Relevant bibliographies by topics / Rho GTPases Signaling

Academic literature on the topic 'Rho GTPases Signaling'

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Published: 7 September 2023

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Journal articles on the topic "Rho GTPases Signaling"

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Mosaddeghzadeh, Niloufar, and Mohammad Reza Ahmadian. "The RHO Family GTPases: Mechanisms of Regulation and Signaling." Cells 10, no. 7 (July 20, 2021): 1831. http://dx.doi.org/10.3390/cells10071831.

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Much progress has been made toward deciphering Rho GTPase functions, and many studies have convincingly demonstrated that altered signal transduction through Rho GTPases is a recurring theme in the progression of human malignancies. It seems that 20 canonical RHO GTPases are likely regulated by three GDIs, 85 GEFs, and 66 GAPs, and eventually interact with >70 downstream effectors. A recurring theme is the challenge in understanding the molecular determinants of the specificity of these four classes of interacting proteins that, irrespective of their functions, bind to common sites on the surface of RHO GTPases. Identified and structurally verified hotspots as functional determinants specific to RHO GTPase regulation by GDIs, GEFs, and GAPs as well as signaling through effectors are presented, and challenges and future perspectives are discussed.
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Mulloy, James C., Jose A. Cancelas, Marie-Dominique Filippi, Theodosia A. Kalfa, Fukun Guo, and Yi Zheng. "Rho GTPases in hematopoiesis and hemopathies." Blood 115, no. 5 (February 4, 2010): 936–47. http://dx.doi.org/10.1182/blood-2009-09-198127.

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AbstractRho family GTPases are intracellular signaling proteins regulating multiple pathways involved in cell actomyosin organization, adhesion, and proliferation. Our knowledge of their cellular functions comes mostly from previous biochemical studies that used mutant overexpression approaches in various clonal cell lines. Recent progress in understanding Rho GTPase functions in blood cell development and regulation by gene targeting of individual Rho GTPases in mice has allowed a genetic understanding of their physiologic roles in hematopoietic progenitors and mature lineages. In particular, mouse gene–targeting studies have provided convincing evidence that individual members of the Rho GTPase family are essential regulators of cell type–specific functions and stimuli-specific pathways in regulating hematopoietic stem cell interaction with bone marrow niche, erythropoiesis, and red blood cell actin dynamics, phagocyte migration and killing, and T- and B-cell maturation. In addition, deregulation of Rho GTPase family members has been associated with multiple human hematologic diseases such as neutrophil dysfunction, leukemia, and Fanconi anemia, raising the possibility that Rho GTPases and downstream signaling pathways are of therapeutic value. In this review we discuss recent genetic studies of Rho GTPases in hematopoiesis and several blood lineages and the implications of Rho GTPase signaling in hematologic malignancies, immune pathology. and anemia.
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Olayioye, Monilola A., Bettina Noll, and Angelika Hausser. "Spatiotemporal Control of Intracellular Membrane Trafficking by Rho GTPases." Cells 8, no. 12 (November 21, 2019): 1478. http://dx.doi.org/10.3390/cells8121478.

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As membrane-associated master regulators of cytoskeletal remodeling, Rho GTPases coordinate a wide range of biological processes such as cell adhesion, motility, and polarity. In the last years, Rho GTPases have also been recognized to control intracellular membrane sorting and trafficking steps directly; however, how Rho GTPase signaling is regulated at endomembranes is still poorly understood. In this review, we will specifically address the local Rho GTPase pools coordinating intracellular membrane trafficking with a focus on the endo- and exocytic pathways. We will further highlight the spatiotemporal molecular regulation of Rho signaling at endomembrane sites through Rho regulatory proteins, the GEFs and GAPs. Finally, we will discuss the contribution of dysregulated Rho signaling emanating from endomembranes to the development and progression of cancer.
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Kjøller, Lars, and Alan Hall. "Signaling to Rho GTPases." Experimental Cell Research 253, no. 1 (November 1999): 166–79. http://dx.doi.org/10.1006/excr.1999.4674.

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Voena and Chiarle. "RHO Family GTPases in the Biology of Lymphoma." Cells 8, no. 7 (June 26, 2019): 646. http://dx.doi.org/10.3390/cells8070646.

