Relevant bibliographies by topics / Rac

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  2. Dissertations / Theses
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Academic literature on the topic 'Rac'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Rac"

1

Lai, Yun-Ju, Jei-Hwa Yu, Braden C. McFarland, and Etty N. Benveniste. "The role of Rac proteins in glioblastoma stem cells." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e13011-e13011. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e13011.

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e13011 Background: Glioblastoma is the grade 4 astrocytoma which is notorious for its highly invasive phenotype, very low survival rate and generally poor responses to conventional therapies. Glioblastoma stem-like cells (GSC), which are usually more resistant to therapeutic treatment, may account for the poor prognosis of this disease. Rac (Ras-related C3 botulinum toxin substrate) is a subfamily of Rho small GTPase which function is regulation of actin cytoskeleton rearrangement. While Rac1 is expressed ubiquitous in different tissues and cells, Rac2 is highly expressed in the mesenchymal subtype of glioblastoma according to the TCGA (the Cancer Genome Atlas) database, and Rac3 is mainly expressed in the brain. Methods: We used Rac proteins overexpressing-glioblastoma cellines derived GSC and Rac proteins specific siRNA harboring-GSC to perform colony formation assay and migration assay. Results: Here we report that Rac proteins overexpressing glioblastoma stem-like cells derived from glioblastoma cell lines have higher proliferation rate and stronger responses to LPA-induced cell migration. Knocking-down their expression by specific siRNA reduces the proliferation and migration of these cells. Instead of Rac1, Rac2 and Rac3 are more effective on promoting proliferation and migration of glioblastoma stem-like cells. Moreover, Rac proteins promote glioblastoma progression is associated with activation of JAK-STAT and ERK pathway. Conclusions: Although Rac1 is the most studied one in the Rac family, and has also been implicated in the progression of different cancers, however, it is homogeneously expressed in all different tissues, and plays important roles in normal cellular functions involving cell movement, such as wound healing, make it not a good candidate for specific drug targeting. According to our results, Rac2 or Rac3 serve as a better potential therapeutic targets for glioblastoma treatment.
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Kalfa, Theodosia A., Suvarnamala Pushkaran, Jose A. Cancelas, James F. Johnson, Deidre Daria, Hartmut Geiger, David A. Williams, and Yi Zheng. "Rac GTPases Regulate Erythropoiesis Both in the Early Steps of Differentiation and in Enucleation." Blood 110, no. 11 (November 16, 2007): 1714. http://dx.doi.org/10.1182/blood.v110.11.1714.1714.

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Abstract Rac GTPases (i.e. Rac1, Rac2 and Rac3), a subfamily of Rho GTPases, control actin organization and have overlapping as well as distinct roles in cell survival, proliferation, and differentiation in various hematopoietic cell lineages (Gu et al, Science 2003, Cancelas et al, Nature Med 2005). Using conditional gene-targeting in mice, we have previously demonstrated that Rac1 and Rac2 deficiency causes anemia with abnormal erythrocyte cytoskeleton and decreased deformability (Kalfa et al, Blood 2006). In the present studies, we found by colony assays that although bone marrow (BM) BFU-E activity was unaltered from that of the wild type (WT) mice, Rac1−/−;Rac2−/− erythroid bursts had a strikingly different morphology appearing as round, small, dense colonies, likely a manifestation of motility defects associated with Rac GTPase deficiency. Total CFU-Es recovered from Rac1−/−;Rac2−/− BM were as low as 25% of that in WT mice (p<0.05). To further assess erythroblast differentiation, BM cells were immunostained with fluorescent label-conjugated anti-CD71 and anti-Ter119, as previously described (Socolovski et al. Blood 2001). Flow cytometry analysis revealed that proerythroblasts and basophilic erythroblasts in the BM were significantly decreased in Rac1−/−;Rac2−/− (∼30–50% of WT content) while the terminal differentiation to orthochromatic erythroblasts was comparable. In vivo BrdU labeling and flow cytometry with 7-AAD and annexin-V in combination with staining for CD71 and Ter119 revealed no difference in proliferation or survival between WT and Rac1−/−;Rac2−/− erythroid cells after the proerythroblast stage. These data suggest that deficiency of Rac1 and Rac2 GTPases affect erythropoiesis mainly at the early stages of BFU-E and CFU-E formation but not during terminal differentiation to orthochromatic erythroblasts. Given the prominent role of Rac GTPases in regulating actin structure, we next evaluated the possible involvement of Rac GTPases in enucleation, the terminal step of erythropoiesis that likely requires significant actin remodeling. We performed quantitative analysis in ex vivo erythropoiesis cultures, by flow cytometry, using SYTO16, a cell-permeable nucleic acid-staining dye. The frequency of enucleated red cells (SYTO16-low, Ter119-positive population) was similar in the WT and the Rac1−/−;Rac2−/− erythroid cultures. However, application of a Rac GTPase inhibitor, NSC23766, to the WT or the Rac1−/−;Rac2−/− erythroid cultures during the enucleation phase resulted in an inhibition of enucleation up to 80% dose-dependently (figure 1). Rac1 and Rac2 deficiency led to a compensatory elevation of Rac3 activity that was effectively suppressed by NSC23766, as demonstrated by immunoblotting in the Rac1−/−;Rac2−/− erythroblasts and effector-domain pull-down studies. Moreover, NSC23766 inhibited Rac1, Rac2, and Rac3 activities as well as actin polymerization of the erythroblasts. Thus, Rac1, Rac2, and Rac3 have redundant but essential roles in supporting actin dynamics necessary for the nucleus extrusion during the enucleation process. Figure Figure
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Engers, R., S. Ziegler, M. Mueller, A. Walter, R. Willers, and H. E. Gabbert. "Prognostic relevance of increased Rac GTPase expression in prostate carcinomas." Endocrine-Related Cancer 14, no. 2 (June 2007): 245–56. http://dx.doi.org/10.1677/erc-06-0036.

