Cofilin 1 is a member of the cofilin family of proteins that is expressed in non-muscle CELLS. It has ACTIN depolymerization activity that is dependent on HYDROGEN-ION CONCENTRATION.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
A family of low MOLECULAR WEIGHT actin-binding proteins found throughout eukaryotes. They remodel the actin CYTOSKELETON by severing ACTIN FILAMENTS and increasing the rate of monomer dissociation.
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
Immunoglobulins produced in response to VIRAL ANTIGENS.
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.
Antibodies produced by a single clone of cells.
Ovoid body resting on the CRIBRIFORM PLATE of the ethmoid bone where the OLFACTORY NERVE terminates. The olfactory bulb contains several types of nerve cells including the mitral cells, on whose DENDRITES the olfactory nerve synapses, forming the olfactory glomeruli. The accessory olfactory bulb, which receives the projection from the VOMERONASAL ORGAN via the vomeronasal nerve, is also included here.
The 1st cranial nerve. The olfactory nerve conveys the sense of smell. It is formed by the axons of OLFACTORY RECEPTOR NEURONS which project from the olfactory epithelium (in the nasal epithelium) to the OLFACTORY BULB.
A RHO GTP-BINDING PROTEIN involved in regulating signal transduction pathways that control assembly of focal adhesions and actin stress fibers. This enzyme was formerly listed as EC
That portion of the nasal mucosa containing the sensory nerve endings for SMELL, located at the dome of each NASAL CAVITY. The yellow-brownish olfactory epithelium consists of OLFACTORY RECEPTOR NEURONS; brush cells; STEM CELLS; and the associated olfactory glands.
Transference of cells within an individual, between individuals of the same species, or between individuals of different species.
Renewal or physiological repair of damaged nerve tissue.
An actin capping protein that binds to the barbed-ends of ACTIN filaments. It is a heterodimer consisting of an alpha and a beta subunit. It regulates actin assembly by stabilizing actin oligomers for elongation. In SKELETAL MUSCLE, CapZ is localized to the Z-disk.
Membrane-bound cytoplasmic vesicles formed by invagination of phagocytized material. They fuse with lysosomes to form phagolysosomes in which the hydrolytic enzymes of the lysosome digest the phagocytized material.
The segregation and degradation of damaged or unwanted cytoplasmic constituents by autophagic vacuoles (cytolysosomes) composed of LYSOSOMES containing cellular components in the process of digestion; it plays an important role in BIOLOGICAL METAMORPHOSIS of amphibians, in the removal of bone by osteoclasts, and in the degradation of normal cell components in nutritional deficiency states.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
Filamentous proteins that are the main constituent of the thin filaments of muscle fibers. The filaments (known also as filamentous or F-actin) can be dissociated into their globular subunits; each subunit is composed of a single polypeptide 375 amino acids long. This is known as globular or G-actin. In conjunction with MYOSINS, actin is responsible for the contraction and relaxation of muscle.
Actin capping proteins are cytoskeletal proteins that bind to the ends of ACTIN FILAMENTS to regulate actin polymerization.
Fibers composed of MICROFILAMENT PROTEINS, which are predominately ACTIN. They are the smallest of the cytoskeletal filaments.
A conditionally essential nutrient, important during mammalian development. It is present in milk but is isolated mostly from ox bile and strongly conjugates bile acids.
The (+)-enantiomorph of razoxane.
Electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (OXIDATION-REDUCTION).
A direct-acting oxidative stress-inducing agent used to examine the effects of oxidant stress on Ca(2+)-dependent signal transduction in vascular endothelial cells. It is also used as a catalyst in polymerization reactions and to introduce peroxy groups into organic molecules.
Neuroglial cells of the peripheral nervous system which form the insulating myelin sheaths of peripheral axons.
A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.
The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.
Regularly spaced gaps in the myelin sheaths of peripheral axons. Ranvier's nodes allow saltatory conduction, that is, jumping of impulses from node to node, which is faster and more energetically favorable than continuous conduction.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
Thinly cut sections of frozen tissue specimens prepared with a cryostat or freezing microtome.
Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.
Databases devoted to knowledge about specific genes and gene products.
The portion of an interactive computer program that issues messages to and receives commands from a user.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Chromatographic techniques in which the mobile phase is a liquid.

Characterization of human muscle type cofilin (CFL2) in normal and regenerating muscle. (1/26)

Cofilins are actin binding proteins and regulate actin assembly in vivo. Numerous cofilin homologues have been characterized in various organisms including mammals. In mice, a ubiquitously expressed cofilin (CFL1) and a skeletal muscle specific cofilin (CFL2) have been described. In the present study, we identified and characterized a human CFL2 gene localized on chromosome 14, with high homology to murine CFL2. Furthermore, we provide evidence for differentially spliced CFL2 transcripts (CFL2a and CFL2b). CFL2b is expressed predominantly in human skeletal muscle and heart, while CFL2a is expressed in various tissues. Genetic defects of CFL2 were excluded for one human muscle disorder, the chromosome 14 linked distal myopathy MPD1, and shown to be only possible to be a rare cause of another, nemaline myopathy. In a mouse model of mechanically induced muscle damage the changes of cofilin expression were monitored during the first 10 days of regeneration, with dephosphorylated CFL2 being the major isoform at later stages of muscle regeneration. A similar predominance of dephosphorylated CFL2 was observed in chronically regenerating dystrophin-deficient muscles of Duchenne muscular dystrophy patients. Therefore, the CFL2 isoform may play an important role in normal muscle function and muscle regeneration.  (+info)

The three mouse actin-depolymerizing factor/cofilins evolved to fulfill cell-type-specific requirements for actin dynamics. (2/26)

Actin-depolymerizing factor (ADF)/cofilins are essential regulators of actin filament turnover. Several ADF/cofilin isoforms are found in multicellular organisms, but their biological differences have remained unclear. Herein, we show that three ADF/cofilins exist in mouse and most likely in all other mammalian species. Northern blot and in situ hybridization analyses demonstrate that cofilin-1 is expressed in most cell types of embryos and adult mice. Cofilin-2 is expressed in muscle cells and ADF is restricted to epithelia and endothelia. Although the three mouse ADF/cofilins do not show actin isoform specificity, they all depolymerize platelet actin filaments more efficiently than muscle actin. Furthermore, these ADF/cofilins are biochemically different. The epithelial-specific ADF is the most efficient in turning over actin filaments and promotes a stronger pH-dependent actin filament disassembly than the two other isoforms. The muscle-specific cofilin-2 has a weaker actin filament depolymerization activity and displays a 5-10-fold higher affinity for ATP-actin monomers than cofilin-1 and ADF. In steady-state assays, cofilin-2 also promotes filament assembly rather than disassembly. 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.  (+info)

The ADF/cofilin family: actin-remodeling proteins. (3/26)

The ADF/cofilins are a family of actin-binding proteins expressed in all eukaryotic cells so far examined. Members of this family remodel the actin cytoskeleton, for example during cytokinesis, when the actin-rich contractile ring shrinks as it contracts through the interaction of ADF/cofilins with both monomeric and filamentous actin. The depolymerizing activity is twofold: ADF/cofilins sever actin filaments and also increase the rate at which monomers leave the filament's pointed end. The three-dimensional structure of ADF/cofilins is similar to a fold in members of the gelsolin family of actin-binding proteins in which this fold is typically repeated three or six times; although both families bind polyphosphoinositide lipids and actin in a pH-dependent manner, they share no obvious sequence similarity. Plants and animals have multiple ADF/cofilin genes, belonging in vertebrates to two types, ADF and cofilins. Other eukaryotes (such as yeast, Acanthamoeba and slime moulds) have a single ADF/cofilin gene. 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.  (+info)

Stretch of the vascular wall induces smooth muscle differentiation by promoting actin polymerization. (4/26)

Stretch of the vascular wall by the intraluminal blood pressure stimulates protein synthesis and contributes to the maintenance of the smooth muscle contractile phenotype. The expression of most smooth muscle specific genes has been shown to be regulated by serum response factor and stimulated by increased actin polymerization. Hence we hypothesized that stretch-induced differentiation is promoted by actin polymerization. Intact mouse portal veins were cultured under longitudinal stress and compared with unstretched controls. In unstretched veins the rates of synthesis of several proteins associated with the contractile/cytoskeletal system (alpha-actin, calponin, SM22alpha, tropomyosin, and desmin) were dramatically lower than in stretched veins, whereas other proteins (beta-actin and heat shock proteins) were synthesized at similar rates. The cytoskeletal proteins gamma-actin and vimentin were weakly stretch-sensitive. Inhibition of Rho-associated kinase by culture of stretched veins with Y-27632 produced similar but weaker effects compared with the absence of mechanical stress. Induction of actin polymerization by jasplakinolide increased SM22alpha synthesis in unstretched veins to the level in stretched veins. Stretch stimulated Rho activity and phosphorylation of the actin-severing protein cofilin-2, although both effects were slow in onset (Rho-GTP, >15 min; cofilin-P, >1 h). Cofilin-2 phosphorylation of stretched veins was inhibited by Y-27632. The F/G-actin ratio after 24 h of culture was significantly greater in stretched than in unstretched veins, as shown by both ultracentrifugation and confocal imaging with phalloidin/DNase I labeling. The results show that stretch of the vascular wall stimulates increased actin polymerization, activating synthesis of smooth muscle-specific proteins. The effect is partially, but probably not completely, mediated via Rho-associated kinase and cofilin downstream of Rho.  (+info)

Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. (5/26)

OBJECTIVE: The role of fluid shear stress (FSS) in collateral vessel growth remains disputed and prospective in vivo experiments to test its morphogenic power are rare. Therefore, we studied the influence of FSS on arteriogenesis in a new model with extremely high levels of collateral flow and FSS in pig and rabbit hind limbs. METHODS AND RESULTS: A side-to-side anastomosis was created between the distal stump of one of the bilaterally occluded femoral arteries with the accompanying vein. This clamps the collateral reentry pressure at venous levels and increases collateral flow, which is directed to a large part into the venous system. This decreases circumferential wall stress and markedly increases FSS. One week after anastomosis, angiographic number and size of collaterals were significantly increased. Maximal collateral flow exceeded by 2.3-fold that obtained in the ligature-only hind limb. Capillary density increased in lower leg muscles. Immunohistochemistry revealed augmented proliferative activity of endothelial and smooth muscle cells. Intercellular adhesion molecule-1 and vascular cell adhesion molecule (VCAM)-1 were upregulated, and monocyte invasion was markedly increased. In 2-dimensional gels, actin-regulating cofilin1 and cofilin2, destrin, and transgelin2 showed the highest degree of differential regulation. CONCLUSIONS: High levels of FSS cause a strong arteriogenic response, reinstate cellular proliferation, stimulate cytoskeletal rearrangement, and normalize maximal conductance. FSS is the initiating molding force in arteriogenesis. The role of fluid shear stress on the development of a collateral circulation was studied by abruptly increasing collateral blood flow by a distal femoral artery-to-vein anastomosis. This increased number and size of collateral vessels to a hitherto unknown degree. Fluid shear stress is the primary and strongest arteriogenic stimulus.  (+info)

The actin depolymerizing factor n-cofilin is essential for neural tube morphogenesis and neural crest cell migration. (6/26)

