Gotowe bibliografie tematyczne / GTPase

Gotowa bibliografia na temat „GTPase”

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

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Artykuły w czasopismach na temat "GTPase"

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Irving, Helen R. "Abscisic acid induction of GTP hydrolysis in maize coleoptile plasma membranes". Functional Plant Biology 25, nr 5 (1998): 539. http://dx.doi.org/10.1071/pp98009.

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Since receptor-coupled G proteins increase GTP hydrolysis (GTPase) activity upon ligands binding to the receptor, a study was undertaken to determine if abscisic acid (ABA) induced such an effect. Plasma membranes isolated from etiolated maize (Zea mays L.) coleoptiles were enriched in GTPase activity relative to microsomal fractions. Vanadate was included in the assay to inhibit the high levels of vanadate sensitive low affinity GTPases present. Under these conditions, GTPase activity was enhanced by Mg2+, stimulated by mastoparan, and inhibited by GTPγS indicating the presence of either monomeric or heterotrimeric G proteins. The combination of NaF and AlCl3 is expected to inhibit heterotrimeric G protein activity but had little effect on GTPase activity in maize coleoptile membranes. Cholera toxin enhanced basal GTPase activity, confirming the presence of heterotrimeric G proteins in maize plasma membranes. Pertussis toxin also slightly enhanced basal GTPase activity in maize membranes. Abscisic acid enhanced GTPase activity optimally at 5 mmol/L Mg2+ in a concentration dependent manner by 1.5-fold at 10 µmol/L and up to three-fold at 100 µmol/L ABA. Abscisic acid induced GTPase activity was inhibited by GTPγS, the combination of NaF and AlCl3, and pertussis toxin. Overall, these results are typical of a receptor-coupled G protein responding to its ligand.
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Herrmann, Andrea, Britta A. M. Tillmann, Janine Schürmann, Michael Bölker i Paul Tudzynski. "Small-GTPase-Associated Signaling by the Guanine Nucleotide Exchange Factors CpDock180 and CpCdc24, the GTPase Effector CpSte20, and the Scaffold Protein CpBem1 in Claviceps purpurea". Eukaryotic Cell 13, nr 4 (31.01.2014): 470–82. http://dx.doi.org/10.1128/ec.00332-13.

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ABSTRACTMonomeric GTPases of the Rho subfamily are important mediators of polar growth and NADPH (Nox) signaling in a variety of organisms. These pathways influence the ability ofClaviceps purpureato infect host plants. GTPase regulators contribute to the nucleotide loading cycle that is essential for proper functionality of the GTPases. Scaffold proteins gather GTPase complexes to facilitate proper function. The guanine nucleotide exchange factors (GEFs) CpCdc24 and CpDock180 activate GTPase signaling by triggering nucleotide exchange of the GTPases. Here we show that CpCdc24 harbors nucleotide exchange activity for both Rac and Cdc42 homologues. The GEFs partly share the cellular distribution of the GTPases and interact with the putative upstream GTPase CpRas1. Interaction studies show the formation of higher-order protein complexes, mediated by the scaffold protein CpBem1. Besides the GTPases and GEFs, these complexes also contain the GTPase effectors CpSte20 and CpCla4, as well as the regulatory protein CpNoxR. Functional characterizations suggest a role of CpCdc24 mainly in polarity, whereas CpDock180 is involved in stress tolerance mechanisms. These findings indicate the dynamic formation of small GTPase complexes and improve the model for GTPase-associated signaling inC. purpurea.
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Humphries, Brock A., Zhishan Wang i Chengfeng Yang. "MicroRNA Regulation of the Small Rho GTPase Regulators—Complexities and Opportunities in Targeting Cancer Metastasis". Cancers 12, nr 5 (28.04.2020): 1092. http://dx.doi.org/10.3390/cancers12051092.

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The small Rho GTPases regulate important cellular processes that affect cancer metastasis, such as cell survival and proliferation, actin dynamics, adhesion, migration, invasion and transcriptional activation. The Rho GTPases function as molecular switches cycling between an active GTP-bound and inactive guanosine diphosphate (GDP)-bound conformation. It is known that Rho GTPase activities are mainly regulated by guanine nucleotide exchange factors (RhoGEFs), GTPase-activating proteins (RhoGAPs), GDP dissociation inhibitors (RhoGDIs) and guanine nucleotide exchange modifiers (GEMs). These Rho GTPase regulators are often dysregulated in cancer; however, the underlying mechanisms are not well understood. MicroRNAs (miRNAs), a large family of small non-coding RNAs that negatively regulate protein-coding gene expression, have been shown to play important roles in cancer metastasis. Recent studies showed that miRNAs are capable of directly targeting RhoGAPs, RhoGEFs, and RhoGDIs, and regulate the activities of Rho GTPases. This not only provides new evidence for the critical role of miRNA dysregulation in cancer metastasis, it also reveals novel mechanisms for Rho GTPase regulation. This review summarizes recent exciting findings showing that miRNAs play important roles in regulating Rho GTPase regulators (RhoGEFs, RhoGAPs, RhoGDIs), thus affecting Rho GTPase activities and cancer metastasis. The potential opportunities and challenges for targeting miRNAs and Rho GTPase regulators in treating cancer metastasis are also discussed. A comprehensive list of the currently validated miRNA-targeting of small Rho GTPase regulators is presented as a reference resource.
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Kötting, Carsten, i Klaus Gerwert. "What vibrations tell us about GTPases". Biological Chemistry 396, nr 2 (1.02.2015): 131–44. http://dx.doi.org/10.1515/hsz-2014-0219.

