TY - JOUR. T1 - The molecular effects of skeletal muscle myosin regulatory light chain phosphorylation. AU - Greenberg, Michael J.. AU - Mealy, Tanya R.. AU - Watt, James D.. AU - Jones, Michelle. AU - Szczesna-Cordary, Danuta. AU - Moore, Jeffrey R.. PY - 2009/8. Y1 - 2009/8. N2 - Phosphorylation of the myosin regulatory light chain (RLC) in skeletal muscle has been proposed to act as a molecular memory of recent activation by increasing the rate of force development, ATPase activity, and isometric force at submaximal activation in fibers. It has been proposed that these effects stem from phosphorylation-induced movement of myosin heads away from the thick filament backbone. In this study, we examined the molecular effects of skeletal muscle myosin RLC phosphorylation using in vitro motility assays. We showed that, independently of the thick filament backbone, the velocity of skeletal muscle myosin is decreased upon phosphorylation due to an increase in the myosin duty cycle. Furthermore, we ...

SILVA, A C R; KENDRICK-JONES, J; REINACH, Fernando de Castro. Construction of a regulatory myosin light chain capable regulation of myosin. Arquivos de Biologia e Tecnologia[S.l: s.n.], 1988 ...

Investigation of protein changes as well as authentication of meat is particularly difficult in processed meat products due to their different composition, complexity and very often inhomogeneity. The aim of this study was to check if the inter-species differences in the expression of myosin light chain (MLC) isoforms observed in raw meat were retained in meat products. MLCs from mixtures of minced meat (16 variants), frankfurters and sausages (15 products) made from cattle, pig, chicken, turkey, duck and goose were analysed by 2DE. Species-specific patterns of MLC isoforms were observed in all the mixtures and processed meat products. Relatively small degradation was observed in the MLCs after processing. Image analysis enabled species identification of the meat in all samples when the content of meat of one species was not lower than 10%. However, it was impossible to differentiate between all the six species under investigation on the basis of individual isoform. It was possible when the ...

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Myosin light chain kinase (MLCK)-dependent phosphorylation of the regulatory light chain (RLC) of cardiac myosin is known to play a beneficial role in heart disease, but the idea of a phosphorylation-mediated reversal of a hypertrophic cardiomyopathy (HCM) phenotype is novel. Our previous studies on transgenic (Tg) HCM-RLC mice revealed that the D166V (Aspartate166 →Valine) mutation-induced changes in heart morphology and function coincided with largely reduced RLC phosphorylation in situ. In this paper, we hypothesized that the introduction of a constitutively phosphorylated Serine15 (S15D) into the hearts of D166V mice would prevent the development of a deleterious HCM phenotype. In support of this notion, MLCK-induced phosphorylation of D166V-mutated hearts was found to rescue some of their abnormal contractile properties. Tg-S15D-D166V mice were generated with the human cardiac RLC-S15D-D166V construct substituted for mouse cardiac RLC and were subjected to functional, structural, and ...

Recent evidence implicates the endosomal sorting complex required for transport (ESCRT) in the regulation of epithelial polarity in Drosophila melanogaster, but the mechanisms responsible for this action remain unclear. Here we show that ESCRTs determine cell orientation during directed migration in human fibroblasts. We find that endosomal retention of α5β1 integrin and its downstream signaling effector Src in ESCRT-depleted cells is accompanied by the failure to activate myosin light chain kinase (MLCK), which thereby cannot phosphorylate myosin regulatory light chain (MRLC). Using this mechanism, ESCRT-depleted fibroblasts fail to orient their Golgi complex to undergo directional migration and show impaired focal adhesion turnover and increased spreading on fibronectin. Consistent with these findings, expression of a phosphomimetic mutant of MRLC in ESCRT-depleted cells restores normal phenotypes during cell spreading and orientation of the Golgi. These results suggest that, through their ...

TY - JOUR. T1 - Dynamic regulation of vascular myosin light chain (MYL9) with injury and aging. AU - Shehadeh, Lina A.. AU - Webster, Keith A.. AU - Hare, Joshua M.. AU - Vazquez-Padron, Roberto I.. N1 - Copyright: Copyright 2012 Elsevier B.V., All rights reserved.. PY - 2011/10/7. Y1 - 2011/10/7. N2 - Background: Aging-associated changes in the cardiovascular system increase the risk for disease development and lead to profound alterations in vascular reactivity and stiffness. Elucidating the molecular response of arteries to injury and age will help understand the exaggerated remodeling of aging vessels. Methodology/Principal Findings: We studied the gene expression profile in a model of mechanical vascular injury in the iliac artery of aging (22 months old) and young rats (4 months old). We investigated aging-related variations in gene expression at 30 min, 3 d and 7 d post injury. We found that the Myosin Light Chain gene (MYL9) was the only gene differentially expressed in the aged versus ...