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Rac proteins of the Rho-like GTPase family, including the ubiquitous Rac1, the hematopoiesis-specific Rac2, and the least-characterized Rac3 play a major role in oncogenic transformation, tumor invasion and metastasis. However, the prognostic relevance of Rac expression in human tumors has not been investigated yet. In the present study, Rac protein expression was analyzed in benign secretory epithelium, high-grade prostatic intraepithelium neoplasia (HG-PIN), and prostate carcinomas of 60 R0-resected radical prostatectomy specimens by semiquantitative immunohistochemistry. Thus, Rac proteins were significantly strongly expressed in HG-PIN (P < 0.001) and prostate carcinomas (P < 0.001) when compared with benign secretory epithelium. Accordingly, all tumor tissues analyzed by isoform-specific real-time PCR (n = 7) exhibited significantly higher RNA expression levels of Rac (i.e. sum of Rac1 and Rac3 expression levels) than the respective benign counterparts (P = 0.018) and this appeared to result mainly from increased expression of the Rac3 isoform as verified by immunoblotting. Univariate analyses showed statistically significant associations of increased Rac protein expression in prostate cancer (P = 0.045), preoperative prostate-specific antigen levels (P = 0.044), pT stage (P = 0.002), and Gleason score (P = 0.001) with decreased disease-free survival (DFS). This prognostic effect of increased protein expression of Rac remained significant even in a multivariate analysis including all these four factors (relative risk = 3.22, 95% confidence interval = 1.04–10.00; P = 0.043). In conclusion, our data suggest that increased Rac protein expression in prostate cancer relative to the corresponding benign secretory epithelium is an independent predictor of decreased DFS and appears to result mainly from increased expression of the Rac3 isoform.
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Cho, Young Jin, Bin Zhang, Vesa Kaartinen, Leena Haataja, Ivan de Curtis, John Groffen, and Nora Heisterkamp. "Generation of rac3 Null Mutant Mice: Role of Rac3 in Bcr/Abl-Caused Lymphoblastic Leukemia." Molecular and Cellular Biology 25, no. 13 (July 1, 2005): 5777–85. http://dx.doi.org/10.1128/mcb.25.13.5777-5785.2005.

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ABSTRACT Numerous studies indirectly implicate Rac GTPases in cancer. To investigate if Rac3 contributes to normal or malignant cell function, we generated rac3 null mutants through gene targeting. These mice were viable, fertile, and lacked an obvious external phenotype. This shows Rac3 function is dispensable for embryonic development. Bcr/Abl is a deregulated tyrosine kinase that causes chronic myelogenous leukemia and Ph-positive acute lymphoblastic leukemia in humans. Vav1, a hematopoiesis-specific exchange factor for Rac, was constitutively tyrosine phosphorylated in primary lymphomas from Bcr/Abl P190 transgenic mice, suggesting inappropriate Rac activation. rac3 is expressed in these malignant hematopoietic cells. Using lysates from BCR/ABL transgenic mice that express or lack rac3, we detected the presence of activated Rac3 but not Rac1 or Rac2 in the malignant precursor B-lineage lymphoblasts. In addition, in female P190 BCR/ABL transgenic mice, lack of rac3 was associated with a longer average survival. These data are the first to directly show a stimulatory role for Rac in leukemia in vivo. Moreover, our data suggest that interference with Rac3 activity, for example, by using geranyl-geranyltransferase inhibitors, may provide a positive clinical benefit for patients with Ph-positive acute lymphoblastic leukemia.
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Thomas, Emily K., Jose A. Cancelas, Heedon Chae, Adrienne D. Cox, Patricia J. Keller, Danilo Perrotti, Paolo Neviani, et al. "Rac GTPases Are Potential Therapeutic Targets in p210-BCR-ABL-Induced Myeloproliferative Disease (MPD)." Blood 110, no. 11 (November 16, 2007): 465. http://dx.doi.org/10.1182/blood.v110.11.465.465.