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Abstract In this review, we discuss how time-resolved Fourier transform infrared (FTIR) spectroscopy is used to understand how GTP hydrolysis is catalyzed by small GTPases and their cognate GTPase-activating proteins (GAPs). By interaction with small GTPases, GAPs regulate important signal transduction pathways and transport mechanisms in cells. The GTPase reaction terminates signaling and controls transport. Dysfunctions of GTP hydrolysis in these proteins are linked to serious diseases including cancer. Using FTIR, we resolved both the intrinsic and GAP-catalyzed GTPase reaction of the small GTPase Ras with high spatiotemporal resolution and atomic detail. This provided detailed insight into the order of events and how the active site is completed for catalysis. Comparisons of Ras with other small GTPases revealed conservation and variation in the catalytic mechanisms. The approach was extended to more nearly physiological conditions at a membrane. Interactions of membrane-anchored GTPases and their extraction from the membrane are studied using the attenuated total reflection (ATR) technique.
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Shan, Shu-ou, Sowmya Chandrasekar i Peter Walter. "Conformational changes in the GTPase modules of the signal reception particle and its receptor drive initiation of protein translocation". Journal of Cell Biology 178, nr 4 (6.08.2007): 611–20. http://dx.doi.org/10.1083/jcb.200702018.

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During cotranslational protein targeting, two guanosine triphosphatase (GTPase) in the signal recognition particle (SRP) and its receptor (SR) form a unique complex in which hydrolyses of both guanosine triphosphates (GTP) are activated in a shared active site. It was thought that GTP hydrolysis drives the recycling of SRP and SR, but is not crucial for protein targeting. Here, we examined the translocation efficiency of mutant GTPases that block the interaction between SRP and SR at specific stages. Surprisingly, mutants that allow SRP–SR complex assembly but block GTPase activation severely compromise protein translocation. These mutations map to the highly conserved insertion box domain loops that rearrange upon complex formation to form multiple catalytic interactions with the two GTPs. Thus, although GTP hydrolysis is not required, the molecular rearrangements that lead to GTPase activation are essential for protein targeting. Most importantly, our results show that an elaborate rearrangement within the SRP–SR GTPase complex is required to drive the unloading and initiate translocation of cargo proteins.
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6

Nur-E-Kamal, M. S., i H. Maruta. "The role of Gln61 and Glu63 of Ras GTPases in their activation by NF1 and Ras GAP." Molecular Biology of the Cell 3, nr 12 (grudzień 1992): 1437–42. http://dx.doi.org/10.1091/mbc.3.12.1437.

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Two distinct GAPs of 120 and 235 kDa called GAP1 and NF1 serve as attenuators of Ras, a member of GTP-dependent signal transducers, by stimulating its intrinsic guanosine triphosphatase (GTPase) activity. The GAP1 (also called Ras GAP) is highly specific for Ras and does not stimulate the intrinsic GTPase activity of Rap1 or Rho. Using GAP1C, the C-terminal GTPase activating domain (residues 720-1044) of bovine GAP1, we have shown previously that the GAP1 specificity is determined by the Ras domain (residues 61-65) where Gln61 plays the primary role. The corresponding domain (residues 1175-1531) of human NF1 (called NF1C), which shares only 26% sequence identity with the GAP1C, also activates Ras GTPases. In this article, we demonstrate that the NF1C, like the GAP1C, is highly specific for Ras and does not activate either Rap1 or Rho GTPases. Furthermore, using a series of chimeric Ras/Rap1 and mutated Ras GTPases, we show that Gln at position 61 of the GTPases primarily determines that NF1C as well as GAP1C activates Ras GTPases, but not Rap1 GTPases, and Glu at position 63 of the GTPases is required for maximizing the sensitivity of Ras GTPases to both NF1C and GAP1C. Interestingly, replacement of Glu63 of c-HaRas by Lys reduces its intrinsic GTPase activity and abolishes the GTPase activation by both NF1C and GAP1C. Thus, the potentiation of oncogenicity by Lys63 mutation of c-HaRas appears primarily to be due to the loss of its sensitivity to the two major Ras signal attenuators (NF1 and GAP1).
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Killoran, Ryan C., i Matthew J. Smith. "Conformational resolution of nucleotide cycling and effector interactions for multiple small GTPases determined in parallel". Journal of Biological Chemistry 294, nr 25 (14.05.2019): 9937–48. http://dx.doi.org/10.1074/jbc.ra119.008653.

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Small GTPases alternatively bind GDP/GTP guanine nucleotides to gate signaling pathways that direct most cellular processes. Numerous GTPases are implicated in oncogenesis, particularly the three RAS isoforms HRAS, KRAS, and NRAS and the RHO family GTPase RAC1. Signaling networks comprising small GTPases are highly connected, and there is some evidence of direct biochemical cross-talk between their functional G-domains. The activation potential of a given GTPase is contingent on a codependent interaction with the nucleotide and a Mg2+ ion, which bind to individual variants with distinct affinities coordinated by residues in the GTPase nucleotide-binding pocket. Here, we utilized a selective-labeling strategy coupled with real-time NMR spectroscopy to monitor nucleotide exchange, GTP hydrolysis, and effector interactions of multiple small GTPases in a single complex system. We provide insight into nucleotide preference and the role of Mg2+ in activating both WT and oncogenic mutant enzymes. Multiplexing revealed guanine nucleotide exchange factor (GEF), GTPase-activating protein (GAP), and effector-binding specificities in mixtures of GTPases and resolved that the three related RAS isoforms are biochemically equivalent. This work establishes that direct quantitation of the nucleotide-bound conformation is required to accurately determine an activation potential for any given GTPase, as small GTPases such as RAS-like proto-oncogene A (RALA) or the G12C mutant of KRAS display fast exchange kinetics but have a high affinity for GDP. Furthermore, we propose that the G-domains of small GTPases behave autonomously in solution and that nucleotide cycling proceeds independently of protein concentration but is highly impacted by Mg2+ abundance.
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Kesseler, Christoph, Julian Kahr, Natalie Waldt, Nele Stroscher, Josephine Liebig, Frank Angenstein, Elmar Kirches i Christian Mawrin. "EXTH-64. SMALL GTPASES IN MENINGIOMAS: PROLIFERATION, MIGRATION, SURVIVAL, POTENTIAL TREATMENT AND INTERACTIONS". Neuro-Oncology 22, Supplement_2 (listopad 2020): ii101. http://dx.doi.org/10.1093/neuonc/noaa215.418.