Inhibitor studies have indicated that MLCK activation, as assessed by MLC phosphorylation, is necessary for TJ regulation secondary to diverse physiological and pathophysiological stimuli (Hopkins et al., 2003; Scott et al., 2002; Turner et al., 2000; Turner et al., 1997; Yuhan et al., 1997; Zolotarevsky et al., 2002). However, the nonspecific nature of pharmacologic agents, the complexity of the stimuli used, and the absence of appropriate experimental models has made it impossible to determine if MLC phosphorylation alone is sufficient to trigger acute downstream regulation of assembled TJs. To address this problem, we developed a model of inducible tMLCK expression in fully differentiated epithelial monolayers, thereby overcoming limitations of previous studies (Gandhi et al., 1997; Hecht et al., 1996). Our data show that induction of tMLCK expression in mature monolayers causes MLC phosphorylation and is sufficient to cause increases in TJ permeability. These changes in TJ function are ...

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Post-activation potentiation (PAP) is a well-described phenomenon with a short half-life (~28 s) that enhances muscle force production at submaximal levels of calcium saturation (i.e., submaximal levels of muscle activation). It has been largely explained by an increased myosin light chain phosphorylation occurring in type II muscle fibers, and its effects have been quantified in humans by measuring muscle twitch force responses to a bout of muscular activity. However, enhancements in (sometimes maximal) voluntary force production detected several minutes after high-intensity muscle contractions are also observed, which are also most prominent in muscles with a high proportion of type II fibers. This effect has been considered to reflect PAP. Nonetheless, the time course of myosin light chain phosphorylation (underpinning

Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Human Myosin Light Chain 3, Alkali, Ventricular, Slow Skeletal (MYL3) in samples from Serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids with no significant corss-reactivity with analogues from other species ...

A regulatory interdependence of expression of proto-oncogenes and muscle specific genes observed in smooth muscle was examined in cardiac muscle during normal development and hypertrophy both in rats and humans. During normal development in rats, myosin light chain 2 expression is very low at prenatal stages, while c-fos expression starts from the early stages of embryonic development. In aorta constricted rats c-fos induction occurs within 30 min whereas myosin light chain 2 expression is sufficiently high only after 3 or 4 days of post operative period. In the case of humans, the expression of myosin light chain 2 as well as c-fos occurs at high levels during embryonic development. Similar results were obtained with tissue samples obtained from patients with cardiac abnormalities. Induction of the c-fos gene in cultured myocytes by 12-O-tetradeeanoylphorbol 13-acetate has no influence on the expression of myosin light chain 2. These studies were extended with studies on c-myc and Β-myosin ...

Garfinkel L.I., Periasamy M., Nadal-Ginard B.. A library of cDNA clones was constructed from adult rat skeletal muscle mRNA, from which a set of contractile protein clones was selected. These clones were identified by sequencing the cDNA inserts and comparing the derived amino acid sequences with published sequences of rabbit contractile proteins. In this manner, clones corresponding to myosin light chains 1, 2, and 3, troponin-C, troponin-T, alpha-tropomyosin, and alpha-actin were identified. A high degree of amino acid sequence conservation was found upon comparison of the rat and rabbit proteins. Using the cDNA clone panel, we analyzed the expression of abundant rat muscle mRNAs. We show that abundant rat muscle mRNAs can be classified into four developmentally regulated groups, based upon their expression at different stages of myogenesis. One class of mRNAs is expressed during all stages of muscle development. Since these mRNAs are also present in nonmuscle tissues, we conclude that they ...

Gregorich ZR, Cai WX, Lin ZQ, Chen AJ, Peng Y, Kohmoto T, Ge Y. Distinct sequences and post-translational modifications in cardiac atrial and ventricular myosin light chains revealed by top-down mass spectrometry. Journal of Molecular and Cellular Cardiology. 2017 ;107:13-21. ...

We have a new publication in press in Molecular Biology of the Cell: Kassianidou, Hughes, et al., Activation of ROCK and MLCK tunes regional stress fiber formation and mechanics via preferential myosin light chain phosphorylation.. ...

Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.

Amino Acid Sequence: MSSKKAKTKT TKKRPQRATS NVFAMFDQSQ IQEFKEAFNM IDQNRDGFID KEDLHDMLAS LGKNPTDAYL DAMMNEAPGP INFTMFLTMF GEKLNGTDPE DVIRNAFACF DEEATGTIQE DYLRELLTTM GDRFTDEEVD ELYREAPIDK KGNFNYIEFT RILKHGAKDK DD ...

Complete information for MYL1 gene (Protein Coding), Myosin Light Chain 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium

Complete information for MYL1 gene (Protein Coding), Myosin Light Chain 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium

MYL12B Human Recombinant produced in E. coli is a single polypeptide chain containing 196 amino acids (1-172) and having a molecular mass of 22.3kDa.MYL12B is fused to a 24 amino acid His-tag at N-terminus & purified by proprietary chromatographic techniques.

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Hi, I have just learned about phasor and laplace analysis of RLC circuits in my engineering course. I am trying to use my knowledge to build an RLC...

Pill with imprint RLC N 075 is White, Round and has been identified as Nature-throid 48.75 mg (¾ Grain). It is supplied by RLC Labs, Inc..

遺伝子「MYL6P3」の詳細情報です。J-GLOBAL 科学技術総合リンクセンターは研究者、文献、特許などの情報をつなぐことで、異分野の知や意外な発見などを支援する新しいサービスです。またJST内外の良質なコンテンツへ案内いたします。

Scallops possess striated and catch adductor muscles, which have different structure and contractile properties. The striated muscle contracts very quickly for swimming, whereas the smooth catch muscle can keep the shells closed for long periods with little expenditure of energy. In this study, we performed proteomic and transcriptomic analyses of differences between the striated (fast) and catch (slow) adductor muscles in Yesso scallop Patinopecten yessoensis. Transcriptomic analysis reveals 1316 upregulated and 8239 downregulated genes in slow compared to fast adductor muscle. For the same comparison, iTRAQ-based proteomics reveals 474 differentially expressed proteins (DEPs), 198 up- and 276 downregulated. These DEPs mainly comprise muscle-specific proteins of the sarcoplasmic reticulum, extracellular matrix, and metabolic pathways. A group of conventional muscle proteins-myosin heavy chain, myosin regulatory light chain, myosin essential light chain, and troponin-are enriched in fast muscle. In

TY - JOUR. T1 - Regulation of myosin light chain kinase and telokin expression in smooth muscle tissues. AU - Herring, B. Paul. AU - El-Mounayri, Omar. AU - Gallagher, Patricia J.. AU - Yin, Feng. AU - Zhou, Jiliang. PY - 2006/11/24. Y1 - 2006/11/24. N2 - The mylk1 gene is a large gene spanning ∼250 kb and comprising at least 31 exons. The mylk1 gene encodes at least four protein products: two isoforms of the 220-kDa myosin light chain kinase (MLCK), a 130-kDa MLCK, and telokin. Transcripts encoding these products are derived from four independent promoters within the mylk1 gene. The kinases expressed from the mylk1 gene have been extensively characterized and function to regulate the activity of nonmuscle and smooth muscle myosin II. Activation of these myosin motors by MLCK modulates a variety of contractile processes, including smooth muscle contraction, cell adhesion, migration, and proliferation. Dysregulation of these processes contributes to a number of diseases. The noncatalytic gene ...

Title: Regulatory Light Chains of Striated Muscle Myosin. Structure, Function and Malfunction. VOLUME: 3 ISSUE: 2. Author(s):Danuta Szczesna-Cordary. Affiliation:Department of Molecular&Cellular Pharmacology, University of Miami School of MedicineRosenstiel Medical Sciences Building R-189, Room 6113, USA. Keywords:regulatory light chains of myosin (rlc), Phosphorylation, skinned fibers, familial hypertrophic, cardiomyopathy (fhc) mutations.. Abstract: Striated (skeletal and cardiac) muscle is activated by the binding of Ca2+ to troponin C and is regulated by the thin filament proteins, tropomyosin and troponin. Unlike in molluscan or smooth muscles, the myosin regulatory light chains (RLC) of striated muscles do not play a major regulatory role and their function is still not well understood. The N-terminal domain of RLC contains a Ca2+-Mg2+-binding site and, analogous to that of smooth muscle myosin, also contains a phosphorylation site. During muscle contraction, the increase in Ca2+ ...