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RHO GTPases are a class of small molecules involved in the regulation of several cellular processes that belong to the RAS GTPase superfamily. The RHO family of GTPases includes several members that are further divided into two different groups: typical and atypical. Both typical and atypical RHO GTPases are critical transducers of intracellular signaling and have been linked to human cancer. Significantly, both gain-of-function and loss-of-function mutations have been described in human tumors with contradicting roles depending on the cell context. The RAS family of GTPases that also belong to the RAS GTPase superfamily like the RHO GTPases, includes arguably the most frequently mutated genes in human cancers (K-RAS, N-RAS, and H-RAS) but has been extensively described elsewhere. This review focuses on the role of RHO family GTPases in human lymphoma initiation and progression.
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Fritz, Rafael Dominik, and Olivier Pertz. "The dynamics of spatio-temporal Rho GTPase signaling: formation of signaling patterns." F1000Research 5 (April 26, 2016): 749. http://dx.doi.org/10.12688/f1000research.7370.1.

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Rho GTPases are crucial signaling molecules that regulate a plethora of biological functions. Traditional biochemical, cell biological, and genetic approaches have founded the basis of Rho GTPase biology. The development of biosensors then allowed measuring Rho GTPase activity with unprecedented spatio-temporal resolution. This revealed that Rho GTPase activity fluctuates on time and length scales of tens of seconds and micrometers, respectively. In this review, we describe Rho GTPase activity patterns observed in different cell systems. We then discuss the growing body of evidence that upstream regulators such as guanine nucleotide exchange factors and GTPase-activating proteins shape these patterns by precisely controlling the spatio-temporal flux of Rho GTPase activity. Finally, we comment on additional mechanisms that might feed into the regulation of these signaling patterns and on novel technologies required to dissect this spatio-temporal complexity.
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Zubor, Pavol, Zuzana Dankova, Zuzana Kolkova, Veronika Holubekova, Dusan Brany, Sandra Mersakova, Marek Samec, et al. "Rho GTPases in Gynecologic Cancers: In-Depth Analysis toward the Paradigm Change from Reactive to Predictive, Preventive, and Personalized Medical Approach Benefiting the Patient and Healthcare." Cancers 12, no. 5 (May 20, 2020): 1292. http://dx.doi.org/10.3390/cancers12051292.

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Rho guanosine triphospatases (GTPases) resemble a conserved family of GTP-binding proteins regulating actin cytoskeleton dynamics and several signaling pathways central for the cell. Rho GTPases create a so-called Ras-superfamily of GTPases subdivided into subgroups comprising at least 20 members. Rho GTPases play a key regulatory role in gene expression, cell cycle control and proliferation, epithelial cell polarity, cell migration, survival, and apoptosis, among others. They also have tissue-related functions including angiogenesis being involved in inflammatory and wound healing processes. Contextually, any abnormality in the Rho GTPase function may result in severe consequences at molecular, cellular, and tissue levels. Rho GTPases also play a key role in tumorigenesis and metastatic disease. Corresponding mechanisms include a number of targets such as kinases and scaffold/adaptor-like proteins initiating GTPases-related signaling cascades. The accumulated evidence demonstrates the oncogenic relevance of Rho GTPases for several solid malignancies including breast, liver, bladder, melanoma, testicular, lung, central nervous system (CNS), head and neck, cervical, and ovarian cancers. Furthermore, Rho GTPases play a crucial role in the development of radio- and chemoresistance e.g. under cisplatin-based cancer treatment. This article provides an in-depth overview on the role of Rho GTPases in gynecological cancers, highlights relevant signaling pathways and pathomechanisms, and sheds light on their involvement in tumor progression, metastatic spread, and radio/chemo resistance. In addition, insights into a spectrum of novel biomarkers and innovative approaches based on the paradigm shift from reactive to predictive, preventive, and personalized medicine are provided.
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Barlow, Haley Rose, and Ondine Cleaver. "Building Blood Vessels—One Rho GTPase at a Time." Cells 8, no. 6 (June 6, 2019): 545. http://dx.doi.org/10.3390/cells8060545.

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Blood vessels are required for the survival of any organism larger than the oxygen diffusion limit. Blood vessel formation is a tightly regulated event and vessel growth or changes in permeability are linked to a number of diseases. Elucidating the cell biology of endothelial cells (ECs), which are the building blocks of blood vessels, is thus critical to our understanding of vascular biology and to the development of vascular-targeted disease treatments. Small GTPases of the Rho GTPase family are known to regulate several processes critical for EC growth and maintenance. In fact, many of the 21 Rho GTPases in mammals are known to regulate EC junctional remodeling, cell shape changes, and other processes. Rho GTPases are thus an attractive target for disease treatments, as they often have unique functions in specific vascular cell types. In fact, some Rho GTPases are even expressed with relative specificity in diseased vessels. Interestingly, many Rho GTPases are understudied in ECs, despite their known expression in either developing or mature vessels, suggesting an even greater wealth of knowledge yet to be gleaned from these complex signaling pathways. This review aims to provide an overview of Rho GTPase signaling contributions to EC vasculogenesis, angiogenesis, and mature vessel barrier function. A particular emphasis is placed on so-called “alternative” Rho GTPases, as they are largely understudied despite their likely important contributions to EC biology.
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Zhang, Zheng, Ming Liu, and Yi Zheng. "Role of Rho GTPases in stem cell regulation." Biochemical Society Transactions 49, no. 6 (December 2, 2021): 2941–55. http://dx.doi.org/10.1042/bst20211071.