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Abstract PURPOSE To evaluate the role of the small GTPases RhoA, Rac1 and Cdc42 in meningiomas as therapeutic targets and their interactions in meningiomas. EXPERIMENTAL DESIGN We analyzed expression of GTPases in human meningioma samples and meningioma cell lines of various WHO grades. Malignant IOMM-Lee meningioma cells were used to generate shRNA mediated knockdowns of GTPases RhoA, Rac1 or Cdc42 and to study knockdown effects on proliferation and migration, as well as analysis of cell morphology by confocal microscopy. The same tests were used to investigate effects of the two inhibitors Fasudil and EHT-1864 of malignant IOMM-Lee, KT21 and benign Ben-Men cells and the effects of these drugs on IOMM-Lee knockdown cells. The effects of GTPase knockdowns and Fasudil treatment were studied in terms of overall survival by intracranial xenografts of mice. Potential interactions of GTPases regarding NF2, mTOR and FAK-Paxillin were examined. RESULTS Small GTPases were upregulated in meningiomas of higher tumor grades. Reduced proliferation and migration could be achieved by GTPase knockdown in IOMM-Lee cells. Additionally, the ROCK-inhibitor Fasudil and Rac1-inhibitor EHT-1864 reduced proliferation in different meningioma cell lines and reduced proliferation and migration independent of GTPase knockdowns/status. Moreover, overall survival in vivo could also be increased by knockdowns of RhoA and Rac1 as well as Fasudil treatment. GTPase expression was affected dependent on the NF2 status but effects were not very distinct, indicating that NF2 is not strongly involved in GTPase regulation in meningiomas. In terms of mTOR and FAK-Paxillin signaling, each GTPase changes those pathways in a different manner. CONCLUSION Small GTPases are important effectors in meningioma proliferation and migration in vitro as well as survival in vivo and their inhibition should be considered as potential treatment option.
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Mohamad Ansor, Nurhuda. "PLANT-DERIVED NATURAL PRODUCTS TARGETING RHO GTPASES SIGNALLING NETWORKS FOR CANCER THERAPY: A REVIEW". Journal of Health and Translational Medicine sp2023, nr 1 (6.06.2023): 116–21. http://dx.doi.org/10.22452/jummec.sp2023no1.10.

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Rho GTPases are intracellular signalling molecules that involve in transducing extracellular stimuli to downstream effector of signalling pathways to elicit cellular functions. Changes in expression level of Rho GTPases and altered activities of GTPase regulators have been reported in a variety of human tumours. These modifications perturb actin cytoskeleton dynamics hence promote cancer cell development and progression. Available evidence suggests that targeting therapeutic targets in Rho GTPase signalling network may reduce the progression of cancer to metastasis stage. Pharmacological modulators of Rho GTPases have been investigated as promising chemotherapeutic intervention, which of these are natural products derived from plants. A brief overview of potential therapeutic compounds from selected plants followed by their roles in altering Rho GTPase signalling in cancer cells will be provided. There is increasing knowledge of newly discovered pharmacological modulators of Rho GTPase from natural sources to suppress cancer growth and metastasis. Future directions should emphasize on evaluating efficacies and appropriate therapeutic doses of the promising Rho GTPase modulators from plants to be used in animal models and clinical trials. Modern techniques should also be considered to improve anticancer drugs properties including increased bioavailability and localization to targeted sites.
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Rubio, I. "Use of the Ras binding domain of c-Raf for biochemical and live-cell analysis of Ras activation". Biochemical Society Transactions 33, nr 4 (1.08.2005): 662–63. http://dx.doi.org/10.1042/bst0330662.

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Small modular GBDs (GTPase-binding domains) derived from GTPase-effector proteins are useful tools for the selective detection of the active GTP-loaded GTPase conformation, be it in biochemical assays or for imaging purposes. Use of GBD probes requires careful consideration of all features of the GDB–GTPase interaction. It is innate to the strong and specific interaction with the GTP-loaded GTPase, that GBDs will protect their partner GTPases from GAP (GTPase-activating protein) action. This feature is likely to cause an increase in cellular Ras-GTP levels, in particular in leucocytes and other cells with high steady-state Ras-GDP/GTP cycling rates. By the same token, high levels of GBD expression will interrupt GTPase-initiated signalling, with implications for the activation of the very same GTPase since feedback regulatory mechanisms can impinge on this process.
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Rozprawy doktorskie na temat "GTPase"

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Normandin, Caroline. "Identification et caractérisation de GTPases Activating Proteins spécifiques à la petite GTPase RAB21". Mémoire, Université de Sherbrooke, 2017. http://hdl.handle.net/11143/11544.