1. Combined histochemical and biochemical single-fibre analyses [Staron & Pette (1987) Biochem. J. 243, 687-693], were used to investigate the rabbit tibialis-anterior fibre population. 2. This muscle is composed of four histochemically defined fibre types (I, IIC, IIA and IIB). 3. Type I fibres contain slow myosin light chains LC1s and LC2 and the slow myosin heavy chain HCI, and types IIA and IIB contain the fast myosin light chains LC1f, LC2f and LC3f and the fast heavy chains HCIIa and HCIIb respectively. 4. A small fraction of fibres (IIAB), histochemically intermediate between types IIA and IIB, contain the fast light myosin chains but display a coexistence of HCIIa and HCIIb. 5. Similarly to the soleus muscle, C fibres in the tibialis anterior muscle contain both fast and slow myosin light chains and heavy chains. The IIC fibres show a predominance of the fast forms and the IC fibres (histochemically intermediate between types I and IIC) a predominance of the slow forms. 6. A total of 60 ...

TY - JOUR. T1 - Differential Regulation of Alternatively Spliced Endothelial Cell Myosin Light Chain Kinase Isoforms by p60Src. AU - Birukov, Konstantin G.. AU - Csortos, Csilla. AU - Marzilli, Lisa. AU - Dudek, Steven. AU - Ma, Shwu Fan. AU - Bresnick, Anne R.. AU - Verin, Alexander D.. AU - Cotter, Robert J.. AU - Garcia, Joe G.N.. PY - 2001/3/16. Y1 - 2001/3/16. N2 - The Ca2+/calmodulin-dependent endothelial cell myosin light chain kinase (MLCK) triggers actomyosin contraction essential for vascular barrier regulation and leukocyte diapedesis. Two high molecular weight MLCK splice variants, EC MLCK-1 and EC MLCK-2 (210-214 kDa), in human endothelium are identical except for a deleted single exon in MLCK-2 encoding a 69-amino acid stretch (amino acids 436-505) that contains potentially important consensus sites for phosphorylation by p60Src kinase (Lazar, V., and Garcia, J. G. (1999) Genomics 57, 256-267). We have now found that both recombinant EC MLCK splice variants exhibit comparable ...

Myosin light chain kinase (MLCK) induces contraction of the perijunctional apical actomyosin ring in response to phosphorylation of the myosin light chain. Abnormal expression of MLCK has been observed in respiratory diseases, pancreatitis, cardiovascular diseases, cancer, and inflammatory bowel disease (IBD). The signaling pathways involved in MLCK activation and triggering of endothelial barrier dysfunction are discussed in this review. The pharmacological effects of regulating MLCK expression by inhibitors such as ML-9, ML-7, microbial products, naturally occurring products, and microRNAs are also discussed. The influence of MLCK in inflammatory diseases starts with endothelial barrier dysfunction. The effectiveness of anti-MLCK treatment may depend on alleviation of that primary pathological mechanism. This review summarizes evidence for the potential benefits of anti-MLCK agents in the treatment of inflammatory disease and the importance of avoiding treatment-related side effects, as MLCK is widely

The smaller subunits of MYOSINS that bind near the head groups of MYOSIN HEAVY CHAINS. The myosin light chains have a molecular weight of about 20 KDa and there are usually one essential and one regulatory pair of light chains associated with each heavy chain. Many myosin light chains that bind calcium are considered calmodulin-like proteins ...

In order to understand the mechanism of defective myofibrilogenesis in muscular dystrophy, we have used the genomic cloned DNA specific for myosin light chain 2A (MLC 2A) to check its expression. The fusion of a partial digest of λLC5, containing the upstream sequence of MLC 2A gene with the expression vector of Psvocat has already been reported. Using this CAT-fused recombinant containing 1.6 kb of MLC 2A gene, we were able to detect the promoter activity in normal heart cells, H9C2 cell line whereas a restricted expression of MLC 2A gene was noticed in muscular dystrophic muscle cells from heart and skeletal. We have also measured the transient transfection efficiency by contransfecting with the plasmid LacZ. Simultaneous assay of β-galactosidase and CAT in the cell extract was performed. With β-galactosidase as control, we confirmed that the promoter activity of MLC 2A gene is inhibited in muscular dystrophy though there is a normal rate of transfection occurred. ...

