Academic literature on the topic 'Endosomal maturation'
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Journal articles on the topic "Endosomal maturation"
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Abenza, Juan F., Antonio Galindo, Mario Pinar, Areti Pantazopoulou, Vivian de los Ríos, and Miguel A. Peñalva. "Endosomal maturation by Rab conversion in Aspergillus nidulans is coupled to dynein-mediated basipetal movement." Molecular Biology of the Cell 23, no. 10 (May 15, 2012): 1889–901. http://dx.doi.org/10.1091/mbc.e11-11-0925.
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We exploit the ease with which highly motile early endosomes are distinguished from static late endosomes in order to study Aspergillus nidulans endosomal traffic. RabSRab7 mediates homotypic fusion of late endosomes/vacuoles in a homotypic fusion- and vacuole protein sorting/Vps41–dependent manner. Progression across the endocytic pathway involves endosomal maturation because the end products of the pathway in the absence of RabSRab7 are minivacuoles that are competent in multivesicular body sorting and cargo degradation but retain early endosomal features, such as the ability to undergo long-distance movement and propensity to accumulate in the tip region if dynein function is impaired. Without RabSRab7, early endosomal Rab5s—RabA and RabB—reach minivacuoles, in agreement with the view that Rab7 homologues facilitate the release of Rab5 homologues from endosomes. RabSRab7 is recruited to membranes already at the stage of late endosomes still lacking vacuolar morphology, but the transition between early and late endosomes is sharp, as only in a minor proportion of examples are RabA/RabB and RabSRab7 detectable in the same—frequently the less motile—structures. This early-to-late endosome/vacuole transition is coupled to dynein-dependent movement away from the tip, resembling the periphery-to-center traffic of endosomes accompanying mammalian cell endosomal maturation. Genetic studies establish that endosomal maturation is essential, whereas homotypic vacuolar fusion is not.
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Delevoye, Cédric, Ilse Hurbain, Danièle Tenza, Jean-Baptiste Sibarita, Stéphanie Uzan-Gafsou, Hiroshi Ohno, Willie J. C. Geerts, et al. "AP-1 and KIF13A coordinate endosomal sorting and positioning during melanosome biogenesis." Journal of Cell Biology 187, no. 2 (October 19, 2009): 247–64. http://dx.doi.org/10.1083/jcb.200907122.
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Specialized cell types exploit endosomal trafficking to deliver protein cargoes to cell type–specific lysosome-related organelles (LROs), but how endosomes are specified for this function is not known. In this study, we show that the clathrin adaptor AP-1 and the kinesin motor KIF13A together create peripheral recycling endosomal subdomains in melanocytes required for cargo delivery to maturing melanosomes. In cells depleted of AP-1 or KIF13A, a subpopulation of recycling endosomes redistributes to pericentriolar clusters, resulting in sequestration of melanosomal enzymes like Tyrp1 in vacuolar endosomes and consequent inhibition of melanin synthesis and melanosome maturation. Immunocytochemistry, live cell imaging, and electron tomography reveal AP-1– and KIF13A-dependent dynamic close appositions and continuities between peripheral endosomal tubules and melanosomes. Our results reveal that LRO protein sorting is coupled to cell type–specific positioning of endosomes that facilitate endosome–LRO contacts and are required for organelle maturation.
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Kim, Sungsu, Yogesh P. Wairkar, Richard W. Daniels, and Aaron DiAntonio. "The novel endosomal membrane protein Ema interacts with the class C Vps–HOPS complex to promote endosomal maturation." Journal of Cell Biology 188, no. 5 (March 1, 2010): 717–34. http://dx.doi.org/10.1083/jcb.200911126.
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Endosomal maturation is critical for accurate and efficient cargo transport through endosomal compartments. Here we identify a mutation of the novel Drosophila gene, ema (endosomal maturation defective) in a screen for abnormal synaptic overgrowth and defective protein trafficking. Ema is an endosomal membrane protein required for trafficking of fluid-phase and receptor-mediated endocytic cargos. In the ema mutant, enlarged endosomal compartments accumulate as endosomal maturation fails, with early and late endosomes unable to progress into mature degradative late endosomes and lysosomes. Defective endosomal down-regulation of BMP signaling is responsible for the abnormal synaptic overgrowth. Ema binds to and genetically interacts with Vps16A, a component of the class C Vps–HOPS complex that promotes endosomal maturation. The human orthologue of ema, Clec16A, is a candidate susceptibility locus for autoimmune disorders, and its expression rescues the Drosophila mutant demonstrating conserved function. Characterizing this novel gene family identifies a new component of the endosomal pathway and provides insights into class C Vps–HOPS complex function.
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Szatmári, Zsuzsanna, Viktor Kis, Mónika Lippai, Krisztina Hegedűs, Tamás Faragó, Péter Lőrincz, Tsubasa Tanaka, Gábor Juhász, and Miklós Sass. "Rab11 facilitates cross-talk between autophagy and endosomal pathway through regulation of Hook localization." Molecular Biology of the Cell 25, no. 4 (February 15, 2014): 522–31. http://dx.doi.org/10.1091/mbc.e13-10-0574.