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L’autophagie est un processus de dégradation et de recyclage des composés cellulaires. Ce mécanisme est nécessaire que ce soit à l’état basal pour éliminer des agrégats protéiques ou des organites endommagés ou en condition de stress, tels que la carence nutritionnelle, l’hypoxie ou encore des traitements anticancéreux. De ce fait, l’autophagie est un processus essentiel à la survie ainsi qu’au maintien de l’homéostasie cellulaire. Connaître les joueurs et comprendre les mécanismes de régulation de l’autophagie sont donc importants. Les GTPases RABs sont des régulateurs importants de ce processus. Celles-ci agissent comme des interrupteurs moléculaires permettant d’exécuter rapidement des fonctions dans la cellule. Les RABs sont activées par des Guanine Nucleotide Exchange Factors (GEF) alors que les GTPase Activating Proteins (GAP) accélèrent la désactivation de la RAB. RAB21 est essentielle dans les étapes tardives de l’autophagie. En effet, RAB21 est activée par la carence nutritionnelle, via sa GEF MTMTR13, et permet le trafic d’une SNARE requise pour le flux autophagique. Lors d’une carence prolongée, l’activité de RAB21 diminue rapidement, suggérant ainsi le rôle d’une GAP dans cette régulation négative. Toutefois, aucune GAP pour RAB21 n’a été identifiée jusqu’à maintenant. Un criblage génétique chez la drosophile a permis d’identifier quelques candidats. Suite à des essais d’interactions protéiques, il s’est avéré que seule la GAP TBC1D25 interagissait avec RAB21. De plus, cette interaction est augmentée en fonction de la carence nutritionnelle. Des immunofluorescences par microscopie confocale ont révélé que l’interaction RAB21-TBC1D25 était située en partie au niveau des endosomes précoces. Par ailleurs, une activation prolongée de RAB5, située sur les endosomes précoces, inhibe l’interaction RAB21-TBC1D25. De plus amples expériences devront être réalisées afin d’expliquer ces résultats. Dans un autre ordre d’idée, RAB21 est surexprimée dans les cellules ayant un flux autophagique élevé ainsi que dans certaines tumeurs de cancer du côlon (données non publiées du laboratoire). L’expression de Tbc1d25 dans ces mêmes tumeurs ne semble pas augmentée, indiquant que TBC1D25 pourrait être un inhibiteur autophagique spécifique aux cellules ayant un flux autophagique élevé. À la lumière des résultats obtenus, TBC1D25 semble être une GAP pour RAB21 qui permet sa régulation négative suivant l’activation de l’autophagie induite par la carence nutritionnelle.
Abstract : Autophagy is defined as the lysosomal degradation and recycling of cellular constituents. At basal levels, autophagy eliminates protein aggregates or damaged organelles. In condition of stress, such as in condition of nutritional deficiency, hypoxia or cancer treatments, autophagy allow cells to adapt and survive. Therefore, autophagy is an essential system required for survival and maintenance of cellular homeostasis. It is thus essential to identify the cellular entities and mechanisms regulating this process. RAB GTPases were identified as master regulators of autophagy. These particular proteins act as molecular switches for the rapid execution of cellular responses. RABs are activated by Guanine Nucleotide Exchange Factors (GEF) whereas GTPase Activating Proteins (GAP) accelerates RAB deactivation. RAB21 is essential in the late stages of autophagy. Indeed, RAB21 is activated by nutritional deficiency, via its GEF MTMTR13, to allow trafficking of a SNARE required for autophagic flux. During starvation, RAB21 is deactivated which suggest that a GAP could negatively regulate RAB21 activity. However, to date no GAP for RAB21 has been identified. An eye modifier genetic screen in Drosophila was performed to identify potential RAB21 GAPs and some candidates were identified. As a result of this screen, the GAP TBC1D25 was identified as interacting with RAB21. Moreover, this interaction was increased by starvation. Proximity ligation assays revealed that the RAB21-TBC1D25 interaction partially localized at early endosomes. Moreover, prolonged activation of RAB5, located at early endosomes, inhibited RAB21-TBC1D25 interaction. Further experiments will be carried out to explain these results. With respect to the roles of autophagy in cancer, RAB21 was shown to be overexpressed in cells with high autophagic flux as well as in some colon cancer tumors. Importantly, the expression of Tbc1d25 in these same tumors does not appear to be increased, indicating that TBC1D25 could be an autophagic inhibitor specific to cells with a high autophagic flow. My work suggests that TBC1D25 could function as a GAP to negatively regulate RAB21 activity in condition of prolonged starvation.
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Visvikis, Orane. "GTPase Rac1 et ubiquitination". Paris 5, 2007. http://www.theses.fr/2007PA05P622.

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Cette thèse a été consacrée à l’étude de la régulation par ubiquitination d’une protéine de signalisation cellulaire, la GTPase Rac1. J’ai montré que l’ubiquitination dégradative de Rac1 affecte peu son variant d’épissage Rac1b, et qu’elle requiert l'activité JNK, stimulée par Rac1 mais non par Rac1b. En parallèle, j’ai mis en évidence une ubiquitination non dégradative de Rac1 qui pourrait contribuer à l’internalisation bactérienne lors de l’invasion. En recherchant l’enzyme responsable de l’ubiquitination spécifique de Rac1, j’ai pu identifier la protéine à domaine RING finger Unkempt comme un nouvel effecteur de Rac1. Cette ubiquitine ligase potentielle, activée par Rac1, serait impliquée dans l’ubiquitination du facteur BAF60b appartenant au complexe chromatinien SWI/SNF. J’ai par ailleurs observé que Rac1 stimule la mono-ubiquitination de l’histone H2A. Ainsi, la GTPase Rac1 serait impliquée dans une ou plusieurs voie(s) de signalisation inédite(s) contrôlant le remodelage de la chromatine
This thesis has been dedicated to the study of the regulation by ubiquitination of a signaling protein, the Rac1 GTPase. I have shown that the degradative ubiquitination of Rac1 affects poorly its splice variant Rac1b, and requires JNK activity, which is stimulated by Rac1 but not by Rac1b. In addition, I have described a non-degradative ubiquitination of Rac1, which could participate in pathogen endocytosis during bacterial infection. Searching for the enzyme responsible for specific Rac1 ubiquitination, I have identified a RING finger protein, Unkempt, as a new effector of Rac1. I have shown that this potential ubiquitin ligase, which is activated by Rac1, could be involved in the ubiquitination of BAF60b, a component of the chromatin remodeling complex SWI/SNF. Moreover, I have observed that Rac1 stimulates histone H2A mono-ubiquitination. Thus, Rac1 GTPase could be involved in novel pathways by controlling chromatin remodeling
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Peurois, François. "Activation des petites GTPases à la périphérie des membranes". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLN037.