The Ca(2+)-dependent kinase myosin light chain kinase (MLCK) is the activator of smooth muscle contraction. In addition, it has been reported to be involved in Ca(2+) channel regulation in cultured cells, and we previously showed that the MLCK inhibitor ML-7 decreases arginine vasopressin (AVP)-induced Ca(2+) influx in rat aorta. This study was designed to investigate whether MLCK is involved in Ca(2+) regulation in resistance artery smooth muscle cell, which plays a major role in the control of blood pressure. As ML compounds were shown to have off-target effects, MLCK was downregulated by transfection with a small interfering RNA targeting MLCK (MLCK-siRNA) in rat small resistance mesenteric artery (RMA) and in the rat embryonic aortic cell line A7r5. Noradrenaline-induced contraction and Ca(2+) signal were significantly depressed in MLCK-siRNA compared to scramble-siRNA-transfected RMA. Contraction and Ca(2+) signal induced by high KCl and voltage-activated Ca(2+) current were also ...

Muscle contraction results from the cyclic interaction of myosin and actin by coupling energy of adenosine triphosphate (ATP) hydrolysis. During muscle contraction myosin and actin interact with each other through a structure called cross-bridge. Despite intense structural studies, the organisation of myosin cross-bridges on myosin filaments is not well understood. Myosin regulatory light chain (RLC) is one of the prominent proteins present at the lever arm domain of cross-bridges. Phosphorylation of RLC modulates cellular functions including muscle contraction. Moreover, RLC mutation is associated with cardiomyopathy. To understand the role of RLC in muscle contraction, high-resolution structure in its sarcomeric environment is required. Currently available high-resolution structure of myosin is inadequate to understand the role of RLC. A novel electron microscopy (EM) labelling technique based on APEX2, an engineered variant of soybean ascorbate peroxidase (APEX) protein is a promising ...

In previous studies, blockade or gene deletion of either myosin light chain kinase (MLCK) or the mechanogated transient receptor potential vanilloid 4 (TRPV4) channel attenuated mechanical lung injury. To determine their effects on calcium entry, rat pulmonary microvascular endothelial cells (RPMVEC) were labeled with fluo-4 and calcium entry initiated with the TRPV4 agonist, 4α-phorbol 12, 13-didecanoate (4αPDD). Mean calcium transients peaked at ~25 sec and persisted ~500 sec. The 4αPDD response was essentially abolished in calcium-free media, or after pretreatment with the MLCK inhibitor, ML-7. ML-7 also attenuated the 4αPDD-induced inward calcium current measured directly using whole-cell patch clamp. Pretreatment with dynasore, an inhibitor of dynamin produced an initial calcium transient followed by a 4αPDD transient of unchanged peak intensity. Automated averaging of areas under the curve (AUC) of calcium transients in individual cells indicated total calcium activity with a ...

To understand how cytokinesis is regulated during mitosis, we tested cyclin-p34cdc2 for myosin-II kinase activity, and investigated the mitotic-specific phosphorylation of myosin-II in lysates of Xenopus eggs. Purified cyclin-p34cdc2 phosphorylated the regulatory light chain of cytoplasmic and smooth muscle myosin-II in vitro on serine-1 or serine-2 and threonine-9, sites known to inhibit the actin-activated myosin ATPase activity of smooth muscle and nonmuscle myosin (Nishikawa, M., J. R. Sellers, R. S. Adelstein, and H. Hidaka. 1984. J. Biol. Chem. 259:8808-8814; Bengur, A. R., A. E. Robinson, E. Appella, and J. R. Sellers. 1987. J. Biol. Chem. 262:7613-7617; Ikebe, M., and S. Reardon. 1990. Biochemistry. 29:2713-2720). Serine-1 or -2 of the regulatory light chain of Xenopus cytoplasmic myosin-II was also phosphorylated in Xenopus egg lysates stabilized in metaphase, but not in interphase. Inhibition of myosin-II by cyclin-p34cdc2 during prophase and metaphase could delay cytokinesis until ...

calmodulin-dependent protein kinase activity, myosin light chain kinase activity, structural constituent of cytoskeleton, protein phosphorylation

TY - JOUR. T1 - The occurrence of myosin light chain kinase in non-muscle tissues. AU - Miyamoto, E.. AU - Matsui, K.. AU - Fukunaga, K.. PY - 1981/1/1. Y1 - 1981/1/1. UR - http://www.scopus.com/inward/record.url?scp=0019412942&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0019412942&partnerID=8YFLogxK. U2 - 10.2220/biomedres.2.341. DO - 10.2220/biomedres.2.341. M3 - Article. AN - SCOPUS:0019412942. VL - 2. SP - 341. EP - 346. JO - Biomedical Research (Japan). JF - Biomedical Research (Japan). SN - 0388-6107. IS - 3. ER - ...

