Local expression of migration inhibitory factor and Th1 type cytokine mRNA in sporotrichosis lesions.
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Actins↗
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Results for “Chain Migration”
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Analysis of the CHK2 gene in lymphoid malignancies.
The CHK2 gene encodes a protein kinase that is important for the regulation of cell cycle arrest after DNA damage. CHK2 acts downstream of ataxia teleangiecstasia mutated (ATM), modulates the function of p53 and may help mediate cell cycle arrest at G2/M by phosphorylation of Cdc25C. Recently, the human homolog of the checkpoint kinase Cds1 (CHK2) has been suggested to be a tumor suppressor gene. Heterozygous germline mutations have been reported in Li-Fraumeni syndrome (LFS), a highly penetrant familial cancer phenotype, and in sporadic colon cancer. LFS is associated with the development of lymphoid malignancies, especially childhood ALL. Therefore, we analyzed the DNA from 143 lymphoid malignancies to determine whether they had mutations of the CHK2 gene. The 14 exons of CHK2 were studied by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) and sequencing of aberrantly migrating bands. One missense mutation changing serine to phenylalanine (codon 428) in an evolutionarily highly conserved domain was found in a non-Hodgkin's aggressive lymphoma. Another point mutation in the non-coding region was identified in one of adult T-cell leukemias (ATL) samples. This result suggests that mutation of the CHK2 gene may rarely be involved in the development of selected lymphomas.
Adult↗
Distribution of alphavbeta3, alphavbeta5 integrins and the integrin associated protein--IAP (CD47) in human glomerular diseases.
The alphav integrins present on the membrane of numerous cells, mediate attachment to matrix proteins, cell proliferation, migration and survival. We studied the expression of alphav integrinis and CD47 (a beta3 chain integrin associated protein) in various forms of glomerulonephritis (GN) characterized by mesangial proliferation and/or increased mesangial matrix. In normal glomeruli, epithelial cells expressed alphavbeta3, alphavbeta5 and CD47; endothelial cells expressed alpha5beta1 and CD47; mesangial cells expressed alphavbeta5, CD47, and to a less extent alphavbeta3. In acute post infectious GN (APIGN), membrano-proliferative GN (MPGN) and diabetic nephropathy(DN), we observed that the beta3 chain, normally expressed by mesangial cells, was not detectable in the mesangium while its expression by epithelial cells was not modified. Parallel to the disappearance of alphavbeta3, the CD47 expression was decreased on the mesangial cells in MPGN, APIGN and DN. The expression of alphavbeta5 was clearly increased on podocytes and on proliferating mesangial cells in APIGN. By contrast, the mesangial expression of alphavbeta was normal or decreased in DN. The alpha5 chain of integrin, absent on normal mesangial cell, was expressed on proliferating mesangial cells in MPGN and APIGN. Thus, we observed modifications of alphavbeta3 and alphavbeta5 expression during human GN. The modulations of alphavbeta3 and alphavbeta5 expression differed according to the different glomerular cell types and were not parallel in glomerular cells: alphavbeta3 was decreased (and alphavbeta5 unchanged) on proliferating mesangial cells and alphavbeta5 was increased (and alphavbeta3 unchanged) in podocytes. This may reflect the existence of two distinct regulatory pathways.
Antibodies, Monoclonal↗
In vivo roles of integrins during leukocyte development and traffic: insights from the analysis of mice chimeric for alpha 5, alpha v, and alpha 4 integrins.
Mice chimeric for integrins alpha(5), alpha(V), or alpha(4) were used to dissect the in vivo roles of these adhesion receptors during leukocyte development and traffic. No major defects were observed in the development of lymphocytes, monocytes, or granulocytes or in the traffic of lymphocytes to different lymphoid organs in the absence of alpha(5) or alpha(V) integrins. However, in agreement with previous reports, the absence of alpha(4) integrins produced major defects in development of lymphoid and myeloid lineages and a specific defect in homing of lymphocytes to Peyer's patches. In contrast, the alpha(4) integrin subunit is not essential for localization of T lymphocytes into intraepithelial and lamina propria compartments in the gut, whereas one of the partners of alpha(4), the beta(7) chain, has been shown to be essential. However, alpha(4)-deficient T lymphocytes cannot migrate properly during the inflammatory response induced by thioglycolate injection into the peritoneum. Finally, in vitro proliferation and activation of lymphocytes deficient for alpha(5), alpha(V), or alpha(4) integrins upon stimulation with different stimuli were similar to those seen in controls. These results show that integrins play distinct roles during in vivo leukocyte development and traffic.