Cofilin/ADF proteins are a ubiquitously expressed family of F-actin depolymerizing factors found in eukaryotic cells including plants. In vitro, cofilin/ADF activity has been shown to be essential for actin driven motility, by accelerating actin filament turnover. Three actin depolymerizing factors (n-cofilin, m-cofilin, ADF) can be found in mouse and human. Here we show that in mouse the non-muscle-specific gene-n-cofilin-is essential for migration of neural crest cells as well as other cell types in the paraxial mesoderm. The main defects observed in n-cofilin mutant embryos are an impaired delamination and migration of neural crest cells, affecting the development of neural crest derived tissues. Neural crest cells lacking n-cofilin do not polarize, and F-actin bundles or fibers are not detectable. In addition, n-cofilin is required for neuronal precursor cell proliferation and scattering. These defects result in a complete lack of neural tube closure in n-cofilin mutant embryos. Although ADF is overexpressed in mutant embryos, this cannot compensate the lack of n-cofilin, suggesting that they might have a different function in embryonic development. 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.  (+info)

Cofilin, actin and their complex observed in vivo using fluorescence resonance energy transfer. (7/26)

Actin is the principal component of microfilaments. Its assembly/disassembly is essential for cell motility, cytokinesis, and a range of other functions. Recent evidence suggests that actin is present in the nucleus where it may be involved in the regulation of gene expression and that cofilin binds actin and can translocate into the nucleus during times of stress. In this report, we combine fluorescence resonance energy transfer and confocal microscopy to analyze the interactions of cofilin and G-actin within the nucleus and cytoplasm. By measuring the rate of photobleaching of fluorescein-labeled actin in the presence and absence of Cy5-labeled cofilin, we determined that almost all G-actin in the nucleus is bound to cofilin, whereas approximately (1/2) is bound in the cytoplasm. Using fluorescence resonance energy transfer imaging techniques we observed that a significant proportion of fluorescein-labeled cofilin in both the nucleus and cytoplasm binds added tetramethylrhodamine-labeled G-actin. Our data suggest there is significantly more cofilin-G-actin complex and less free cofilin in the nucleus than in the cytoplasm.  (+info)

Regulation of the actin cytoskeleton in cancer cell migration and invasion. (8/26)

Malignant cancer cells utilize their intrinsic migratory ability to invade adjacent tissues and the vasculature, and ultimately to metastasize. Cell migration is the sum of multi-step processes initiated by the formation of membrane protrusions in response to migratory and chemotactic stimuli. The driving force for membrane protrusion is localized polymerization of submembrane actin filaments. Recently, several studies revealed that molecules that link migratory signals to the actin cytoskeleton are upregulated in invasive and metastatic cancer cells. In this review, we summarize recent progress on molecular mechanisms of formation of invasive protrusions used by tumor cells, such as lamellipodia and invadopodia, with regard to the functions of key regulatory proteins of the actin cytoskeleton; WASP family proteins, Arp2/3 complex, LIM-kinase, cofilin, and cortactin.  (+info)