Circular RNA Myosin Light Chain Kinase (MYLK) Promotes Prostate Cancer Progression through Modulating Mir-29a Expression - Article statistics #908009

The inhibition of myosin light chain phosphatase (MLCP) enhances smooth muscle contraction at a constant [Ca2+]. There are two components, myosin-binding subunit of MLCP (MBS) and CPI17, thought to be responsible for the inhibition of MLCP by external stimuli. The phosphorylation of MBS at Thr-641 and of CPI17 at Thr-38 inhibits the MLCP activity in vitro. Here we determined the changes in the phosphorylation of MBS and CPI17 after agonist stimulation in intact as well as permeabilized smooth muscle strips using phosphorylation-site-specific antibodies as probes. The CPI17 phosphorylation transiently increased after agonist stimulation in both alpha-toxin skinned and intact fibres. The time course of the increase in CPI17 phosphorylation after stimulation correlated with the increase in myosin regulatory light chain (MLC) phosphorylation. The increase in CPI17 phosphorylation was significantly diminished by Y27632, a Rho kinase inhibitor, and GF109203x, a protein kinase C inhibitor, suggesting that both

TY - JOUR. T1 - The paradox of smooth muscle physiology. AU - Woodrum, David A.. AU - Brophy, Colleen M.. PY - 2001/5/25. Y1 - 2001/5/25. N2 - Vascular smooth muscle tone is controlled by a balance between the cellular signaling pathways that mediate the generation of force (contraction) and the release of force (relaxation). The signaling events that activate contraction include Ca2+-dependent myosin light chain phosphorylation. The signaling events that mediate relaxation include the removal of a contractile agonist (passive relaxation) and activation of cyclic nucleotide-dependent signaling pathways in the continued presence of a contractile agonist (active relaxation). The major questions that remain in contractile physiology include (1) how is tonic force maintained when intracellular Ca2+ levels and myosin light chain phosphorylation have returned to basal levels; and (2) what is the mechanism of cyclic nucleotide-dependent relaxation? This review focuses on these specific controversies ...

Toxoplasma gondii is an obligate intracellular parasite that enters cells by a process of active penetration. Host cell penetration and parasite motility are driven by a myosin motor complex consisting of four known proteins: TgMyoA, an unconventional Class XIV myosin; TgMLC1, a myosin light chain; and two membrane-associated proteins, TgGAP45 and TgGAP50. Little is known about how the activity of the myosin motor complex is regulated. Here, we show that treatment of parasites with a recently identified small-molecule inhibitor of invasion and motility results in a rapid and irreversible change in the electrophoretic mobility of TgMLC1. While the precise nature of the TgMLC1 modification has not yet been established, it was mapped to the peptide Val46-Arg59. To determine if the TgMLC1 modification is responsible for the motility defect observed in parasites after compound treatment, the activity of myosin motor complexes from control and compound-treated parasites was compared in an in vitro ...

Contractile agonists can mobilize Ca2+ from both intracellular and extracellular stores in smooth muscle. This study addresses the role of Ca2+ mobilization as it relates to the complex manner by which Ca2+ regulates the contractile system in smooth muscle. In swine carotid media, both histamine and phenylephrine produced initial rapid increases in myosin phosphorylation and stress. Stress was sustained for the duration of the stimulus while myosin phosphorylation slowly declined to steady-state levels. Removal of extracellular Ca2+ or elimination of cellular Ca2+ influx did not dramatically reduce the initial rapid increase in myosin phosphorylation produced by either agonist but reduced steady-state levels of myosin phosphorylation to basal values. Initial rapid increases in stress were seen, but stress was not maintained. Following depletion of Ca2+ from sarcoplasmic reticulum, muscle activation by Ca2+ influx in the presence of phenylephrine occurred without an initial transient in myosin ...