Animals↗
Size of the polyadenylic acid region of newly synthesized globin messenger ribonucleic acid.
The size of the polyadenylic acid region of newly synthesized globin mRNA was determined on mRNA isolated from nucleated erythroid spleen cells of anemic mice. The globin mRNA was purified by a combination of affinity chromatography on oligodeoxythymidylate-cellulose (oligo-(dT)-cellulose) and sucrose density gradient centrifugation. The purified RNA was shown to be globin mRNA by virtue of its ability to direct the synthesis of mouse alpha- and beta-globin chains in a cell-free system and by the presence of two bands migrating identically with authentic mouse alpha- and beta-globin mRNA when subjected to electrophoresis in polyacrylamide gels in the presence of formamide. When labeled for 1 hour with [3H]adenosine, the newly synthesized radioactive mRNA also migrated as two bands in these gels but they moved slower than the main bands suggesting that they have higher molecular weights. The polyadenylic acid region of the mRNA was isolated from the T1 and pancreatic RNase digestion mixture by acrylamide sodium dodecyl sulfate gel electrophoresis. The polyadenylic acid region was found to contain approximately 150 adenylate residues. As it is known that globin mRNA isolated from reticulocytes contains only 40 to 60 residues, it follows that at least 150 adenylic acid residues are added to the globin mRNA soon after its synthesis and that some of these are removed during the subsequent maturation of the erythroid cell.
Adenine Nucleotides↗
[Genetic changes in liver metastasis of colorectal cancer and their clinical application].
It has been confirmed that several genes are involved in each step of liver metastasis of colorectal cancer. This article reviews recent highlights in this field. The expression of c-erbB2 or Rho protein in colorectal cancer tissues correlates closely with liver metastasis. Suppressor genes such as nm23, DCC, and DPC4 may play a role in the suppression of liver metastasis. On the other hand, the E-cadherin-catenin system, carbohydrate chains, selectin, and variant CD44 are known to play an important role in cells migration from the primary lesion, the adhesion of tumor cells to endothelial cells, and cell motility. These adhesion molecules may be a biological marker of liver metastasis. In addition, treatment targeting these genes will be a potent therapy for liver metastasis in the future.
Colorectal Neoplasms↗
Macrophage migration inhibitory factor gene polymorphism is associated with sarcoidosis in biopsy proven erythema nodosum.
OBJECTIVE: To assess whether polymorphism of the macrophage migration inhibitory factor (MIF) gene at the position -173 is implicated in the development of sarcoidosis. METHODS: Twenty-eight patients with biopsy proven erythema nodosum (EN) associated with sarcoidosis, 70 patients with biopsy proven EN related to other etiologies, and 122 healthy matched controls from the Lugo region of Northwest Spain were studied. Patients and controls were genotyped for a single nucleotide polymorphism in the 5'-flanking region at position -173 of the MIF gene, using SNapshot ddNTP primer extension, followed by capillary electrophoresis (ABI 3100). RESULTS: A significantly increased frequency of the C mutant allele was observed in patients with EN secondary to sarcoidosis compared to controls (p = 0.0016; p(corr) = 0.0032; OR 2.78, 95% CI 1.45, 5.35) and also compared to patients with EN unrelated to sarcoidosis (p = 0.0004; p(corr) = 0.0008; OR 3.72, 95% CI 1.75, 7.87). Patients with EN carrying an MIF 173 C allele were found to have an increased risk of sarcoidosis (57% in EN secondary to sarcoidosis vs 24% in patients with EN related to other etiologies; p = 0.002; p(corr) = 0.004; OR 4.16, 95% CI 1.64, 10.50). CONCLUSION: This is the first attempt to assess the influence of MIF genetic polymorphism at position -173 in the development of sarcoidosis. The MIF 173 C allele is associated with a significantly increased risk of developing sarcoidosis in patients with EN.
Adolescent↗
[Association of the polymorphism of macrophage migration inhibitory factor gene with coronary heart disease in Chinese population].