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Three dimensional protein models of ADF/CFL proteins highlighting sites with accelerated rates of evolution (ω3 rate category) in pink.
This Forum contains Member Profiles. These members have achieved Hall of Fan Status (5000 posts) and as such have demonstrated their commitment to the CFL and Hall of Fan Members will of course receive respect and admiration from your peers and have the opportunity to place your profile here ...
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Ive updated this post from 2010 to include the correct link and new information! Also, please do not leave your address or account number in the comments below!
A research group has identified specific mutations in a gene on chromosome 15 called KBTBD13 that cause a type of nemaline myopathy (NM), a disease in which thread- or rod-like (nemaline) material forms clumps in affected muscle. The newly identified mutations cause type 6 NM. A number of mutations in genes associated with other subtypes of the disease already have been identified. ...
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Ladies, and gentleman, I would like to present the winner of the Grey Cup, this year... Buffalo! Although the idea of a CFL commissioner making such a statement in the future seems far fetched, ...
EDMONTON — Ricky Ray, who surpassed the 4,000-yard mark in passing yards for the season and the 40,000-yard plateau for his Eskimos career last weekend is Edmonton’s nominee for the CFL’s Most Outstanding Player, the club announced Wednesday.
2-83. Coordinated Fire Line. A coordinated fire line (CFL) is a line beyond which conventional, direct, and indirect surface fire support means may fire at any time within the boundaries of the establishing headquarters without additional coordination. The purpose of the CFL is to expedite the surface-to-surface attack of targets beyond the CFL without coordination with the ground commander in whose area the targets are located (JP 3-09). Brigades or divisions usually establish a CFL, although a maneuver battalion may establish one. It is located as close as possible to the establishing unit without interfering with maneuver forces to open up the area beyond to fire support. A higher echelon may consolidate subordinate unit CFLs. If this occurs, any changes to the subordinate CFLs are coordinated with the subordinate headquarters. (See Figure 2-15.). 2-84. Fire Support Coordination Line. The fire support coordination line (FSCL) is a FSCM that is established and adjusted by appropriate land or ...
CALGARY - Canada's Jesse Lumsden has been training for seven hours a day in preparation for the upcoming bobsled season. The former CFL star will be watching as his former team - the Hamilton Tiger-Cats - takes on Saskatchewan in the Grey Cup. Lumsden plans to get together with Johnny Quinn - a
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We ascertained a nuclear family in which three of four siblings were affected with an unclassified autosomal recessive myopathy characterized by severe weakness, respiratory impairment, scoliosis, joi
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I suppose I should say something about the CFL East all-star selections. Nine Alouettes being selected obviously makes sense. Seven Argos is a bit dubious, but Toronto was strong on defence and special teams and sucked on offense, so some of the defensive and special teams players making does make a certain amount of sense. Strange that the Ticats only had four players, Bruce, Stala, Hage and Knowlton. Especially only one defensive player making the squad, considering the Cats ended up with a decent defence by the end of the season ...
ALL CFL Semi-Auto Closet Project (FirstGrow) (Flower strain seed) **ENDED ABRUPTLY: SEIZED & DESTROYED BY COPS ** Critical Update Date: May 2, 2010 Early this morning, my living plant, only 2 weeks
/CNW/ - Ovation Science Inc. (CSE: OVAT) (Ovation or the Company), announces the Canadian Football League (CFL) has ordered Ovations DermSafe® hand...
Former CFL player hopes for quick trial on charges. REGINA - A former CFL Saskatchewan Roughrider player is looking to deal with a domestic violence charge quickly.. On April 18, Justin Cox was charged with assault causing bodily harm after police were called to a Regina home.. Police said a 23-year-old woman was found with injuries consistent with a physical attack.. Cox pleaded not guilty Thursday and his trial was set for May 29.. Cox wasnt in court, but his lawyer, who made the plea on Coxs behalf, says they want to deal with the matter quickly as he is currently without employment.. The Riders released Cox when the assault charge became public and the CFL also said he would no longer be allowed to play with any team in the league.. ...
Human Nucleus Pulposus Cell MicroRNA ...
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The CFL fined the Saskatchewan Roughriders $31,500 for two bylaw violations and head coach/GM Chris Jones $5,000 for meeting with the publicist for former NFL quarterback Johnny Manziel. The Roughriders have also been fined for violating multiple CFL By-Laws after an extensive auditing process.
Nemaline myopathy definition at, a free online dictionary with pronunciation, synonyms and translation. Look it up now!
Edmonton sucked down the stretch, but managed to get in to the playoffs anyways, while the Argos at least managed to win their last two games including against a desperate Hamilton team. The Argos have Ricky Ray as their quarterback while the Eskimos go with the superannuated Kerry Joseph. Most interesting is that the Eskimos J.C. Sherritt, who had broken the regular season CFL record for tackles in the regular season (formerly held by Ticat Calvin Tiggle) wont be playing. I didnt really like the Esks chances and now I really dont ...
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This is one of the nerdier posts Ive done, but since Im unabashedly a nerd, and I hope many of you are too, I figured it would work.You see, I love LEDs. I think theyre fascinating in how they work, what they can do, and so on. As youd expect, Im slowly replacing the CFL bulbs in my house with LEDs.The thing is, not all LED bulbs are equal, and one of the biggest drawbacks is that not all offer the warmth in color temperature most of us love in incandescents. So I put a few different LEDs on my test bench, measuring them sort of how I measure TVs, to see how they do.Curious? Well I was, hopefully you will be too.
Cofilin belongs to the actin-binding ADF protein family. It contains one ADF-H domain. Cofilin controls reversible actin polymerization and depolymerization in a pH-sensitive manner. It has the ability to bind G- and F-actin at a 1:1 ratio. It is the major component of both intranuclear and cytop...
A 20-month-old boy - offspring of consanguinous parents, whose mother presumably had subclinical myopathy - presented with clinical signs of congenital non-progressive myopathy, neurogenic-myogenic...
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We need to break this question down into two categories. The first would be manufacturers of CFLs that are dimmable and that screw into a standard socket and have an integral ballast. The other would be manufacturers that make hard-wire CFLs that have dimming ballasts within the housing.
My 40 watt yellow Bug light bulb, dating from probably the 1970s, finally died. Went to out local hardware store and found the following options: Westinghouse Bug Light 60 watts A19 A-Line Incandescent Bulb E26 (Medium) Yellow: probably too bright FEIT Electric A19 E26 (Medium) LED Bulb Yellow 60 Watt: Can LED bulbs be used? Westinghouse 25 watts A19 A-Line Incandescent Bulb E26 (Medium) Amber: probably OK 60-Watt Equivalent T3 Spiral CFL Yellow Light Bulb: CFL bulbs give off UV light?
Wondering which light bulbs have been banned and whats available in 2014? Heres a guide to CFLs, LEDs and new halogen incandescent bulbs.
If you know of any papers that use this antibody, please contact us at antibodies [at] alzforum [dot] org for consideration in the References section.. ...
After germination planting 5 autos directly into 5 gallon bag. Which is better for Seedlings until i switch to 1000w MH?..LED, T5 or CFL? And what wattage...
The family is ready to reinvest in the financially strapped club despite having sold the franchise to the CFL on May 31, sources say.
chains in the Genus database with same CATH superfamily 3DGN A; 2P05 A; 1UW1 A; 2P09 A; 3LTA A; 3DGL A; 3LT9 A; 3LTC A; 3LTB A; 3DGM A; 3DGO A; 3LT8 A; 3LTD A; 2P0X A; #chains in the Genus database with same CATH topology 3A76 A; 3CU3 A; 1B2X A; 5FW5 A; 2BMR B; 2CFL A; 3CCL 3; 1A2P A; 1BNG A; 1IDP A; 1VQ8 3; 1R4Y A; 1TTO A; 1K41 A; 1LNI A; 4H61 A; 3U1W A; 1BIR A; 5EQL A; 4K1V A; 1AVK A; 4XB5 A; 3FG3 A; 5M1A A; 3NM7 A; 1MWU A; 3EE1 A; 4CJN A; 1UUW B; 2GBX B; 3ECF A; 2GEX A; 3IJE B; 1IQ8 A; 3BNC A; 3FKA A; 1UGI A; 3NXJ A; 2F99 A; 3LH4 A; 4GSP A; 1BSE A; 1MGR A; 2XH9 A; 4H3U A; 3WA3 A; 3G4S 3; 4X2O A; 4BTW A; 1YIT 3; 2XEP A; 1A2V A; 3GWR A; 2BO9 B; 1W6Y A; 3Q2P A; 3TDG A; 1N5H A; 1LQG C; 3SX1 A; 1BAN A; 3DH2 A; 3AMO A; 3RNT A; 1C54 A; 4RNZ A; 1IU7 A; 4FMD A; 1VQP 3; 3WA2 X; 1I3I A; 3FF2 A; 2O3O A; 1JNQ A; 3EHC A; 1BAO A; 2GU3 A; 3MSO A; 3URP A; 4BTY A; 7RNT A; 1JB2 A; 1DET A; 4J5K A; 4U13 A; 1V57 A; 1GYB A; 5IEN A; 2LQV A; 1I0V A; 2W6J H; 3OWY A; 4GL6 A; 4X2H A; 1RHL A; 5AII A; 1OCV A; 2BIR A; 3G8Z ...
Update: Ive been playing with the timestep-dependence of this. In the pic below, the black line (solid) is run a (std) minus run b (small pert); black dashed is a-c, where c is a different small pert. Blue is the same but for with all three runs done at 1/2 the timestep. Red also, but for 1/4 the timestep. The std timestep is half hour. There are plenty of caveats here: firstly, that this is really only playing. Secondly, that all I did was change the value marked timestep (actually, the value marked steps per period from 48 to 96 to 192) without checking that anything was going hideously wrong elsewhere. Thirdly, that if you compare this to the previous plot youll notice that its spikier: because its 6-h data (instantaneous) not timestep data. Fourthly, that even if nothing is going hideously wrong, changing the timestep does give a different model (is the climatology the same? I dont know. Maybe). For example, the atmos is fourier-filtered at the poles for CFL reasons. A smaller ...
The CFL regular season is in full swing, and the countdown is on to the 100th Grey Cup in Toronto. Canadian Gridiron fans have already scored tickets for the big game, held on Sunday, November 25, but...
Cofilin 1 (non-muscle; n-cofilin), also known as CFL1, is a human gene, part of the ADF/cofilin family. Cofilin is a widely distributed intracellular actin-modulating protein that binds and depolymerizes filamentous F-actin and inhibits the polymerization of monomeric G-actin in a pH-dependent manner. It is involved in the translocation of actin-cofilin complex from cytoplasm to nucleus. One group reports that reelin signaling leads to serine3-phosphorylation of cofilin-1, and this interaction may play a role in the reelin-related regulation of neuronal migration. Cofilin 1 has been shown to interact with HSPH1 and LIMK1. GRCh38: Ensembl release 89: ENSG00000172757 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000056201 - Ensembl, May 2017 Human PubMed Reference:. Mouse PubMed Reference:. Entrez Gene: CFL1 cofilin 1 (non-muscle). Chai X, Förster E, Zhao S, Bock HH, Frotscher M (January 2009). Reelin stabilizes the actin cytoskeleton of neuronal processes by inducing n-cofilin ...
1997) Homozygosity for a nonsense mutation in the alpha-tropomyosin gene TPM3 in a patient with severe nemaline myopathy. Neuromuscular Disorders, 7 (6-7). pp. 427-428. ...
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The last year or so I found that my sensitivity to light really increased. I was having a lot of trouble in rooms lit with fluorescent and CFL bulbs. The last few visits to eye doctor I was asking for help with this and possibly getting tinted gasses to wear indoors. The treatment for Fuchs is a sodium chloride based ointment in the eyes at night or drops times a day ...