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During autophagy, double-membrane autophagosomes deliver sequestered cytoplasmic content to late endosomes and lysosomes for degradation. The molecular mechanism of autophagosome maturation is still poorly characterized. The small GTPase Rab11 regulates endosomal traffic and is thought to function at the level of recycling endosomes. We show that loss of Rab11 leads to accumulation of autophagosomes and late endosomes in Drosophila melanogaster. Rab11 translocates from recycling endosomes to autophagosomes in response to autophagy induction and physically interacts with Hook, a negative regulator of endosome maturation. Hook anchors endosomes to microtubules, and we show that Rab11 facilitates the fusion of endosomes and autophagosomes by removing Hook from mature late endosomes and inhibiting its homodimerization. Thus induction of autophagy appears to promote autophagic flux by increased convergence with the endosomal pathway.
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Casanova, James E., and Bettina Winckler. "A new Rab7 effector controls phosphoinositide conversion in endosome maturation." Journal of Cell Biology 216, no. 10 (September 19, 2017): 2995–97. http://dx.doi.org/10.1083/jcb.201709034.
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Endosome maturation requires a coordinated change in the Rab GTPase and phosphoinositide composition of the endosomal membrane. In this issue, Liu et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201705151) identify WDR91 as a ubiquitous Rab7 effector that inhibits phosphatidylinositol 3-kinase activity on endosomes and is critical for endosome maturation, viability, and dendrite growth of neurons in vivo.
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Chotard, Laëtitia, Ashwini K. Mishra, Marc-André Sylvain, Simon Tuck, David G. Lambright, and Christian E. Rocheleau. "TBC-2 Regulates RAB-5/RAB-7-mediated Endosomal Trafficking inCaenorhabditis elegans." Molecular Biology of the Cell 21, no. 13 (July 2010): 2285–96. http://dx.doi.org/10.1091/mbc.e09-11-0947.
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During endosome maturation the early endosomal Rab5 GTPase is replaced with the late endosomal Rab7 GTPase. It has been proposed that active Rab5 can recruit and activate Rab7, which in turn could inactivate and remove Rab5. However, many of the Rab5 and Rab7 regulators that mediate endosome maturation are not known. Here, we identify Caenorhabditis elegans TBC-2, a conserved putative Rab GTPase-activating protein (GAP), as a regulator of endosome to lysosome trafficking in several tissues. We show that tbc-2 mutant animals accumulate enormous RAB-7–positive late endosomes in the intestine containing refractile material. RAB-5, RAB-7, and components of the homotypic fusion and vacuole protein sorting (HOPS) complex, a RAB-7 effector/putative guanine nucleotide exchange factor (GEF), are required for the tbc-2(−) intestinal phenotype. Expression of activated RAB-5 Q78L in the intestine phenocopies the tbc-2(−) large late endosome phenotype in a RAB-7 and HOPS complex-dependent manner. TBC-2 requires the catalytic arginine-finger for function in vivo and displays the strongest GAP activity on RAB-5 in vitro. However, TBC-2 colocalizes primarily with RAB-7 on late endosomes and requires RAB-7 for membrane localization. Our data suggest that TBC-2 functions on late endosomes to inactivate RAB-5 during endosome maturation.
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Sun, Ming, Gary Luong, Faiz Plastikwala, and Yue Sun. "Abstract 155: An endosomal type Igamma PIP 5-kinase controls endosome maturation, lysosome function, and autophagy by modulating Rab7a." Cancer Research 82, no. 12_Supplement (June 15, 2022): 155. http://dx.doi.org/10.1158/1538-7445.am2022-155.
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Abstract Endosomes are major protein-sorting stations in cells. Defects in endosomal sorting are implicated in various human pathologies, such as cancer and neurodegenerative disorders. The small GTPase Ras-related protein Rab-7a (Rab7a) serves as a key organizer of the endosomal-lysosomal system. However, molecular mechanisms controlling Rab7a activation levels and subcellular translocation are still poorly defined. Here, we demonstrate that type Igamma phosphatidylinositol phosphate 5-kinase i5 (PIPKIgammai5), an endosome-localized enzyme that produces phosphatidylinositol 4,5-bisphosphate (PI4,5P2), directly interacts with Rab7a and plays critical roles in the control of endosomal-lysosomal system. The loss of PIPKIgammai5 blocks Rab7a recruitment to early endosomes, which prevents the maturation of early to late endosomes. In this way, PIPKIgammai5 is required for Epidermal Growth Factor Receptor (EGFR) sorting from endosomes to lysosomes, which controls the down-regulation of EGFR signaling. Furthermore, PIPKIgammai5 loss disturbs retromer complex connection with Rab7a, which blocks the retrograde sorting of Cation-independent Mannose 6-Phosphate Receptor (CI-MPR) from late endosomes. This leads to the decreased sorting of hydrolases to lysosomes. Thus, loss of PIPKIgammai5 causes lysosome dysfunction and reduces the autophagic degradation. By modulating retromer-Rab7a connection, PIPKIgammai5 is also required for the recruitment of the GTPase-activating protein (GAP) TBC1 domain family member 5 (TBC1D5) to late endosomes, which controls the conversion of Rab7a from the active state to the inactive state. Altogether, PIPKIgammai5 is critical for the modulation of Rab7a activity, localization, and function in the endosomal-lysosomal system. Citation Format: Ming Sun, Gary Luong, Faiz Plastikwala, Yue Sun. An endosomal type Igamma PIP 5-kinase controls endosome maturation, lysosome function, and autophagy by modulating Rab7a [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 155.