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The future of regenerative medicine relies on our understanding of stem cells which are essential for tissue/organ generation and regeneration to maintain and/or restore tissue homeostasis. Rho family GTPases are known regulators of a wide variety of cellular processes related to cytoskeletal dynamics, polarity and gene transcription. In the last decade, major new advances have been made in understanding the regulatory role and mechanism of Rho GTPases in self-renewal, differentiation, migration, and lineage specification in tissue-specific signaling mechanisms in various stem cell types to regulate embryonic development, adult tissue homeostasis, and tissue regeneration upon stress or damage. Importantly, implication of Rho GTPases and their upstream regulators or downstream effectors in the transformation, migration, invasion and tumorigenesis of diverse cancer stem cells highlights the potential of Rho GTPase targeting in cancer therapy. In this review, we discuss recent evidence of Rho GTPase signaling in the regulation of embryonic stem cells, multiple somatic stem cells, and cancer stem cells. We propose promising areas where Rho GTPase pathways may serve as useful targets for stem cell manipulation and related future therapies.
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Guo, Daji, Xiaoman Yang, and Lei Shi. "Rho GTPase Regulators and Effectors in Autism Spectrum Disorders: Animal Models and Insights for Therapeutics." Cells 9, no. 4 (March 31, 2020): 835. http://dx.doi.org/10.3390/cells9040835.

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The Rho family GTPases are small G proteins that act as molecular switches shuttling between active and inactive forms. Rho GTPases are regulated by two classes of regulatory proteins, guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Rho GTPases transduce the upstream signals to downstream effectors, thus regulating diverse cellular processes, such as growth, migration, adhesion, and differentiation. In particular, Rho GTPases play essential roles in regulating neuronal morphology and function. Recent evidence suggests that dysfunction of Rho GTPase signaling contributes substantially to the pathogenesis of autism spectrum disorder (ASD). It has been found that 20 genes encoding Rho GTPase regulators and effectors are listed as ASD risk genes by Simons foundation autism research initiative (SFARI). This review summarizes the clinical evidence, protein structure, and protein expression pattern of these 20 genes. Moreover, ASD-related behavioral phenotypes in animal models of these genes are reviewed, and the therapeutic approaches that show successful treatment effects in these animal models are discussed.
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Dissertations / Theses on the topic "Rho GTPases Signaling"

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Fransson, Åsa. "Cell signaling by Rho and Miro GTPases : Studies of Rho GTPases in Cytoskeletal Reorganizations and of Miro GTPases in Mitochondrial Dynamics." Doctoral thesis, Uppsala University, Ludwig Institute for Cancer Research, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8514.

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The Ras superfamily of GTPases embraces six major branches of proteins: the Ras, Rab, Ran, Arf, Rho and Miro subfamilies. The majority of GTPases function as binary switches that cycle between active GTP-bound and inactive GDP-bound states. This thesis will focus primarily on the biological functions of the Rho and Miro proteins. The Rho GTPases control the organization of the actin cytoskeleton and other associated activities, whereas the Miro GTPases are regulators of mitochondrial movement and morphology.

A diverse array of cellular phenomena, including cell movement and intracellular membrane trafficking events, are dependent on cytoskeletal rearrangements mediated by Rho GTPases. Although human Rho GTPases are encoded by 20 distinct genes, most studies involving Rho GTPases have focused on the three representatives RhoA, Rac1 and Cdc42, which each regulate specific actin-dependent cellular processes. In an effort to compare the effects of all Rho GTPase members in the same cell system, we transfected constitutively active Rho GTPases in porcine aortic endothelial (PAE) cells and examined their effects on the organization of the actin cytoskeleton. We identified a number of previously undetected roles of the different members of the Rho GTPases. Moreover, we demonstrated that the downstream effectors of Rho GTPases have a broader specificity than previously thought.