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Abstract The p210-BCR-ABL fusion protein is a constitutively active tyrosine kinase that is necessary and sufficient for the development of chronic myelogenous leukemia (CML). ABL-kinase inhibitors such as imatinib mesylate (Gleevec, STI571) potently block BCR-ABL activation, but the continued presence of leukemic stem cells and the emergence of imatinib-resistant BCR-ABL mutants suggest that ABL kinase inhibitors alone cannot completely eradicate disease. Rac GTPases have been implicated in BCR-ABL-mediated proliferation in cell lines and regulate many of the same signaling pathways as BCR-ABL, suggesting that these proteins could be additional therapeutic targets in CML. We have found that Rac1, Rac2, and, to a lesser extent, Rac3 were hyperactivated in CD34+ cells purified from the peripheral blood of two CML patients. To better study the role of Rac in BCR-ABL disease development, murine hematopoietic stem cells (HSC) genetically deficient in Rac1 and/or Rac2 were transduced with a retroviral vector expressing p210-BCR-ABL. Wild type (WT) and Rac1−/− mice experienced similar disease progression [median survival 23 ± 6 days (n=30) and 22 ± 4 days (n=8), respectively], Rac2−/− mice exhibited significantly attenuated development of BCR-ABL-mediated MPD [median survival 43 ± 27 days (n=18); p<0.001], and Rac1−/−;Rac2−/− animals showed markedly prolonged survival [median survival 92 ± 34 days (n=19); p<0.001]. p210-BCR-ABL WT, Rac1−/−, and Rac2−/− mice had elevated circulating myeloblasts 30 days post-transplant, while Rac1−/−;Rac2−/− mice had normal peripheral blood morphology. Attenuation of disease in Rac2- and Rac1/Rac2-deficient animals correlated with severely diminished activation of BCR-ABL-induced signaling pathways, including p44/42 and p38 ERK, JNK, CrkL, and Akt. The leukemogenesis impairment induced by Rac deficiency did not appear to be due to loss of p210-BCR-ABL vector integration, as clonal analysis of leukemic bone marrow from mice in each genotype by LAM-PCR showed similar, oligoclonal reconstitution of p210-BCR-ABL expressing cells. Interestingly, bone marrow cells obtained from Rac1/Rac2-deficient animals that developed late leukemia showed marked hyperactivation of Rac3 and initiated disease in recipients with a latency of three weeks, suggesting that leukemia-initiating cells were able to engraft, in spite of Rac1/Rac2 deficiency. Treatment of BCR-ABL-expressing murine HSC with NSC23766, a rationally-designed Rac-specific small molecule antagonist, potently inhibited cell proliferation in vitro and increased the survival of leukemic animals treated in vivo, compared to PBS control-treated animals (p<0.05). NSC23766 also inhibited the growth of an imatinib-resistant p210-BCR-ABL-T315I-expressing Ba/F3 leukemic cell line by 90%, compared to <5% by imatinib alone, blocked the growth of primary human chronic phase Rac-hyperactivated CML blast colonies by 80% in vitro, and inhibited survival of these cells in NOD-SCID mice. These results suggest that individual Rac proteins play both unique and combinatorial roles in stem cell transformation and may represent unique targets for therapy of BCR-ABL-persistent and imatinib-resistant CML.
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Shutes, Adam, Cercina Onesto, Virginie Picard, Bertrand Leblond, Fabien Schweighoffer, and Channing J. Der. "Specificity and Mechanism of Action of EHT 1864, a Novel Small Molecule Inhibitor of Rac Family Small GTPases." Journal of Biological Chemistry 282, no. 49 (October 11, 2007): 35666–78. http://dx.doi.org/10.1074/jbc.m703571200.

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There is now considerable experimental evidence that aberrant activation of Rho family small GTPases promotes the uncontrolled proliferation, invasion, and metastatic properties of human cancer cells. Therefore, there is considerable interest in the development of small molecule inhibitors of Rho GTPase function. However, to date, most efforts have focused on inhibitors that indirectly block Rho GTPase function, by targeting either enzymes involved in post-translational processing or downstream protein kinase effectors. We recently determined that the EHT 1864 small molecule can inhibit Rac function in vivo. In this study, we evaluated the biological and biochemical specificities and biochemical mechanism of action of EHT 1864. We determined that EHT 1864 specifically inhibited Rac1-dependent platelet-derived growth factor-induced lamellipodia formation. Furthermore, our biochemical analyses with recombinant Rac proteins found that EHT 1864 possesses high affinity binding to Rac1, as well as the related Rac1b, Rac2, and Rac3 isoforms, and this association promoted the loss of bound nucleotide, inhibiting both guanine nucleotide association and Tiam1 Rac guanine nucleotide exchange factor-stimulated exchange factor activity in vitro. EHT 1864 therefore places Rac in an inert and inactive state, preventing its engagement with downstream effectors. Finally, we evaluated the ability of EHT 1864 to block Rac-dependent growth transformation, and we determined that EHT 1864 potently blocked transformation caused by constitutively activated Rac1, as well as Rac-dependent transformation caused by Tiam1 or Ras. Taken together, our results suggest that EHT 1864 selectively inhibits Rac downstream signaling and transformation by a novel mechanism involving guanine nucleotide displacement.
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Pai, Sung-Yun, Chaekyun Kim, and David A. Williams. "Rac GTPases in Human Diseases." Disease Markers 29, no. 3-4 (2010): 177–87. http://dx.doi.org/10.1155/2010/380291.

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Rho GTPases are members of the Ras superfamily of GTPases that regulate a wide variety of cellular functions. While Rho GTPase pathways have been implicated in various pathological conditions in humans, to date coding mutations in only the hematopoietic specific GTPase,RAC2, have been found to cause a human disease, a severe phagocytic immunodeficiency characterized by life-threatening infections in infancy. Interestingly, the phenotype was predicted by a mouse knock-out ofRAC2and resembles leukocyte adhesion deficiency (LAD). Here we review Rho GTPases with a specific focus on Rac GTPases. In particular, we discuss a new understanding of the unique and overlapping roles of Rac2 in blood cells that has developed since the generation of mice deficient in Rac1, Rac2 and Rac3 proteins. We propose that Rac2 mutations leading to disease be termed LAD type IV.
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Heyworth, P. G., U. G. Knaus, J. Settleman, J. T. Curnutte, and G. M. Bokoch. "Regulation of NADPH oxidase activity by Rac GTPase activating protein(s)." Molecular Biology of the Cell 4, no. 11 (November 1993): 1217–23. http://dx.doi.org/10.1091/mbc.4.11.1217.