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He, Jing, Jennifer L. Johnson, Jlenia Monfregola, Mahalakshmi Ramadass, Kersi Pestonjamasp, Gennaro Napolitano, Jinzhong Zhang, and Sergio D. Catz. "Munc13-4 interacts with syntaxin 7 and regulates late endosomal maturation, endosomal signaling, and TLR9-initiated cellular responses." Molecular Biology of the Cell 27, no. 3 (February 2016): 572–87. http://dx.doi.org/10.1091/mbc.e15-05-0283.
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The molecular mechanisms that regulate late endosomal maturation and function are not completely elucidated, and direct evidence of a calcium sensor is lacking. Here we identify a novel mechanism of late endosomal maturation that involves a new molecular interaction between the tethering factor Munc13-4, syntaxin 7, and VAMP8. Munc13-4 binding to syntaxin 7 was significantly increased by calcium. Colocalization of Munc13-4 and syntaxin 7 at late endosomes was demonstrated by high-resolution and live-cell microscopy. Munc13-4–deficient cells show increased numbers of significantly enlarged late endosomes, a phenotype that was mimicked by the fusion inhibitor chloroquine in wild-type cells and rescued by expression of Munc13-4 but not by a syntaxin 7–binding–deficient mutant. Late endosomes from Munc13-4-KO neutrophils show decreased degradative capacity. Munc13-4–knockout neutrophils show impaired endosomal-initiated, TLR9-dependent signaling and deficient TLR9-specific CD11b up-regulation. Thus we present a novel mechanism of late endosomal maturation and propose that Munc13-4 regulates the late endocytic machinery and late endosomal–associated innate immune cellular functions.
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Arlt, Henning, Kathrin Auffarth, Rainer Kurre, Dominik Lisse, Jacob Piehler, and Christian Ungermann. "Spatiotemporal dynamics of membrane remodeling and fusion proteins during endocytic transport." Molecular Biology of the Cell 26, no. 7 (April 2015): 1357–70. http://dx.doi.org/10.1091/mbc.e14-08-1318.
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Organelles of the endolysosomal system undergo multiple fission and fusion events to combine sorting of selected proteins to the vacuole with endosomal recycling. This sorting requires a consecutive remodeling of the organelle surface in the course of endosomal maturation. Here we dissect the remodeling and fusion machinery on endosomes during the process of endocytosis. We traced selected GFP-tagged endosomal proteins relative to exogenously added fluorescently labeled α-factor on its way from the plasma membrane to the vacuole. Our data reveal that the machinery of endosomal fusion and ESCRT proteins has similar temporal localization on endosomes, whereas they precede the retromer cargo recognition complex. Neither deletion of retromer nor the fusion machinery with the vacuole affects this maturation process, although the kinetics seems to be delayed due to ESCRT deletion. Of importance, in strains lacking the active Rab7-like Ypt7 or the vacuolar SNARE fusion machinery, α-factor still proceeds to late endosomes with the same kinetics. This indicates that endosomal maturation is mainly controlled by the early endosomal fusion and remodeling machinery but not the downstream Rab Ypt7 or the SNARE machinery. Our data thus provide important further understanding of endosomal biogenesis in the context of cargo sorting.
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Friedman, Jonathan R., Jared R. DiBenedetto, Matthew West, Ashley A. Rowland, and Gia K. Voeltz. "Endoplasmic reticulum–endosome contact increases as endosomes traffic and mature." Molecular Biology of the Cell 24, no. 7 (April 2013): 1030–40. http://dx.doi.org/10.1091/mbc.e12-10-0733.
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The endosomal pathway is responsible for plasma membrane cargo uptake, sorting, and, in many cases, lysosome targeting. Endosome maturation is complex, requiring proper spatiotemporal recruitment of factors that regulate the size, maturity, and positioning of endosomal compartments. In animal cells, it also requires trafficking of endosomes on microtubules. Recent work has revealed the presence of contact sites between some endosomes and the endoplasmic reticulum (ER). Although these contact sites are believed to have multiple functions, the frequency, dynamics, and physical attributes of these contacts are poorly understood. Here we use high-resolution three-dimensional electron microscopy to reveal that ER tubules wrap around endosomes and find that both organelles contact microtubules at or near membrane contact sites. As endosomes traffic, they remain bound to the ER, which causes the tubular ER to rearrange its structure around dynamic endosomes at contact sites. Finally, as endosomes transition through steps of maturation, they become more tightly associated with the ER. The major implication of these results is that endosomes mature and traffic while coupled to the ER membrane rather than in isolation.