In a screen for novel Ras-like GTPases, we identified the Miro GTPases (Mitochondrial Rho). In our characterization of Miro, we established that these proteins influence mitochondrial morphology and serve functions in the transport of mitochondria along the microtubule system. Additionally, we provided evidence that Miro can be under control of calcium signaling pathways. Mitochondria are highly dynamic organelles that undergo continuous change in shape and distribution. Defects in mitochondrial dynamics are associated with several neurodegenerative diseases. In conclusion, our findings have contributed to a deeper understanding of the biological roles of Rho and Miro GTPases.

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Fransson, Åsa. "Cell signaling by Rho and Miro GTPases : studies of Rho GTPases in cytoskeletal reorganizations and of Miro GTPases in mitochondrial dynamics /." Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8514.

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Chan, Man-lok Mandy, and 陳文樂. "A study of RhoV and PAK4 signaling in hepatocarcinogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47053434.

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Sipes, Nisha Schuler. "Cdc42 signaling in extracellular matrix remodeling in three dimensions." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1253622562.

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Picard, Mariêve. "The role of the small Rho GTPases in the signaling mechanisms mediated by the netrin-1 receptor UNC5a." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19255.

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Netrin-1 is a bifunctional chemotropic cue that attracts or repels different classes of axons through the Deleted in Colorectal Cancer (DCC) and the UNC5 receptors (UNC5a, b, c and d). DCC is implicated in mediating both responses whereas UNC5 receptors are strictly involved in the repulsive events. The intracellular molecular mechanisms underlying axon growth and guidance are still unclear but it is known that this process requires remodeling of the actin cytoskeleton. There is now compelling evidence that Rho GTPases, in particular RhoA, Rac1 and Cdc42, are important signaling elements within the neuronal growth cone and we hypothesize that they link netrin-1-mediated UNC5a signaling to cytoskeletal remodeling and repulsion. In the first part of this thesis, we have demonstrated that overexpression of UNC5a or a mutant lacking the cytoplasmic tail of the receptor in N1E-115 neuroblastoma cells expressing netrin-1, stimulated the formation of neurites in a netrin-1-dependent manner. Rho GTPase activation assays in COS-7 cells expressing UNC5a also showed a transient 1.5-, 2- and 9-fold increase in the levels of activated Rac1, Cdc42 and RhoA, respectively, after two minutes of netrin-1 stimulation. Fluorescence Resonance Energy Transfer (FRET) in N1E-115 cells revealed that UNC5a strongly activated RhoA at neurite tips and activated Rac1 in the absence of its cytoplasmic domain, suggesting the presence of a signaling partner. These results demonstrate that Rho GTPases are important signaling components of the netrin-1 receptor UNC5a. In the second part, we have investigated the implication of Rac1, Cdc42 and RhoA in the netrin-1-mediated inhibitory effect of embryonic mouse dorsal root ganglia (DRG) axons. We found that netrin
Les nétrines sont des facteurs chémotropiques qui attirent ou repoussent différentes classes d'axones en agissant via les récepteurs DCC et UNC5 (UNC5a, b, c et d). DCC est impliqué dans l'attraction et dans la répulsion du cône de croissance tandis que les récepteurs UNC5 sont impliqués seulement dans la répulsion. Les mécanismes intracellulaires régissant le guidage axonal sont encore très peu connus. Cependant, il est clair que le mouvement dynamique du cône de croissance via le remodelage de son cytoskelette d'actine est requis durant les événements de guidage. Les activités des GTPases Rho, en particulier RhoA, Rac1 et Cdc42, font parties des mécanismes moléculaires qui régissent la migration axonale et nous croyons que ces protéines jouent un rôle primordial durant les événements de répulsion induits par le récepteur UNC5a. Dans la première partie de ce mémoire, nous avons démontré que UNC5a ainsi qu'un mutant tronqué de son domaine cytoplasmique induisent la formation de neurites dans les cellules murines de neuroblastomes, suivant la liaison de la nétrine-1. De plus, UNC5a augmente de 1.5, 2 et 9 fois le niveau d'activation de Rac1, Cdc42 et RhoA, respectivement, après deux minutes de stimulation avec la nétrine-1 dans les fibroblastes. Nous démontrons également par « Fluorescence Resonance Energy Transfer » (FRET) que UNC5a active fortement RhoA à l'extrémité de la neurite et active également Rac1, lorsque tronqué de son domaine cytoplasmique, suggérant la possibilité que le récepteur agisse via un partenaire. Ces résultats indiquent que les GTPases Rho sont des éléments majeurs de la signalisation de la nétrine-1 et de son récepteur UNC5a. Dans la seconde partie, nous
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Hoop, Alyssa N. "Rho-Family GTPase Signaling in the Nervous System: An Analysis of the C. elegans RhoGEF UNC-73." University of Toledo / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1404733888.