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Activation of the NADPH oxidase of phagocytic cells requires the action of Rac2 or Rac1, members of the Ras superfamily of GTP-binding proteins. Rac proteins are active when in the GTP-bound form and can be regulated by a variety of proteins that modulate the exchange of GDP for GTP and/or GTP hydrolysis. The p190 Rac GTPase Activating Protein (GAP) inhibits human neutrophil NADPH oxidase activity in a cell-free assay system with a K1 of approximately 100 nM. Inhibition by p190 was prevented by GTP gamma S, a nonhydrolyzable analogue of GTP. Similar inhibition was seen with a second protein exhibiting Rac GAP activity, CDC42Hs GAP. The effect of p190 on superoxide (O2-) formation was reversed by the addition of a constitutively GTP-bound Rac2 mutant or Rac1-GTP gamma S but not by RhoA-GTP gamma S. Addition of p190 to an activated oxidase produced no inhibitory effect, suggesting either that p190 no longer has access to Rac in the assembled oxidase or that Rac-GTP is not required for activity once O2- generation has been initiated. These data confirm the role of Rac in NADPH oxidase regulation and support the view that it is the GTP form of Rac that is necessary for oxidase activation. Finally, they raise the possibility that NADPH oxidase may be regulated by the action of GAPs for Rac proteins.
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Pestonjamasp, Kersi N., Carol Forster, Chunxiang Sun, Elisabeth M. Gardiner, Ben Bohl, Orion Weiner, Gary M. Bokoch, and Michael Glogauer. "Rac1 links leading edge and uropod events through Rho and myosin activation during chemotaxis." Blood 108, no. 8 (October 15, 2006): 2814–20. http://dx.doi.org/10.1182/blood-2006-01-010363.

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Abstract Chemotactic responsiveness is crucial to neutrophil recruitment to sites of infection. During chemotaxis, highly divergent cytoskeletal programs are executed at the leading and trailing edge of motile neutrophils. The Rho family of small GTPases plays a critical role in cell migration, and recent work has focused on elucidating the specific roles played by Rac1, Rac2, Cdc42, and Rho during cellular chemotaxis. Rac GTPases regulate actin polymerization and extension of the leading edge, whereas Rho GTPases control myosin-based contraction of the trailing edge. Rac and Rho signaling are thought to crosstalk with one another, and previous research has focused on mutual inhibition of Rac and Rho signaling during chemotaxis. Indeed, polarization of neutrophils has been proposed to involve the activity of a negative feedback system where Rac activation at the front of the cell inhibits local Rho activation, and vice versa. Using primary human neutrophils and neutrophils derived from a Rac1/Rac2-null transgenic mouse model, we demonstrate here that Rac1 (and not Rac2) is essential for Rho and myosin activation at the trailing edge to regulate uropod function. We conclude that Rac plays both positive and negative roles in the organization of the Rhomyosin “backness” program, thereby promoting stable polarity in chemotaxing neutrophils.
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Miyano, Kei, Hirofumi Koga, Reiko Minakami, and Hideki Sumimoto. "The insert region of the Rac GTPases is dispensable for activation of superoxide-producing NADPH oxidases." Biochemical Journal 422, no. 2 (August 13, 2009): 373–82. http://dx.doi.org/10.1042/bj20082182.

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Rac1 and Rac2, which belong to the Rho subfamily of Ras-related GTPases, play an essential role in activation of gp91phox/Nox2 (cytochrome b-245, β polypeptide; also known as Cybb), the catalytic core of the superoxide-producing NADPH oxidase in phagocytes. Rac1 also contributes to activation of the non-phagocytic oxidases Nox1 (NADPH oxidase 1) and Nox3 (NADPH oxidase 3), each related closely to gp91phox/Nox2. It has remained controversial whether the insert region of Rac (amino acids 123–135), unique to the Rho subfamily proteins, is involved in gp91phox/Nox2 activation. In the present study we show that removal of the insert region from Rac1 neither affects activation of gp91phox/Nox2, which is reconstituted under cell-free and whole-cell conditions, nor blocks its localization to phagosomes during ingestion of IgG-coated beads by macrophage-like RAW264.7 cells. The insert region of Rac2 is also dispensable for gp91phox/Nox2 activation at the cellular level. Although Rac2, as well as Rac1, is capable of enhancing superoxide production by Nox1 and Nox3, the enhancements by the two GTPases are both independent of the insert region. We also demonstrate that Rac3, a third member of the Rac family in mammals, has an ability to activate the three oxidases and that the activation does not require the insert region. Thus the insert region of the Rac GTPases does not participate in regulation of the Nox family NADPH oxidases.
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Dissertations / Theses on the topic "Rac"

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Maximano, Filipe Manuel Correia. "Armus : A novel link between Rac and Rab small GTPases." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526397.

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Sadou, Amel. "Cross-talk between ral and rac pathways in the control of cell migration." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T010.