OBJECTIVE: Inflammation is involved in the process of coronary heart disease (CHD). Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine which can inhibit the random migration of macrophages and concentrate macrophages at the inflammatory site, and is thought to play an important role in cell mediated immunity. The present study is to investigate the association of the -173 G/C polymorphism of MIF gene with the outcome of the CHD. METHODS: One hundred and thirty-eight patients with coronary angiography (CAG) proved CHD were studied, and 163 healthy matched controls in Guangdong were studied. Patients and controls were genotyped for a single nucleotide polymorphism in the 5'-flanking region at position -173 of the MIF gene, using PCR-RFLP analysis, followed by DNA sequencing identification. RESULTS: Only MIF -173G/G and MIF -173G/C genotypes were detected in CHD patients and controls. The MIF -173 G allele was detected in 0.966 of normal controls and 0.917 of patients, while MIF -173 C allele was detected in 0.034 of normal controls and 0.083 of patients. Individuals possessing a MIF-173*C genotype have an increased risk of CHD (16.7% versus 6.8%) (OR: 2.764, 95% CI: 1.295-5.899; P= 0.007). CONCLUSION: These results suggest that MIF -173G /C polymorphism was associated with CHD in Chinese population, the MIF -173C allele might be a risk factor for CHD in Chinese Han nationality.
Adult↗
Functions associated with the C1q receptor.
Information gathered from various sources indicates that the receptor for human C1q is expressed on a wide range of normal and cultured cell lines. Similarly, the functions mediated by the C1qR are as diverse as the cells that express the molecule. On B lymphocytes, for instance, the C1qR is known to mediate cellular cytotoxicity, induce an anti-proliferative response, inhibit synthesis of IL-1 and modulate the synthesis of Ig, whereas on PMNs and monocytes the C1qR participates in the increase of oxidative metabolism and enhancement of phagocytosis of opsonized target particles. Endothelial cells which form an important barrier between blood and vascular basement membrane use their C1qR to localize C1q bearing immune complexes into the basement membrane and thus initiate an inflammatory response. Human diploid fibroblasts express two types of C1qRs: a low affinity C1qR for the collagen-like domain and a small subpopulation expressing high affinity C1qR which binds to the globular region of C1q. Since the high affinity subpopulation manifests characteristics of fibroblasts participating in wound healing and tissue regeneration, the C1qR on these cells may play an important role at sites of inflammation. Recently, binding of C1q to the C1qR on mouse fibroblasts was shown to induce chemotaxis and K+ conductance activation with an increase in cytosolic Ca2+. Although isolation of C1qR from every cell type has not been accomplished as yet, partial characterization of highly purified C1qR from Raji cells and platelets indicate that at least on these cell types, the structure of the molecule is similar. Both molecules are anionic, single chain glycoproteins of approximately 67-70 kDA and upon reduction on SDS-PAGE migrate to an apparent 80-85 kDa indicative of the presence of disulfide bonds. The sedimentation coefficient was estimated to be 2.4-4.2S for platelet C1qR and 4.2S for that of Raji. Equilibrium isoelectric focusing showed the Raji cell C1qR to migrate with a pI of 5.5-6.0. Because the Raji C1qR reveals two components when analyzed by two dimensional SDS-PAGE, the possibility that the C1qR may be a doublet of two apparent 70 kDa molecules only one of which contains relatively more intrachain disulfide bonds is being raised.
Animals↗
Urokinase receptor. An activation antigen in human T lymphocytes.