Dissertations / Theses on the topic "Endosomal maturation"
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Djeddi, Abderazak. "Caractérisation cellulaire et fonctionnelle de l’autophagie : interactions avec la voie de maturation endosomale chez Caenorhabditis elegans." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA112036.
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L’autophagie est une voie catabolique durant laquelle des constituants cytoplasmiques sont engloutis dans des vésicules à double membrane nommées autophagosomes. Elle sert à éliminer les protéines mal repliées ou les agrégats protéiques, à détruire les organites défectueux comme les mitochondries, le réticulum endoplasmique et les peroxysomes mais aussi des pathogènes intracellulaires. Le matériel séquestré dans les autophagosomes est ensuite envoyé, pour dégradation, vers le lysosome. La dégradation du matériel séquestré génère des nucléotides, des acides aminés et des acides gras qui seront recyclés en vue de la synthèse de macromolécules et de la génération d’ATP.Dans cette étude nous explorons l’aspect cellulaire et fonctionnel de la voie de l’autophagie chez Caenorhabditis elegans. Nous montrons que le génome du nématode contient deux homologues du gène autophagique de levure Atg8. Ces homologues codent pour les protéines LGG-1 et LGG-2 qui sont des protéines des membranes des autophagosomes. Ces protéines agissent de façon synergique dans les processus physiologiques impliquant l’autophagie, en l’occurrence, la longévité et la formation des larves dauer.Nous montrons également que l’autophagie est impliquée dans le maintien de l’homéostasie cellulaire chez les mutants ESCRT. Les complexes ESCRT sont impliqués dans l’adressage des protéines ubiquitinées vers les corps multi vésiculaires pour les dégrader. Les mutants ESCRT se caractérisent par des altérations cellulaires et développementales. Nos résultats indiquent que l’inactivation des ESCRT cause une augmentation du flux autophagique. L’inactivation de l’autophagie dans ces mutants exacerbe les défauts cellulaires alors que son induction protège de la dégradationMacroautophgagy is a catabolic process involved in the clearance of cellular components in the lysosome when cells face starvation conditions. This eukaryotic process requires the formation of double membrane vesicles named autophagosomes. Autophagy is implicated in the elimination of misfolded proteins, protein aggregates and long-lived or damaged organelles such as mitochondria, endoplasmic reticulum and peroxysomes. It is alos required for the clearance of intracellular pathogens. The material enclosed inside autophagososmes in degraded in the lysosome: nucleotides, amino-acids and fatty-acids are generated and reused for neosynthesis of macromolecules and ATP.In the present study, we are exploring the cellular and functional aspects of the autophagic pathway in Caenorhabditis elegans. We show that the genome of the worm contain two homologues of the Yeast autophagic gene, Atg8. These homlogues encode for two proteins namely, LGG-1 and LGG-2, which localize to the autophagosomal membranes. We have shown that this two proteins act synergistically in dauer formation and longevity.We have also shown that autophagy play an important role in maintaining cell homeostasis in endosomal maturation mutans. These latter mutants show defects in the ESCRT coplexes (Endosomal Sorting Complex Required for Transport). ESCRT complexes are required the recycling of cell surface receptors and for the sorting of ubiquitinated prtoteins into the multivesicular bodies. Mutations in the ESCRTs cause cellular et developmental defects. In our study, we show that autophagy is induced in these mutants and play a beneficial role in correcting cellular defects
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Hunt, Piper Reid. "Evidence for a maturation model of endosomal trafficking derived from analysis of human fibroblasts." Available to US Hopkins community, 2002. http://wwwlib.umi.com/dissertations/dlnow/3068170.
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Hannemann, Mandy [Verfasser], Stefan [Akademischer Betreuer] Eimer, Reinhard [Akademischer Betreuer] Jahn, and Nils [Akademischer Betreuer] Brose. "Dense-core vesicle maturation at the Golgi-endosomal interface in Caenorhabditis elegans / Mandy Hannemann. Gutachter: Stefan Eimer ; Reinhard Jahn ; Nils Brose. Betreuer: Stefan Eimer." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2012. http://d-nb.info/1043608400/34.
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Stroud, Evelyn Joy. "Kinetic analysis of endosome processing : maturation of early endosomes and vesicular traffic to lysosomes." Master's thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27043.
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The present study was undertaken to establish the mechanism(s) involved in the endocytic pathway, in particular, early endosome processing and delivery to the lysosomes. Two models for endosome processing have previously been proposed in the literature, namely the maturation and vesicular traffic models. The general consensus has been an early phase of intermingling of the endocytic contents markers within early endosomes that mature to form non-fusogenic late endosomes (maturation model). This maturation phase is followed by a segregation phase where intermingling of contents between vesicles no longer takes place. To establish the mechanism(s) involved in early endosome processing and delivery to lysosomes, a kinetic analysis was made using results from cellular fluid-phase uptake assays. This unique approach offers an alternative view to previous studies on the mechanisms in operation during endocytic processing. The results and conclusions made could thus confirm or disprove previously proposed mechanisms.
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GIUSTRA, MARCO DAVIDE. "Synthesis of multi-branched polymers for the stabilization of metallic nanoparticles." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/366171.
