesleff I, Partanen J, et al. The three mouse actin-depolymerizing factor/cofilins evolved to fulfill cell-type-specific requirements for actin dynamics. Mol Biol Cell. 2002;13:183-94 pubmed..Taken together, these data suggest that the three biochemically distinct mammalian ADF/cofilin isoforms evolved to fulfill specific requirements for actin filament dynamics in different cell types. ..
- Boengler K, Pipp F, Broich K, Fernandez B, Schaper W, Deindl E. Identification of differentially expressed genes like cofilin2 in growing collateral arteries. Biochem Biophys Res Commun. 2003;300:751-6 pubmed..In summary, our data showed an augmented expression level of genes contributing to different fundamental processes of arteriogenesis. ..
- Zhang Q, Lee H, Han J, Kang S, Lee N, Baik M, et al. Differentially expressed proteins associated with myogenesis and adipogenesis in skeletal muscle and adipose tissue between bulls and steers. Mol Biol Rep. 2012;39:953-60 pubmed publisher..repeat domain-containing protein 1 (ANKRD1) and heat shock protein beta 1 (HSPB1) that were up-regulated and cofilin 2 (CFL2) that was down-regulated, and also identified two down-regulated proteins in adipose tissue, transaldolase ..
- Agrawal P, Joshi M, Savic T, Chen Z, Beggs A. Normal myofibrillar development followed by progressive sarcomeric disruption with actin accumulations in a mouse Cfl2 knockout demonstrates requirement of cofilin-2 for muscle maintenance. Hum Mol Genet. 2012;21:2341-56 pubmed publisher..Overall, cofilin-2, although not critical for muscle development, is essential for muscle maintenance. ..
- Galkin V, Orlova A, Kudryashov D, Solodukhin A, Reisler E, Schröder G, et al. Remodeling of actin filaments by ADF/cofilin proteins. Proc Natl Acad Sci U S A. 2011;108:20568-72 pubmed publisher..Our results show the structural plasticity of actin, suggest that other actin-binding proteins may also induce large but different conformational changes, and show that F-actin cannot be described by a single molecular model. ..
- Gurniak C, Perlas E, Witke W. The actin depolymerizing factor n-cofilin is essential for neural tube morphogenesis and neural crest cell migration. Dev Biol. 2005;278:231-41 pubmed..Our data suggest that in mammalian development, regulation of the actin cytoskeleton by the F-actin depolymerizing factor n-cofilin is critical for epithelial-mesenchymal type of cell shape changes as well as cell proliferation. ..
- Won K, Park S, Park T, Lee C, Lee H, Choi W, et al. Cofilin phosphorylation mediates proliferation in response to platelet-derived growth factor-BB in rat aortic smooth muscle cells. J Pharmacol Sci. 2008;108:372-9 pubmed
- Nakashima K, Sato N, Nakagaki T, Abe H, Ono S, Obinata T. Two mouse cofilin isoforms, muscle-type (MCF) and non-muscle type (NMCF), interact with F-actin with different efficiencies. J Biochem. 2005;138:519-26 pubmed..These results suggest that MCF interacts with F-actin with higher affinity than NMCF, and although both of them are involved in the regulation of actin assembly in developing myotubes, the two proteins may play somewhat different roles. ..
- Vainshtein A, Kazak L, Hood D. Effects of endurance training on apoptotic susceptibility in striated muscle. J Appl Physiol (1985). 2011;110:1638-45 pubmed publisher..In addition, training can attenuate oxidative stress-induced apoptotic signaling in a tissue-specific manner, with an effect that is most prominent in cardiac muscle. ..
- Maciver S, Hussey P. The ADF/cofilin family: actin-remodeling proteins. Genome Biol. 2002;3:reviews3007 pubmed..Phylogenetic analysis of the ADF/cofilins reveals that, with few exceptions, their relationships reflect conventional views of the relationships between the major groups of organisms. ..
- Ren J, Albinsson S, Hellstrand P. Distinct effects of voltage- and store-dependent calcium influx on stretch-induced differentiation and growth in vascular smooth muscle. J Biol Chem. 2010;285:31829-39 pubmed publisher..Compartmentation of Ca(2+) entry pathways appears as one mechanism whereby extracellular and membrane signals influence smooth muscle phenotype regulation, with MEF2 as a focal point. ..
- Kurita S, Gunji E, Ohashi K, Mizuno K. Actin filaments-stabilizing and -bundling activities of cofilin-phosphatase Slingshot-1. Genes Cells. 2007;12:663-76 pubmed..SSH1 thus has the potential to regulate actin filament dynamics and organization in cells via F-actin-stabilizing and -bundling activities, in addition to its ability to dephosphorylate cofilin. ..
- Li Z, Liang J, Wu W, Yu X, Yu J, Weng X, et al. Leptin activates RhoA/ROCK pathway to induce cytoskeleton remodeling in nucleus pulposus cells. Int J Mol Sci. 2014;15:1176-88 pubmed publisher..These findings may provide novel insights into the pathogenic mechanism of obesity-associated lumbar disc degeneration. ..
- Dai Y, Bongalon S, Tian H, Parks S, Mutafova Yambolieva V, Yamboliev I. Upregulation of profilin, cofilin-2 and LIMK2 in cultured pulmonary artery smooth muscle cells and in pulmonary arteries of monocrotaline-treated rats. Vascul Pharmacol. 2006;44:275-82 pubmed
- Albinsson S, Nordström I, Hellstrand P. Stretch of the vascular wall induces smooth muscle differentiation by promoting actin polymerization. J Biol Chem. 2004;279:34849-55 pubmed..The effect is partially, but probably not completely, mediated via Rho-associated kinase and cofilin downstream of Rho. ..
- Kuramitsu Y, Wang Y, Okada F, Baron B, Tokuda K, Kitagawa T, et al. Malignant progressive tumor cell clone exhibits significant up-regulation of cofilin-2 and 27-kDa modified form of cofilin-1 compared to regressive clone. Anticancer Res. 2013;33:3661-5 pubmed..001). These results suggested that the 27-kDa protein recognized by the antibody against cofilin-1 is a possible biomarker for progressive tumor cells. ..