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Buy anti-PRKDC antibody, Rabbit Myosin Light Chain 2 Polyclonal Antibody-NP_001075109.1 (MBS857334) product datasheet at MyBioSource, Primary Antibodies. Application: Immunohistochemistry (IHC)

DISCUSSION. Myosin RLC phosphorylation at Ser19 (P-RLC) is sufficient to fully activate SMMII and NMII (reviewed in [27]), however frequently observed RLC di-phosphorylation at Thr18/Ser19 (PP-RLC) (reviewed in [28]) may be responsible for prolonged myosin activation because of significantly slower RLC dephosphorylation [29]. Based on these findings, mono-phosphorylation at Ser19 and/or di-phosphorylation at Thr18/Ser19 are widely used to biochemically characterize myosin II motor activity and its involvement in (patho)physiological responses.. A variety of experimental approaches has been developed for analysis of P-RLC and PP-RLC. One of these approaches is electrophoretic separation of non-phosphorylated RLC, P-RLC, and PP-RLC followed by staining with a protein dye and densitometric analysis of the stained protein bands. RLC phospho-species can be separated by isoelectric focusing in the presence of pyrophosphate [9], urea/glycerol polyacrylamide electrophoresis [10], or recently introduced ...

anti-Myosin Regulatory Light Chain 2, Smooth Muscle Isoform (MYL9) (pThr19), (AA 10-25) antibody (Cy5.5) ABIN753243 from antibodies-online

The study by Sato et al9 raises important questions of how the RhoA-Rho-kinase pathway is activated after the insult of hemorrhage, how MLCP activity is regulated in general, and whether these mechanisms are altered in various pathological states. MLCP is affected not only by various signaling cascades that might alter the state of phosphorylation of MBS, but there are also multiple sites for regulation by protein factors that could modify the interactions among the subunit domains involved in MLCP targeting and catalysis. There is evidence for modulation of MLCP activity by either activator or repressor proteins, whose activity is modified by phosphorylation. A potential activator protein is telokin, which comprises an independently expressed C-terminal domain of MLCK.12 13 It is not clear whether telokin acts by modifying the activity of MLCP directly or indirectly by interactions with MLC. Whatever the case, its activity as a promoter of MLCP activity is amplified when telokin is ...

As described shortly after its discovery, CT-1 promotes cardiac myocyte hypertrophy by directing sarcomere assembly in series.3 At the ventricular structural level, in-series sarcomeric assembly leads to eccentric hypertrophy and chamber dilatation. Thus, increased myocardial expression of CT-1 immediately became a candidate for the molecular basis of pathological hypertrophy and remodeling in dilated cardiomyopathy phenotypes. The cardiac myocyte protective effects were also appreciated early in the investigation of CT-1s biological properties.4 Mice with genetic ablation of gp130 have hypoplastic hearts,5 which suggests a role for CT-1 or other IL-6-type cytokines in normal cardiac development. However, mice with ventricular myocyte-restricted knockout of gp130 using a ventricular myosin light chain 2 promoter that drives a Cre/lox recombination/knockout system from early in development have no cardiac abnormalities at birth,6 indicating that the hypoplastic heart phenotype of generalized ...

Asthma is associated with airway obstruction, airway inflammation, and bronchoconstriction. Immune cell infiltration and their production of inflammatory cytokines, such as interleukin (IL)-13, IL-17A, and tumor necrosis factor-α (TNF-α), increase airway smooth muscle contractility by increasing the calcium sensitivity of a pathway involving the guanosine triphosphatase RhoA, the kinase ROCK2, myosin light chain phosphatase, and myosin light chain. Mfge8 is an integrin-binding and phosphatidylserine-binding protein that functions in the clearance of apoptotic cells. Comparison of wild-type and mfge8-deficient mice in a mouse model of asthma (induced by ovalbumin) revealed that the mfge8-deficient mice had increased pulmonary resistance, a measure of airway hyperresponsiveness, but the abundance of infiltrated immune cells, the types of cells present, and the abundance of the inflammatory cytokines were the same between the two genotypes of mice. Isolated tracheal rings from the ...