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È fondamentale progettare e monitorare tutte le fasi preparative di un sistema di drug delivery in modo tale da raggiungere un determinato sito bersaglio. Ogni parte di un nanocarrier influenza sé stesso e l'ambiente circostante. Inoltre, per ottenere campioni monodispersi, il rivestimento e le eventuali funzionalizzazioni sono fondamentali per determinare la stabilità colloidale, prevedere il comportamento in un sistema biologico e raggiungere il target di interesse. In particolar modo, la razionalizzazione dei meccanismi di internalizzazione e la quantificazione dei carrier nei siti intracellulari è ancora oggi un tema di grande interesse in ambito nanomedico.
In questo lavoro, è stata presentata una classe di polimeri multidentati di facile sintesi mostrando un'ampia applicabilità in combinazione con nanoparticelle (NPs) metalliche. I polimeri multidentati sono stati coinvolti in tre diversi progetti. Il primo progetto mirava a presentare un polimero multidentato come modello generale da applicare nel rivestimento di superfici metalliche. Per dimostrarlo sono stati effettuati diversi test prendendo in considerazione la composizione e la dimensione delle NPs. Questo polimero è stato confrontato con altri due tipi di rivestimenti comuni in letteratura. I dati ottenuti mostrano come il nuovo rivestimento fornisca una maggiore stabilità colloidale. In secondo luogo, sono stati ottenuti miglioramenti dal punto di vista della tossicità e della bio-funzionalizzazione.
Nel secondo progetto, la catena polimerica è stata modificata con un altro ligando per ampliare il campo di applicazione di questi polimeri. La scelta della molecola è basata sull'affinità per alcune superfici metalliche. In questo caso la molecola scelta è il 4-amminotiofenolo, spesso utilizzata per applicazioni SERS. Inizialmente, il polimero è stato studiato rivestendo diversi tipi di NPs metalliche (oro e argento) e sono state eseguite analisi SERS. Le dimensioni e la forma hanno giocato un ruolo chiave, in particolare con le nanoparticelle cubiche concave risultando promettenti agenti diagnostici. Nella seconda parte del progetto, le nanoparticelle cubiche d'argento sono state utilizzate come modello per la valutazione del traffico cellulare e della maturazione endosomiale. Dei test preliminari sono stati effettuati a diversi pH (per emulare le variazioni di pH nelle fasi evolutive dell'endosoma) e studi in vitro sono stati eseguiti per verificare l'uptake delle NPs nelle cellule HeLa.
Il terzo progetto mirava a utilizzare il polimero sintetizzato come precursore nella sintesi di nanoparticelle anisotropiche. La forma ottenuta inizialmente è stata quella di un petalo, ma aumentando la temperatura, i petali si sono assemblati a nanofiori con un diametro al di sopra di 100 nm. La presenza del polimero SERS-attivo rende queste nanoparticelle ottimi candidati per questa tipologia di applicazione.Designing and monitoring all the preparation steps of a drug delivery system is essential to achieve a specific target. Each part of a nanocarrier affects the batch itself and the surrounding environment. In addition, to obtain monodispersed samples, the coating and any functionalization are crucial to determine the colloidal stability, to predict the behavior with a biological system, and the reaching of the target site. In particular, the achievement of intracellular sites by rationalizing the internalization mechanisms and quantifying the carriers in the target is still today a hot topic in the nanomedical field. Here, a class of multidentate polymers was presented: a simple way to synthesize them and show their broad applicability in combination with metal NPs. Multi-branched polymers were involved in three projects. The first project aimed to present a multidentate polymer as a general model to be applied in the coating of metal surfaces. To prove this, several tests were carried out by modulating the composition and size of the NPs. This easily synthesized polymer has been compared with two types of coatings common in literature. The obtained data show how the new surfactant provides high colloidal stable nanoparticles. Secondly, this leads to improvements from the point of view of toxicity and bio-functionalization. In the second project, the ligands polymer chain was modified to increase the range of application. Moreover, the choice of the ligand was based on the affinity for certain metal surfaces. In this case, the molecule is 4-aminotiophenol which is often used for SERS applications. Initially, the versatility of the polymer was investigated by coating different types of metallic NPs (gold and silver) and then SERS analyses were performed. Size and shape played a key role, especially with cubic concave nanoparticles that are promising for diagnostics application. In the second part of the project, cubic silver nanoparticles were used as a model for the evaluation of cell trafficking and endosomal maturation. Preliminary tests of NPs have been carried out at different pH (to emulate the pH variations in the endosomal evolution stages) and in vitro studies to check the nanoparticles uptake in HeLa cells were performed. The third project aimed to use the designed polymer as precursor in the synthesis of anisotropic nanoparticles. The shape obtained is a petal form. Subsequently, with the increase of the temperature, the petals assembled to nanoflowers above 100 nm. The presence of the active SERS polymer makes these nanoparticles, excellent candidates for this application.
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Shah, Ankur H. "Adenovirus RIDalpha Regulates Endosome Maturation by Mimicking GTP-Rab7." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1181051279.