The ability of activated T lymphocytes to extravasate and reach inflammatory and malignant foci in the tissues is a basic function of cellular immunity. Recent evidence strongly suggests that the urokinase receptor (uPAR) holds a central position in the development of human two-chain urokinase-mediated pericellular proteolysis and matrix degradation, an important element in cell migration. In this report we establish uPAR as a pan T cell activation Ag. As determined by FACS analysis, CD3+ lymphocytes from healthy donors exhibited no significant uPAR expression. In contrast, patients (e.g., HIV-positive donors) showed distinct uPAR expression, confined to HLA-DR+ cells, in up to 80% of all T cells. In vitro activation by PMA caused a rapid up-regulation of membrane uPAR in all healthy donor T cells and was accompanied by enhanced receptor synthesis and elevated uPAR mRNA levels. A similar induction resulted from activation via the TCR/CD3 complex using mitogens (PHA, and Con A), anti-CD3 antibodies, and alloantigen. Receptor expression at single cell level was also modulated by a number of cytokines. IL-2, IL-4 and IL-7 increased uPAR presentation on 20 to 50% of the T cell population, and combined stimulation of bulk cultures demonstrated an additive effect of IL-2 and IL-7, whereas the response to each of the two was inhibited by IL-4. In addition, TGF-beta 1 substantially reduced the uPAR expression in T cell cultures responding to PHA, IL-2, and IL-7. Irrespective of the activating reagent, the T cells appeared to produce the same molecular uPAR species, but the affinity of uPAR expressed in PMA blasts was decreased, presumably because of a differential location at the cell surface. All activated cultures showed co-expression of uPAR and CD25. The finding that the urokinase receptor is an activation Ag may suggest that cell-associated plasminogen activation is involved in extravasation and migration of activated T cells.
Base Sequence↗
Mutations in the type II 3beta-hydroxysteroid dehydrogenase (HSD3B2) gene can cause premature pubarche in girls.
OBJECTIVE: Most previous studies have failed to demonstrate any mutations in the type II 3beta hydroxysteroid dehydrogenase (HSD3B2) gene in patients satisfying the hormonal criteria of nonclassic 3beta-hydroxysteroid dehydrogenase deficiency, suggesting that a mutant 3beta-hydroxysteroid dehydrogenase protein is not the cause of this disorder. We screened the HSD3B2 gene for mutations in girls with premature pubarche and a hormonal diagnosis of 3beta-hydroxysteroid dehydrogenase deficiency. DESIGN: From 30 girls with premature pubarche, we selected 9 whose ACTH-stimulated 17-hydroxypregnenolone levels were elevated (> or =6 SD) and screened the HSD3B2 gene for mutations. MEASUREMENTS: All patients were submitted to a standard ACTH stimulation test. Serum steroids were measured and compared to the mean level of pubertal stage matched control subjects. The four exons and exon-intron boundaries of the HSD3B2 gene were amplified by polymerase chain reaction and screened for mutations by denaturing gradient gel electrophoresis. The fragments with abnormal migration on denaturing gradient gel electrophoresis were directly sequenced. RESULTS: A homozygous T259M mutation was identified in one girl and a new compound heterozygous G129R/P222H mutation was identified in two sisters. The highest ACTH-stimulated 17-hydroxypregnenolone levels, 147, 339 and 351 nmol/l, were found in those patients with mutations in the HSD3B2 gene. In the patients without mutations, ACTH-stimulated 17-hydroxypregnenolone ranged from 48 to 111 nmol/l. ACTH-stimulated dehydroepiandrosterone levels had an overlap among the girls with and without mutations and the normal controls. CONCLUSIONS: Premature pubarche can be caused by mutations in the type II 3beta hydroxysteroid dehydrogenase gene.
17-alpha-Hydroxypregnenolone↗
The multifocality of bronchioloalveolar lung carcinoma: evidence and implications of a multiclonal origin.
Bronchioloalveolar lung carcinoma (BAC) is a unique type of lung cancer with distinguishing pathologic, biologic, epidemiologic, and perhaps etiologic features that set it apart from all other forms of lung cancer, including general adenocarcinoma, into which it is traditionally grouped. Recent studies at our institution have demonstrated a near exponential increase in BAC cases with 25% showing evidence of multifocality. Although some theories suggest that this multifocality is caused by intrapulmonary aerosol/aspiration or lymphatic spread, this study provides evidence for multiclonality as the basis for some cases of multifocal BAC by exploiting a novel strategy for clonality determinations that involves polymerase chain reaction amplification of a 511-base pair region located within the first intron of the human hypoxanthine phosphoribosyltransferase gene, a site that contains inactive X chromosomal obligately methylated HpaII/MspI sites and single-base allelic polymorphisms in 5 to 10% of females. BAC cells, obtained by enzymatic dissociation of different fresh/paraffin-embedded tumoral foci from polymorphic individuals with multilobar or bilateral BAC, were sorted to homogeneity with a fluorescein-conjugated anticarcinoembryonic antigen and then subjected to genomic DNA extraction and HpaII digestion before polymerase chain reaction amplification and subsequent analysis of the product on denaturing gradient gel electrophoresis. The differing migrations of the single homoduplexes generated were indicative of BAC clonal nonidentity or multiclonality in three separate cases. The demonstration of multiclonality in some cases of BAC provides an alternate explanation for multifocality.