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Saint-Cyr, Proulx Étienne. "Role of the Rho GTPases in the signaling mechanisms regulated by the axon guidance cue Netrin-1 receptors deleted in colorectar cancer and Unc5H1." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98788.

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Chemotropic cues guide the migrating axons of neurons in the developing nervous system. Netrins are bifunctional guidance cues, attracting or repelling different classes of axons. The attraction to netrins is mediated by DCC whereas repulsion is achieved through Unc5H receptors. In this thesis, we demonstrate that Rho GTPases are required for embryonic spinal commissural axon outgrowth induced by Netrin-1. Using N1E-115 neuroblastoma cells, we have found that Rac1 and Cdc42 activities are required for DCC-induced neurite outgrowth. In fibroblasts, DCC was found to trigger actin reorganization through activation of Rac1. Moreover, we show that Unc5H1 triggers actin reorganization through activation of RhoA in fibroblasts. Using N1E-115 cells we found that Unc5H1 induces neurite outgrowth in a Rac1- and Cdc42-dependent manner. The studies presented in this thesis demonstrate that Rho GTPases are major signaling components of Netrin-1 receptors DCC and Unc5H1.
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Silva, Gisele Espinha Teixeira da. "Sinalização da GTPase RhoA nas respostas celulares após estresse genotóxico promovido por radiação ultravioleta." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-19102016-165552/.

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A via de sinalização da GTPase RhoA atua em diversos processos celulares. Para avaliar o comportamento de RhoA, após estresse causado por radiação ultravioleta, foram gerados clones mutantes que expressam RhoA em seu estado constitutivamente ativo e dominante negativo. Após exposição das linhagens à radiação ultravioleta, observou-se uma maior sensibilidade e um maior tempo de recuperação das linhagens quando a atividade de RhoA é reduzida. Estes prejuízos no reparo prejudicaram a proliferação e sobrevivência celular quando da deficiência na atividade de RhoA. Em linhagens deficientes na via de NER, percebemos que estas linhagens possuem uma capacidade ainda mais reduzida de reparo quando a atividade de RhoA é inibida.
The RhoA GTPase signaling pathway acts on many cellular processes. To evaluate this possible RhoA function after stress caused by ultraviolet radiation, mutant clones expressing RhoA in its constitutively active or dominant negative forms were generated. After exposure of the cells to ultraviolet radiation, cell lines showed a higher sensitivity and a delayed recovery capacity when the RhoA activity is reduced. The impaired repair reduced the cells proliferation and survival under RhoA deficiency. In cell lines deficient in NER pathway, we notice that these cell lines, have a further reduced ability to repair damaged DNA under RhoA inhibition.
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Osaki, Juliana Harumi. "O papel de RhoA e Rac1 GTPases nas respostas celulares após danos no DNA induzidos por radiação ionizante gama." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-22092015-075415/.