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Wang, Xiaolin. "Analysis of candidate regulators of TBC-2 and endosome maturation in «Caenorhabditis elegans»." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114348.
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The Rab5 and Rab7 GTPases are key regulators of endosome to lysosome trafficking, whose activities are positively regulated by Rab Guanine nucleotide Exchange Factors and negatively regulated by GTPase Activating Proteins (GAP). In this thesis, the nematode Caenorhabditis elegans was used as a model system to study regulation of Rab GTPase-mediated endosomal trafficking, for simple genetics and easy visualization of organelles under Differential Interference Contrast (DIC) and confocal optics. It was previously demonstrated that TBC-2 functions as a RAB-5 GAP. Loss of tbc-2 activity results in the formation of enlarged late endosomes in the intestine that require the activities of RAB-5, RAB-7 and components of the homotypic fusion and vacuole protein sorting (HOPS) complex. TBC-2 colocalizes with RAB-7 on late endosomes, and requires RAB-7 for membrane localization. My hypothesis is that RAB-7 recruits TBC-2 to late endosomes to inactivate RAB-5 and possibly RAB-7 itself, to facilitate early to late endosome maturation. The vh8 mutant was previously identified in the lab as a suppressor of the tbc-2(-) phenotype and displaces GFP::RAB-7 from vesicular membranes. It is possible that vh8 encodes for a potential RAB-7 GEF. To investigate the molecular identity of vh8, I tested candidate genes by RNAi. While none of the candidates appear to be vh8, I did find that the HOPS core complex is required for the tbc-2(-) phenotype. ARL-8, and its human homolog arl8b, have recently been shown to be important for late endosome to lysosome trafficking. To investigate whether ARL-8 is required for TBC-2 mediated early to late endosome trafficking, I performed RNAi experiments. The results of which suggest that ARL-8 functions downstream of TBC-2. ARL-8 is required for the tbc-2(-) large late endosome phenotype, but is not required for membrane localization of either TBC-2 or RAB-7.In mammalian cells, the Rac1 GTPase is able to bind Armus, a human homolog of TBC-2. That raises the possibility that RAB-7 recruits CED-10/Rac1 via TBC-2. However, I observe that in tbc-2(tm2241) mutant animals, CED-10 is still localized to vesicles. It suggests that CED-10 might be recruited to membrane via other mechanism. Active CED-10 is also crucial for phagocytosis and clearance of apoptotic cell corpses. CED-10 can be activated by the CED-5/CED-12 complex, which is proposed to be recruited and activated by PI(3,5)P2. Work from this thesis suggests that the active state might not be a requirement for CED-10 localization, as ced-5 RNAi does not change the localization of CED-10.Les GTPases Rab5 et Rab7 participent à la régulation du traffic des endosomes. L'activité de ces protéines est régulée positivement par les "Rab Guanine nucleotide Exchange Factors" (GEF) et régulée négativement par les "GTPase Activating Proteins" (GAP). Dans ce projet, le nematode Caenorhabditis elegans a été utilisé comme modèle pour étudier la régulation du traffic endosomal médié par les Rab GTPase car celui-ci est un bon modèle génétique et permet une visualisation des organites à l'aide de microscopie à constraste d'interférence différentielle et de microscopie confocale. Il a été démontré dans la passé que TBC-2 fonctionne en tant que GAP pour RAB-5. La perte de l'activité de tbc-2 résulte en la formation d'endosomes tardifs élargis dans les intestins des nématodes, qui requièrent normalement l'activité de RAB-5, RAB-7 et des constituants du complexe "homotypic fusion and vacuole protein sorting" (HOPS). TBC-2 se retrouve avec RAB-7 sur les endosomes tardifs et nécessite RAB-7 pour sa localisation sur la membrane. Notre hypothèse était que RAB-7 recrute TBC-2 aux endosomes tardifs pour inactiver RAB-5 et possiblement RAB-7, ce qui facilite la maturation des endosomes en endosomes tardifs. Le mutant vh8 a préalablement été identifié dans le laboratoire en tant que suppresseur du phénotype tbc2(-) et cause le déplacement de GFP::RAB-7 des membranes vésiculaires. Il est possible que vh8 exprime un potentiel GEF de RAB-7. Pour trouver l'identité moléculaire de vh8, nous avons testé les gènes candidats à l'aide d'ARN d'interférence (ARNi). Malgré qu'aucun des candidats ne semblaient être vh8, nous avons découvert que le complexe central de HOPS est nécessaire au phénotype tbc-2(-). ARL-8 et son homolog humain arl8b ont récessement été démontrés comme étant importants dans le traffic des endosomess tardifis aux lysosomes. Pour vérifier si ARL-8 est requis dans le traffic des endosomes médiés par TBC-2. Nos travaux à l'aide d'ARNi suggèrent qu'ARL-8 fonctionne en aval de TBC-2. ARL-8 est nécessaire à l'apparition du phénotype tbc-2(-), mais n'est pas requis pour la localisation de TBC-2 et RAB-7 à la membrane. Dans les cellules de mammifères, la GTPase Rac1 peut se lier à Armus, un homologue humain de TBC-2. Ceci suggère que RAB-7 pourrait recruter CED-10/RAC1 par l'entremise de TBC-2. Par contre, nous observons que chez les nématodes tbc-2(tm2241), CED-10 est toujours localisé sur les vésicules. Ceci suggère que CED-10 pourrait être recruté à la membrane par d'autres mécanismes. Un CED-10 activé est aussi nécessaire à la phagocytose et à la dégradation des corps cellulaires apoptotiques. CED-10 peut être activé par le complexe CED-5/CED-12, qui est possiblement recruté et activé par PI(3,5)P2. Nos travaux suggèrent par contre que l'activation de CED-10 n'est pas obligatoire à sa localisation, car l'ARNi de ced-5 ne change pas la localisation de CED-10.