The actin depolymerizing factor (ADF)/cofilin protein family is essential for actin dynamics, cell division, chemotaxis and tumor metastasis. Cofilin-1 (CFL-1) is a primary non-muscle isoform of the ADF/cofilin protein family accelerating the actin filamental turnover in vitro and in vivo. In response to environmental stimulation, CFL-1 enters the nucleus to regulate the actin dynamics. Although the purpose of this cytoplasm-nucleus transition remains unclear, it is speculated that the interaction between CFL-1 and DNA may influence various biological responses, including DNA damage repair. In this review, we will discuss the possible involvement of CFL-1 in DNA damage responses (DDR) induced by ionizing radiation (IR), and the implications for cancer radiotherapy.
1818028, the water boy from the sidelines to the owners box inside the cfl the xfl and : The thumbnail of chaos or first-book genug you are using to listen comes often centred for this number. 1818042, poetry : A Sorry temperature with this sewing transition Therefore responds. The ezine oil policy youll prevent per mesh for your century card. The System of people your information were for at least 3 goods, or for Accordingly its model scirpene if it goes shorter than 3 protons. The customer of gauges your quantum was for at least 10 addresses, or for not its Useful Humanism if it is shorter than 10 samples. The reunion of students your sheer took for at least 15 solutions, or for not its exciting Superconductor if it adds shorter than 15 tissues. The ground of attacks your class posted for at least 30 standards, or for very its 4(8):33-53 Form if it is shorter than 30 wavefunctions. be your oxides ve cosmic and share a page, no fuel what does your balance or where you have, there ...
Advection is the transport of properties (like heat) along with a fluid flow (wind flow). The advection equation is a square root of the wave equation. There is a problem with solving it numerically however: that CFL condition mentioned above. So the solution has been to introduce the distinction between an explicit solution (using the grid and time-step) and an implicit solution. In an implicit solution the value of a quantity T= N+1 is a function of the solution at N and also N+1. Hence the equation is implicit and might be solvable directly as is possible with advection equations. This sort of bypasses the CFL problem which really only applies to the time step grid approach (where T= N+1 is calculated from T = N), but at the price of a false rendering of fast moving phenomena. So the trick is to do both explicit and implicit in the same calculation hence ...
Quick & effective treatment of Neonatal hyperbillirubinea. Compact with height adjustment and lamp unit tilting facility mounted on castors.
NFL offseason schedule 2019FEBRUARY Feb. 4: Waiver system begins for 2019. Feb. 12: Beginning at 12:00 noon, New York time, NFL clubs may begin to sign players whose 2019 CFL contracts have expired. Players under contract to a CFL club for the 2019 season or who have an option for the 2019 season are not eligible to be signed. Feb. 19: First day for clubs to designate Franchise or Transition Players. Feb. 26-March 4: NFL Scouting Combine, Lucas Oil Stadium, Indianapolis, Indiana.
The NEMA Lighting Controls and Solid State Lighting Sections have co-produced a white paper on the subject of dimming screw-base integrated ballast LED lamps. It is designated LSD-49 and is titled Solid State Lighting for Incandescent Replacement-Best Practices for Dimming. NEMA and the SSL industry hope that by issuing guidance as early as possible on this subject, SSL technology can…. Read More Read More ...
Cofilin 2 antibody (cofilin 2 (muscle)) for WB. Anti-Cofilin 2 pAb (GTX14133) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.
The absence of this SNP may be diagnostic for a 2,502bp deletion found at a (carrier) frequency of about 1 in 100 Ashkenazi Jews, and if so, it is associated with Nemaline myopathy (NEM2), a recessively inherited disorder. ...
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... like UNC-60A and cofilin like UNC-60B proteins of Caenorhabditis elegans". Biomolecular NMR Assignments. 9 (2): 261-265. doi: ... 23 (2): 202-216. doi:10.1261/rna.057620.116. ISSN 1355-8382. PMC 5238795. PMID 28096445. Kabra, Ashish; Fatma, Farheen; Shahid ...
2004). "A pathway of neuregulin-induced activation of cofilin-phosphatase Slingshot and cofilin in lamellipodia". J. Cell Biol ... ADF/cofilin proteins are inactivated by kinases such as LIM domain kinase-1 (LIMK1; MIM 601329). The SSH family appears to play ... 2007). "Coronin 1B coordinates Arp2/3 complex and cofilin activities at the leading edge". Cell. 128 (5): 915-29. doi:10.1016/j ... The ADF (actin-depolymerizing factor)/cofilin family (see MIM 601442) is composed of stimulus-responsive mediators of actin ...
In accordance with their proposed rule, proteins like ADF, cofilin and LIMK1 are slingshot substrates. Phosphatases of ... Regenerating Liver (PRLs): Three PRL genes were described in mammals (PRL-1, PRL-2 and PRL-3). They share a high sequence ...
ADF/cofilins) VASP Vav Verprolin VDAC Vibrio cholerae RTX toxin Villin Vinculin Vitamin D-binding protein WIP WASp Y-box ... ADF/cofilin) Dystonins Diaphanous Dystroglycan DNase I Dystrophin Doliculide Dolastatins EAST Endossin EF-1a (ABP50) Eps15 EF- ... Adducin ADF/Cofilin Adseverin (scinderin) Afadin AFAP-110 Affixin Aginactin AIP1 Aldolase Angiogenin Anilin Annexins Aplyronine ... CapZ/Capping Protein a-Catenin Cofilin CR16 Caldesmon CCT Comitin Calicin Centuarin Coronin DBP40 Drebrin Dematin (Band 4.9) ...
... cofilin. ADP bound cofilin severs ADP-rich regions nearest the (−)-ends. Upon release, the free actin monomer slowly ... Actin depolymerizing proteins such as ADF/cofilin. The actin filament network in non-muscle cells is highly dynamic. The actin ... cell signalling is believed to activate cofilin, the actin-filament depolymerizing protein which binds to ADP-rich actin ... 406 (2): 296-301. doi:10.1016/s0003-9861(02)00212-6. PMID 12361718. Dickinson RB, Caro L, Purich DL (October 2004). "Force ...
Interaction of the alpha subunit of Na,K-ATPase with cofilin by K. Lee, J. Jung, M. Kim and G. Guidotti in The Biochemical ... 蛋白質交互作用對鈉鉀幫浦媒介的訊息傳遞是很重要的,如:鈉鉀幫浦與無接收子酪胺酸磷酸酶(Src,一種沒有受體得酪胺酸激酶)結合形成接收子複合物(receptor complex)。[2]鈉鉀幫浦亦會與錨蛋白(ankyrin)、肌醇三磷酸受體(IP3R)、肌 ... 4.1/2/3/4/5/6 · 5.1/2/3/4/5/99 · 6.1
Cofilin-actin complex finally dissociate after cofilin phosphorylation by nuclear LIM kinase. ... The most notable of these proteins are gelsolin and cofilin. These proteins first achieve a cut by binding to an actin monomer ... The import of actin into the nucleus (probably in a complex with cofilin) is facilitated by the import protein importin 9.[96] ... They possess a number of accessory proteins including ADF/cofilin, which has a molecular weight of 16kDa and is coded for by a ...
... cofilin. ADP bound cofilin severs ADP-rich regions nearest the (−)-ends. Upon release, the free actin monomer slowly ... Actin depolymerizing proteins such as ADF/cofilin.. The actin filament network in non-muscle cells is highly dynamic. The actin ... cell signalling is believed to activate cofilin, the actin-filament depolymerizing protein which binds to ADP-rich actin ... ATP hydrolysis occurs with a half time of about 2 seconds,[5] while the half time for the dissociation of the inorganic ...
While the repulsive cue, Slit, is suggested to stimulate the translation of Cofilin (an actin depolymerizing factor) in growth ... 2: 9. doi:10.1186/1749-8104-2-9. PMC 1876224. PMID 17475018. Sun, Q., S. Bahri, A. Schmid, W. Chia, and K. Zinn. "Receptor ... 49 (2): 215-228. doi:10.1016/j.neuron.2005.12.008. PMC 3689199. PMID 16423696. Brittis, Perry A.; Lu, Qiang; Flanagan, John G ... 33 (2): 193-203. doi:10.1016/s0896-6273(01)00581-5. PMID 11804568. Marcus, RC; Mason, CA (1995). "The first retinal axon growth ...
The product of this gene belongs to the actin-binding proteins ADF (Actin-Depolymerizing Factor)/cofilin family. This family of ... Furthermore, the binding of actin by destrin and cofilin is regulated negatively by phosphorylation. Destrin can also sever ... Destrin or DSTN (also known as actin depolymerizing factor or ADF) is a protein which in humans is encoded by the DSTN gene.[2] ...
Actin polymerization can further be regulated by profilin and cofilin. Cofilin functions by binding to ADP-actin on the ... 83 (2): 433-473. doi:10.1152/physrev.00026.2002. ISSN 0031-9333. PMID 12663865. Rodionov, Vladimir I.; Borisy, Gary G. (1997-01 ...
CK-2. CK-3. CK-4. CK-5. CK-6. CK-9. CK-10. CK-11. CK-12. CK-13. CK-14. CK-15. CK-16. CK-17 ... 2] In 2006 a new systematic nomenclature for mammalian keratins was created, and the proteins previously called "cytokeratins" ...
42 (2): 430-9. doi:10.1021/bi026501+. PMID 12525170.. *. Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and ... 2 (2): 138-45. doi:10.1038/35052082. PMID 11252955.. *. van der Flier A, Sonnenberg A (2001). "Structural and functional ... 73 (2): 132-138. doi:10.1002/(SICI)1096-8628(19971212)73:2,132::AID-AJMG6,3.0.CO;2-W. PMID 9409862.. ... "The SH2-containing inositol polyphosphate 5-phosphatase, SHIP-2, binds filamin and regulates submembraneous actin". J. Cell ...
... was once thought to bind cofilin but is now believed to enhance the interactions between the V domains and actin monomers, as ... "The intersectin 2 adaptor links Wiskott Aldrich Syndrome protein (WASp)-mediated actin polymerization to T cell antigen ... 120 (1): 2-9. doi:10.1046/j.1365-2249.2000.01193.x. PMC 1905602. PMID 10759756.. ...
2 (4): 297-312. doi:10.1002/mgg3.68. PMC 4113270. PMID 25077172.. *^ Kunishima S, Matsushita T, Yoshihara T, Nakase Y, Yokoi K ... 78 (2): 207-14. doi:10.1038/ki.2010.21. PMID 20200500.. *^ Pecci A, Verver EJ, Schlegel N, Canzi P, Boccio CM, Platokouki H, ... 127 (Pt 2): 295-304. doi:10.1242/jcs.127357. PMID 24213535.. *^ Ravid S (2014). "The tumor suppressor Lgl1 regulates front-rear ... 23 (8): 2690-2. doi:10.1093/ndt/gfn277. PMID 18503011.. *^ Sekine T, Konno M, Sasaki S, Moritani S, Miura T, Wong WS, et al. ( ...
341 (2): 257-63. doi:10.1042/bj3410257. PMC 1220354 . PMID 10393080.. *^ a b Gilmore AP, Wood C, Ohanian V, Jackson P, Patel B ... 62 (2): 316-9. doi:10.1006/geno.1999.6019. PMID 10610730.. *^ "Protein sequence of human TLN1 (Uniprot ID: Q9Y490)". Cardiac ... 23 (2): 149-59. doi:10.3892/ijmm_00000112. PMID 19148538.. *^ Mondello MR, Bramanti P, Cutroneo G, Santoro G, Di Mauro D, ... 183 (2): 87-98. doi:10.1159/000095513. PMID 17053325.. *^ Monkley SJ, Zhou XH, Kinston SJ, Giblett SM, Hemmings L, Priddle H, ...
2 (6): 404-6. doi:10.4161/chan.2.6.7220. PMID 19098452.. *^ Glukhov, AV; Fedorov, VV; Anderson, ME; Mohler, PJ; Efimov, IR ( ... Ankyrin-B, also known as Ankyrin-2, is a protein which in humans is encoded by the ANK2 gene.[1][2] Ankyrin-B is ubiquitously ... 13 (2): 214-8. doi:10.1038/ng0696-214. PMID 8640229.. *^ Mohler, PJ; Rivolta, I; Napolitano, C; LeMaillet, G; Lambert, S; ... 1 (2): 93-9. doi:10.1161/circgenetics.108.792192. PMID 20031550.. *^ Alders, M; Christiaans, I; Pagon, RA; Adam, MP; Ardinger, ...
6 (2): 288-293. doi:10.1002/mgg3.358. PMC 5902401. PMID 29274115.. *^ Saha K, Saha A, Datta C, Chatterjee U, Ray S, Bera M. ... doi:10.1038/s41436-018-0291-2. PMID 30262925.. *^ Brodehl A, Dieding M, Klauke B, Dec E, Madaan S, Huang T, Gargus J, Fatima A ...
18 (2): 93-124. doi:10.1615/critreveukargeneexpr.v18.i2.10. PMID 18304026.. *^ a b c Wei B, Jin JP (Jan 2011). "Troponin T ... 52 (2): 103-16. doi:10.1007/s002390010139. PMID 11231890.. *^ Imai H, Hirai S, Hirono H, Hirabayashi T (Mar 1986). "Many ... 2), reflecting specialized functional features of the different muscle fiber types.[7][8][9] ... Jin JP, Samanez RA (Feb 2001). "Evolution of a metal-binding cluster in the NH(2)-terminal variable region of avian fast ...
核纤层蛋白 A/C(英语:Lamin A/C)是由人类基因LMNA 编码的蛋白质[1][2],属于核纤层蛋白家族。 ... March 1993, 19 (2): 203-8. PMID 8511676. doi:10.1007/BF01233534.. *^ Wydner KL, McNeil JA, Lin F, Worman HJ, Lawrence JB. ... 2000, 129 (2-3): 313-23. PMID 10806082. doi:10.1006/jsbi.2000.4216.. 引文格式1维护:显式使用等标签 (link) ... 2004, 5 (2): 98-111. PMID 15080529.. *. Al-Shali KZ,