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Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Regulation of skeletal muscle development and organization is a complex process that is not fully understood. Here, we focused on amphiphysin 2 (BIN1, also known as bridging integrator-1) and dynamin 2 (DNM2), two ubiquitous proteins implicated in membrane remodeling and mutated in centronuclear myopathies (CNMs). We generated Bin1-/- Dnm2+/- mice to decipher the physiological interplay between BIN1 and DNM2. While Bin1-/- mice die perinatally from a skeletal muscle defect, Bin1-/- Dnm2+/- mice survived at least 18 months, and had normal muscle force and intracellular organization of muscle fibers, supporting BIN1 as a negative regulator of DNM2. We next characterized muscle-specific isoforms of BIN1 and DNM2. While BIN1 colocalized with and partially inhibited DNM2 activity during muscle maturation, BIN1 had no effect on the isoform of DNM2 found in adult muscle. Together, these results indicate that BIN1 and DNM2 regulate muscle development and organization, function through a common pathway, ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Treatment options are limited for severe asthma, and the need for additional therapies remains great. Previously, we demonstrated that integrin αvβ6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression of the murine ortholog of human chymase. Here, we determined that chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair tension transmission in airway smooth muscle (ASM). Additionally, we identified a pathway that can be therapeutically targeted to mitigate the effects of airway hyperresponsiveness. Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due to alterations in calcium homeostasis or myosin light chain phosphorylation. Rather, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylation. Disruption of integrin ligation with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no ...

Next, we focused on intermediate signaling molecules that are implicated in the mediation of cell motility and calcium signaling. Compared with control cells, MECs treated with recMFAP5 had higher expression of phosphorylated FAK (p-FAK) (Y861), p-PLC-γ1 (Y783), p-PKCθ (T538), p-ERK1/2 (T202/Y204), phosphorylated myosin regulatory light chain 2 (p-MLC2) (T18/S19), phosphorylated cyclic AMP-responsive element-binding protein (p-CREB) (S133), c-Jun, and p-c-Jun (S73), which may have led to the upregulation of LPP expression and thus increased cell motility and permeability (Figure 7G).. Because our data demonstrated that MFAP5-induced microvascular endothelial cell motility was suppressed in cells that had been pretreated with an anti-αVβ3 integrin antibody (Figure 7H) and that MFAP5-upregulated p-FAK (Y861) expression was suppressed in cells that had been pretreated with BAPTA-AM (1,2-bis-[2-aminophenoxy]-ethane-N,N,N′,N′-tetraacetic acid, tetraacetoxymethyl ester) (Supplemental Figure 9A ...

Bakin, A. V., Safina, A., Rinehart, C., Daroqui, C., Darbary, H., Helfman, D. M. (October 2004) A critical role of tropomyosins in TGF-beta regulation of the actin cytoskeleton and cell motility in epithelial cells. Molecular Biology of the Cell, 15 (10). pp. 4682-4694. ISSN 1059-1524 Kim, E. J., Helfman, D. M. (August 2003) Characterization of the metastasis-associated protein, S100A4 - Roles of calcium binding and dimerization in cellular localization and interaction with myosin. Journal of Biological Chemistry, 278 (32). pp. 30063-30073. ISSN 0021-9258 Pawlak, G., Helfman, D. M. (November 2002) Anchorage-independent activation of ERK1/2 depends on myosin light chain kinase-mediated regulation of myosin II. Molecular Biology of the Cell, 13. 158A-158A. ISSN 1059-1524 Pawlak, G., Helfman, D. M. (July 2002) MEK mediates v-Src-induced disruption of the actin cytoskeleton via inactivation of the Rho-ROCK-LIM kinase pathway. Journal of Biological Chemistry, 277 (30). pp. 26927-26933. ISSN 0021-9258 ...

Rabbit polyclonal Myosin Light Chain 2 antibody validated for WB, ELISA, IHC, ICC/IF and tested in Rat. Referenced in 8 publications and 1 independent review…

Acosta-Herrera M, Pino-Yanes M, Ma SF, Barreto-Luis A, Corrales A, Cumplido J, Pérez-Rodríguez E, Campo P, Eng C, García-Robaina JC, Quintela I, Villar J, Blanca M, Carracedo Á, Carrillo T, Garcia JG, Torgerson DG, Burchard EG, Flores C. Fine mapping of the myosin light chain kinase (MYLK) gene replicates the association with asthma in populations of Spanish descent. J Allergy Clin Immunol. 2015 Oct; 136(4):1116-8.e9 ...

CCL19/21 induced PI3K-dependent phosphorylation of Akt/protein kinase B, activation of the Rho/Rho-associated coiled-coil forming protein kinases/myosin light chain pathway and MAPKs phosphorylation ...

We offer new ways of deriving the expressions reported in our previous work for assessing the quality of pairwise models. Rotational spectroscopy of the atmospheric photo-oxidation product o-toluic acid and its monohydrate. MLC phosphorylation in MKs is regulated by Rho-associated kinase ...

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Well, nearly 11 weeks in and I am starting to get the light headedness that people sometimes talk about. I didnt think I would be getting it yet as I am...