Adenocarcinoma, Bronchiolo-Alveolar↗
Neural stem cell migration toward gliomas in vitro.
Various in vivo studies demonstrated a migration tendency of neural stem cells (NSCs) toward gliomas, making these cells a potential carrier for delivery of therapeutic genes to disseminated glioma cells. We analyzed which factors determine NSC migration and invasion in vitro. Conditioned media prepared from 10 different human glioma cell lines, as well as 13 different tumor-associated growth factors, were analyzed for their chemotactic effects on murine C17.2 NSCs. The growth factor receptor status was analyzed by reverse transcriptase-polymerase chain reaction. Invasion of NSCs into multicellular tumor spheroids generated from 10 glioma cell lines was quantified. NSCs displayed a heterogeneous migration pattern toward glioma spheroids as well as toward glioma-cell-conditioned medium. Chemotactic migration was stimulated up to fivefold by conditioned medium as compared to controls. In coculture assays, NSC invasion varied from single cell invasion into glioma spheroids to complete dissemination of NSCs into glioma spheroids of different cell lines. Among 13 different growth factors, scatter factor/hepatocyte growth factor (SF/HGF) was the most powerful chemoattractant for NSCs, inducing a 2.5-fold migration stimulation. An antibody against SF/HGF inhibited migratory stimulation induced by conditioned media. NSC migration can be stimulated by various growth factors, similar to glioma cell migration. The extent to which NSCs infiltrate three-dimensional glioma cell aggregates appears to depend on additional factors, which are likely to include cell-to-cell contacts and interaction with extracellular matrix proteins.
Animals↗
Expression of extraocular myosin heavy chain in rabbit laryngeal muscle.
The intrinsic laryngeal muscles of mammals are functionally heterogeneous, some of these muscles (e.g. the thyroarytenoid) contract extremely rapidly, like extraocular muscle, whilst others (e.g. the cricothyroid) contract as fast as limb fast muscle. The extraordinarily rapid contraction speed of extraocular muscles is associated with a fast myosin not found in limb muscles. In this work we explored the possibility that the thyroarytenoid muscle may also express this extraocular-specific fast myosin by raising a monoclonal antibody (mab 4A6) against its heavy chain. Electrophoretic separation of native isomyosins revealed that both the extraocular and the thyroarytenoid have two similar bands migrating ahead of bands found in limb fast or cricothyroid myosins. These two bands bound mab 4A6. The thyroarytenoid muscle can be divided into two divisions, a vocalis division which is important in phonation and an external division which functions in closing the glottis. Fibres in the vocalis are heterogeneous, some stain with mab 4A6, whilst others stain with mabs against limb myosin heavy chains. Fibres in the external division stain almost homogeneous with mab 4A6. The immunohistochemical staining pattern in the cricothyroid muscle resembled that of fast limb muscle: no fibres stained with mab 4A6. Thus, the high speed of contraction of the thyroarytenoid is associated with the same myosin heavy chain found in extraocular muscles, this characteristic is presumably an evolutionary adaptation for rapid closure of the glottis to enhance airway defense mechanisms.
Animals↗
Inhibition of tendon cell migration by dexamethasone is correlated with reduced alpha-smooth muscle actin gene expression: a potential mechanism of delayed tendon healing.
Local corticosteroid injection is commonly used to treat sports-related tendon injuries. However, isolated cases of tendon rupture following injection suggest that this treatment may impair the healing process. Tendon healing requires the migration of tendon cells to the repair site, followed by the proliferation and synthesis of the extracellular matrix. This study was designed to determine the effect of dexamethasone on the migration of tendon cells intrinsic to rat Achilles tendon at concentrations similar to those typically used for local injection treatment. Furthermore, the existence of a correlation between this effect and the expression of the contractile actin isoform, alpha-smooth muscle (SM) actin, which is associated with cell motility, was also examined. Using cultured tendon cells, migration was evaluated by counting the number of initial outgrowths from the tendon explants and by transwell filter migration assay. The distribution and assembly of alpha-SM actin were assessed by immunocytochemistry. The mRNA and protein expressions of alpha-SM actin were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. Dose-dependent dexamethasone inhibition was demonstrated for both tendon cells outgrowth from the explants, ex vivo, and migration of tendon cells through the transwell filter, in vitro. Immunocytochemical staining revealed significant decreases in both the amount and assembly of alpha-SM actin in cells. Suppression of mRNA expression and protein level of alpha-SM actin was revealed from RT-PCR and Western blot analyses. In conclusion, dexamethasone inhibits tendon cell migration that is correlated with decreased gene expression of alpha-SM actin.