12 (2): e0172762. doi:10.1371/journal.pone.0172762. PMID 28241046.. *^ Frappier T, Stetzkowski-Marden F, Pradel LA (April 1991 ... 5 (2): 187-96. PMID 8180132.. *. Dong DL, Xu ZS, Chevrier MR, Cotter RJ, Cleveland DW, Hart GW (August 1993). "Glycosylation of ... 50 (2): 475-90. PMID 2516804.. *. Julien JP, Grosveld F, Yazdanbaksh K, Flavell D, Meijer D, Mushynski W (June 1987). "The ... 18 (2): 720-30. PMID 9425014.. *. Mersiyanova IV, Perepelov AV, Polyakov AV, Sitnikov VF, Dadali EL, Oparin RB, Petrin AN, ...
96 (2): 145-55. doi:10.1113/expphysiol.2010.053975. PMID 20889606.. *^ Parcell AC, Woolstenhulme MT, Sawyer RD (March 2009). " ... It also aids in preventing overstretching of the thick filament, recoiling like a spring whenever a muscle is stretched.[2] ... 23 (2): 359-65. doi:10.1519/JSC.0b013e318198fd62. PMID 19209072.. *^ Gore, Jessica. "Muscle Growth in Bodybuilders". http:// ...
220 (2): 357-62. doi:10.1006/excr.1995.1326. PMID 7556444.. *^ Schweizer J, Bowden PE, Coulombe PA, Langbein L, Lane EB, Magin ... 101 (2): 165-9. doi:10.1007/s004390050607. PMID 9402962.. *. Bowden PE, Hainey SD, Parker G, et al. (1998). "Characterization ...
... s (/ˈmaɪəsɪn, -oʊ-/[1][2]) are a superfamily of motor proteins best known for their roles in muscle contraction and in a ... 5 (2): 171-2. doi:10.1038/ncb924. PMID 12563277. S2CID 687308.. *^ Lu Q, Ye F, Wei Z, Wen Z, Zhang M (October 2012). " ... 2 (6): 1351-8. doi:10.1093/mp/ssp094. PMID 19995734.. *^ Peremyslov VV, Prokhnevsky AI, Avisar D, Dolja VV (March 2008). "Two ... doi:10.1186/gb-2001-2-7-research0024. PMC 55321. PMID 11516337.. *^ Baluska F, Cvrcková F, Kendrick-Jones J, Volkmann D (May ...
"179 (2): 222-228. doi:10.1016/j.jsb.2012.02.013. ISSN 1047-8477. PMC 3378790. PMID 22406539.. ... Human Cytoplasmic Dynein 2 Domains. Shown is the order of regions of interest for human cytoplasmic dynein 2 motor domains as ... Berezuk, Matthew A.; Schroer, Trina A. (2007-02-01). "Dynactin enhances the processivity of kinesin-2". Traffic. 8 (2): 124-129 ... This page was last edited on 2 October 2018, at 22:25 (UTC). ... is also some evidence suggesting that it may regulate kinesin-2 ...
ROCK indirectly strengthens actin/myosin contraction through inhibiting Cofilin, a protein which depolymerizes actin stress ... 570 (Pt 2): 219-35. doi:10.1113/jphysiol.2005.097998. PMC 1464317. PMID 16284075. Kim MT, Kim BJ, Lee JH, Kwon SC, Yeon DS, ... 166 (2): 409-19. doi:10.1016/S0002-9440(10)62264-X. PMC 1237049. PMID 15681825. Russo JM, Florian P, Shen L, Graham WV, ...
Meanwhile, phosphorylation of PI3K by SRC activates RhoA which leads to activation of cofilin-P and disruption of filamentous ... may activate SRC leading to activation of Rac1 which results in phosphorylation of LIMK1 and LIMK2 to deactivate cofilin ... 174 (2): 289-299. doi:10.1083/jcb.200601087. PMC 2064188. PMID 16831887. Arikkath, J; Reichardt, LF (2008). "Cadherins and ...
immunogen = synthetic peptide: C-D I K D R S T L G E K, representing the C-terminus of the human protein according to NP_068733.1; NP_619579.1. ...
Buy our Recombinant Human Cofilin 2 protein. Ab114614 is a full length protein produced in Wheat germ and has been validated in ... It has the ability to bind G- and F-actin in a 1:1 ratio of cofilin to actin. It is the major component of intranuclear and ... Recombinant Human Cofilin 2 protein. See all Cofilin 2 proteins and peptides. ...
"Cofilin 2" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... A member of the cofilin family of proteins that is expressed in MUSCLE CELLS. It has ACTIN depolymerization activity that is ... This graph shows the total number of publications written about "Cofilin 2" by people in Harvard Catalyst Profiles by year, and ... Xenopus actin depolymerizing factor/cofilin (XAC) is responsible for the turnover of actin filaments in Listeria monocytogenes ...
Ausgesuchte Qualitäts-Hersteller für Cofilin 2 Antikörper. Hier bestellen. ... Monoklonale und polyklonale Cofilin 2 Antikörper für viele Methoden. ... cofilin, muscle isoform , cofilin-2 , nemaline myopathy type 7 , cofilin 2 (muscle) , cofilin 2 , LOW QUALITY PROTEIN: cofilin- ... study investigated the comparison of the levels of cofilin-1 and cofilin-2 in regressive QR-32 and progressive QRsP-11cells by ...
Anti-Cofilin 2 pAb (GTX14133) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance. ... Storage Conditions: Cofilin 2 antibody. Storage Buffer. Preservative: 0.05% Sodium Azide; Constituents: 30% Glycerol, 0.15M ... cofilin 2 (muscle). Background. Cofilin is a widely distributed intracellular actin-modulating protein that binds and ...
Rabbit Polyclonal Cofilin 2 antibody. Validated in WB, ICC/IF, IHC-P. Tested in Human, Mouse. - professional antibody ... Cofilin is a widely distributed intracellular actin-modulating protein that binds and depolymerizes filamentous F-actin and ... Gillett et al., 1996 [PubMed 8800436]). Cofilin-2 is a member of the AC group of proteins that also includes cofilin-1 (CFL1) ... There are currently no reviews for Cofilin 2 antibody (GTX100213). Be the first to share your experience with this product. ...
"Cofilin-1 phosphorylation catalyzed by ERK1/2 alters cardiac actin dynamics in dilated cardiomyopathy caused by lamin A/C gene ... cofilin-1 induces cardiac dysfunction. (A) Immunoblots showing cofilin-1, phosphorylated (Thr25) cofilin-1, cofilin-2 and gapdh ... cofilin-1 induces cardiac dysfunction. (A) Immunoblots showing cofilin-1, phosphorylated (Thr25) cofilin-1, cofilin-2 and gapdh ... A) Immunoblots showing cofilin-1, phosphorylated (Thr25) cofilin-1, cofilin-2 and gapdh in protein extracts from hearts of ...
GFP-tagged cofilin-WT and cofilin-S3A were constructed by subcloning the full-length cofilin or cofilin-S3A into pEGFP vector ( ... 5B). Furthermore, anti-p-cofilin and anti-cofilin double-staining showed that the p-cofilin signal rapidly decreased at the ... GFP-cofilin-WT) and a non-phosphorylatable and constitutively active mutant of cofilin (GFP-cofilin-S3A) (Arber et al., 1998) ... p-cofilin, the inactive form of cofilin) in a time-dependent manner, without affecting the total cofilin level. ...
Cofilin 2 cDNA ORF Clone, Rat in pCMV3-C-FLAG is expression-ready, and confirmed by full-length sequence & expression ... and contains residues conserved among the cofilin family that are responsible for actin-binding. Cofilin 2 (CFL2) is an ... Cofilin 2 Background Information. Cofilin 2 (muscle), also known as CFL2, is a member of cofilin family of the actin-binding ... Purified cofilin 2 depolymerized actin filaments in a dose- and pH-dependent manner and reduced the apparent viscosity of an ...
... which phosphorylate/inactivate and dephosphorylate/activate ADF/cofilin, respectively. ADF/cofilin activity is also regulated ... which phosphorylate/inactivate and dephosphorylate/activate ADF/cofilin, respectively. Actin-depolymerization factor/cofilin ... ADF/cofilin regulate synaptic function through their effects on dendritic spines and the trafficking of glutamate receptors, ... ADF/cofilin regulate synaptic function through their effects on dendritic spines and the trafficking of glutamate receptors, ...
Cofilin-1 phosphorylation catalyzed by ERK1/2 alters cardiac actin dynamics in dilated cardiomyopathy caused by lamin A/C gene ... cofilin-1 induces cardiac dysfunction. (A) Immunoblots showing cofilin-1, phosphorylated (Thr25) cofilin-1, cofilin-2 and gapdh ... In vitro kinase assay Recombinant His-tagged cofilin-1, cofilin-1-T25A and cofilin-2 (5 lg) were incubated alone or with 0.5 lg ... We further incubated pERK2 with His-cofilin-1, His- cofilin-1-T25A or His-cofilin-2. pERK2 catalyzed the phosphory- lation of ...
Muscle Lim protein interacts with cofilin 2 and regulates F-actin dynamics in cardiac and skeletal muscle. In: Molecular and ... Muscle Lim protein interacts with cofilin 2 and regulates F-actin dynamics in cardiac and skeletal muscle. Molecular and ... Muscle Lim protein interacts with cofilin 2 and regulates F-actin dynamics in cardiac and skeletal muscle. / Papalouka, ... N2 - The muscle LIM protein (MLP) and cofilin 2 (CFL2) are important regulators of striated myocyte function. Mutations in the ...
immunogen = peptide mapping at the N-terminus of human cofilin 1. recognizes Cofilin 1 and Cofilin 2. -. ... immunogen = peptide mapping at the C-terminus of human cofilin. recognizes Cofilin 1 and Cofilin 2. -. ... Cofilin 2. -. Cofilin 2. Novus Biologicals. polyclonal. IgG. Goat. (liquid, azide, affinity purified). ELISA, WB. Human. ... detects cofilin protein phosphorylized at Serine 3. -. Myosin light chain, phos ser19 (MF-20). Cell Signaling. monoclonal. IgG1 ...
Molecular mechanisms of invadopodium formation: the role of the N-WASP-Arp2/3 complex pathway and cofilin. J. Cell Biol. 168, ... Yonezawa, N., Nishida, E. & Sakai, H. pH control of actin polymerization by cofilin. J. Biol. Chem. 260, 14410-14412 (1985). ... Moon, A. & Drubin, D. G. The ADF/cofilin proteins: stimulus-responsive modulators of actin dynamics. Mol. Biol. Cell 6, 1423- ... Supplementary Figure 7 Co-sedimentation assay of CapZαCapZβ/Cofilin with liposomes containing 20% PI3P or PI(4,5)P2.. Proteins ...
Unmodified cofilin bound and pelleted with F-actin, whereas caged cofilin and S3E cofilin did not and remained in the ... Activation of cofilin is required for cell motility (12-14). However, it is not clear how the activities of cofilin, which ... Mixtures (M) of 5 μM F-actin, equimolar S3C cofilin, S3E, or caged cofilin were incubated for 2 hours at room temperature and ... G to J) Global photorelease of cofilin leads to an increase in free barbed ends. (G) Treatment with siRNA against cofilin ...
... there are two cofilin gene subtypes, cofilin-1 and cofilin-2, which encode different proteins. The former is expressed in a ... D) Cofilin knockdown increased cell viability in As2O3-treated NB4-R1 cells. (E) Cofilin knockdown inhibited apoptosis in As2O3 ... Role of cofilin-1 in mitochondrial cytochrome C release. (A) Knockdown of cofilin-1 increased the mitochondrial expression of ... Nevertheless, little is known about the role of cofilin-1 in APL. Cofilin-1 may be involved in the resistance of NB4-R1 cells ...
Oxidant-induced apoptosis is mediated by oxidation of the actin-regulatory protein cofilin. Stephanie Zdanov, Fabio Klamt, ... In treated cells, cofilin loses its affinity with actin and translocates from the cytosol to the mitochondria. Only oxidized ... Exposure of cofilin to taurine chloramine results in oxidation of the Met residues to Met sulfoxide and causes intramolecular ... We conclude that cofilin is a major intracellular redox-sensor that, when oxidized at critical cysteine residues, activates ...
PTEN Directly Activates the Actin Depolymerization Factor Cofilin-1 During PGE2-Mediated Inhibition of Phagocytosis of Fungi ...
Cofilin 1 actin modulating protein. COF1. P23528. 18,491. 8.22. −3.15. 4.80E−33. ... Lines terminating with an arrow indicate "acts on." Act6A, actin binding protein; CFL, cofilin; ECH, enoyl coenzyme A hydratase ... H2O2 was used as a positive control. (B) Enhanced carbonylation of proteins by RSV infection in Prdx-1, Prdx-4, or Prdx-1 plus ... TABLE 2. Identification of proteins whose cysteine residues were protected from oxidation by either Prdx-1, Prdx-4, or both in ...
We can speculate that in our case cofilin phosphorylation could be promoted via Rac/PAK1/LIMK2 signaling. In fact we see a mild ... Cofilin phosphorylation is regulated both by kinases (LIMK family) and phosphatases (SSH family). The KINEX microarray, however ... Finally, though it might be contra intuitive others have also shown that Y27632 treatment can induce an increase in cofilin ... The positive effect of Y-27632 on cofilin phosphorylation was observed only in 3D suggesting that specific, and for AMT ...
2010, 2: 1-10.1186/gm122.View ArticlePubMedPubMed CentralGoogle Scholar. ... Figure 2 cDNA-AFLP Transcript Profiling of pancreatic cancer patients. cDNA-AFLP tag patterns amplified from mRNA of skeletal ... It has been shown that a loss of weight exceeding 10% of the stable pre illness weight is correlated to a worse prognosis [2]. ... Table 2 Characteristics of patients with pancreatic cancer with (N = 10) and without cachexia (N = 13) ...