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Le mode de coordination parmi les différentes molécules qui régulent la migration reste très peu connu. Ce travail traite de deux voies de transduction régulant la migration: la voie Rac1/WRC (Wave Regulatory Complex) qui contrôle la formation du réseau d’actine au front des cellules migrantes, et la voie RalB/exocyst, dont les mécanismes moléculaires de son implication dans la motilité cellulaire étaient inconnus au début de cette thèse. Rac1 et RalB sont des petites protéines G des familles Rho et Ras, respectivement. Les complexes WRC et exocyst sont leurs effecteurs directs.Au cours de la recherche de connexions entre l’exocyst et des régulateurs de la migration, nous avons trouvé que deux sous-unités de l’exocyst, Exo70 et Sec6, interagissent directement in vitro avec Abi et Cyfip, respectivement, deux sous unités du WRC. De plus, nous avons trouvé que les sous-unités de l’exocyst peuvent interagir in vitro avec le WRC entier. Nous avons également montré que ces deux complexes s’associent in vivo. Sur le plan fonctionnel, l’exocyst est requis pour le positionnement du complexe WRC au front des cellules migrantes. D’autre part, nous avons également trouvé que deux autres sous- unités de l’exocyst Sec8 et Exo84, interagissent avec SH3BP1 (une RhoGAP) en double hybride et en co-immunoprécipitation. SH3BP1 se localise au front des cellules migrantes, et cette localisation dépend de l’exocyst. De façon intéressante, in vivo, la voie RalB/exocyst/SH3BP1 cible spécifiquement Rac1, et non Cdc42. Grâce à plusieurs approches, nous concluons que SH3BP1 est requis pour inactiver Rac1 au front. Dans notre modèle nous proposons que RalB/exocyst règulerait la migration cellulaire en véhiculant au front de migration deux éléments majeurs de la signalisation de Rac1 : son complexe effecteur WRC, qui stimule la nucléation de filaments d’actine et son régulateur négatif SH3BP1, une GAP qui promeut l’inactivation et le cycle GDP/GTP de Rac1. En conclusion, ce travail fournit de nouvelles connexions moléculaires et fonctionnelles entre l’exocytose polarisée et la dynamique de l’actine au cours de la motilité cellulaire
Very little is known about the coordination and the integration among the different regulators of the motility process. This work deals with two migration-regulatory pathways: the Rac1/WRC (Wave Regulatory Complex) pathway that drives the formation of the actin polymerization network at the front of motile cells; and RalB/exocyst pathway for which the molecular mechanisms underlying its implication in cell motility were still largely unknown at the beginning of this thesis. Rac1 and RalB are small GTPases of the Rho and Ras family, respectively. WRC and exocyst complexes are their direct effectors.In searching for connections between the exocyst and migration regulators, we found that two subunits of the exocyst, Exo70 and Sec6, interact directly in vitro with two subunits of the WRC, Abi and Cyfip, respectively. Moreover, we found that exocyst subunits can interact in vitro with the whole fully-assembled WRC complex. We also showed that these two complexes associate in vivo. Functionally, the exocyst was required for WRC complex positioning at the front of migrating cells.On the other hand, we also found that two other subunits of the exocyst, Sec8 and Exo84, interact with SH3BP1 (a RhoGAP protein) by two-hybrid assay and by co-immunoprecipitation. SH3BP1 localizes at the leading edge and this localization is dependent on the exocyst. Interestingly, in vivo, the RalB/exocyst/SH3BP1 pathway specifically targets Rac1, and not Cdc42. By a combination of approaches we concluded that SH3BP1 is required to inactivate Rac1 at the front.In our model we propose that RalB/exocyst regulates cell migration by driving to the leading edge two key signaling elements of the Rac1 pathway: its effector WRC, that stimulates actin filament nucleation, and its negative regulator SH3BP1, a GAP promoting Rac1 inactivation and GDP/GTP cycling. In conclusion, this work provides novel molecular and functional links between polarized exocytosis and actin dynamics during cell motility
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SADOU, AMEL. "CROSS-TALK BETWEEN RAL AND RAC PATHWAYS IN THE CONTROL OF CELL MIGRATION." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/214614.

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SUMMARY (English) Very little is known about the coordination and the integration among the different regulators of the motility process. This work deals with two migration-regulatory pathways: the Rac1/WRC (Wave Regulatory Complex) pathway that drives the formation of the actin polymerization network at the front of motile cells; and RalB/exocyst pathway for which the molecular mechanisms underlying its implication in cell motility were still largely unknown at the beginning of this thesis. Rac1 and RalB are small GTPases of the Rho and Ras family, respectively. WRC and exocyst complexes are their direct effectors. In searching for connections between the exocyst and migration regulators, we found that two subunits of the exocyst, Exo70 and Sec6, interact directly in vitro with two subunits of the WRC, Abi and Cyfip, respectively. Moreover, we found that exocyst subunits can interact in vitro with the whole fully-assembled WRC complex. We also showed that these two complexes associate in vivo. Functionally, the exocyst was required for WRC complex positioning at the front of migrating cells. On the other hand, we also found that two other subunits of the exocyst, Sec8 and Exo84, interact with SH3BP1 (a RhoGAP protein) by two-hybrid assay and by co-immunoprecipitation. SH3BP1 localizes at the leading edge and this localization is dependent on the exocyst. Interestingly, in vivo, the RalB/exocyst/SH3BP1 pathway specifically targets Rac1, and not Cdc42. By a combination of approaches we concluded that SH3BP1 is required to inactivate Rac1 at the front. In our model we propose that RalB/exocyst regulates cell migration by driving to the leading edge two key signaling elements of the Rac1 pathway: its effector WRC, that stimulates actin filament nucleation, and its negative regulator SH3BP1, a GAP promoting Rac1 inactivation and GDP/GTP cycling. In conclusion, this work provides novel molecular and functional links between polarized exocytosis and actin dynamics during cell motility.
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Di, Niro Gaetano. "Recycled aggregate concrete (RAC) for structural purposes." Thesis, University of Strathclyde, 1999. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=21124.

