Gotowe bibliografie tematyczne / RhoA

Gotowa bibliografia na temat „RhoA”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 6 lipca 2024

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Artykuły w czasopismach na temat "RhoA"

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Saracaloglu, Ahmet, Seniz Demiryürek, Sabit Kimyon, Alper Mete, Ebru Temiz, Gülper Nacarkahya, Oguzhan Saygili, Kıvanc Güngör i Abdullah Tuncay Demiryürek. "RHO Gene Polymorphisms in Patients with Pterygium". Proceedings 2, nr 25 (6.12.2018): 1572. http://dx.doi.org/10.3390/proceedings2251572.

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Pterygium is one of the most common ocular surface diseases, and characterized by inflammatory infiltrates, proliferation, fibrosis, angiogenesis, and extracellular matrix breakdown. We investigated the association of polymorphisms in the RHO genes RHOA, RHOB, RHOC, RHOD, and RND3 (RHOE). The results of this study demonstrate for the first time the association of RHO genes with the pterygium. We displayed that the RHO gene polymorphisms were significantly associated with pterygium in the Turkish population.
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Guasch, Rosa M., Peter Scambler, Gareth E. Jones i Anne J. Ridley. "RhoE Regulates Actin Cytoskeleton Organization and Cell Migration". Molecular and Cellular Biology 18, nr 8 (1.08.1998): 4761–71. http://dx.doi.org/10.1128/mcb.18.8.4761.

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ABSTRACT The actin cytoskeleton is regulated by Rho family proteins: in fibroblasts, Rho mediates the formation of actin stress fibers, whereas Rac regulates lamellipodium formation and Cdc42 controls filopodium formation. We have cloned the mouse RhoE gene, whose product is a member of the Rho family that shares (except in one amino acid) the conserved effector domain of RhoA, RhoB, and RhoC. RhoE is able to bind GTP but does not detectably bind GDP and has low intrinsic GTPase activity compared with Rac. The role of RhoE in regulating actin organization was investigated by microinjection in Bac1.2F5 macrophages and MDCK cells. In macrophages, RhoE induced actin reorganization, leading to the formation of extensions resembling filopodia and pseudopodia. In MDCK cells, RhoE induced the complete disappearance of stress fibers, together with cell spreading. However, RhoE did not detectably affect the actin bundles that run parallel to the outer membranes of cells at the periphery of colonies, which are known to be dependent on RhoA. In addition, RhoE induced an increase in the speed of migration of hepatocyte growth factor/scatter factor-stimulated MDCK cells, in contrast to the previously reported inhibition produced by activated RhoA. The subcellular localization of RhoE at the lateral membranes of MDCK cells suggests a role in cell-cell adhesion, as has been shown for RhoA. These results suggest that RhoE may act to inhibit signalling downstream of RhoA, altering some RhoA-regulated responses, such as stress fiber formation, but not affecting others, such as peripheral actin bundle formation.
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Königs, Volker, Richard Jennings, Thomas Vogl, Markus Horsthemke, Anne C. Bachg, Yan Xu, Kay Grobe i in. "Mouse Macrophages Completely Lacking Rho Subfamily GTPases (RhoA, RhoB, and RhoC) Have Severe Lamellipodial Retraction Defects, but Robust Chemotactic Navigation and Altered Motility". Journal of Biological Chemistry 289, nr 44 (11.09.2014): 30772–84. http://dx.doi.org/10.1074/jbc.m114.563270.

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RhoA is thought to be essential for coordination of the membrane protrusions and retractions required for immune cell motility and directed migration. Whether the subfamily of Rho (Ras homolog) GTPases (RhoA, RhoB, and RhoC) is actually required for the directed migration of primary cells is difficult to predict. Macrophages isolated from myeloid-restricted RhoA/RhoB (conditional) double knock-out (dKO) mice did not express RhoC and were essentially “pan-Rho”-deficient. Using real-time chemotaxis assays, we found that retraction of the trailing edge was dissociated from the advance of the cell body in dKO cells, which developed extremely elongated tails. Surprisingly, velocity (of the cell body) was increased, whereas chemotactic efficiency was preserved, when compared with WT macrophages. Randomly migrating RhoA/RhoB dKO macrophages exhibited multiple small protrusions and developed large “branches” due to impaired lamellipodial retraction. A mouse model of peritonitis indicated that monocyte/macrophage recruitment was, surprisingly, more rapid in RhoA/RhoB dKO mice than in WT mice. In comparison with dKO cells, the phenotypes of single RhoA- or RhoB-deficient macrophages were mild due to mutual compensation. Furthermore, genetic deletion of RhoB partially reversed the motility defect of macrophages lacking the RhoGAP (Rho GTPase-activating protein) myosin IXb (Myo9b). In conclusion, the Rho subfamily is not required for “front end” functions (motility and chemotaxis), although both RhoA and RhoB are involved in pulling up the “back end” and resorbing lamellipodial membrane protrusions. Macrophages lacking Rho proteins migrate faster in vitro, which, in the case of the peritoneum, translates to more rapid in vivo monocyte/macrophage recruitment.
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Han, Jian, Li Li, Jiongyu Hu, Lili Yu, Yingru Zheng, Jianxin Guo, Xiuhui Zheng, Ping Yi i Yuanguo Zhou. "Epidermal Growth Factor Stimulates Human Trophoblast Cell Migration through Rho A and Rho C Activation". Endocrinology 151, nr 4 (11.02.2010): 1732–42. http://dx.doi.org/10.1210/en.2009-0845.

