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Relevant bibliographies by topics / Regulation of Cdc42

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Dissertations / Theses

Academic literature on the topic 'Regulation of Cdc42'

Author: Grafiati

Published: 25 May 2024

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Dissertations / Theses on the topic "Regulation of Cdc42"

1

Ravichandran, Yamini. "Cdc42 isoforms : localization, functions and regulation." Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS405.

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Les mutations sont responsables de diverses pathologies du développement, en particulier chez les patients atteints de maladies rares ou pour lesquels il n’y a pas de diagnostic clinique clair. Cdc42 est une protéine clé pour la polarité cellulaire, une étape cruciale de nombreux processus cellulaires, comme la migration cellulaire, la division cellulaire ou la réponse immunitaire. Les mutations de Cdc42 entrainent une variété de pathologies, par exemple des dérégulations de la croissance ou de la morphologie faciale ainsi que des anomalies immunologiques, hématologiques et du développement ne

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2

Lu, Ruifeng, and Jean M. Wilson. "Rab14 specifies the apical membrane through Arf6-mediated regulation of lipid domains and Cdc42." NATURE PUBLISHING GROUP, 2016. http://hdl.handle.net/10150/622499.

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The generation of cell polarity is essential for the development of multi-cellular organisms as well as for the function of epithelial organs in the mature animal. Small GTPases regulate the establishment and maintenance of polarity through effects on cytoskeleton, membrane trafficking, and signaling. Using short-term 3-dimensional culture of MDCK cells, we find that the small GTPase Rab14 is required for apical membrane specification. Rab14 knockdown results in disruption of polarized lipid domains and failure of the Par/aPKC/Cdc42 polarity complex to localize to the apical membrane. These ef

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3

Murali, Arun [Verfasser]. "Role of XIAP in ubiquitin mediated regulation of Cdc42 and other Rho GTPases / Arun Murali." Mainz : Universitätsbibliothek Mainz, 2019. http://d-nb.info/1191286649/34.

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4

Francis, Monika K. "Regulation of GRAF1 membrane sculpting function during cell movement." Doctoral thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-111213.

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All eukaryotic cells rely on endocytic events to satisfy a constant need for nutrient and fluid uptake from their surroundings. Endocytosis-dependent turnover of cell surface constituents also serves to control signal transduction and establish morphological changes in response to extracellular stimuli. During endocytosis, distinct protein machineries re-sculpt the plasma membrane into vesicular carriers that enclose molecules that are to be taken up into the cell. Besides those produced from the canonical clathrin-mediated endocytic machinery, it is becoming increasingly clear that other memb

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5

Mutavchiev, Delyan Rumenov. "Regulation of fission yeast cell polarity by stress-response pathways." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29006.

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Cell polarisation is a key biological process crucial for the functioning of essentially all cells. Regulation of cell polarity is achieved through various processes determined by both internal and external factors. An example of the latter is that cell polarity can be disrupted or lost as a consequence of a variety of external stresses. When facing such stresses, cells adapt to unfavourable conditions by activating a range of molecular signalling pathways, collectively termed ‘stress response’. Despite the connections between external stress and cell polarity, whether stress-response signalli

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6

Langer, Torben [Verfasser]. "Der Einfluss des Tumorsuppressorproteins Merlin auf die Regulation der beiden Rho-GTPasen Rac2 und Cdc42 / Torben Langer." Ulm : Universität Ulm. Medizinische Fakultät, 2013. http://d-nb.info/1036215121/34.

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7

Ye, Xiangcang. "Role of a CDC42 homologous gene in the regulation of cell polarity and morphogenic transitions in Wangiella dermatitidis /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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8

Primeau, Martin. "Novel mechanisms of regulation of the Cdc42 GTPase- activating protein CdGAP/ARHGAP31, a protein involved in cell migration and adhesion." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96901.

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The Rho GTPases form a family of enzymes that control numerous cellular processes including cell migration and proliferation through effects on the cytoskeleton, membrane trafficking and cell adhesion. The activity of these molecular switches is modulated by GTPase-activating proteins (GAPs), a group of negative-regulators which includes Cdc42-GTPase-Activating Protein (CdGAP). This protein specifically negatively-regulates the Rho GTPases Cdc42 and Rac1. In this study, we show that CdGAP is regulated by lipid-, protein- and intramolecular-interactions. First, we demonstrate that a polybasic r

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9

Ofo, Enyinnaya. "Flourescent biosensor-based, Cdc42 activity imaging for understanding the regulation of Epidermal Growth Receptor (EGFR) signalling in head and neck cancer." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/flourescent-biosensorbased-cdc42-activity-imaging-for-understanding-the-regulation-of-epidermal-growth-receptor-egfr-signalling-in-head-and-neck-cancer(32081fef-10f1-4a3e-ac33-67afbbf78376).html.

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The Epidermal Growth Factor Receptor (EGFR) is overexpressed in several solid tumours including squamous cell carcinoma of the head & neck (SCCHN). Drugs that directly block the action of EGFR are currently available. However, a major unanswered question is; how best to select patients most likely to respond to these new treatments, as the response rate to EGFR-targeted mono-therapy in SCCHN, as well as other solid tumours, such as lung and colorectal cancer, is very low. Resistance to EGFR therapy may stem from aberrant receptor trafficking. Cdc42 is known to affect EGFR downregulation by

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10

Bretou, Marine. "Regulation of the dynamics of the fusion pore : importance of the SNARE protein synaptobrevin 2 and of the Rho GTPase Cdc42." Paris 7, 2010. http://www.theses.fr/2010PA077157.

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L'exocytose nécessite la formation d'un pore de fusion. Le pore initial est étroit ; seules de petites molécules sont libérées. Quand le pore s'élargit les macromolécules sont libérées. J'ai étudié le rôle de deux protéines sur la dilatation du pore: la protéine SNARE synaptobrévine 2 (Syb2), et la Rhô GTPase Cdc42. L'assemblage des SNAREs fournirait l'énergie nécessaire à la fusion. L'insertion d'un espacer dans le domaine juxtamembranaire de Syb2 ne modifie pas la fréquence des événements d'exocytose détectés par ampérométrie à 1|jM [Ca2+], mais empêche l'apparition d'une composante de sécré

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