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Menager, Mickaël. "Rôles de hMunc13-4 et Rab27a dans la maturation et l'exocytose des granules cytotoxiques." Paris 7, 2008. http://www.theses.fr/2008PA077102.
Full textAbstract:
L'étude de différentes pathologies du système immunitaire associée à l'apparition d'un syndrome hémophagocytaire nous a permis de mettre en évidence un rôle déterminant de la fonction cytotoxique des lymphocytes T CD8+ dans le maintien de l'homéostasie lymphocytaire. Dans pratiquement toutes les pathologies génétiquement caractérisées qui évoluent vers l'apparition d'un syndrome hémophagocytaire, un effecteur de la voie cytotoxique dépendante des granules est mis en cause. C'est le cas en particulier des défauts en protéines hMunc13-4 et Rab27a, impliquées dans l'apparition d'une lymphohistiocytose familiale de type 3 et d'un syndrome de Griscelli. Ce travail permet de montrer que la fonction cytotoxique des lymphocytes T cytotoxiques et des cellules Natural Killer nécessite la coopération entre deux types d'organelles : les granules cytotoxiques contenant les effecteurs de la lyse (granzymes, Perforine. . ) et des vésicules dîtes « d'exocytose » de type endosomal, véhiculant les effecteurs de Pexocytose (Rab27a et hMunc13-4). Ces résultats suggèrent l'existence d'un phénomène de maturation rapide des granules lytiques, induit par la formation de la synapse immunologique. Nous mettons également en évidence une nouvelle isoforme de Slp2a, Slp2a-hem, interagissant avec la forme active de Rab27a et impliquée dans les processus d'arrimage des vésicules au niveau de la synapse immunologique. Nous montrons l'existence d'une interaction entre hMunc13-4 et Rab27a dans les cellules cytotoxiques, qui coordonnerait les étapes d'arrimage et d'amorçage de la fusion des granules cytotoxiques au niveau de la synapse immunologiqueSeveral human inherited disorders are characterized by a functional impairment of the granule dependent cytotoxic pathway. Molecular characterization of these human conditions allowed to identify critical effectors of this cytotoxic pathway and highlighted the essential role of the cytotoxic activity in lymphocyte homeostasis. According to our previous work, the protein hMunc13-4 and Rab27a are one of these effectors which anomalies lead to Hemophagocytic Syndrom, in the context of Familial Hemophagocytic Lymphohistiocytosis type 3 and Griscelli Syndrome type 2. Here we show that the granule-dependent cytotoxic fonction of cytotoxic T lymphocytes and Natural Killer cells requires the cooperation of two types of organelles, the lytic granule and an endosomal-like "exocytic vesicle". In a first step of the secretory pathway, hMunc!3-4, independently of Rab27a, mediates assembly of recycling and late endosomal structures to constitute a pool of endosomal vesicles engaged into the regulated exocytic pathway. Cytotoxic-target cell recognition induces a rapid polarization of both types of organelles, which overlap and likely fuse at the cell-cell contact. In addition, hMunc13-4 has been identified as one of the effectors of Rab27a, potentially Connecting granule docking to granule priming at the Immunological Synapse. We have also shown that Rab27a recruits a previously unknown hematopoietic form of Slp2a (Slp2a-hem) on vesicular structures in peripheral CTLs. Following CTL-target cell conjugate formation, the Slp2a-hem/Rab27a complex colocalizes with perforin-containing granules at the immunological synapse, where it binds to the plasma membrane through its C2 domains
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Basque, Julie. "Modification pharmacologique de l'environnement calcique et du pH acide du système trans-Golgi network/endosomes afin d'inhiber la maturation du pro-TGF[bêta]1." Mémoire, Université de Sherbrooke, 2007. http://savoirs.usherbrooke.ca/handle/11143/3914.