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This study investigated the roles of Rho protein in epidermal growth factor (EGF)-induced trophoblast cell migration and its mechanism. Using choriocarcinoma cell lines JEG-3 and JAR and first-trimester human chorionic villus explant cultures on matrigel, we examined EGF-mediated stimulation of trophoblast migration. EGF is shown to have a dose-dependent effect on trophoblast migration. A low concentration of EGF (1 ng/ml) has a stimulatory effect on cell migration, whereas high concentrations of EGF (100 ng/ml) shows an inhibitory effect. EGF (1 ng/ml) activates RhoA and RhoC, but not RhoB, through elevated protein levels and activity. EGF-induced migration was shown to be inhibited by either cell-permeable C3 exoenzyme transferase or selective RhoA or RhoC small interfering RNAs. The inhibition was not mitigated by the addition of EGF, suggesting that RhoA and RhoC play an important role in trophoblast migration and are obligatory for EGF action. Treatment of JEG-3 and JAR cells with RhoA small interfering RNA induced F-actin cytoskeleton disruption and cell shrinkage, which is consistent with the effect of C3 exoenzyme transferase, and this action was not mitigated by EGF treatment. RhoC small interfering RNA had no apparent effect on the F-actin arrangement, suggesting that RhoA but not RhoC takes part in the EGF-induced migration through F-actin rearrangement. These results indicate that RhoA and RhoC play more important roles than RhoB in EGF-mediated migration of trophoblast cells, and RhoA but not RhoC regulates this migration through F-actin cytoskeleton reorganization.
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Tsubaki, Masanobu, Shuuji Genno, Tomoya Takeda, Takuya Matsuda, Naoto Kimura, Yuuma Yamashita, Yuusuke Morii, Kazunori Shimomura i Shozo Nishida. "Rhosin Suppressed Tumor Cell Metastasis through Inhibition of Rho/YAP Pathway and Expression of RHAMM and CXCR4 in Melanoma and Breast Cancer Cells". Biomedicines 9, nr 1 (4.01.2021): 35. http://dx.doi.org/10.3390/biomedicines9010035.

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The high mortality rate of cancer is strongly correlated with the development of distant metastases at secondary sites. Although Rho GTPases, such as RhoA, RhoB, RhoC, and RhoE, promote tumor metastasis, the main roles of Rho GTPases remain unidentified. It is also unclear whether rhosin, a Rho inhibitor, acts by suppressing metastasis by a downstream inhibition of Rho. In this study, we investigated this mechanism of metastasis in highly metastatic melanoma and breast cancer cells, and the mechanism of inhibition of metastasis by rhosin. We found that rhosin suppressed the RhoA and RhoC activation, the nuclear localization of YAP, but did not affect ERK1/2, Akt, or NF-κB activation in the highly metastatic cell lines B16BL6 and 4T1. High expression of YAP was associated with poor overall and recurrence-free survival in patients with breast cancer or melanoma. Treatment with rhosin inhibited lung metastasis in vivo. Moreover, rhosin inhibited tumor cell adhesion to the extracellular matrix via suppression of RHAMM expression, and inhibited SDF-1-induced cell migration and invasion by decreasing CXCR4 expression in B16BL6 and 4T1 cells. These results suggest that the inhibition of RhoA/C-YAP pathway by rhosin could be an extremely useful therapeutic approach in patients with melanoma and breast cancer.
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Tseliou, Melpomeni, Ahmed Al-Qahtani, Saud Alarifi, Saad H. Alkahtani, Christos Stournaras i George Sourvinos. "The Role of RhoA, RhoB and RhoC GTPases in Cell Morphology, Proliferation and Migration in Human Cytomegalovirus (HCMV) Infected Glioblastoma Cells". Cellular Physiology and Biochemistry 38, nr 1 (2016): 94–109. http://dx.doi.org/10.1159/000438612.

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Background/Aims: Rho GTPases are crucial regulators of the actin cytoskeleton, membrane trafficking and cell signaling and their importance in cell migration and invasion is well- established. The human cytomegalovirus (HCMV) is a widespread pathogen responsible for generally asymptomatic and persistent infections in healthy people. Recent evidence indicates that HCMV gene products are expressed in over 90% of malignant type glioblastomas (GBM). In addition, the HCMV Immediate Early-1 protein (IE1) is expressed in >90% of tumors analyzed. Methods: RhoA, RhoB and RhoC were individually depleted in U373MG glioblastoma cells as well as U373MG cells stably expressing the HCMV IE1 protein (named U373MG-IE1 cells) shRNA lentivirus vectors. Cell proliferation assays, migration as well as wound-healing assays were performed in uninfected and HCMV-infected cells. Results: The depletion of RhoA, RhoB and RhoC protein resulted in significant alterations in the morphology of the uninfected cells, which were further enhanced by the cytopathic effect caused by HCMV. Furthermore, in the absence or presence of HCMV, the knockdown of RhoB and RhoC proteins decreased the proliferation rate of the parental and the IE1-expressing glioblastoma cells, whereas the knockdown of RhoA protein in the HCMV infected cell lines restored their proliferation rate. In addition, wound healing assays in U373MG cells revealed that depletion of RhoA, RhoB and RhoC differentially reduced their migration rate, even in the presence or the absence of HCMV. Conclusion: Collectively, these data show for the first time a differential implication of Rho GTPases in morphology, proliferation rate and motility of human glioblastoma cells during HCMV infection, further supporting an oncomodulatory role of HCMV depending on the Rho isoforms' state.
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Saracaloglu, Ahmet, Seniz Demiryürek, Sabit Kimyon, Alper Mete, Ebru Temiz, Gülper Nacarkahya, Betül Düzen, Oguzhan Saygili, Kıvanc Güngör i Abdullah Tuncay Demiryürek. "Protein Expressions of the Small GTPase Rho Proteins in Pterygial Tissue and Leukocytes of Patients with Pterygium". Proceedings 2, nr 25 (6.12.2018): 1571. http://dx.doi.org/10.3390/proceedings2251571.

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Pterygium is a benign fibrovascular proliferation that develops from the conjunctiva and invades the cornea. The etiology of this disorder remains unclear. Current treatment of pterygium is surgical. The postoperative recurrence rate of pterygium is reported be high. To the best of our knowledge, these results are the first to demonstrate the contribution of proteins expressions of the small GTPase Rho proteins in patients with pterygium. Our data showed that leukocyte RhoA, RhoB, RhoD, and RhoE protein expressions were markedly elevated in primary pterygium. However, no significant modifications were noted in pterygial tissues.
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Jackson, Ben, Karine Peyrollier, Esben Pedersen, Astrid Basse, Richard Karlsson, Zhipeng Wang, Tine Lefever i in. "RhoA is dispensable for skin development, but crucial for contraction and directed migration of keratinocytes". Molecular Biology of the Cell 22, nr 5 (marzec 2011): 593–605. http://dx.doi.org/10.1091/mbc.e09-10-0859.