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Les petites GTPases sont des régulateurs majeurs de nombreux processus cellulaires. La dérégulation de l’activation des petites GTPases est à l’origine de nombreuses maladies comme, entre autres, certains diabètes et cancers. In vivo, l’activation des petites GTPases se fait par des facteurs d’échange nucléotidiques (GEF), qui interagissent avec les GTPases à la périphérie des membranes cellulaires. Au delà d’un simple lieu de co-localisation, les membranes biologiques possèdent des propriétés physico-chimiques impactant directement l’activation des petites GTPases par les GEFs. Ce projet de thèse s’articule autour de trois axes, 1) proposer une stratégie expérimentale pour mesurer quantitativement les effets des membranes dans cette activation, 2) établir un modèle d’activation à la périphérie des membranes du GEF EPAC1, cible thérapeutique de maladies cardiaques 3) caractériser des petites molécules inhibitrices connues d’ArfGEF dans un contexte membranaire. Les résultats ont montré que les membranes modifiaient l’efficacité catalytique des GEFs, et questionnait leur spécificité vis à vis des petites GTPases. Les membranes apparaissent également comme de véritables actrices de l’activation d’EPAC1 en coopération avec l’AMPc. Ces effets pourraient être expliqués par une colocalisation entre GEFs et GTPases à la surface des membranes, l’induction d’un réarrangement conformationnel du GEF par les membranes, une modification de la diffusion latérale des GEF, ou encore une géométrie catalytiquement avantageuse du complexe GEF-GTPase-membrane. Enfin comprendre et expliciter l’implication des membranes dans cette activation amène à imaginer de nouvelles stratégies d’inhibition thérapeutique
Small GTPases are major regulators of many cellular processes. Nucleotide exchange factors (GEF) activate small GTPases. Deregulation of the activation of small GTPases is at the origin of several diseases, such as certain diabetes and cancers. GTPases and GEFs interact together at the periphery of cell membranes. Beyond a simple place of co-localization, biological membranes have physicochemical properties directly impacting the activation of small GTPases by GEFs. This thesis project is based on three axes, 1) to propose an experimental strategy to quantitatively measure the effects of membranes in this activation 2) to establish a model of the activation at the periphery of membranes of the GEF EPAC1, a therapeutic target in heart diseases, 3) to characterize known ArfGEF inhibitory small molecules in a membrane context. The results showed that membranes modified GEF catalytic efficiency, and questioned their specificity towards small GTPases. The membranes also appear as partners for the activation of EPAC1 in cooperation with cAMP. These effects could be explained by a co-localization between GEF and GTPases on the membranes surfaces, a conformational rearrangement of the GEF induced by membranes, a modification of lateral diffusion of the GEF, or a catalytically advantageous geometry of the GEF-GTPase-membrane complex. Finally, understanding the involvement of membranes in this activation leads us to imagine new therapeutic inhibition strategies
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Chan, King-chung Fred, i 陳敬忠. "Functional characterization of StAR-related lipid transfer domain containing 13 (DLC 2) RhoGAP in the nervous system". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278449.

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Chan, King-chung Fred. "Functional characterization of StAR-related lipid transfer domain containing 13 (DLC 2) RhoGAP in the nervous system". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278449.

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Keller, Laura. "Conception de nano-anticorps conformationnels comme nouveaux outils d'étude de l'activité des GTPases de la sous-famille RHOA". Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30005/document.

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Les GTPases de la sous famille RHOA participent à la régulation de nombreuses voies de signalisation qui contrôlent la dynamique du cytosquelette cellulaire et une grande diversité de fonctions telles que la prolifération, la division, la migration et la polarité cellulaires. Ce sont de véritables interrupteurs moléculaires qui, en réponse à un stimulus, changent de conformation tridimensionnelle pour activer leurs protéines effectrices cibles. Elles existent donc sous deux formes, une forme inactive liant le GDP et une forme active, liant le GTP. La proportion de forme active est extrêmement régulée au niveau spatial et temporel dans une cellule et représente moins de 10% de sa totalité. Depuis près de 20 ans, le seul outil disponible pour étudier leur activation est constitué par le domaine de liaison d'un effecteur, le RBD. Peu stable, faiblement soluble et peu adaptable, de nouveaux outils sont nécessaires afin de mieux comprendre la fine régulation de ces protéines. Les anticorps à simple domaine, VHH ou nanobodies, sont caractérisés par leur stabilité, solubilité, haut rendement de production et versatilité de fonctionnalisation. A partir d'une nouvelle banque d'anticorps à simple domaine optimisée pour la production d'intracorps, nous avons isolés différents clones capables de reconnaître in vitro et de bloquer in cellulo la forme active de ces protéines. L'un de ces clones permettra le développement d'un nouvel outil de mesure de l'activité de ces protéines in vitro tandis qu'un autre, in cellulo, permettra de mieux comprendre la régulation spatiale et temporelle des protéines endogènes
RHOA small GTPase belongs to a subfamily acting as a molecular switch activating major signaling pathways that regulate cytoskeletal dynamics and a variety of cellular responses such as cell cycle progression, cytokinesis, migration and polarity. RHOA activity resides in a few percent of GTP loaded protein, which is finely tuned by a crosstalk between regulators of the GTPase cycle. Manipulating a single RHO at the expression level often induces imbalance in the activity of other RHO GTPases, suggesting that more specific tools targeting these active pools are needed to decipher RHOA functions in time and space. We decided to use single domain antibodies, also known as VHH or nanobodies, as a new tool for studying RHOA activation. We produced and screened a novel fully synthetic phage display library of humanized nanobodies (NaLi-H1) to develop conformational sensors of the GTP loaded active conformation of RHO subfamily. We obtained several high affinity nanobodies against RHOA's active form which we characterized as RHO active antibodies in vitro and RHO signaling blocking intrabodies in cellulo. These new tools will facilitate and improve our current knowledge of this peculiar protein subfamily and will be a paradigm for the study of other RHO related small GTPases
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Tillement, Vanessa. "Régulation de la GTPase RHOB par phosphorylation". Toulouse 3, 2005. http://www.theses.fr/2005TOU30175.