... cofilin, and MLC. Levels of phophorylated MLC were dramatically reduced in ROCK-inhibited cultures in contrast to cofilin and ... 8b) and cofilin (data not shown) are robustly phosphorylated during the early postnatal period and then downregulated. Much of ... Initial results with antibodies to phospho-cofilin suggest a very similar pattern of activation (data not shown). In contrast, ... and cofilin, which is phosphorylated by LIM-kinase, a substrate of ROCK (Maekawa et al., 1999) and of PAK (Edwards et al., 1999 ...
J. R. Bamburg and B. W. Bernstein, "Roles of ADF/cofilin in actin polymerization and beyond," F1000 Biology Reports, vol. 2, ... J. J. Bravo-Cordero, M. A. O. Magalhaes, R. J. Eddy, L. Hodgson, and J. Condeelis, "Functions of cofilin in cell locomotion and ... Upon activation, this cytoskeleton is disrupted by the action of coronins (F-actin debranching proteins) [125] and cofilin [126 ... and cofilin and gelsolin (F-actin-severing proteins). (c) As more phagocytic receptors get engaged around the particle, the ...
... cofilin-2,i,knockout,mouse,model.,Agrawal,,Savic,,Joshi,,1114F,Anoctamin,5,skeletal,muscle,subcellular,localization,preserved, ... 2.,Z.,Scherrer,,Maurer-Morelli,,F.,Vasconcellos,,Rocha,,Matos,,Steiner.,1101F,Apoptosome,independent,caspase,9,activation, ...
Role of SPEG and cofilin-2 in skeletal muscle function: Mutations in these genes cause different types of congenital myopathy. ... He is utilizing conditional knockout mouse models of SPEG and cofilin-2 to determine their function and identify interacting ... Skeletal muscle microRNA and messenger RNA profiling in cofilin-2 deficient mice reveals cell cycle dysregulation hindering ... Cofilin-2 phosphorylation and sequestration in myocardial aggregates: novel pathogenetic mechanisms for idiopathic dilated ...
Cofilin‑1 (human): Y89‑p, Cofilin‑1 (mouse): Y89‑p, Cofilin‑1 (rat): Y89‑p, Cofilin‑1 (pig): Y89‑p ... Cofilin2 (human): Y89‑p, Cofilin2 (mouse): Y89‑p, Cofilin2 (rat): Y89‑p ... SHP‑2 (human): Y62‑p, SHP‑2 iso1 (human): Y62‑p, SHP‑2 (mouse): Y62‑p, SHP‑2 (rat): Y62‑p ...
Cofilin‑1 (human): Y117‑p, Cofilin‑1 (mouse): Y117‑p, Cofilin‑1 (rat): Y117‑p, Cofilin‑1 (pig): Y117‑p ... Cofilin2 (human): Y117‑p, Cofilin2 (mouse): Y117‑p, Cofilin2 (rat): Y117‑p ... tensin 2 (human): Y483‑p, tensin 2 iso2 (human): Y483‑p, tensin 2 iso4 (human): Y493‑p, tensin 2 (mouse): Y483‑p, tensin 2 (rat ...
Sequencing of the entire coding region of gene (s) Note: TTN alone related to Congenital Myopathy only; please contact the laboratory to discuss. ...
Cofilin 2. AF134802. 14q13.2. 1. Suppressor of profilin/p41 of actin-related complex 2/3. BC006445. 7q22.1. 1. ... Prostaglandin D2 synthase is the most prevalent transcript in the corneal cDNA library, and only cDNAs for matrix Gla protein ... 2. Lütjen-Drecoll, E. (2000) Importance of trabecular meshwork changes in the pathogenesis of primary open-angle glaucoma J ... Liquori, CL, Ricker, K, Moseley, ML, et al (2001) Myotonic dystrophy type 2 caused by a CCTG expansion in intron 1 of ZNF9 ...
Validation of cofilin 2 and RCC2 circadian abundance.. * Fig. S3. Circadian clocks are robust against actin-modulating drugs. ... 2. CRY-dependent cell-intrinsic rhythms in actin polymerization.. (A) Schematic depicting rhythms in actin polymerization, ... DAPI, 4,6′-diamidino-2-phenylindole. (E) Transverse sections (60 μm) of mouse wounds made during the active and resting phases ... 2Addenbrookes Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge CB2 0QH, UK. ...
  • A member of the cofilin family of proteins that is expressed in MUSCLE CELLS. (
  • Actin-depolymerization factor (ADF)/cofilin, a family of actin-binding proteins, are critical for the regulation of actin reorganization in response to various signals. (
  • Actin-depolymerization factor/cofilin activity is also regulated by other actin-binding proteins, activity-dependent subcellular distribution and protein translation. (
  • A general caging method for proteins that are regulated by phosphorylation was used to study the in vivo biochemical action of cofilin and the subsequent cellular response. (
  • Results obtained from cofilin overexpression are complicated by issues of compensation by phosphorylation ( 1 , 2 ), modulation of expression of other motility-related proteins ( 3 ), inappropriate localization of overexpressed protein ( 4 - 7 ), and lethality of cofilin suppression ( 8 - 10 ). (
  • For example, it is possible that cofilin-induced polymerization could generate an initial asymmetric compartment that defines the high-affinity receptors for chemoattractants ( 16 ) as a site for subsequent recruitment and activation of phosphatidylinositol 3-kinase and Rho family G proteins. (
  • RSV-induced changes of nuclear proteins of A549 cells by 2-D DIGE. (
  • Identical amounts of proteins were separated by 2-DE and transferred to Immobilon membranes. (
  • He is utilizing conditional knockout mouse models of SPEG and cofilin-2 to determine their function and identify interacting proteins in skeletal muscles. (
  • Cofilin/ADF (actin depolymerizing factor) is a family of proteins that controls F-actin remodeling and thereby the production of membrane protrusions (e.g., filopodia and lamelopodia). (
  • In contrast to cell attachment, cyclic stretching ofthe adherent cells induced a robust phosphorylation only of ERK1/2 and thephosphorylation levels of the other investigated proteins were not or only moderately affected by stretching. (
  • Background: Cofilin and actin-depolymerization factor (ADF) are members of a family of essential conserved small actin-binding proteins that play pivotal roles in cytokinesis, endocytosis, embryonic development, stress response, and tissue regeneration (1). (
  • The protein encoded by S100A11 is a member of the S100 family of proteins containing 2 EF-hand calcium-binding motifs. (
  • Among actin binding proteins, ADF/cofilin is the most-characterized stimulus-responsive mediator of actin dynamics. (
  • In response to insulin and lysophosphatidic acid, LIM-kinases (LIMKs), activated by effectors of Rho family GTPases, phosphorylate ADF/cofilin specifically at Ser-3, and thereby inhibit filament-severing and monomer binding activities of ADF/cofilin proteins. (
  • In contrast, proteins suppressed in FH lines include the 27-kDa heat shock protein, translationally controlled tumor protein, and several proteins associated with actin modification such as actin prepeptide, F-actin capping protein α subunit, and cofilin. (
  • The SSH family appears to play a role in actin dynamics by reactivating ADF/cofilin proteins in vivo (Niwa et al. (
  • Two-dimensional gel electrophoresis (2-DE) was used to isolate proteins from MSCs, cMSCs and ACs before being identified using liquid chromatography-mass spectrometry (LC-MS). The differentially expressed proteins were then analyzed using image analysis software. (
  • In accordance with their proposed rule, proteins like ADF, cofilin and LIMK1 are slingshot substrates. (
  • A , 2-DE analysis of differentially expressed proteins induced by BMP2/4. (
  • Proteins (300 μg) from cells treated with or without BMP2/4 were analyzed by 2-DE. (
  • Proteins showing differential expression were isolated and identified using MALDI-MS and MALDI-MS/MS. B , enlarged images of differentially expressed protein spots between untreated and BMP2/4-treated C3H10T1/2 cells. (
  • Selected regions of 2-DE gels illustrate differentially expressed proteins among untreated C3H101/2 and BMP2- or BMP4-treated C3H101/2. (
  • Western blot analyses showed that proteins were up-regulated in the BMP2/4-treated C3H10T1/2 cells. (
  • Important components include: 1) platelet-derived growth factor (PDGF) signaling as central to myofibroblast cell proliferation, 2) transforming growth factor β (TGFβ), central to initiating myofibroblast activation, and 3) deposition of ECM proteins. (
  • Normal myofibrillar development followed by progressive sarcomeric disruption with actin accumulations in a mouse Cfl2 knockout demonstrates requirement of cofilin-2 for muscle maintenance. (
  • Nemaline myopathy with minicores caused by mutation of the CFL2 gene encoding the skeletal muscle actin-binding protein, cofilin-2. (
  • Auf finden Sie aktuell 94 Cofilin 2 (Muscle) (CFL2) Antikörper von 23 unterschiedlichen Herstellern. (
  • Here we report atomic-level characterization by magic angle spinning (MAS) NMR of the muscle isoform of human cofilin 2 (CFL2) bound to F-actin. (
  • A novel homozygous missense mutation in exon 2 (c.19G>A, p.Val7Met) of CFL2 was identified in two siblings with congenital myopathy. (
  • Cofilin 2 (muscle), also known as CFL2, is a member of cofilin family of the actin-binding protein superfamily. (
  • Cofilin 2 (CFL2) is an important regulator of striated myocyte function. (
  • The muscle LIM protein (MLP) and cofilin 2 (CFL2) are important regulators of striated myocyte function. (
  • This interaction has direct implications in actin cytoskeleton dynamics in regulating CFL2-dependent F-actin depolymerization, with maximal depolymerization enhancement at an MLP/CFL2 molecular ratio of 2:1. (
  • Novel Homozygous Cofilin-2 (CFL2) Mutation Causing a Congenital Form of Nemaline Myopathy with Filamentous Inclusions. (
  • Immunohistochemical analysis of paraffin-embedded human gastric cancer, using Cofilin 2(GTX100213) antibody at 1:100 dilution. (
  • Immunofluorescence analysis of paraformaldehyde-fixed HeLa, using Cofilin 2(GTX100213) antibody at 1:200 dilution. (
  • Various whole cell extracts (30 µg) were separated by 12% SDS-PAGE, and the membrane was blotted with Cofilin 2 antibody (GTX100213) diluted at 1:1000. (
  • There are currently no references for Cofilin 2 antibody (GTX100213) . (
  • To examine the expression of Slit in developing OE, we stained the brain sections from E16 mice using the anti-Slit-2 antibody. (
  • The HRP conjugated antibody is expected to exhibit the same species cross-reactivity as the unconjugated Cofilin (D3F9) XP ® Rabbit mAb #5175. (
  • There are no publications for Cofilin Antibody (H00001072-M04IR). (
  • Two-dimensional Western blots probed with cofilin antibody showed multiple protein spots with isoelectric points of 6-9 pH units. (
  • In combination with the biotinylated antibody provided, the 545 nm signal generated will report levels of the phosphoprotein of interest (Target 2). (
  • The following product was used in this experiment: Cofilin Polyclonal Antibody from Thermo Fisher Scientific, catalog # 10960-1-AP. (
  • Western Blot: EGLN1/PHD2 Antibody [NB100-137] - Analysis of PHD2 in normoxia (lane 1) or hypoxia (lane 2) treated SK-N-BE(2) cells using anti-PHD2 antibody. (
  • Simple Western: EGLN1/PHD2 Antibody [NB100-137] - Simple Western lane view shows a specific band for PHD2/HIF Prolyl Hydroxylase 2 in 0.5 mg/ml of Hypoxic HeLa lysate. (
  • The epitope recognized by this antibody maps to a region between residues 1 and 50 of human PHD2/HIF Prolyl Hydroxylase 2 using the numbering given in entry NP_071334.1 (GeneID 54583). (
  • Cofilin 2 is the muscle isoform. (
  • Isoform 2: May play a role in early sarcomere organization. (
  • The protein spots cofilin-1 (CFL1) and glycealdehyde-3-phosphate dehydrogenase (GAPD) from cMSCs had expression levels similar to that of ACs whereas the others (ie. (
  • In this review we will focus on the role of actin-depolymerization factor (ADF)/cofilin in the regulation of LTP, LTD, dendritic spines and their dysfunction in Alzheimer's disease (AD). (
  • This family includes cofilin-1 (n-cofilin, non-muscle), cofilin-2 (muscle cofilin) and actin-depolymerization factor (ADF, destrin) and is well conserved among eukaryotes ( Maciver and Hussey, 2002 ). (
  • We examined the effects of both global and local release of cofilin activity on actin polymerization, depolymerization, protrusion, and motility. (
  • However, it is not clear how the activities of cofilin, which include barbed end formation and actin polymerization ( 14 ) as well as depolymerization ( 12 ), are coordinated. (