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RhoA is a small guanosine-5’-triphosphatase (GTPase) suggested to be essential for cytokinesis, stress fiber formation, and epithelial cell–cell contacts. In skin, loss of RhoA was suggested to underlie pemphigus skin blistering. To analyze RhoA function in vivo, we generated mice with a keratinocyte-restricted deletion of the RhoA gene. Despite a severe reduction of cofilin and myosin light chain (MLC) phosphorylation, these mice showed normal skin development. Primary RhoA-null keratinocytes, however, displayed an increased percentage of multinucleated cells, defective maturation of cell–cell contacts. Furthermore we observed increased cell spreading due to impaired RhoA-ROCK (Rho-associated protein kinase)-MLC phosphatase-MLC–mediated cell contraction, independent of Rac1. Rho-inhibiting toxins further increased multinucleation of RhoA-null cells but had no significant effect on spreading, suggesting that RhoB and RhoC have partially overlapping functions with RhoA. Loss of RhoA decreased directed cell migration in vitro caused by reduced migration speed and directional persistence. These defects were not related to the decreased cell contraction and were independent of ROCK, as ROCK inhibition by Y27632 increased directed migration of both control and RhoA-null keratinocytes. Our data indicate a crucial role for RhoA and contraction in regulating cell spreading and a contraction-independent function of RhoA in keratinocyte migration. In addition, our data show that RhoA is dispensable for skin development.
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Riento, Kirsi, Rosa M. Guasch, Ritu Garg, Boquan Jin i Anne J. Ridley. "RhoE Binds to ROCK I and Inhibits Downstream Signaling". Molecular and Cellular Biology 23, nr 12 (15.06.2003): 4219–29. http://dx.doi.org/10.1128/mcb.23.12.4219-4229.2003.

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ABSTRACT RhoE belongs to the Rho GTPase family, the members of which control actin cytoskeletal dynamics. RhoE induces stress fiber disassembly in a variety of cell types, whereas RhoA stimulates stress fiber assembly. The similarity of RhoE and RhoA sequences suggested that RhoE might compete with RhoA for interaction with its targets. Here, we show that RhoE binds ROCK I but none of the other RhoA targets tested. The interaction of RhoE with ROCK I was confirmed by coimmunoprecipitation of the endogenous proteins, and the two proteins colocalized on the trans-Golgi network in COS-7 cells. Although RhoE and RhoA were not able to bind ROCK I simultaneously, RhoE bound to the amino-terminal region of ROCK I encompassing the kinase domain, at a site distant from the carboxy-terminal RhoA-binding site. Overexpression of RhoE inhibited ROCK I-induced stress fiber formation and phosphorylation of the ROCK I target myosin light chain phosphatase. These data suggest that RhoE induces stress fiber disassembly by directly binding ROCK I and inhibiting it from phosphorylating downstream targets.
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Pronk, Manon C. A., Jan S. M. van Bezu, Geerten P. van Nieuw Amerongen, Victor W. M. van Hinsbergh i Peter L. Hordijk. "RhoA, RhoB and RhoC differentially regulate endothelial barrier function". Small GTPases 10, nr 6 (26.09.2017): 466–84. http://dx.doi.org/10.1080/21541248.2017.1339767.

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Rozprawy doktorskie na temat "RhoA"

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Chinestra, Patrick. "Conception de biosenseurs des protéines RhoA, RhoB, RhoC". Toulouse 3, 2012. http://thesesups.ups-tlse.fr/1715/.

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Notre équipe s'intéresse à la compréhension des mécanismes de dérégulation des voies de signalisation cellulaire dans la survenue et la maintenance des processus tumoraux, ainsi que leurs conséquences dans la réponse aux thérapies antitumorales. Nous nous intéressons particulièrement aux protéines Rho et à leurs régulateurs. Ils interviennent dans les voies de signalisation des récepteurs cellulaires conduisant à des modifications de l'adhérence, de la prolifération, de la motilité et de la balance survie/mort cellulaire. Les protéines RhoA, RhoB et RhoC sont des petites GTPases passant d'un état actif (liées au GTP) à un état inactif (liées au GDP) et dont l'homologie est proche de 85%. La surexpression des protéines RhoA et RhoC a été décrite dans un grand nombre de tumeurs; à l'inverse, on observe une diminution de l'expression de RhoB dans le mélanome et dans le cancer du poumon. La conception de fragments d'anticorps sélectifs de la conformation active des Rho, appelés biosenseurs, permettant d'évaluer l'activation de ces protéines in situ dans des coupes de tissus sains et cancéreux, pourrait aboutir à un usage pronostique de ces outils voire à la définition de nouveaux marqueurs thérapeutiques et permettrait de répondre à des questions plus fondamentales comme leurs localisations cellulaire, leur rôle dans la migration cellulaire, leur activation spatio-temporelle. A partir du scFvC1 sélectif de la conformation active des trois protéines RhoA, RhoB et RhoC et isolé précédemment dans l'équipe, nous avons créé une banque secondaire par mutagénèse aléatoire et opéré une sélection par phage display avec un objectif double : 1°) augmenter l'affinité du scFvC1 pour améliorer ses capacités d'interaction avec les protéines Rho actives natives en vue d'améliorer ses performances en immunohistologie ainsi que pour une utilisation intracellulaire. 2°) sélectionner des variants spécifiques de chaque Rho malgré leur très forte homologie. Nous montrons que la stratégie mise en œuvre permet d'augmenter l'affinité des scFv et de modifier leur sélectivité puisqu'un variant se lie préférentiellement à RhoA et RhoC. De plus, contrairement au svFvC1, ces scFv sont immunoprécipitants pour les Rho actives produites dans des cellules eucaryotes. En parallèle, nous avons mis au point une méthodologie permettant le marquage d'un scFv anti-RhoB obtenu au laboratoire, par l'action d'un dérivé fluorescent de la biotine sur une intéine exprimée en fusion C-terminale du scFv. Ceci permettra d'améliorer les techniques immunohistologiques avec des biosenseurs fluorescents
Our team is interested in understanding the mechanisms of deregulation of cell signaling pathways in the development and maintenance of tumor processes and their consequences in response to anti-tumor therapies. We focuse on Rho proteins as well as on their regulators. They are involved in signaling pathways of cell receptors leading to changes in adhesion, proliferation, motility and balance survival / cellular death. RhoA, RhoB and RhoC are small GTPases switching from an active state (GTP-bound) to an inactive state (GDP-bound) and the homology of which is close to 85%. Overexpression of RhoA and RhoC protein has been described in many tumors; in contrast, there was a decreased expression of RhoB in melanoma and lung cancer. Engineering antibody fragment specific of Rho active conformations, namely biosensors, would allow in situ assessment of these proteins activation in healthy or tumour samples. These tools could be further developed towards diagnosis or prognosis usage, or could even define novel therapeutics markers and be used to answer more fundamental question as their cellular localization, their role in cell migration, or their spatio-temporal activation. Starting from the scFvC1 previously isolated in the group and which is selective for RhoA, RhoB and RhoC active conformations, we have created by random mutagenesis a second library and performed a phage display selection with two aims: 1°) increase the C1 scFv affinity to enhance its interaction potential with active native Rho proteins in order to improve its performance in immuno-histology or to use it as an intracellular antibody. 2°) select variants with a selectivity towards strictly only one of the three Rho excluding the others despite their strong homology. We show that our strategy allowed an affinity increase of scFv and also a selectivity modulation as one variant preferentially binds RhoA and C. Moreover, in contrast to scFvC1 these scFvs immuno-precipitate active endogenous Rho Proteins in eukaryotic cells. In parallel, we have established a method allowing the labelling of an anti-RhoB scFv from the lab, by fusing it to an intein that induce covalent binding of a biotin fluorescent analogue. This approach will improve immuno-histological techniques using fluorescent biosensors
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Huppertz, Tilman [Verfasser]. "Charakterisierung der Rekrutierungsdomäne der kleinen Rho-GTPasen RhoA und RhoC / Tilman Huppertz". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023697491/34.