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RhoB appartient à la famille Rho (RhoA, RhoB et RhoC) des GTPases de faible poids moléculaire, régulées par un cycle de liaison au GDP et GTP. Nous avons mis en évidence que RhoB est régulée également par phosphorylation. Contrairement à RhoA, qui est phosphorylée par la PKA, RhoB est, elle spécifiquement phosphorylée par la Caséine kinase 1 (CK1) et la Calmoduline kinase II in vitro et in vivo. Des études en spectrométrie de masse nous ont permis de montrer que CK1 phosphoryle RhoB dans son extrémité C-terminale sur la sérine 185. L'utilisation d'inhibiteurs de CK1 a permis de montrer que la phosphorylation de RhoB CK1-dépendante inhibe sa liaison à un des ses effecteurs, donc probablement son activité. Des résultats préliminaires suggèrent fortement que la phosphorylation de RhoB par CK1 est impliquée dans la régulation du trafic du récepteur à l'EGF suite à son internalisation par l'EGF
RhoB belongs to the Rho family (RhoA, RhoB and RhoC) of the low molecular weight GTPases, regulated by cycling between GDP and GTP bound state. We have shown that RhoB is also regulated by phosphorylation. On contrast to RhoA, which is phosphorylated by PKA, RhoB is specifically phosphorylated by Casein kinase 1 (CK1) and Calmodulin kinase II in vitro and in vivo. Mass spectrometry analysis has shown that CK1 phosphorylates RhoB on its C-terminal sequence on serine 185. With CK1 inhibitors we have shown that CK1-mediated phosphorylation of RhoB inhibits its binding to one of its effector, thus inhibiting its activity. Finally, preliminary results strongly suggest that RhoB phosphorylation by CK1 is implicated in the regulation of the intracellular trafficking of internalized EGF receptor
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Paul, Florian [Verfasser]. "Developing quantitative GTPase affinity purification (qGAP) to identify interaction partners of Rho GTPases / Florian Paul". Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1069532711/34.

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Paul, Florian Ernst Rudolf Benjamin [Verfasser]. "Developing quantitative GTPase affinity purification (qGAP) to identify interaction partners of Rho GTPases / Florian Paul". Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1069532711/34.

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Koraïchi, Faten. "Etude de l'activation de la GTPase RhoB par complémentation split-GFP tripartite". Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30081.

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RhoB est une petite GTPase rapidement activée par les facteurs de croissance et les stress cellulaires, qui régule des processus biologiques fondamentaux comme la migration, l'angiogenèse, la réparation de l'ADN, l'apoptose ainsi que la réponse à des thérapeutiques anticancéreuses. L'activité des petites GTPases est finement régulée par leur localisation subcellulaire. Cependant, l'activation de RhoB en cellules vivantes n'avait jamais été investiguée. Ce travail a permis d'adapter et de valider une méthode innovante d'analyse des interactions protéine-protéine par complémentation split-GFP tripartite, pour la détection sensible et spécifique de l'activation des petites GTPases en cellules vivantes. Nous avons ensuite développé un modèle cellulaire optimisé par la combinaison de la technologie split-GFP tripartite et d'un intracorps anti-GFP amplificateur de fluorescence, pour détecter la régulation de l'activation de RhoB avec une haute résolution spatiale. Ce biosenseur a mis en évidence la translocation de la forme active de RhoB en réponse au sérum à partir des endosomes pour s'accumuler au niveau de la membrane plasmique, révélant ainsi une nouvelle plateforme de signalisation membranaire de RhoB. Ce biosenseur permettra d'analyser le profil d'activation de RhoB et d'autres petites GTPases, sous d'autres stimulations ou dans différents contextes cellulaires, et d'identifier leurs partenaires et les modulateurs de leur activation
RhoB is a small GTPase that is rapidly activated in response to growth factors and cellular stress. It regulates fundamental biological processes such as cell migration, angiogenesis, DNA repair, apoptosis and response to anticancer therapies. Small GTPases activity is tightly regulated by their subcellular localization. However, RhoB activation had never been investigated in living cells. In this work, we have adapted and validated an innovative method of protein-protein interactions analysis using tripartite split-GFP complementation, for the sensitive and specific detection of small GTPases activation in living cells. Then, we developed an optimized cellular model by combining the tripartite split-GFP technology with an anti-GFP intrabody fluorescence-enhancer to detect the regulation of RhoB activation with high spatial resolution. This biosensor highlighted the translocation of active RhoB from endosomes to accumulate at the plasma membrane upon serum stimulation, revealing a novel membrane signaling platform of RhoB. Future studies based on this biosensor will enable the analysis of RhoB activation profile and other small GTPases upon various stimuli or in different cellular contexts, as well as the identification of the GTPases partners and activation modulators
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Książki na temat "GTPase"

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Manser, Ed, i Thomas Leung. GTPase Protocols. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592592813.

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Joan, Marsh, i Goode Jamie, red. The GTPase superfamily. Chichester: Wiley, 1993.

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Rush, Mark, i Peter D’Eustachio, red. The Small GTPase Ran. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1501-2.

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Corda, D., H. Hamm i A. Luini. GTPase-controlled molecular machines. Rome: Ares-Serono Symposia Publications, 1994.

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Holmes, L. P. Gtpase protocols: The ras superfamily. [Place of publication not identified]: Humana, 2010.

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Ed, Manser, i Leung Thomas, red. GTPase protocols: The Ras superfamily. Totowa, N.J: Humana Press, 2002.

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Zhang, Xin. Multistate GTPase Control Co-translational Protein Targeting. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4419-7808-0.

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Marsh, Joan, i Jamie Goode, red. Ciba Foundation Symposium 176 - The GTPase Superfamily. Chichester, UK: John Wiley & Sons, Ltd., 1993. http://dx.doi.org/10.1002/9780470514450.