Full textAbstract:
La fibrose pulmonaire idiopathique (FPI) est une maladie chronique et progressive où aucun traitement efficace n'existe à jour.La FPI se définit comme un désordre épithéliale-fibroblaste caractérisé par la présence excessive de facteurs profibrotiques dont majoritairement du facteur de croissance tumorale de type [bêta]1 (TGF[bêta]1) qui entraîne des effets néfastes importants au niveau de la production de matrice extracellulaire. Le TGF[bêta]1 est une cytokine 'homodimérique de 25 kDa qui est initialement synthétisée à partir d'un précurseur nommé pré-pro-TGF[bêta]1. Suite au clivage du peptide signal, le précurseur est clivé au site [indice supérieur 275]Arg-His-Arg-Arg[indice supérieur 278] par la furine, une enzyme de la famille des sérines protéases lors de son passage dans le trans-Golgi network (TGN). Puisque la furine est impliquée dans la maturation du TGF[bêta]1 et que cette enzyme requiert la présence de calcium et d'un pH acide dans le TGN pour la maturation de ses substrats, nous avons étudié l'effet d'agents modifiant l'environnement calcique à pH acide du système TGN/endosomes sur la diminution de la maturation du TGF[bêta]1. Par buvardage de type Western à l'aide d'un anticorps neutralisant dirigé contre le précurseur complet du TGF[bêta]1 (50 kDa) et la pro-région LAP (40 kDa), nous avons observé que la modification du pH du TGN suite à l'incubation de la lignée cellulaire épithéliale alvéolaire A549 avec la bafilomycine, le NH[indice inférieur 4]Cl et la monensine diminuait la maturation du pro-TGF[bêta]1. De plus, un dosage antigénique (ELISA) du TGF[bêta]1 a permis de montrer que cette diminution de la maturation causait ainsi une diminution du niveau de TGF[bêta]1 mature retrouvé dans le milieu extracellulaire des cellules A549. De façon similaire, nous avons montré que des médicaments (le la classe des anti-malariens (chloroquine, hydroxychloroquine, azithromycine et amodiaquine), considérés comme des bases faibles, avaient la capacité de diminuer de façon significative la maturation et donc le niveau de TGF[bêta]1 mature des cellules A549 et des cellules gliales T98G de façon dose-dépendante. Par la suite, nous avons montré par buvardage de type Western et par ELISA que la modification de l'environnement calcique du TGN suite à l'exposition de la lignée cellulaire A549 avec les molécules A23187, EGTA et thapsigargine diminuait la maturation et donc le niveau de TGF[bêta]1 mature. De la même façon, nous avons observé que la doxycycline, un antibiotique de la classe (les tétracyclines connu pour être un chélateur de calcium, diminuait la maturation et le niveau de TGF[bêta]1 des cellules A549.
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Basque, Julie. "Modification pharmacologique de l'environnement calcique et du pH acide du système trans-Golgi network/endosomes afin d'inhiber la maturation du pro-TGFB[bêta]1." [S.l. : s.n.], 2007.
Find full textBook chapters on the topic "Endosomal maturation"
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Podinovskaia, Maria, and Anne Spang. "The Endosomal Network: Mediators and Regulators of Endosome Maturation." In Endocytosis and Signaling, 1–38. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96704-2_1.
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Murphy, Robert F., Mario Roederer, David M. Sipe, Cynthia Corley Cain, and Russell B. Wilson. "Endosomal pH Regulation and the Maturation Model for Lysosome Biogenesis." In Endocytosis, 91–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_11.
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Mulligan, Ryan J., Chan Choo Yap, and Bettina Winckler. "Endosomal Transport to Lysosomes and the Trans-Golgi Network in Neurons and Other Cells: Visualizing Maturational Flux." In Methods in Molecular Biology, 595–618. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2639-9_36.
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Manil-Ségalen, Marion, Emmanuel Culetto, Renaud Legouis, and Christophe Lefebvre. "Interactions Between Endosomal Maturation and Autophagy." In Methods in Enzymology, 93–118. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-397926-1.00006-8.
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Benarroch, Eduardo E. "Vesicular Trafficking." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 106–25. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0007.
Full textAbstract:
Normal cell function depends on the appropriate synthesis, maturation, sorting, and delivery of fully processed proteins and other macromolecules to specific intracellular compartments; uptake of material from the cell exterior; and regulated intracellular processing and degradation of proteins, lipids, complex carbohydrates, abnormal aggregates, and senescent organelles. These fundamental functions involve secretory, endocytic, and autophagic pathways. The secretory pathway is responsible for protein maturation, sorting, and delivery of transmembrane and secreted proteins from their site of synthesis to their final destinations. Synaptic vesicle exocytosis is a special form of secretion that allows rapid communication between neurons. The endocytic pathway starts with the internalization of material via endosomes. Endosomal content can be transported back to the cell body, recycled to cell compartments, or delivered for degradation by the lysosome. Abnormal protein aggregates or damaged organelles undergo autophagy, which involves formation of an autophagosome and degradation by the lysosome. Impaired vesicular trafficking is a fundamental mechanism in a large number of neurodegenerative disorders, including hereditary spastic paraplegia, lower motor neuron syndromes, and Parkinson disease.
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Rai, Ashim, Divya Pathak, and Roop Mallik. "Dynein in Endosome and Phagosome Maturation." In Handbook of Dynein, 225–50. Jenny Stanford Publishing, 2019. http://dx.doi.org/10.1201/9780429021312-9.
Full textConference papers on the topic "Endosomal maturation"
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Hu, Xian. "A Fast Projection Imaging Method for the Quantification of the Dynamics of Endosome Maturation." In European Light Microscopy Initiative 2021. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.elmi2021.74.
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