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Zandvakili, Inuk. "RhoA as a Potential Target in Lung Cancer". University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1445342196.

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Will, Laura Christine [Verfasser]. "Charakterisierung der Interaktion von p120ctn mit den Rho-GTPasen RhoA und RhoC / Laura Christine Will". Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1178320073/34.

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Will, Laura [Verfasser]. "Charakterisierung der Interaktion von p120ctn mit den Rho-GTPasen RhoA und RhoC / Laura Christine Will". Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1178320073/34.

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Soliman, Hesham. "The RhoA/Rho kinase pathway in diabetic cardiomyopathy". Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43439.

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Diabetes mellitus leads to a unique pathological entity termed diabetic cardiomyopathy, the mechanisms of which have not been fully defined. In diabetic rat hearts, RhoA expression is increased and the RhoA/ROCK pathway is activated, while ROCK inhibition acutely improves contractile function of diabetic hearts. The mechanisms underlying this improvement and those responsible for the detrimental activation of RhoA/ROCK were investigated here. Nitric oxide (NO) has been reported to upregulate RhoA expression in smooth muscle, and previous reports showed that iNOS expression is increased in diabetic rat hearts. In the first part of this thesis, the hypothesis that in diabetic cardiomyopathy, iNOS induction is responsible for increased RhoA expression was investigated. The results demonstrate that increased NO production from iNOS induction leads to RhoA upregulation in the diabetic heart and in isolated cardiomyocytes, contributing to the RhoA/ROCK mediated contractile dysfunction by increasing the total pool of RhoA available for activation. In diabetic rat hearts, PKCβ₂ activation induces iNOS expression, leading to increased nitrosative/oxidative stress. This suggests that PKCβ2 might positively regulate RhoA expression, although in preliminary experiments inhibition of ROCK itself reduced RhoA expression. Therefore, in the second part, the hypothesis that PKCβ₂/iNOS and RhoA/ROCK interact together to form a positive feedback loop was tested. The results show that RhoA/ROCK overactivation is sustained by a positive feedback loop that involves PKCβ₂ activation and iNOS induction. This feedback loop requires an intact actin cytoskeleton and plays a key role in elevating superoxide production in diabetic rat hearts. In the third part, the hypothesis that ROCK inhibition augments contraction by improving Ca²⁺ signaling was tested. Inhibition of ROCK improved contractile function and abolished the diabetes-induced delayed aftercontractions in isolated cardiomyocytes, in association with an improvement in Ca²⁺ transients. Overall, the results show that in diabetic cardiomyopathy, overactivation of RhoA/ROCK contributes to contractile dysfunction by sustaining PKCβ2 activation, iNOS induction and superoxide production via a positive feedback loop that leads to impaired intracellular Ca²⁺ homeostasis. Inhibition of ROCK disrupts the loop, resulting in decreased oxidative stress, and improved Ca²⁺ handling and cardiomyocyte contraction, suggesting that ROCK inhibition might be a novel approach in treating diabetic cardiomyopathy.
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Srivastava, Kirtiman. "Pathophysiological role of RhoA/Rho-kinase under oxygen-glucose deprivation/reperfusion and hyperglycaemia". Thesis, University of Nottingham, 2013. http://eprints.nottingham.ac.uk/13533/.