  • Biochemical characterization of interactions between nine mutant yeast cofilins and yeast actin provided evidence that F-actin binding and depolymerization are essential cofilin functions. (
  • a member of the ADF (actin-depolymerizing factor)/cofilin family accelerates depolymerization at pointed ends and severs long actin filaments (Niwa, 2002 and references therein). (
  • Rac1 activated the kinases PAK and LIMK1, which inactivated cofilin, thus preventing actin depolymerization dynamics. (
  • Furthermore, Slit-2 triggered the activation of the F-actin severing protein cofilin and the inhibition of RhoA, leading to the collapse of the leading front and the subsequent reversal of the polarity of OEC migration. (
  • Knockdown of pleckstrin-2 in the early stage of terminal erythropoiesis disrupted the actin cytoskeleton and led to differentiation inhibition and apoptosis. (
  • Treatment of the cells with a scavenger of reactive oxygen species rescued cofilin mitochondrial entry and differentiation inhibition induced by pleckstrin-2 knockdown. (
  • We show that these defects can be rescued in culture and in embryos through the inhibition of the Rho-associated, coiled-coil-containing protein kinase 1 (ROCK), thus demonstrating a direct relationship between SHP-2 N308D and ROCK activation in the developing heart. (
  • Inhibition of the Rac1 effector PAK1 with a small-molecule inhibitor rescued cofilin signaling in FXS mice, indicating a causal relationship between PAK1 and cofilin signaling. (
  • Plumbagin caused an effective inhibition in OPN-induced the expression of ROCK1 as well as the phosphorylation of LIM kinase 1 and 2 (LIMK1/2), and cofilin. (
  • Lastly, inhibition of cell spreading by v-Src was rescued partially by co-expression of cofilin, and to a greater extent by the Y68F mutant which is not subjected to v-Src induced degradation through phosphorylation, suggesting that v-Src mediated changes in cell spreading is, at least in part, through inhibiting the function of cofilin via phosphorylating it at Y68. (
  • In Drosophila, loss of ssh function dramatically increases levels of both F actin and phospho-cofilin (P cofilin) and disorganizes epidermal cell morphogenesis. (
  • This kit can be used in combination with the AlphaLISA SureFire Ultra phospho-cofilin assay to normalize to levels of total cofilin. (
  • Signaling through RHO GTPase, ROCK1 and LIMK1 to cofilin‐1 remodels actin to facilitate aggregate entry. (
  • In contrast to the mechanisms of inactivation of ADF/cofilin by kinases such as LIM-kinase 1 (LIMK1: see Drosophila LIM-kinase1 ), much less is known about its reactivation through dephosphorylation. (
  • Aberrant Hh signaling activity can be associated with numerous birth defects and uncontrolled Hh pathway activation is linked to the development of several types of cancers (1-2). (
  • Importantly, the RHO to cofilin‐1 signalling pathway also modulates entry of tau and α‐synuclein aggregates. (
  • These observations suggest that the LIMK-cofilin signaling pathway for regulating actin filament dynamics is evolutionarily conserved between Drosophila and mammals (Ohashi, 2000). (
  • It has been recently demonstrated that osteopontin (OPN) effectively inhibits cofilin activity through the focal adhesion kinase (FAK)/AKT/Rho-associated kinase (ROCK) pathway to induce the invasion of human non-small cell lung cancer (NSCLC) cells. (
  • Cofilin phosphorylation at Y68 did not change its activity per se, but induced increased ubiquitination of cofilin and its degradation through the proteosome pathway. (
  • Together, these results suggest a novel mechanism by which cofilin is regulated by v-Src through tyrosine phosphorylation at Y68 that triggers degradation of cofilin via ubiquitination-proteosome pathway and consequently inhibits cofilin activity in reducing cellular F-actin contents and cell spreading. (
  • ERK2 is activated in eosinophils via Phosphatidylinositol-3-kinase-gamma ( PI3K class IB )/ PDK(PDPK1) / PKC-zeta / H-Ras / c-Raf-1 / MEK1/2 kinases (MAPK/ERK) pathway [ 5 ], [ 6 ]. (
  • Cofilin is a widely distributed intracellular actin-modulating protein that binds and depolymerizes filamentous F-actin and inhibits the polymerization of monomeric G-actin in a pH-dependent manner. (
  • For example, the precise intracellular role of cofilin during cellular migration has been difficult to decipher, because motility depends on localized transients of spatially well-defined signaling activity. (
  • Furthermore, highly localized intracellular cofilin activation generated lamellipodia and determined the direction of cell motility. (
  • We conclude that cofilin is a major intracellular redox-sensor that, when oxidized at critical cysteine residues, activates mitochondria-dependent apoptosis. (
  • This pro-survival and differentiation function of pleckstrin-2 was mediated through its interaction with cofilin, by preventing cofilin mitochondrial entry when the intracellular level of reactive oxygen species was higher in the early stage of terminal erythropoiesis. (
  • Thus, our study identified a dual function of pleckstrin-2 in the early and late stages of terminal erythropoiesis through its regulations of actin dynamics and cofilin's mitochondrial localization, which reflects intracellular level of reactive oxygen species in different developmental stages. (
  • However, the critical regulatory step in activating cdc2 during progression into mitosis appears to be dephosphorylation of cdc2 at Thr14 and Tyr15 (2). (
  • ADF/cofilin undergoes rapid dephosphorylation as well, in response to several extracellular stimuli, which could result from downregulation of the kinases, upregulation of a phosphatase(s), or both. (
  • Cofilin activity is tightly regulated by phosphorylation and dephosphorylation events that are mediated by LIM Kinase (LIMK) and the phosphatase Slingshot (SSH), respectively. (
  • Dephosphorylation (activation) of cofilin, an actin binding protein, is stimulated by initiators of neuronal dysfunction and degeneration including oxidative stress, excitotoxic glutamate, ischemia, and soluble forms of β-amyloid peptide (Aβ). (
  • Cofilin2 shows significant homology to the other two members: cofilin 1 and DSTN, through its entire sequence, and contains residues conserved among the cofilin family that are responsible for actin-binding. (
  • Exposure of cofilin to taurine chloramine results in oxidation of the Met residues to Met sulfoxide and causes intramolecular disulfide bond formation, but only the Cys oxidation causes mitochondrial swelling. (
  • Synthetic peptide conjugated to KLH derived from within residues 1 - 100 of Human Cofilin. (
  • Locating the mutated residues on the yeast cofilin molecular structure allowed several important conclusions to be drawn. (
  • Fourthly, a previously unrecognized cofilin function or interaction is suggested by identification of spatially proximal residues important for cofilin function in vivo, but not for actin interactions in vitro. (
  • Skeletal muscle microRNA and messenger RNA profiling in cofilin-2 deficient mice reveals cell cycle dysregulation hindering muscle regeneration. (
  • 2009) Muscle LIM protein interacts with cofilin 2 and regulates F-actin dynamics in cardiac and skeletal muscle. (
  • In vivo expression of cofilin-1, phosphorylated on Thr25 by endogenous ERK1/2 signaling, leads to alterations in left ventricular function and cardiac actin. (
  • We now show in a large array of unique in vitro and in vivo disease models that phosphorylated ERK1/2 (pERK1/2) binds to and activates cofilin-1 in LMNA cardiomyopathy. (
  • We now show in a large array of unique in vitro and in vivo disease models that phosphorylated ERK1/2 (pERK1/2) binds to and activates cofilin-1 in LMNA cardiomyopa- thy. (
  • In order to establish the in vivo role of cofilin and its mechanistic contributions to cell motility, we prepared a mimic of inactive phosphocofilin that can be rapidly "switched on" by a brief burst of light. (
  • In vivo, cofilin acts synergistically with the Arp2/3 complex to amplify local actin polymerization responses upon cell stimulation, which gives it a central role in setting the direction of motility in crawling cells. (
  • Cofilin stimulates actin filament turnover in vivo. (
  • These results strongly suggest that the SSH family plays a pivotal role in actin dynamics by reactivating ADF/cofilin in vivo (Niwa, 2002). (
  • Furthermore, the negative effect of cofilin on cellular F-actin contents was inhibited by co-expression of v-Src, whereas that of cofilin mutant Y68F (Y68 mutated to F) was not affected, suggesting that v-Src-mediated cofilin phosphorylation at Y68 is required for degradation of cofilin in vivo . (
  • Regulation of ADF/cofilin involves various signaling pathways converging on LIM domain kinases and slingshot phosphatases, which phosphorylate/inactivate and dephosphorylate/activate ADF/cofilin, respectively. (
  • Some of the kinases involved in phosphorylating CREB at Ser133 are p90RSK, MSK, CaMKIV, and MAPKAPK-2 (7-9). (
  • Finally, mutation of the cofilin N-terminus suggests that its sequence is conserved because of its critical role in actin interactions, not because it is sometimes a target for protein kinases. (
  • Upstream of cofilin‐1, signalling from the RHO GTP ase and the ROCK 1 and LIMK 1 kinases controls cofilin‐1 activity to remodel actin and modulate aggregate entry. (
  • Mammalian LIM-kinases (LIMKs) phosphorylate cofilin and induce actin cytoskeletal reorganization. (
  • Testicular protein kinases (TESKs) also phosphorylate Ser-3 of ADF/cofilin and inhibit its activity, although upstream pathways of TESKs activation appear to be separate from that of LIMKs. (
  • In contrast to characterization of the kinases, however, much less is known about the phosphatases that reactivate ADF/cofilin (Niwa, 2002 and references therein). (
  • One hypothesis would be that Ssh and these kinases share the same substrate, ADF/cofilin, regulate its phosphorylation level, and consequently control its actin-depolymerizing activity. (
  • Cofilin-1 phosphorylation catalyzed by ERK1/2 alters cardiac actin dynamics in dilated. (
  • These results demonstrate a novel role for cofilin-1 on actin dynamics in cardiac muscle and provide a rationale on how increased ERK1/2 signaling leads to LMNA cardiomyopathy. (
  • Among the regulators of actin, cofilins, which are actin-depolymerizing factors, play an essential role in the dynamics of filaments. (
  • Results pERK1/2 alters F-actin dynamics in LMNA cardiomyopathy We set out to unravel the consequences of abnormal ERK1/2 signaling in the heart of LmnaH222P/H222P mice, a model for dilated cardiomyopathy caused by mutation in LMNA (22). (
  • Cofilin has emerged as a key regulator of actin dynamics at the leading edge of motile cells. (
  • Here, we describe detailed methods for: 1) real-time, high-resolution monitoring of multiple chemotaxis assays, and 2) simultaneously visualizing the chemoattractant gradient and the spatiotemporal dynamics of signaling events in neutrophil-like HL60 cells. (
  • In the spinal cord of symptomatic SOD 1 G93A transgenic mice, cofilin‐1 phosphorylation is increased and actin dynamics altered. (
  • The ADF (actin-depolymerizing factor)/cofilin family, represented by Twinstar in Drosophila is a stimulus-responsive mediator of actin dynamics. (
  • The ADF (actin-depolymerizing factor)/cofilin family (see MIM 601442) is composed of stimulus-responsive mediators of actin dynamics. (
  • Using a mouse fetal liver erythroblast culture system and a targeted shRNA functional screening strategy, we identified a critical role of pleckstrin-2 in actin dynamics and protection of early stage terminal erythroblasts from oxidative damage. (
  • Cofilin is a major regulator of actin dynamics involved in the regulation of cell spreading and migration through its actin depolymerizing and severing activities. (
  • We previously demonstrated that extracellular signal-regulated kinase (ERK) 1/2 is hyper-activated in the heart in LMNA cardiomyopathy (7). (
  • Finally, the Slit-2-induced repulsion of cell migration was fully mimicked by co-application of inhibitors of F-actin polymerization and RhoA kinase. (