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A, Kahn Richard, red. ARF family GTPases. Dordrecht: Kluwer Academic Publishers, 2003.

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1949-, Balch William Edward, Der Channing J i Hall A, red. Regulators and effectors of small GTPases. San Diego: Academic Press, 2000.

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Części książek na temat "GTPase"

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Del Pulgar, Teresa Gómez, i Juan Carlos Lacal. "GTPase". W Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2533-2.

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Del Pulgar, Teresa Gómez, i Juan Carlos Lacal. "GTPase". W Encyclopedia of Cancer, 1968–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_2533.

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Pulgar, Teresa Gómez Del, i Juan Carlos Lacal. "GTPase". W Encyclopedia of Cancer, 1609–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2533.

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Konstantinidis, Diamantis G., i Theodosia A. Kalfa. "Rac GTPase". W 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., i Theodosia A. Kalfa. "Rac GTPase". W 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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Dempsey, Brian R., Anne C. Rintala-Dempsey, Gary S. Shaw, Yuan Xiao Zhu, A. Keith Stewart, Jaime O. Claudio, Constance E. Runyan i in. "Small GTPase". W Encyclopedia of Signaling Molecules, 1752. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101254.

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McCormick, F. "GTPase Activating Proteins". W GTPases in Biology I, 345–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78267-1_23.

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Ting, T. D., R. H. Lee i Y. K. Ho. "The GTPase Cycle: Transducin". W GTPases in Biology II, 99–117. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78345-6_7.

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Stevens, Ellen V., i Channing J. Der. "Overview of Rho GTPase History". W The Rho GTPases in Cancer, 3–27. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1111-7_1.

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Leung, Roland, i Michael Glogauer. "Rho GTPase Techniques in Osteoclastogenesis". W Methods in Molecular Biology, 167–79. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-442-1_12.

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Streszczenia konferencji na temat "GTPase"

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

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Cell migration is achieved by the dynamic feedback interactions between traction forces generated by the cell and exerted onto the underlying extracellular matrix (ECM), and intracellular mechano-chemical signaling pathways, e.g., Rho GTPase (RhoA, Rac1, and Cdc42) activities [1,2,3]. These components are differentially distributed within a cell, and thus the coordination between tractions and mechanotransduction (i.e, RhoA and Rac1 activities) must be implemented at a precise spatial and temporal order to achieve optimized, directed cell migration [4,5]. Recent studies have shown that focal adhesions at the leading edge exert strong tractions [6], and these traction sites are co-localized with focal adhesion sites [7]. Further, by using the fluorescence resonance energy transfer (FRET) technology coupled with genetically encoded biosensors, researchers reported that Rho GTPases, such as RhoA [8], Rac1 [9], and Cdc42 [10] are maximally activated at the leading edge, suggesting the leading edge of the cell as its common functional site for Rho GTPase activities. All these works, however, were done separately, and the relationship between tractions and mechanotransduction during cell migration has not been demonstrated directly because of the difficulty in simultaneously recording tractions and mechanotransduction in migrating cells, precluding direct comparison between these results. Furthermore, these studies have been conducted by monitoring cells on glass coverslips, the stiffness of which is ∼ 65 giga pascal (GPa), at least three to six order higher than the physiological range of ECM stiffness. Although it is increasingly accepted that ECM stiffness influences cell migration, it is not known exactly how physiologically relevant ECM stiffness (order of kPa range) affects the dynamics of RhoA and Rac1 activities. For a complete understanding of the mechanism of mechano-chemical signaling in the context of cell migration, the dynamics and interplay between biomechanical (e.g., tractions) and biochemical (e.g., Rho GTPase) activities should be visualized within the physiologically relevant range of ECM stiffness.
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Mondal, Subhanjan, Said Goueli i Kevin Hsiao. "Abstract C204: GTPase/GAP/GEF-Glo™: A bioluminescent system to measure GTPase, GAP, and GEF activities." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c204.

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Mondal, Subhanjan, i Said A. Goueli. "Abstract B44: GTPase/GAP/GEF-Glo™: A bioluminescent system to measure GTPase, GAP, and GEF activities". W Abstracts: AACR Special Conference on RAS Oncogenes: From Biology to Therapy; February 24-27, 2014; Lake Buena Vista, FL. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.rasonc14-b44.

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Schulze, J., L. Heinkele, M. Steffens, A. Warnecke, T. Lenarz, I. Just i A. Rohrbeck. "Rho-GTPase und p38 vermittelte Neuroprotektion in Spiralganglienzellen". W Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641056.

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Weber, Igor. "Oscillatory dynamics of small GTPase Rac1 in motile cells". W European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.1187.

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Acosta, Lehi, Aaron Rogers, Jingfu Peng, Alan Mueller, Zongzhong Tong, Donghan Shin, Jae Hyuk Yoo i in. "Abstract 4367: The small GTPase ARF6 is necessary for melanomagenesis". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4367.

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Schulze, J., L. Heinkele, M. Steffens, A. Warnecke, T. Lenarz, I. Just i A. Rohrbeck. "Rho-GTPase and p38 mediated neuroprotection in spiral ganglion cells". W Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641057.

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Jakobs, K. H., P. Gierschik i R. Grandt. "THE ROLE OF GTP-BINDING PROTEINS EXHIBITING GTPase ACTIVITY IN PLATELET ACTIVATION". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644773.