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Introduction: Oxygen-glucose deprivation (OGD)±reperfusion and hyperglycaemia exacerbate the ischaemic cerebral injuries during or after a stroke. The key biochemical events associated with these pathologies include excessive cytoskeletal remodelling, modulation of tight junction proteins and the induction of oxidative stress. Recently, the overactivities of protein kinase C (PKC), RhoA/Rho-kinase, and pro-oxidant NADPH oxidase have been shown to account for the development of these events and the consequent disruption of human blood-brain barrier (BBB) integrity. Objectives: This thesis focused on the putative roles of RhoA/Rho-kinase signalling in OGD and OGD+reperfusion-evoked modulation of cytoskeletal remodelling, tight junction proteins and oxidative stress in human brain microvascular endothelial cells (HBMEC). The effects of hyperglycaemia-mediated PKC overactivities in modulating the RhoA/Rho-kinase pathway with reference to the aforementioned parameters i.e. cytoskeletal remodelling and tight junction protein expression and localisation have also been the focus of this thesis. Methods: For the OGD studies, the HBMEC were exposed to normoxia (controls), OGD (4, 20 hours) alone and followed by reperfusion (20 hours). The HBMEC-human astrocyte (HA) cocultures were established to mimic human BBB before exposing them to the experimental conditions. The integrity and function of HBMEC-HA cocultures were measured by transendothelial electrical resistance (TEER) and flux of permeability markers sodium fluorescein (NaF) and Evan’s blue-labelled albumin (EBA), respectively. For the hyperglycaemia studies, the HBMEC monolayers and the cocultures were exposed to normoglycaemia (5.5 mM D-glucose), hyperglycaemia (25 mM D-glucose), and hyperglycaemia with inhibitors of Rho-kinase, PKC, PKC-α, PKC-β, PKC-βII, PKC-δ; and the BBB integrity and function were measured by the TEER and flux studies, respectively. Fold differences in the protein expression or activity of RhoA, Rho-kinase-2, mono- and di-phosphorylated myosin light chain-2 (MLC2), total MLC2, gp91-phox (a pivotal NADPH oxidase subunit), catalase, occludin, claudin-5, zonula occludens-1 (ZO-1), β-catenin, and vinculin were either measured by in-cell or ordinary Western analyses. Results from the OGD studies: OGD compromised the barrier integrity as observed by decreases in TEER values and concomitant increases in flux of EBA and NaF across the cocultures. Transfection of HBMEC with constitutively active RhoA also decreased the TEER and increased the NaF paracellular permeability, whereas inactivation of RhoA by anti-RhoA-IgG electroporation exerted barrier protective effects. Moreover, OGD alone and after constitutively active RhoA transfection introduced stress fibres in HBMEC, which were abrogated by inactivation of RhoA and the specific inhibition of its main effector Rho-kinase by Y-27632. In addition, dramatic increases in the protein expressions of RhoA-GTP, Rho-kinase-2, gp91-phox, and antioxidant catalase were observed in HBMEC exposed to OGD+reperfusion conditions. These along with increases in the NADPH oxidase activity and total superoxide anion levels confirmed the oxidative stress in HBMEC under these experimental conditions. A marked rise in the protein expressions of claudin-5 and β-catenin observed after OGD (20 hours) alone and followed by reperfusion may represent the effects of oxidative stress on tight and adherens junction proteins stability, respectively. These results also concurred with marked decreases in TEER and concomitant increases in the flux of EBA across the in vitro models of human BBB exposed to OGD±reperfusion conditions when compared with the controls. Cotreatment with Y-27632 under OGD±reperfusion normalised the protein expressions of RhoA, Rho-kinase-2, gp91-phox, claudin-5, catalase; activities of RhoA and NADPH oxidase; and total superoxide anions levels, alongside improving the expression of occludin and the coculture integrity under the OGD±reperfusion conditions. Results from the hyperglycaemia studies: Hyperglycaemia also increased RhoA-GTP, Rho-kinase-2, mono- and di-phosphorylated MLC2 protein levels and total PKC activity. These changes were consistent with the actin stress fibre formations, ZO-1 and occludin redistribution from HBMEC periphery. Hyperglycaemia-mediated endothelial-barrier dysfunction was further characterised by reduction in TEER and elevation in flux of EBA. Glucose normalisation, RhoA neutralisation by anti-RhoA-IgG electroporation and Rho-kinase-2 inhibition by Y-27632 normalised all abovementioned protein expressions, restored actin and tight junction protein localisations and barrier integrity. Cotreatment of HBMEC with hyperglycaemia and a general PKC inhibitor namely, bisindolylmaleimide-I normalised the Rho-kinase-2, mono- and di-phosphorylated MLC2 levels. Moreover, specific inhibitors of PKC-α (Ro-32-0432), PKC-β (LY333531), PKC-βII (CGP53353) attenuated the PKC overactivity, normalised all protein expressions, restored actin localisation and improved barrier integrity. In addition, the PKC-α and PKC-β siRNA transfections mimicked the effects of the specific inhibitors and attenuated the hyperglycaemia-evoked RhoA-GTP, mono- and di-phosphorylated MLC2 protein levels and stress fibre formations. Conclusions: The RhoA/Rho-kinase overactivities compromise the endothelial-barrier integrity, in part, by modulating the cytoskeletal remodelling and inducing the NADPH oxidase-evoked oxidative stress under OGD±reperfusion pathology. Moreover, hyperglycaemia-mediated increases in PKC-α and PKC-β activities exacerbate the endothelial-barrier dysfunction by modulating RhoA/Rho-kinase signalling pathway. Summary: These findings support the hypothesis that OGD±reperfusion and hyperglycaemia perturb BBB integrity through regulation of RhoA/Rho-kinase activity and modulation of cytoskeletal reorganisation, oxidative stress and tight junction protein expressions or localisations.
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Ard, Ryan. "Regulation of RhoA Activation and Actin Reorganization by Diacylglycerol Kinase". Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22669.