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O mecanismo pelo qual uma célula responde a algum dano no seu material genético é extremamente importante. Isto ocorre pela rápida ativação da maquinaria de reparo de danos no DNA, a qual é composta por uma rede intrincada de sinalização proteica, culminando no reparo do DNA; porém se o dano for irreparável ocorre ativação de mecanismos de morte celular. RhoA,e Rac1 pertencem a família das pequenas proteínas sinalizadoras Rho GTPases, as quais atuam como interruptores moleculares ciclando entre estado ativo (ligada a GTP) e inativo (ligada a GDP). Os componentes desta família estão relacionados ao controle dos mais diversos processos celulares como, por exemplo, remodelamento do citoesqueleto, migração, adesão, endocitose, progressão do ciclo celular e oncogênese. No entanto, apesar das proteínas Rho GTPases estarem envolvidas em um amplo espectro de atividades biológicas, há poucas informações sobre seu papel na manutenção da integridade genômica quando células são submetidas a algum agente genotóxico. Para investigar o envolvimento das GTPases RhoA e Rac1 nas respostas de células submetidas a radiação gama, foram gerados, a partir de células de carcinoma de cervix humano - HeLa, sublinhagens clonais mutantes de RhoA e Rac1 expressando exogenamente RhoA constitutivamente ativa (HeLa-RhoA V14), RhoA dominante negativa (HeLa-RhoA N19), Rac1 constitutivamente ativa (HeLa-Rac1 V12) e Rac1 dominante negativa (HeLa-Rac N17). Após estas linhagens celulares serem expostas a diferentes doses de radiação gama, observamos que ambas GTPases, RhoA e Rac1, são ativadas em resposta aos efeitos da radiação. Além disso, a modulação da atividade destas enzimas, através das mutações, levou a uma alteração das respostas celulares frente aos danos no DNA, como uma redução da capacidade de reparar quebras simples e duplas nas fitas do DNA. Por outro lado, a deficiência de RhoA ou Rac1 GTPase levou a uma redução da ativação de Chk1 e Chk2 ou da fosforilação da histona H2AX, respectivamente, prejudicando os mecanismos de detecção de danos no DNA e levando as células a permanecerem mais tempo nos pontos de checagem G1/S e/ou G2/M do ciclo celular. Esses fatores contribuíram de modo expressivo para a redução da proliferação e sobrevivência celular levando as células à morte. Por fim, ensaios celulares de reparo de danos de um DNA exógeno através de mecanismos de Recombinação Homóloga (HR) e Recombinação Não-Homóloga de extremidades (NHEJ), demonstraram que a inibição da atividade de RhoA reduz significativamente a eficiência de ambas vias de reparo. Desta maneira, este trabalho demonstra e reforça a existência de mais um viés de atuação das pequenas GTPases RhoA e Rac1, agora em células HeLa, nas respostas celulares aos danos induzidos por exposição a radiação gama, modulando a sobrevivência, proliferação e indiretamente modulando resposta ao reparo do DNA através da via de Recombinação Homóloga e Não-Homóloga
The mechanism by which a cell responds to DNA damage is extremely important. This occurs by a quick activation of the DNA damage repair machinery, which consists of an intricate protein signaling network culminating in DNA repair. But if the damages are irreparable occurs there is activation of cell death mechanisms. RhoA and Rac1 belong to family of small Rho GTPases, signaling proteins that act as molecular switches cycling between the active state (GTP-bound) and inactive state (GDP-bound). Members of this family are implicated in the control of diverse cellular process such as cytoskeletal remodeling, migration, adhesion, endocytosis, cell cycle progression, and oncogenesis. However, despite Rho proteins are involved in a broad spectrum of biological activities, there is just a few information about their roles in the maintenance of genomic integrity, that is, when the cells are subjected to some kinf of genotoxic agent. To investigate the involvement of the GTPases RhoA and Rac1 in cellular responses to gamma radiation, we generated from human cervix carcinoma cells - HeLa, clonal sublines of RhoA and Rac1 mutants, exogenous and stably expressing the constitutively active RhoA (HeLa-RhoA V14), the dominant negative RhoA (HeLa-RhoA N19), the constitutively active Rac1 (HeLa-Rac1 V12) and the dominant negative Rac1 (HeLa-Rac1 N17). After all these cell lines have been exposed to different doses of gamma radiation, we found that both GTPases, RhoA and Rac1, are activated in response to the radiation effects. Furthermore, the modulation of two enzymes activity, by using the mutant clones, led to a change in cellular responses to the DNA damage, as the reduction in the capacity of repairing DNA single and double strand breaksr. On the other hand, the deficiency of RhoA or Rac1 GTPase led to a reduction of Chk1 and Chk2 activation, or on the phosphorylation of histone H2AX, respectively, hindering the mechanisms of DNA damage detection and arresting cells in the G1/S and/or G2/M checkpoints of cell cycle. These factors significantly contributed to the reduction of cell proliferation and survival, leading cells to death. Finally, cellular assays of DNA damage repair of exogenous DNA by Homologous Recombination (HR) and Non-Homologous End Joining (NHEJ), demonstrated that RhoA inhibition significantly reduced the repair efficiency of both pathways. Thus, this work demonstrates and reinforces the existence of other biological functions of small GTPases RhoA and Rac1 in HeLa cells, by regulating cellular responses to DNA damage induced by exposure to gamma radiation, modulating the survival, proliferation and indirectly modulating the response to DNA damage repair pathway through the Homologous Recombination and Non-Homologous Recombination
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Marshall, Andrew Keith. "Signalling through Rho GTPases in cardiomyocytes." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/6962.