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The possibility of using demolished concrete waste as aggregate in fresh concrete in the production of prestressed concrete beams is checked in this research. As opposed to the use for road foundations or as fill-in material the use of the Recycled Aggregate (RA) for concrete structures requires more tests and processing of results. In fact to be able to use a material for construction it is essential to assess more than just its compressive strength. After the physical and chemical characteristics of the RA and the properties of both the wet and hardened Recycled Aggregate Concrete (RAC) have been determined, it is important to check if the mathematical models and numerical correlation normally used for design of ordinary concrete (such as mix-design procedure, design codes, non-linear analysis) are suitable for RAC. For this reason the main task of this investigations has been to ensure that RAC has satisfactory mechanical performance for structural use and later to guarantee a consistency of the results using methods checked for RAC. A mix-design procedure suitable for RAC to attain the desired workability and the target strength was the first step. Tests on durability of RA and RAC have been performed and the results reported. Finally three 15.0 metres span prestressd beams cast with different percentages of RA (one with 100% of RA, one with 100% of Natural Aggregate NA, and one with 50% of RA and 50% of NA) have been tested. The results show that it is practicable to make prestressed concrete elements using concrete made with Recycled Aggregate and that these elements can have satisfactory and predictable mechanical performance.
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Brentzel, Kelvin, Patrick Coronado, Barbie Brown, Parminder Ghuman, and Carol Harris. "A Regional Application Center (RAC) Ingest System." International Foundation for Telemetering, 1999. http://hdl.handle.net/10150/607319.

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International Telemetering Conference Proceedings / October 25-28, 1999 / Riviera Hotel and Convention Center, Las Vegas, Nevada
Over the next ten years, NASA’s Earth Science Enterprise Program is scheduled to deploy a series of remote sensing satellites that require high-rate downlinks. As part of the program, a goal has been defined to provide the user community with a low-cost solution for receiving this Earth Science spaceborne remotely sensed data. This paper describes one approach, the High-Rate Ingest System (HRIS), which can serve as a gateway between the satellites and the information systems. HRIS is capable of ingesting a UQPSK downlink at rates up to 200Mbps in real-time and provide a level 0 data product with rapid turnaround. The commercial components of the HRIS include a high performance 3.1-meter antenna system, a DEC Alpha workstation, and a RAID storage system. Within the DEC Alpha workstation are advanced technology hardware and software components that will become available for commercialization. The paper describes the architecture and proposed application of the HRIS as a complete end-to-end ingest solution for regional sites. In addition, collaborative commercial efforts and technologies, along with Goddard’s technology prototyping efforts will also be presented as part of HRIS.
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Fan, Wing-Tze. "Characterization of Ras-GRF2, a bifunctional guanine nucleotide exchange factor for the Ras and Rac GTPases." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ63720.pdf.

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Sadou, Amel. "Connexions entre les voies ral et rac dans le contrôle de la migration cellulaire." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00701484.

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Le mode de coordination parmi les différentes molécules qui régulent la migration reste très peu connu. Ce travail traite de deux voies de transduction régulant la migration: la voie Rac1/WRC (Wave Regulatory Complex) qui contrôle la formation du réseau d'actine au front des cellules migrantes, et la voie RalB/exocyst, dont les mécanismes moléculaires de son implication dans la motilité cellulaire étaient inconnus au début de cette thèse. Rac1 et RalB sont des petites protéines G des familles Rho et Ras, respectivement. Les complexes WRC et exocyst sont leurs effecteurs directs.Au cours de la recherche de connexions entre l'exocyst et des régulateurs de la migration, nous avons trouvé que deux sous-unités de l'exocyst, Exo70 et Sec6, interagissent directement in vitro avec Abi et Cyfip, respectivement, deux sous unités du WRC. De plus, nous avons trouvé que les sous-unités de l'exocyst peuvent interagir in vitro avec le WRC entier. Nous avons également montré que ces deux complexes s'associent in vivo. Sur le plan fonctionnel, l'exocyst est requis pour le positionnement du complexe WRC au front des cellules migrantes. D'autre part, nous avons également trouvé que deux autres sous- unités de l'exocyst Sec8 et Exo84, interagissent avec SH3BP1 (une RhoGAP) en double hybride et en co-immunoprécipitation. SH3BP1 se localise au front des cellules migrantes, et cette localisation dépend de l'exocyst. De façon intéressante, in vivo, la voie RalB/exocyst/SH3BP1 cible spécifiquement Rac1, et non Cdc42. Grâce à plusieurs approches, nous concluons que SH3BP1 est requis pour inactiver Rac1 au front. Dans notre modèle nous proposons que RalB/exocyst règulerait la migration cellulaire en véhiculant au front de migration deux éléments majeurs de la signalisation de Rac1 : son complexe effecteur WRC, qui stimule la nucléation de filaments d'actine et son régulateur négatif SH3BP1, une GAP qui promeut l'inactivation et le cycle GDP/GTP de Rac1. En conclusion, ce travail fournit de nouvelles connexions moléculaires et fonctionnelles entre l'exocytose polarisée et la dynamique de l'actine au cours de la motilité cellulaire.
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Bishop, Anne Louise. "Functional analysis of the Rac binding protein POSH." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248466.