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Rho GTPases are critical regulators of actin cytoskeletal dynamics. The three most well characterized Rho GTPases, Rac1, RhoA and Cdc42 share a common inhibitor, RhoGDI. It is only recently becoming clear how upstream signals cause the selective release of individual Rho GTPases from RhoGDI. For example, our laboratory showed that diacylglycerol kinase zeta (DGKz), which converts diacylglycerol (DAG) to phosphatidic acid (PA), activates PAK1-mediated RhoGDI phosphorylation on Ser-101/174, causing selective Rac1 release and activation. Phosphorylation of RhoGDI on Ser-34 by PKCa has recently been demonstrated to selectively release RhoA, promoting RhoA activation. Here, I show DGKz is required for optimal RhoA activation and RhoGDI Ser-34 phosphorylation. Both were substantially reduced in DGKz-null fibroblasts and occurred independently of DGKz activity, but required a function DGKz PDZ-binding motif. In contrast, Rac1 activation required DGKz-derived PA, but not PDZ-interactions, indicating DGKz regulates these Rho GTPases by two distinct regulatory complexes. Interestingly, RhoA bound directly to the DGKz C1A domain, the same region known to bind Rac1. By direct interactions with RhoA and PKCa, DGKz was required for the efficient co-precipitation of these proteins, suggesting it is important to assemble a signalling complex that functions as a RhoA-specific RhoGDI dissociation complex. Consequently, cells lacking DGKz exhibited decreased RhoA signalling downstream and disrupted stress fibers. Moreover, DGKz loss resulted in decreased stress fiber formation following the expression of a constitutively active RhoA mutant, suggesting it is also important for RhoA function following activation. This is consistent with the ability of DGKz to bind both active and inactive RhoA conformations. Collectively, these findings suggest DGKz is central to two distinct Rho GTPase activation complexes, each having different requirements for DGKz activity and PDZ interactions, and might regulate the balance of Rac1 and RhoA activity during dynamic changes to the actin cytoskeleton.
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Bendris, Nawal. "Nouvelles fonctions de la Cycline A2 : régulation de l’invasion cellulaire et de la transition épithéliomésenchymateuse". Thesis, Montpellier 2, 2011. http://www.theses.fr/2011MON20079.

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L'agressivité des cancers est souvent liée au pouvoir métastatique des cellules tumorales et la dissémination de ces dernières peut survenir suite à un phénomène appelé la transition épithéliomésenchymateuse. Une analyse de l'expression de la Cycline A2 conduite sur des échantillons humains de tumeurs primaires colorectales et de leurs métastases correspondantes révèle que cette protéine est moins abondante dans ces dernières. Le travail décrit dans cette thèse a permis de relier la Cycline A2 au remodelage du cytosquelette d'Actine dans les fibroblastes. Cette régulation requiert la localisation cytoplasmique de la molécule ainsi que son domaine N-terminal qui ne lie pas les CDKs. Nos expériences suggèrent que cette nouvelle activité est la conséquence d'une liaison directe entre la GTPase RhoA et la Cycline A2. La présence de cette dernière augmente l'activation de RhoA par sa GEF in vitro. L'utilisation de cellules épithéliales mammaires normales a permis l'identification d'un autre partenaire, RhoC. Dans ce contexte cellulaire, l'invalidation de la Cycline A2 diminue l'activation de RhoA et, renforce celle de RhoC ce qui conduit à une augmentation de l'invasion cellulaire en matrice de collagène. Ces cellules acquièrent aussi des propriétés mésenchymateuses caractéristiques de l'EMT, et ce phénotype est exacerbé par la présence de RasV12. Ce travail établit donc l'existence de nouvelles fonctions pour la Cycline A2 qui viennent compléter le tableau de régulation de la motilité par les protéines du cycle cellulaire et contribuent à une meilleure compréhension de son rôle dans le cancer
Cancer aggressiveness is often associated with metastases occurrence and their dissemination can arise following an epithelial to mesenchymal transition (EMT). Cyclin A2 expression is lower in metastases relative to primary colon adenocarcinoma of matched human tumors. This manuscript describes new links between Cyclin A2 and Actin cytoskeleton remodeling in fibroblasts. This regulation requires a cytoplasmic localization of the protein and its N-terminal domain, which is unable to bind CDKs. This new Cyclin A2 activity appears to be mediated by its binding to RhoA. Accordingly, the activity of its GEF is potentiated when Cyclin A2 is present, in vitro. Furthermore, we used a normal mammary epithelial cell line and identified another Cyclin A2 partner, RhoC. Cyclin A2 depletion in this context leads to a reciprocal RhoGTPase activation where RhoA activation is impaired and that of RhoC is increased. Moreover, cell invasiveness is increased in a collagen matrix following Cyclin A2 knockdown in these cells. In addition, the epithelial cells acquire mesenchymal properties, which are exarcerbated by the expression of RasV12 and are characteristic of an EMT. Our work completes the network involving cell cycle proteins in motility. These novel functions of Cyclin A2 will hopefully help to understand the impact of its deregulation in cancer
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Keller, Laura. "Conception de nano-anticorps conformationnels comme nouveaux outils d'étude de l'activité des GTPases de la sous-famille RHOA". Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30005/document.

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Les GTPases de la sous famille RHOA participent à la régulation de nombreuses voies de signalisation qui contrôlent la dynamique du cytosquelette cellulaire et une grande diversité de fonctions telles que la prolifération, la division, la migration et la polarité cellulaires. Ce sont de véritables interrupteurs moléculaires qui, en réponse à un stimulus, changent de conformation tridimensionnelle pour activer leurs protéines effectrices cibles. Elles existent donc sous deux formes, une forme inactive liant le GDP et une forme active, liant le GTP. La proportion de forme active est extrêmement régulée au niveau spatial et temporel dans une cellule et représente moins de 10% de sa totalité. Depuis près de 20 ans, le seul outil disponible pour étudier leur activation est constitué par le domaine de liaison d'un effecteur, le RBD. Peu stable, faiblement soluble et peu adaptable, de nouveaux outils sont nécessaires afin de mieux comprendre la fine régulation de ces protéines. Les anticorps à simple domaine, VHH ou nanobodies, sont caractérisés par leur stabilité, solubilité, haut rendement de production et versatilité de fonctionnalisation. A partir d'une nouvelle banque d'anticorps à simple domaine optimisée pour la production d'intracorps, nous avons isolés différents clones capables de reconnaître in vitro et de bloquer in cellulo la forme active de ces protéines. L'un de ces clones permettra le développement d'un nouvel outil de mesure de l'activité de ces protéines in vitro tandis qu'un autre, in cellulo, permettra de mieux comprendre la régulation spatiale et temporelle des protéines endogènes
RHOA small GTPase belongs to a subfamily acting as a molecular switch activating major signaling pathways that regulate cytoskeletal dynamics and a variety of cellular responses such as cell cycle progression, cytokinesis, migration and polarity. RHOA activity resides in a few percent of GTP loaded protein, which is finely tuned by a crosstalk between regulators of the GTPase cycle. Manipulating a single RHO at the expression level often induces imbalance in the activity of other RHO GTPases, suggesting that more specific tools targeting these active pools are needed to decipher RHOA functions in time and space. We decided to use single domain antibodies, also known as VHH or nanobodies, as a new tool for studying RHOA activation. We produced and screened a novel fully synthetic phage display library of humanized nanobodies (NaLi-H1) to develop conformational sensors of the GTP loaded active conformation of RHO subfamily. We obtained several high affinity nanobodies against RHOA's active form which we characterized as RHO active antibodies in vitro and RHO signaling blocking intrabodies in cellulo. These new tools will facilitate and improve our current knowledge of this peculiar protein subfamily and will be a paradigm for the study of other RHO related small GTPases
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Książki na temat "RhoA"

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Krepinsky, Joan Caroline. Nitric oxide inhibits stretch-induced MAPK activation in mesangial cells through RhoA inactivation. Ottawa: National Library of Canada, 2003.