Achilles Tendon↗
Myosin I from mammalian smooth muscle is regulated by caldesmon-calmodulin.
A single-headed monomeric myosin (myosin I) was isolated from pig urinary bladder smooth muscles and purified to homogeneity. Myosin I from smooth muscle is composed of a 110-kDa heavy chain and three 17-kDa light chains. The heavy chain from smooth muscle myosin I does not cross-react with the antibody against conventional myosin (myosin II) from smooth muscle, but it does show antigenic similarity to adrenal medulla myosin I heavy chain. The light chain from smooth muscle myosin I is similar to calmodulin in molecular weight, amino acid composition, and migration on SDS-polyacrylamide gel electrophoresis in the presence of Ca2+. The high salt ATPase activity of myosin I in the presence of CaCl2 is higher than that in K(+)-EDTA. Smooth muscle actin causes a 5-10-fold activation of the Mg-ATPase activity of myosin I. In the presence of Ca2+, exogenous calmodulin enhances the actin-activated ATPase activity of myosin I, and the increased activity is associated with the binding of exogenous calmodulin to myosin I heavy chain. A maximum of 4 mol of light chains/mol of myosin I heavy chain is observed in the presence of exogenous calmodulin. Caldesmon, a calmodulin/actin-binding protein, inhibits the actin-activated ATPase activity of myosin I. This inhibition is reversed by exogenous calmodulin in the presence of Ca2+. The actin activation of myosin I ATPase exhibits around 50% Ca2+ sensitivity in the presence of exogenous calmodulin. When caldesmon is bound to actin, Ca2+ sensitivity is increased to 80% in the presence of calmodulin. Therefore, smooth muscle caldesmon, which is thought to play a role in the regulation of actin activation of myosin II, also regulates the actin activation of myosin I ATPase in smooth muscle.
Actins↗
Cloning of the cDNA encoding human nonmuscle myosin heavy chain-B and analysis of human tissues with isoform-specific antibodies.
Previously, we reported the sequence of cDNA clones encoding amino acids 63 through 723 of the human nonmuscle myosin heavy chain-B isoform. In this paper, we present the derived sequence of the remaining 1303 amino acids along with 5' and 3' untranslated sequences. We made use of the differences between the derived nonmuscle myosin heavy chain-A and -B amino acid sequences to raise isoform-specific antibodies. Immunoblot analysis reveals a differential expression of both myosin heavy chain isoforms in a variety of human adult and foetal tissues and cells. When extracts of human adult aorta were subjected to gel electrophoresis, two distinct Coomassie Blue-stained bands and a fused band were seen migrating at approximately 200 kDa. These bands can be detected with four different specific antibodies recognizing the two different smooth muscle myosin heavy chain isoforms (204 kDa and 200 kDa) and the two different nonmuscle myosin heavy chain isoforms (A and B). Using immunohistochemistry, we confirmed the presence of the four different isoforms in adult and foetal aortas.
Amino Acid Sequence↗
[Activation of smooth muscle myosin by the non-kinase role of myosin light chain kinase].
Myosin light chain kinase (MLCK) is a regulatory protein for smooth muscle contraction, which acts by phosphorylating 20-kDa myosin light chain (MLLC20) to activate the myosin ATPase activity. Although this mode of action is well-established, there are numberous reports of smooth muscle contraction that is not associated with MLC20 phosphorylation. The kinase activity for the phosphorylation is localized at the central part of MLCK, which is also furnished with actin-binding activity at its N terminal and myosin-binding activity at its C terminal. I will overview as to how such multifunctional properties of MLCK modify the actin-myosin interaction and presents our observations that the phosphorylation is not obligatory in induction of smooth muscle contraction and migration.
Animals↗