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Rooney, Claire. "A role for the Rac GEF, STEF, in cell migration, polarization and Ras-induced transformation." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492898.

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Tiam1 (for T-lymphoma invasion and metastasis-inducing protein) belongs to the Rho GEF family of proteins. In response to growth factors and cell-substrate interactions, Tiam1 selectively activates Rac. Using a two stage chemical carcinogenesis protocol (DMBA/TPA) it was previously shown that mice lacking Tiam1 are resistant to the development of Ras-induced skin tumours, suggestmg an important role for Tiam1/Rac signalling in tumourigenesis in vivo.
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Ni, Wenjun. "Involvement of Rac GTPase in p53-deficiency mediated lymphomagenesis." Cincinnati, Ohio : University of Cincinnati, 2006. http://rave.ohiolink.edu/etdc//view?acc_num=ucin1155831060.

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Books on the topic "Rac"

1

RAC Rally. London: Partridge, 1989.

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Club, Royal Automobile, ed. RAC Greece. London: G.Philip, 1989.

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Club, Royal Automobile, ed. RAC Italy. London: G.Philip, 1989.

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AutomobileClub, Royal, ed. RAC France & Belgium. London: G.Philip, 1989.

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Club, RoyalAutomobile, ed. RAC hotel guide. Croydon: RAC Motoring Services., 1988.

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Club, Royal Automobile, ed. RAC hotel guide. London: RAC Motoring Services for the Royal Automobile Club., 1987.

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Club, Royal Automobile. RAC hotel guide. Croydon: RAC Motoring Services., 1988.

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Club, Royal Automobile, ed. RAC Continental motoring guide and directory of RAC appointed hotels. Croydon: Royal Automobile Club, 1985.

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Hussain, Syed Jaffar, Tariq Farooq, Riyaj Shamsudeen, and Kai Yu. Expert Oracle RAC 12c. Berkeley, CA: Apress, 2013. http://dx.doi.org/10.1007/978-1-4302-5045-6.

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N, Morrison Gerald, and Reliability Analysis Center (U.S.), eds. RAC thermal management guidebook. Rome,NY: Reliability Analysis Center, 1995.

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Book chapters on the topic "Rac"

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Gass, Saul I., and Carl M. Harris. "RAC." In Encyclopedia of Operations Research and Management Science, 687. New York, NY: Springer US, 2001. http://dx.doi.org/10.1007/1-4020-0611-x_848.

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Chernoff, Jonathan. "Rac 1." In Cancer Therapeutic Targets, 817–21. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_24.

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Shaw, Steve, and Martin Bach. "RAC Concepts." In Pro Oracle Database 11g RAC on Linux, 27–61. Berkeley, CA: Apress, 2010. http://dx.doi.org/10.1007/978-1-4302-2959-9_2.

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Shaw, Steve, and Martin Bach. "RAC Architecture." In Pro Oracle Database 11g RAC on Linux, 63–95. Berkeley, CA: Apress, 2010. http://dx.doi.org/10.1007/978-1-4302-2959-9_3.

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Konstantinidis, Diamantis G., and Theodosia A. Kalfa. "Rac GTPase." In Encyclopedia of Signaling Molecules, 4408–14. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_597.

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Konstantinidis, Diamantis G., and Theodosia A. Kalfa. "Rac GTPase." In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_597-1.

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Chernoff, Jonathan. "Rac 1." In Cancer Therapeutic Targets, 1–5. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_24-2.

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Martemyanov, Kirill A., Pooja Parameswaran, Irene Aligianis, Mark Handley, Marga Gual-Soler, Tomohiko Taguchi, Jennifer L. Stow, et al. "Rac GTPases." In Encyclopedia of Signaling Molecules, 1557–62. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_597.

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Irvine, William M. "RAC, Russia." In Encyclopedia of Astrobiology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-642-27833-4_5343-1.

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Knaus, Ulla G., Alison Bamberg, and Gary M. Bokoch. "Rac and Rap GTPase Activation Assays." In Neutrophil Methods and Protocols, 59–67. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-467-4_5.

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Conference papers on the topic "Rac"

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Papadopoulos, Panos, Thanasis Loukopoulos, Ioannis Anagnostopoulos, Nikolaos Tziritas, and Michael Vassilakopoulos. "RAC." In PCI '15: 19th Panhellenic Conference on Informatics. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2801948.2801978.

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Kieselmann, Olga, Arno Wacker, and Gregor Schiele. "k-rAC." In ARES '17: International Conference on Availability, Reliability and Security. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3098954.3103154.

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Ni, Yuanjiang, Ji Jiang, Dejun Jiang, Xiaosong Ma, Jin Xiong, and Yuangang Wang. "S-RAC." In SYSTOR '16: International Conference on Systems and Storage. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2928275.2928284.

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Skilton, P. "RAC telematics services development." In IEE Seminar Driver Information Systems: Influencing Your Route. IEE, 1999. http://dx.doi.org/10.1049/ic:19990471.