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Endothelin-1 (ET-1) promotes changes in gene/protein expression in cardiomyocytes leading to hypertrophy. This results from activation of intracellular signalling pathways including small G proteins that activate protein kinases. Thus, ET-1 activates RhoA that stimulates ROCK and PKN, and Ras that promotes activation of extracellular signal-regulated kinases 1/2 (ERK1/2). Microarrays were used to dissect the roles of ERK1/2 vs RhoA in the cardiomyocyte transcriptomic response to ET-1 using PD184352 and C3 endotoxin from C. botulinum (C3T) for selective inhibition of the ERK1/2 cascade and RhoA, respectively. Microarray data were analysed using GeneSpring and data were validated by qPCR. ERK1/2 signalling positively regulated ~65% of the early gene expression response to ET-1 with a small (~2%) negative effect, whereas RhoA signalling positively regulated ~11% of the early gene expression response to ET-1 with a greater (~14%) negative contribution. Of RNAs non-responsive to ET-1, 66 or 448 were regulated by PD184352 or C3T, respectively, indicating that RhoA had a more significant effect on baseline RNA expression. mRNAs upregulated by ET-1 encoded several receptor ligands (e.g. Ereg, Areg) and transcription factors (e.g. Abra/STARS, Srf) that potentially propagate the response. Published studies suggest that PKN1 (activated by RhoA) is important in cardiomyocyte gene expression. Adenoviruses were generated to overexpress FLAG-tagged PKN1 in cardiomyocytes for protein kinase studies. Unexpectedly, PKN1 was not activated by ET-1, but was activated by oxidative stress, insulin, or hyperosmotic shock, stimuli that do not activate RhoA. Thus, PKN1 is not necessarily an effector of RhoA in cardiomyocytes. In conclusion, ERK1/2 dominates over RhoA in the early transcriptomic response to ET-1. RhoA plays a major role in maintaining baseline RNA expression but, as with upregulation of Abra/Srf by ET-1, RhoA may regulate changes in RNA expression over longer times. However, the effects of RhoA on cardiomyocyte gene expression are unlikely to be mediated through PKN1.
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Books on the topic "Rho GTPases Signaling"

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Ciano-Oliveira, Caterina Di. Signaling pathways linking osmotic stress to adaptive responses: Roles for Rho family GTPases. 2006.

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Book chapters on the topic "Rho GTPases Signaling"

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Karnoub, Antoine E., Emily J. Chenette, and Channing J. Der. "RHO Proteins in RAS Signaling and Transformation." In RAS Family GTPases, 143–67. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/1-4020-4708-8_7.

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Hajicek, Nicole, Barry Kreutz, and Tohru Kozasa. "Signaling through Galpha12/13 and RGS-RhoGEFs." In The Rho GTPases in Cancer, 59–76. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1111-7_4.

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Zhu, Shizhen, and Boon Chuan Low. "Using Zebrafish for Studying Rho GTPases Signaling In Vivo." In Methods in Molecular Biology, 321–37. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-442-1_21.

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Chiariello, Mario, Jose P. Vaqué, Piero Crespo, and J. Silvio Gutkind. "Activation of Ras and Rho GTPases and MAP Kinases by G-Protein-Coupled Receptors." In MAP Kinase Signaling Protocols, 137–50. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-795-2_8.

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Hu, Bo, Marc Symons, Bodour Salhia, Shannon P. Fortin, Nhan L. Tran, James Rutka, and Shi-Yuan Cheng. "Rho GTPases and Their Activators, Guanine Nucleotide Exchange Factors (GEFs): Their Roles in Glioma Cell Invasion." In Signaling Pathways and Molecular Mediators in Metastasis, 143–69. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2558-4_6.

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Liu, Jian-Qin, and Katsunori Shimohara. "A Novel Programmable Molecular Computing Method Based on Signaling Pathways Regulated by Rho-GTPases in Living MDCK Epithelial Mammalian Cells." In Lecture Notes in Computer Science, 312–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-30217-9_32.

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Fujita, Yasuyuki, and Vania Braga. "Epithelial Cell Shape and Rho Small GTPases." In Signalling Networks in Cell Shape and Motility, 144–58. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/047001766x.ch12.

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Aspenström, Pontus. "BAR Domain Proteins Regulate Rho GTPase Signaling." In Protein Reviews – Purinergic Receptors, 33–53. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/5584_2018_259.

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Eisenmann, Kathryn M., Jun Peng, Bradley J. Wallar, and Arthur S. Alberts. "Rho GTPase-Formin Pairs in Cytoskeletal Remodelling." In Signalling Networks in Cell Shape and Motility, 206–22. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/047001766x.ch16.

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Feltrin, Daniel, and Olivier Pertz. "Assessment of Rho GTPase Signaling During Neurite Outgrowth." In Methods in Molecular Biology, 181–94. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-442-1_13.

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Conference papers on the topic "Rho GTPases Signaling"

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

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Abstract:
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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Sun, Hui-Chuan, Jian-Yang Ao, Zong-Tao Chai, and Yuan-Yuan Zhang. "Abstract 4168: Robo1 promotes angiogenesis through CDC42/Rho GTPases signaling pathway in hepatocellular carcinoma." In 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.am2015-4168.