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Siegert, Peter. Pasteurella multocida toxin prevents osteoblast differentiation by transactivation of the MAP-kinase cascade via the Gaq/11 - p63RhoGEF - RhoA axis. Freiburg: Universität, 2013.

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Rempel, Byron. No limits: The amazing life story of Rhona and Rhoda Wurtele : Canada's olympian skiing pioneers. [Westmount, QC?]: Twinski Publications, 2007.

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Société d'histoire et de généalogie des Pays-d'en-Haut, red. No limits: The amazing life story of Rhona and Rhoda Wurtele, Canada's olympian skiing pioneers. Wyd. 2. [Montréal]: Éditions Histoire Québec, 2009.

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Johnson, Clifford. What is a rhea? Wisconsin Rapids, WI (3824 St. John's Rd., Wisconsin Rapids 54494): Design Wise Graphics, 1991.

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Clifford, Johnson. What is a rhea? Wyd. 2. Stevens Point, WI (330 W. Cedar St., Stevens Point 54481): Design Works Graphics, 1994.

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Little, Jean. Stanley & Rhoda. London: Picture Lions, 1992.

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Société d'histoire et de généalogie des Pays-d'en-Haut, red. Sans limites: La vie exceptionnelle des jumelles Rhona et Rhoda Wurtele, olympiennes et pionnières du ski au Canada. Wyd. 2. [Montréal]: Éditions Histoire Québec, 2009.

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Askevold, David. Rhea ; Jumped out. Toronto: Trinity Square Video, 1986.

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Little, Jean. Stanley and Rhoda. London: Collins, 1991.

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Części książek na temat "RhoA"

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Orgaz, Jose L., i Victoria Sanz-Moreno. "RhoA". W Encyclopedia of Signaling Molecules, 4681–91. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101793.

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Orgaz, Jose L., i Victoria Sanz-Moreno. "RhoA". W Encyclopedia of Signaling Molecules, 1–11. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101793-1.

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Hair, Joseph F., G. Tomas M. Hult, Christian M. Ringle, Marko Sarstedt, Nicholas P. Danks i Soumya Ray. "Evaluation of Reflective Measurement Models". W Classroom Companion: Business, 75–90. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80519-7_4.

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AbstractThe goal of reflective measurement model assessment is to ensure the reliability and validity of the construct measures and therefore provides support for the suitability of their inclusion in the path model. This chapter introduces the key criteria that are relevant in reflective measurement model assessment: indicator reliability, internal consistency reliability (Cronbach’s alpha, reliability coefficient rhoA, and composite reliability rhoC), convergent validity, and discriminant validity. We illustrate their use by means of the SEMinR package and a well-known model on corporate reputation.
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Tabit, Corey E., Qing Mei Wang, Robert Y. L. Zee i James K. Liao. "RhoA/Rho-Associated Kinase as Marker of Cardiovascular Health". W Biomarkers in Cardiovascular Disease, 739–69. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7678-4_17.

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Liao, James K., Qing Mei Wang, Robert Y. L. Zee i Corey E. Tabit. "RhoA/Rho-Associated Kinase as Marker of Cardiovascular Health". W Biomarkers in Cardiovascular Disease, 1–31. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7741-5_17-1.

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Sajib, Md S., Fatema T. Zahra, Racheal G. Akwii i Constantinos M. Mikelis. "Identification of Rho GEF and RhoA Activation by Pull-Down Assays". W Methods in Molecular Biology, 97–109. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0845-6_10.

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Liu, Yianzhu, Jacek Z. Kubiak, Xian C. Li, Rafik M. Ghobrial i Malgorzata Kloc. "Macrophages and RhoA Pathway in Transplanted Organs". W Results and Problems in Cell Differentiation, 365–76. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54090-0_15.

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Santiago-Lopez, Angel J., Claire-Anne Gutekunst i Robert E. Gross. "C3 Transferase Gene Therapy for Continuous RhoA Inhibition". W Methods in Molecular Biology, 267–81. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8612-5_19.

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Ito, Satoru. "Role of RhoA/Rho-kinase and Calcium Sensitivity in Airway Smooth Muscle Functions". W Calcium Signaling In Airway Smooth Muscle Cells, 285–307. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01312-1_15.

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Kloc, Malgorzata, Ahmed Uosef, Jarek Wosik, Jacek Z. Kubiak i Rafik Mark Ghobrial. "RhoA Pathway and Actin Regulation of the Golgi/Centriole Complex". W Results and Problems in Cell Differentiation, 81–93. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-23173-6_5.

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Streszczenia konferencji na temat "RhoA"

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Na, Sungsoo. "Engineering Tools for Studying Coordination Between Biochemical and Biomechanical Activities in Cell Migration". W ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53709.