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Xianyi Li, Victor Plessky, Paul Hartogh, Thomas Weimann, Leonhard Reindl, and V. I. Grigorievsky. "Revisiting of RAC devices." In 2009 IEEE International Ultrasonics Symposium. IEEE, 2009. http://dx.doi.org/10.1109/ultsym.2009.5441936.

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Hartley, K. "Mobile information at the RAC." In IEE Colloquium on `Developments in Personal Systems'. IEE, 1995. http://dx.doi.org/10.1049/ic:19950872.

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Talay, A. Cagatay, and D. Turgay Altilar. "RAC: Range adaptive cognitive radio networks." In 2009 Fourth International Conference on Communications and Networking in China (CHINACOM). IEEE, 2009. http://dx.doi.org/10.1109/chinacom.2009.5339736.

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D'Abreo, Carmeline, Rozanne Arulanandam, Mulu Geletu, and Leda H. Raptis. "Abstract 3136: Activated Src increases total Rac levels and requires Rac and IL6 for full neoplastic transformation." 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.am10-3136.

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Quan Liu and Hang Su. "Improvement in camera calibration based on RAC." In 2007 International Symposium on Intelligent Signal Processing and Communication Systems. IEEE, 2007. http://dx.doi.org/10.1109/ispacs.2007.4445851.

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Wei, Ying, Ruizhe Ye, and Xuhui Chen. "Oracle RAC performance analysis on VMware Virtual SAN." In 2019 IEEE/ACIS 18th International Conference on Computer and Information Science (ICIS). IEEE, 2019. http://dx.doi.org/10.1109/icis46139.2019.8940347.

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Reports on the topic "Rac"

1

Coppola, Anthony. RAC Quarterly. Volume 3, Issue 2. Spring 1993. Fort Belvoir, VA: Defense Technical Information Center, January 1993. http://dx.doi.org/10.21236/ada278435.

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Symons, Marc H. Role of Rac GTPases in Chemokine-Stimulated Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada457469.

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Leng, Jie. Role of RAC GTPases in Tumor Mobility and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 1997. http://dx.doi.org/10.21236/ada337864.

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Delmer, Deborah P., Douglas Johnson, and Alex Levine. The Role of Small Signal Transducing Gtpases in the Regulation of Cell Wall Deposition Patterns in Plants. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7570571.bard.

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The combined research of the groups of Delmer, Levine and Johnson has led to a number of interesting findings with respect to the function of the small GTPase Rac in plants and also opened up new leads for future research. The results have shown: 1) The Rac13 protein undergoes geranylgeranlyation and is also translocated to the plasma membrane as found for Rac in mammals; 2) When cotton Rac13 is highly- expressed in yeast, it leads to an aberrant phenotype reminiscent of mutants impaired in actin function, supporting a role for Rac13 in cytoskeletal organization; 3) From our searches, there is no strong evidence that plants contain homologs of the related CDC42 genes found in yeast and mammals; 4) We have identified a rather unique Rac gene in Arabidopsis that has unusual extensions at both the N- and C-terminal portions of the protein; 5) New evidence was obtained that an oxidative burst characterized by substantial and sustained production of H202 occurs coincident with the onset of secondary wall synthesis in cotton fibers. Further work indicates that the H202 produced may be a signal for the onset of this phase of development and also strongly suggests that Rac plays an important role in signaling for event. Since the secondary walls of plants that contain high levels of lignin and cellulose are the major source of biomass on earth, understanding what signals control this process may well in the future have important implications for manipulating the timing and extent of secondary wall deposition. 6) When the cotton Rac13 promoter is fused to the reporter gene GUS, expression patterns in Arabidopsis indicate very strong and specific expression in developing trichomes and in developing xyelm. Since both of these cell types are engaged in secondary wall synthesis, this further supports a role for Rac in signaling for onset of this process. Since cotton fibers are anatomically defined as trichomes, these data may also be quite useful for future studies in which the trichomes of Arabidopsis may serve as a model for cotton fiber development; the Rac promoter can therefore be useful to drive expression of other genes proposed to affect fiber development and study the effects on the process; 7) The Rac promoter has also been shown to be the best so far tested for use in development of a system for transient transformation of developing cotton fibers, a technique that should have many applications in the field of cotton biotechnology; 8) One candidate protein that may interact with Rac13 to be characterized further in the future is a protein kinase that may be analogous to the PAK kinase that is known to interact with Rac in mammals.
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Symons, Marc. Role of Rac GTPases in Chemokine-Stimulated Breast Carcinoma Metastasis. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada502287.

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Symons, Marc. Role of Rac GTPasas in Chemokine-Stimulated Breast Carcinoma Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada473355.

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Cancelas, Jose. Inhibition of Rac GTPases in the Therapy of Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada510761.

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Aelst, Linda Van. Isolation of Genes in Rac Induced Invasion and Metastasis of Breast Carcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada408834.

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Denson, William, John Farrell, and David Nicholls. Reliable Application of Plastic Encapsulated Microcircuits; RAC Parts Seclection, Application and Control Series. Fort Belvoir, VA: Defense Technical Information Center, January 1996. http://dx.doi.org/10.21236/ada363879.

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Irazoqui, Javier E. Regulation of Cdc42/Rac Signaling in the Establishment of Cell Polarity and Control of Cell Motility. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada434009.

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