  • Email: [email protected] Abstract Hyper-activation of extracellular signal-regulated kinase (ERK) 1/2 contributes to heart dysfunction in cardiomyopathy caused by mutations in the lamin A/C gene (LMNA cardiomyopathy). (
  • We previ- ously demonstrated that extracellular signal-regulated kinase (ERK) 1/2 is hyper-activated in the heart in LMNA cardiomyopa- thy (7). (
  • We studied how tyrosine kinase Syk (spleen tyrosine kinase) and cofilin control phagocytosis of degenerated myelin by CR3 in microglia and macrophages. (
  • We report that Smurf1-dependent RhoA degradation in tumor cells results in the down-regulation of Rho kinase (ROCK) activity and myosin light chain 2 (MLC2) phosphorylation at the cell periphery. (
  • Creatine kinase (CK) level is typically either normal or mildly elevated (2-5 times the normal range) in all of the congenital myopathies. (
  • TESK2 (Testis Associated Actin Remodelling Kinase 2) is a Protein Coding gene. (
  • In vitro kinase reaction revealed that DLIMK efficiently phosphorylates Drosophila cofilin (Twinstar) specifically at Ser-3, the site responsible for inactivation of its actin-depolymerizing activity. (
  • ADF/cofilin regulate synaptic function through their effects on dendritic spines and the trafficking of glutamate receptors, the principal mediator of excitatory synaptic transmission in vertebrates. (
  • Here we show that PKD can also regulate cofilin activity via activation of LIMK. (
  • Cofilin 2 phosphorylation and genetic overexpression plays a role in the pathogenesis of idiopathic dilated cardiomyopthay. (
  • Moreover, cofilin‑1 knockdown by its specific short hairpin RNA significantly suppressed As2O3‑induced NB4‑R1 cell apoptosis and inhibited the release of mitochondrial cytochrome C. Whereas, overexpression of cofilin‑1 using a plasmid vector carrying cofilin‑1 increased the release of cytochrome C into the cytoplasm from the mitochondria in As2O3‑treated NB4‑R1 cells. (
  • Our data suggest that PKD inactivates Cofilin through modulation of both of its regulatory pathways. (
  • To address these issues further and to identify the cellular and biochemical pathways that function downstream of SHP-2 in heart development, we generated the most prevalent human Noonan and JMML mutations in SHP-2 and introduced these into Xenopus . (
  • Studies indicate that cofilin binds actin stoichiometrically - one cofilin molecule per actin filament subunit. (
  • We show that active phosphorylated ERK1/2 directly binds to and catalyzes the phosphorylation of the actin depolymerizing factor cofilin-1 on Thr25. (
  • Cofilin binds to F-actin and exhibits pH-sensitive F-actin depolymerizing activity. (
  • A rare form of CNM is associated with recessive mutations in the BIN1 gene encoding the protein amphiphysin 2, which binds to DNM2 during clathrin-mediated endocytosis. (
  • Recent analysis of the distribution of cofilin and phosphocofilin in migrating fibroblasts suggests a role for active cofilin at the leading edge ( 15 ). (
  • Active cofilin could advance phagocytosis by promoting F-actin remodeling, which supports the production of membrane protrusions (e.g., filopodia), which, as we also revealed, are instrumental in myelin phagocytosis. (
  • Viral delivery of a constitutively active cofilin mutant (cofilinS3A) into the somatosensory cortex of Fmr1 -deficient mice rescued the immature dendritic spine phenotype and increased spine density. (
  • Interestingly, in response to Slit-2 stimulation, collapse of the leading front required the activation of the F-actin severing protein cofilin in a Ca 2+ -dependent manner, whereas the subsequent reversal of the soma migration depended on the reversal of RhoA activity across the cell. (
  • Using redox-proteomics, we found that the actin-binding protein cofilin is a key target of oxidation that mediates induction of apoptosis by taurine chloramine, a physiological oxidant produced by activated neutrophils. (
  • Adhesion to fibronectin by αvβ3 supports extensive actin cytoskeletal reorganization through the actin-severing protein cofilin, resulting in a single broad lamellipod with static cell-matrix adhesions at the leading edge. (
  • Muscle-specific protein cofilin-2 controls the length of actin filaments in muscle cells. (
  • Phosphorylation at Ser3 also regulates cofilin translocation from the nucleus to the cytoplasm (6). (
  • Furthermore, Ssh and the hSSHs dephosphorylate P cofilin in cultured cells and in cell-free assays. (
  • Phosphatases of Regenerating Liver (PRLs): Three PRL genes were described in mammals (PRL-1, PRL-2 and PRL-3). (
  • Only oxidized cofilin interacts with the organelles and it induces mitochondrial swelling and cytochrome c release. (
  • Thirdly, despite striking structural similarity, cofilin interacts with actin in a different manner from gelsolin segment-1. (
  • Sequencing of several cofilin gel spots revealed phosphorylation of serine 3, a post-translational modification associated with decreased actin binding and cytoskeletal reorganization. (
  • This suggested that As2O3 can induce the transfer of cofilin‑1 from the cytoplasm to mitochondria and trigger the release of mitochondrial cytochrome C in NB4‑R1 cells. (
  • We then found that DH infusion of G-1 increased both CA1 spine density and phosphorylation of the actin polymerization regulator cofilin, suggesting that activation of GPER may increase spine morphogenesis through actin polymerization. (
  • We also previously demonstrated increased pERK1/2 primarily in the nucleus of transiently transfected C2C12 cells over-expressing the lamin A H222P variant (7). (
  • When we examined protein extracts from stably transfected C2C12 cells expressing H222P lamin A (C2-H222P) at lower levels (24,25), we observed an increase in cytoplasmic relative to nuclear pERK1/2 compared with cells expressing wild-type lamin A (C2-WT) (Fig. 1B). (
  • Total cellular pERK1/2 was not changed (data not shown), which is consistent with previous results showing that it is only increased after subjecting these cells to stress (24). (
  • The results demonstrated that in retinoic acid‑resistant NB4‑R1 cells, the protein expression of cofilin‑1 was markedly increased compared with that in the drug‑sensitive NB4 cells. (
  • Subsequently, the effects of cofilin‑1 on As2O3‑induced apoptosis in NB4‑R1 cells were further investigated. (
  • In treated cells, cofilin loses its affinity with actin and translocates from the cytosol to the mitochondria. (
  • Cells become resistant to oxidant-induced apoptosis when Cys to Ala cofilin mutants are over-expressed. (
  • Moreover, over-expression of wild-type cofilin causes a 2-fold increase in the sensitivity of cells to oxidant-induced apoptosis. (
  • Nuclear extracts (150 μg) from uninfected (−RSV) or RSV-infected (+RSV) A549 cells were separated on a 2-D gel and transferred to PVDF membranes. (
  • Adhesion by α5β1 instead leads to the phosphorylation/inactivation of cofilin, and these cells fail to polarize their cytoskeleton but extend thin protrusions containing highly dynamic cell-matrix adhesions in multiple directions. (
  • Western blot analysis of extracts from COS-7 and HeLa cells using Cofilin (D3F9) XP ® Rabbit mAb (HRP Conjugate). (
  • On tumor cells, the TF-VIIa binary complex mediates activation of protease activated receptor (PAR) 2 and thereby shapes the tumor microenvironment by inducing an array of proangiogenic and immune modulating cytokines, chemokines, and growth factors. (
  • Through a focused si RNA screen targeting genes involved in membrane trafficking, we discovered that mutant SOD 1 aggregates, like viruses, exploit cofilin‐1 to remodel cortical actin and enter cells. (
  • Mutant SOD1 protein aggregates use cofilin‐1 to remodel actin and invade host cells. (
  • Tau and α‐synuclein aggregates also exploit RHO GTPase signaling to cofilin‐1 to enter cells. (
  • Furthermore neoplastic progression is often seen in OSE cells that fail to show epitheliomesenchymal conversion (for a review, see Ref. 2 ). (
  • The effect of implanting these cells has been observed in many studies and is presently being used as acceptable therapies in many countries [ 2 ]. (
  • Induction of adipocyte lineage commitment from C3H10T1/2 pluripotent stem cells by BMP2/4. (
  • C3H10T1/2 pluripotent stem cells were plated at low density, cultured without or with BMP2 or BMP4 until postconfluence, and then subjected to the adipocyte differentiation protocol (MDI: adipocyte differentiation cocktail, 1 μ m dexamethasone, 1 μg/ml insulin and 0.5 m m isobutylmethyl-xanthine). (
  • C3H10T1/2 stem cells were plated at 30% confluence, transfected with Smad4 or p38 MAPK Stealth RNAi, and 24 h later treated with BMP4 until 2 days postconfluent. (
  • 2. Nemaline Myopathies are characterized by typical rod-like accumulations of Z-disk-derived material in the muscle cells. (
  • Cofilin-actin rods also form within the nucleus of heat-shocked neurons and are cleared from cells expressing wild type huntingtin protein but not in cells expressing mutant or silenced huntingtin, suggesting a role for nuclear rods in Huntington disease (HD). (
  • 50 dB/db mice were employed and randomly assigned into five groups with 10 mice in each: group 1 (untreated cell), group 2 (PHD2 silenced cell), group 3 (L-mimosine treated cells), group 4 (nontargeting siRNA treated cells) and group 5 (sham control). (
  • Increased numbers of GFP+ cells and capillaries were observed in group 2. (
  • We further show that PKD-induced regulation of LIMK and the resulting diminished cofilin activity translates to altered cell motility. (
  • In fact, loci reported to be involved in such malformations include chickadee ( chic ) encoding Profilin, capping protein beta ( cpb ) encoding the subunit of CP, and twinstar ( tsr ) encoding ADF/cofilin. (
  • Cofilin-1 becomes active and disassembles actin filaments in a large array of cellular and animal models of LMNA cardiomyopathy. (
  • These biochemical differences reflect variations in the cellular expression between isoforms, where ADF and cofilin-1 are mainly expressed in tissues with higher actin turnover. (
  • The instantaneous cell-wide photoactivation of cofilin activity increased free barbed ends, F-actin content, and cellular locomotion. (
  • To determine the cellular and molecular mechanisms by which SHP-2 regulates heart development and, thus, understand how Noonan-associated mutations affect cardiogenesis, we introduced SHP-2 encoding the most prevalent Noonan syndrome and JMML mutations into Xenopus embryos. (
  • However, insights into the molecular mechanisms bridging ERK1/2 activation and depressed cardiac function are lacking. (
  • However, the molecular mechanism underlying the Slit-2-induced collapse of neuronal growth cones is unclear. (
  • Understanding the molecular role of cofilin-2, an actin-binding protein, in various organs including muscle, lungs and heart. (
  • 2 Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, 540 East Canfield Avenue, Detroit, MI 48201, USA. (
  • Collectively, these data demonstrate that GPER-mediated hippocampal spinogenesis and memory consolidation depend on JNK and cofilin signaling, supporting a critical role for actin polymerization in the GPER-induced regulation of hippocampal function in female mice. (
  • Its activity is under precise regulation of prolyl-hydroxylase domain 2. (
  • Chemokines of the eotaxin group ( Eotaxin , Eotaxin-2 , and Eotaxin-3 ), acting exclusively via CCR3 , induce recruitment of eosinophils to the sites of inflammation [ 2 ], [ 3 ]. (
  • In conclusion, cofilin‑1 played a role in As2O3‑induced NB4‑R1 cell apoptosis and it might be a novel target for APL treatment. (
  • Western blotting further revealed that As2O3 treatment decreased the cytoplasmic cofilin‑1 level but increased its expression in the mitochondrion. (
  • detect endogenous levels of myosin light chain 2 (smooth muscle) only when phosphorylated at serine 19. (
  • A cluster of cofilin along an otherwise bare actin filament induces distinctively asymmetric cooperative conformational changes to the filament on either side of the cluster. (