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Shi, Geng-Xian, Ling Jin, Michelle L. Matter, Santosh Kesari, and Joe W. Ramos. "Abstract 1363: RSK2 provokes invasive signaling in glioblastoma through LARG-dependent activation of Rho GTPases." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1363.

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Wan, Qiaoqiao, Eunhye Cho, Seungman Park, Bumsoo Han, Hiroki Yokota, and Sungsoo Na. "Visualizing Chondrocyte Mechanotransduction in 3D." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14484.

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Chondrocytes are the only cell type present in the articular cartilage and their response to mechanical stimuli influences the maintenance and remodeling of the cartilage. Numerous studies have shown that the balance between anabolic and catabolic responses of the chondrocytes to mechanical loading is dependent on the loading intensities (reviewed in ref. [1]). Moderate, physiological loading, for instance, increases synthetic activity of the extracellular matrix (ECM) such as collagen type II, aggrecan, and proteoglycan, while decreasing the catabolic activity of degradative enzymes such as matrix metalloproteinases (MMPs) and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) [2,3]. In contrast to moderate loading, static or high-intensity loading has been shown to degrade the cartilage resulting from inhibition of matrix synthesis and up-regulation of catabolic activities [3,4]. Therefore, the importance of these load-dependent signaling pathways involved in the maintenance and remodeling of the cartilage is widely accepted. However, the underlying mechanisms as to how varying magnitudes of mechanical stimuli trigger differential signaling activities that consequently lead to selective gene expression are not clear. FAK and Src are considered to be the main mechanotransduction signaling proteins at the cell-ECM adhesion sites and their activities influence various structural and signaling changes within the cell, including cytoskeletal organization, migration, proliferation, differentiation, and survival [5]. Accumulating evidence has shown that Src and FAK play crucial roles in regulating cartilage maintenance and degeneration and their activation stimulates matrix catabolic genes and activity [6,7]. Rho family GTPases such as RhoA and Rac1 play critical roles in fundamental processes including morphogenesis, polarity, movement, and cell division [8]. They also contribute to cartilage development and degradation [9,10]. Despite these studies, much remains to be elucidated on how load-induced Src and FAK participate in chondrocyte functions, and how their interactions are linked and regulated in connection to the activities of RhoA and Rac1 under different loading conditions. In this study, we use fluorescence resonance energy transfer (FRET)-based biosensors to monitor activities of Src and FAK as well as individual GTPases and evaluate the potential linkage of a network of these signaling molecules under different loading conditions.
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Mansour, Mariam, Sue Haupt, Ai-Leen Chan, Nathan Godde, Alexandra Rizzitelli, Sherene Loi, Franco Caramia, et al. "Abstract A72: The E3-ligase E6AP represses breast cancer metastasis through regulation of ECT2-Rho-GTPases signaling." In Abstracts: AACR Special Conference: Advances in Breast Cancer; October 17-20, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.advbc15-a72.

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Kurisetty, Vittal, Trinath P. Das, Rama S. Reddy, Jessica Stiles, Brad Bryan, and Chendil Damodaran. "Abstract 5329: The role of miR-301-3P in the regulation of Rho GTPases mediated EMT signaling in castration resistant prostate cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5329.

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Balraj, P., N. S. Ambhore, N. A. Borkar, C. M. Pabelick, Y. S. Prakash, and S. Venkatachalem. "Kisspeptin Attenuates Airway Smooth Muscle Cell Migration by Regulating Rho GTPase Signaling Pathway." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1229.

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Little, Andrew C., Pragathi Pathanjeli, Zhifen Wu, Liwei Bao, Laura Goo, Joel A. Yates, and Sofia D. Merajver. "Abstract 4518: IL-4/IL-13 stimulated tumor-associated macrophages enhance breast cancer cell invasion through Rho-GTPase signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4518.

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Little, Andrew C., Pragathi Pathanjeli, Zhifen Wu, Liwei Bao, Laura Goo, Joel A. Yates, and Sofia D. Merajver. "Abstract 4518: IL-4/IL-13 stimulated tumor-associated macrophages enhance breast cancer cell invasion through Rho-GTPase signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4518.

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Schrecengost, Randy S., Ashley L. Wilson, Michael S. Guerrero, and Amy H. Bouton. "Abstract 5135: Breast cancer antiestrogen resistance-3 influences breast cancer cell migration by regulating Rac and Rho GTPase signaling." In 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.am10-5135.

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