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Cell migration is achieved by the dynamic feedback interactions between traction forces generated by the cell and exerted onto the underlying extracellular matrix (ECM), and intracellular mechano-chemical signaling pathways, e.g., Rho GTPase (RhoA, Rac1, and Cdc42) activities [1,2,3]. These components are differentially distributed within a cell, and thus the coordination between tractions and mechanotransduction (i.e, RhoA and Rac1 activities) must be implemented at a precise spatial and temporal order to achieve optimized, directed cell migration [4,5]. Recent studies have shown that focal adhesions at the leading edge exert strong tractions [6], and these traction sites are co-localized with focal adhesion sites [7]. Further, by using the fluorescence resonance energy transfer (FRET) technology coupled with genetically encoded biosensors, researchers reported that Rho GTPases, such as RhoA [8], Rac1 [9], and Cdc42 [10] are maximally activated at the leading edge, suggesting the leading edge of the cell as its common functional site for Rho GTPase activities. All these works, however, were done separately, and the relationship between tractions and mechanotransduction during cell migration has not been demonstrated directly because of the difficulty in simultaneously recording tractions and mechanotransduction in migrating cells, precluding direct comparison between these results. Furthermore, these studies have been conducted by monitoring cells on glass coverslips, the stiffness of which is ∼ 65 giga pascal (GPa), at least three to six order higher than the physiological range of ECM stiffness. Although it is increasingly accepted that ECM stiffness influences cell migration, it is not known exactly how physiologically relevant ECM stiffness (order of kPa range) affects the dynamics of RhoA and Rac1 activities. For a complete understanding of the mechanism of mechano-chemical signaling in the context of cell migration, the dynamics and interplay between biomechanical (e.g., tractions) and biochemical (e.g., Rho GTPase) activities should be visualized within the physiologically relevant range of ECM stiffness.
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Duong-Quy, Sy, Thong Hua-Huy, Pierre Dao, Nhat-Nam Le-Dong i Anh Tuan Dinh-Xuan. "Downregulation Of ENOS Expression And Activity by RhoA/Rho-kinase Pathway In Moderate COPD Patients". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5247.

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Osterziel, Richard, Michael Döbrönti, Anja Schulz-Kuhnt, Cord Brakebusch, Rocío López-Posadas, Stefan Wirtz, Markus Neurath i Imke Atreya. "ILC2s in der mukosalen Entzündung: Fehlender Einfluss der kleinen Rho GTPasen Rac1, RhoA und Cdc42". W 50. Jahrestagung der Gesellschaft für Gastroenterologie in Bayern e.V. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1764098.

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Ryu, Byung-Kyu, Min-Goo Lee, Min-Ju Kang, Tae-Kyu Ha, Jikhyon Han, Nam-Gu Her, Seong-In Chung i Sung-Gil Chi. "Abstract 5068: Identification of RASSF1A as a novel RhoA antagonist: direct interaction with and Smurf1-mediated ubiquitination of RhoA". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5068.

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Millar, Fraser, Robert Hynds, Kate Gowers, Colin Butler, Laura Succony, Krishna Kolluri, Samuel Janes i Adam Giangreco. "LSC Abstract – Human bronchial epithelial cell migration is dependent on the RhoA effector protein Rho-associated kinase". W ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pp217.

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Belaid, Amine, Papa Diogop N'diaye, Michaël Cerezo, Patrick Brest, Daniel J. Klionsky, Georges F. Carle, Paul Hofman i Baharia Mograbi. "Abstract A224: Autophagy and SQSTM1 on the RHOA(d) again." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a224.

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Schaafsma, Dedmer, Sarah A. Maltby, Behzad Yeganeh, Sujata Basu, Karol D. McNeill, Gerald L. Stelmack, Helmut Unruh i Andrew J. Halayko. "The RhoA-Rho Kinase Axis Contributes To Hyperreactivity Of Airway Smooth Muscle From Allergen Naive Caveolin-1 Knockout Mice". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4127.

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Rodrigues, Paulo, Irati Macaya, Sarah Bazzocco, Elena Andretta, Rocco Mazzolini, Higinio Dopeso, Silvia Mateo-Lozano i in. "Abstract 2058: RHOA inactivation enhances Wnt signaling and promotes colorectal cancer". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2058.

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Misek, Sean A., Kathleen A. Gallo i Richard R. Neubig. "Abstract 5895: Targeting RhoA-regulated gene transcription in drug-resistant melanoma". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5895.

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Rackow, A. R., G. Zapas, R. Clough i R. M. Kottmann. "Activation of TDAG8 Prevents Myofibroblast Differentiation via Inhibition of RhoA Signaling". W American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4413.

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Raporty organizacyjne na temat "RhoA"

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Falk, A. Comment on Extracting alpha from B to rho rho. Office of Scientific and Technical Information (OSTI), październik 2003. http://dx.doi.org/10.2172/826521.

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Bevan, A. Measurements of sin2 alpha phi_2 from B to pi pi, rho pi and rho rho Modes. Office of Scientific and Technical Information (OSTI), listopad 2004. http://dx.doi.org/10.2172/839802.

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Aubert, B. Observation of e+e- Annihilations into the C=+1 Hadronic Final States \rho^0\rho^0 and \phi\rho^0. Office of Scientific and Technical Information (OSTI), czerwiec 2006. http://dx.doi.org/10.2172/885278.

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Li, H. Constraints on the CKM Angle alpha in the B to rho rho Decays. Office of Scientific and Technical Information (OSTI), listopad 2004. http://dx.doi.org/10.2172/839589.

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Aubert, B. Improved Measurement of the CKM Angle alpha Using B0 to rho+rho- Decays. Office of Scientific and Technical Information (OSTI), marzec 2005. http://dx.doi.org/10.2172/839874.

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Aubert, B. Search for the Decay B{sup 0} --> {rho}{sup 0} {rho}{sup 0}. Office of Scientific and Technical Information (OSTI), sierpień 2004. http://dx.doi.org/10.2172/829731.

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Kamasani, Uma R., i George Prendergast. Mechanism of RhoB/FTI Action in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, maj 2004. http://dx.doi.org/10.21236/ada446332.

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Rane, Neena S., i George C. Prendergast. Mechanism of RhoB/FTI Action in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, maj 2002. http://dx.doi.org/10.21236/ada412302.

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Corbin, D. R., M. M. Eddy, L. Abrams, G. A. Jones i G. D. Stucky. Flexibility of the Zeolite RHO Framework. Neutron Powder Structural Characterization of Ca-Exchanged Zeolite RHO. Fort Belvoir, VA: Defense Technical Information Center, lipiec 1988. http://dx.doi.org/10.21236/ada197195.

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Jessop, Colin P. Study of B -> psi rho. Office of Scientific and Technical Information (OSTI), czerwiec 2003. http://dx.doi.org/10.2172/813223.

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