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Activation of platelets by agonists acting via cell surface-located receptors apparently involves as an early event in transmembrane signalling an interaction of the agonist-occupied receptor with a guanine nucleotide-binding regulatory protein (G-protein). The activated G-protein, then, transduces the information to the effector molecule, being responsible for the changes in intracellular second messengers. At least two changes in intracellular signal molecules are often found to be associated with platelet activation by agonists, i.e., increases in inositol trisphosphate and diacylglycerol levels caused by activation of a polyphosphoinositide-specific phospholipase C and decrease in cyclic AMP concentration caused by inhibition of adenylate cyclase.Both actions of platelet-activating agents apparently involve G-proteins as transducing elements. Generally, the function of a G-protein in signal transduction can be measured either by its ability to regulate the activity of the effector molecule (phospholipase C or adenylate cyclase) or the binding affinity of an agonist to its specific receptor or by the abitlity of the G-protein to bind and hydrolyze GTP or one of its analogs in response to agonist-activated receptors. Some platelet-activating agonists (e.g. thrombin) can cause both adenylate cyclase inhibition and phospholipase C activation, whereas others induce either inhibition of adenylate cyclase (e.g. α2-adrenoceptor agonists) or activation of phospholipase C (e.g. stable endoperoxide analogs) . It is not yet known whether the simultaneous activation of two signal transduction systems is due to activation of two separate G-proteins by one receptor, to two distinct receptors activating each a distinct G-protein or to activation of two effector molecules by one G-protein.For some of the G-proteins, rather specific compounds are available causing inactivation of their function. In comparison to Gs, the stimulatory G-protein of the adenylate cyclase system, the adenylate cyclase inhibitory Gi-protein is rather specifically inactivated by ADP-ribosylation of its a-subunit by pertussis toxin, “unfortunately” not acting in intact platelets, and by SH-group reactive agents such as N-ethylmaleimide and diamide, apparently also affecting the Giα-subunit. Both of these treatments completely block α2-adrenoceptor-induced GTPase stimulation and adenylate cyclase inhibition and also thrombin-induced inhibition of adenylate cyclase. In order to know whether the G-protein coupling receptors to phospholipase C is similar to or different from the Gi-protein, high affinity GTPase stimulation by agents known to activate phospholipase C was evaluated in platelet membranes. The data obtained indicated that GTPase stimulation by agents causing both adenylate cyclase inhibition and phospholipase C activation is reduced, but only partially, by the above mentioned Gi-inactivating agents, while stimulation of GTPase by agents stimulating only phospholipase C is not affected by these treatments. These data suggested that the G-protein regulating phospholipase C activity in platelet membranes is different from the Gi-protein and may also not be a substrate for pertussis toxin. Measuring thrombin stimulation of inositol phosphate and diacylglycerol formation in saponin-permeabilized platelets, apparently contradictory data were reported after pertussis toxin treatment, being without effect or causing even an increase in thrombin stimulation of inositol phosphate formation (Lapetina: BBA 884, 219, 1986) or being inhibitory to thrombin stimulation of diacylglycerol formation (Brass et al.: JBC 261, 16838, 1986). These data indicate that the nature of the phospholipase C-related G-protein(s) is not yet defined and that their elucidation requires more specific tools as well as purification and reconstitution experiments. Preliminary data suggest that some antibiotics may serve as useful tools to characterize the phospho-lipase-related G-proteins. The possible role of G-protein phosphorylation by intracellular signal molecule-activated protein kinases in attenuation of signal transduction in platelets will be discussed.
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Pusapati, Ganesh Varma, An Rykx, Sandy Vandoninck, Johan van Lint, Guido Adler i Thomas Seufferlein. "Abstract 296: Protein kinase D regulates Rho GTPase activity through rhotekin". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-296.

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Okura, Hidehiro, Brian J. Golbourn, Amanda J. Luck, Christian A. Smith i James T. Rutka. "Abstract 4038: Role of the Rho-GTPase CDC42 in glioma migration". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4038.

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Raporty organizacyjne na temat "GTPase"

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Simpson, Kaylene J. Rho GTPase Involvement in Breast Cancer Migration and Invasion. Fort Belvoir, VA: Defense Technical Information Center, marzec 2005. http://dx.doi.org/10.21236/ada435395.

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Simpson, Kaylene J. Rho GTPase Involvement in Breast Cancer Migration and Invasion. Fort Belvoir, VA: Defense Technical Information Center, marzec 2007. http://dx.doi.org/10.21236/ada469757.

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Yang, Zhenbiao. ROP GTPase Signaling in The Hormonal Regulation of Plant Growth. Office of Scientific and Technical Information (OSTI), maj 2013. http://dx.doi.org/10.2172/1080178.

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Kandpal, Rajendra P., i G. M. Nagaraja. Involvement of a Novel Rho GTPase Activating Protein in Breast Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2001. http://dx.doi.org/10.21236/ada404607.

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Band, Vimia. Human Mammary Epithelial Cell Transformation by Rho GTPase through a Novel Mechanism. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2008. http://dx.doi.org/10.21236/ada500910.

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Kleer, Celina G. Detection of Metastatic Potential in Breast Cancer by RhoC-GTPase and WISP3 Proteins. Fort Belvoir, VA: Defense Technical Information Center, maj 2005. http://dx.doi.org/10.21236/ada442688.

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Kleer, Celina G. Detection of Metastatic Potential in Breast Cancer by RhoC-GTPase and WISP3 Proteins. Fort Belvoir, VA: Defense Technical Information Center, maj 2006. http://dx.doi.org/10.21236/ada456604.

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Kleer, Celina G. Detection of Metastatic Potential in Breast Cancer by RhoC-GTPase and WISP3 Proteins. Fort Belvoir, VA: Defense Technical Information Center, maj 2004. http://dx.doi.org/10.21236/ada426448.

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Kleer, Celina G. Detection of Metastatic Potential in Breast Cancer by RhoC-GTPase and WISP3 Proteins. Fort Belvoir, VA: Defense Technical Information Center, maj 2003. http://dx.doi.org/10.21236/ada422281.

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Kleer, Celina G. Detection of Metastatic Potential in Breast Cancer by RhoC-GTPase and WISP3 Proteins. Fort Belvoir, VA: Defense Technical Information Center, maj 2007. http://dx.doi.org/10.21236/ada473395.

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