Academic literature on the topic 'Endosome'
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Journal articles on the topic "Endosome"
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Liu, Kai, Ruxiao Xing, Youli Jian, et al. "WDR91 is a Rab7 effector required for neuronal development." Journal of Cell Biology 216, no. 10 (2017): 3307–21. http://dx.doi.org/10.1083/jcb.201705151.
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Early-to-late endosome conversion, which is essential for delivery of endosomal cargoes to lysosomes, requires switching of early endosome–specific Rab5 and PtdIns3P to late endosome–specific Rab7 and PtdIns(3,5)P2. In this study, we identify the WD40-repeat protein WDR91 as a Rab7 effector that couples Rab switching with PtdIns3P down-regulation on endosomes. Loss of WDR91 greatly increases endosomal PtdIns3P levels, arresting endosomes at an intermediate stage and blocking endosomal–lysosomal trafficking. WDR91 is recruited to endosomes by interacting with active guanosine triphosophate–Rab7 and inhibits Rab7-associated phosphatidylinositol 3-kinase activity. In mice, global Wdr91 knockout causes neonatal death, whereas brain-specific Wdr91 inactivation impairs brain development and causes postnatal death. Mouse neurons lacking Wdr91 accumulate giant intermediate endosomes and exhibit reduced neurite length and complexity. These phenotypes are rescued by WDR91 but not WDR91 mutants that cannot interact with Rab7. Thus, WDR91 serves as a Rab7 effector that is essential for neuronal development by facilitating endosome conversion in the endosome–lysosome pathway.
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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 (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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Schmid, S., R. Fuchs, M. Kielian, A. Helenius, and I. Mellman. "Acidification of endosome subpopulations in wild-type Chinese hamster ovary cells and temperature-sensitive acidification-defective mutants." Journal of Cell Biology 108, no. 4 (1989): 1291–300. http://dx.doi.org/10.1083/jcb.108.4.1291.
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During endocytosis in Chinese hamster ovary (CHO) cells, Semliki Forest virus (SFV) passes through two distinct subpopulations of endosomes before reaching lysosomes. One subpopulation, defined by cell fractionation using free flow electrophoresis as "early endosomes," constitutes the major site of membrane and receptor recycling; while "late endosomes," an electrophoretically distinct endosome subpopulation, are involved in the delivery of endosomal content to lysosomes. In this paper, the pH-sensitive conformational changes of the SFV E1 spike glycoprotein were used to study the acidification of these defined endosome subpopulations in intact wild-type and acidification-defective CHO cells. Different virus strains were used to measure the kinetics at which internalized SFV was delivered to endosomes of pH less than or equal to 6.2 (the pH at which wild-type E1 becomes resistant to trypsin digestion) vs. endosomes of pH less than or equal to 5.3 (the threshold pH for E1 of the SFV mutant fus-1). By correlating the kinetics of acquisition of E1 trypsin resistance with the transfer of SFV among distinct endosome subpopulations defined by cell fractionation, we found that after a brief residence in vesicles of relatively neutral pH, internalized virus encountered pH less than or equal to 6.2 in early endosomes with a t1/2 of 5 min. Although a fraction of the virus reached a pH of less than or equal to 5.3 in early endosomes, most fus-1 SFV did not exhibit the acid-induced conformational change until arrival in late endosomes (t1/2 = 8-10 min). Thus, acidification of both endosome subpopulations was heterogeneous. However, passage of SFV through a less acidic early endosome subpopulation always preceded arrival in the more acidic late endosome subpopulation. In mutant CHO cells with temperature-sensitive defects in endosome acidification in vitro, acidification of both early and late endosomes was found to be impaired at the restrictive temperature (41 degrees C). The acidification defect was also found to be partially penetrant at the permissive temperature, resulting in the inability of any early endosomes in these cells to attain pH less than or equal to 5.3. In vitro studies of endosomes isolated from mutant cells suggested that the acidification defect is most likely in the proton pump itself. In one mutant, this defect resulted in increased sensitivity of the electrogenic H+ pump to fluctuations in the endosomal membrane potential.
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Liu, Kai, Youli Jian, Xiaojuan Sun, et al. "Negative regulation of phosphatidylinositol 3-phosphate levels in early-to-late endosome conversion." Journal of Cell Biology 212, no. 2 (2016): 181–98. http://dx.doi.org/10.1083/jcb.201506081.
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Phosphatidylinositol 3-phosphate (PtdIns3P) plays a central role in endosome fusion, recycling, sorting, and early-to-late endosome conversion, but the mechanisms that determine how the correct endosomal PtdIns3P level is achieved remain largely elusive. Here we identify two new factors, SORF-1 and SORF-2, as essential PtdIns3P regulators in Caenorhabditis elegans. Loss of sorf-1 or sorf-2 leads to greatly elevated endosomal PtdIns3P, which drives excessive fusion of early endosomes. sorf-1 and sorf-2 function coordinately with Rab switching genes to inhibit synthesis of PtdIns3P, allowing its turnover for endosome conversion. SORF-1 and SORF-2 act in a complex with BEC-1/Beclin1, and their loss causes elevated activity of the phosphatidylinositol 3-kinase (PI3K) complex. In mammalian cells, inactivation of WDR91 and WDR81, the homologs of SORF-1 and SORF-2, induces Beclin1-dependent enlargement of PtdIns3P-enriched endosomes and defective degradation of epidermal growth factor receptor. WDR91 and WDR81 interact with Beclin1 and inhibit PI3K complex activity. These findings reveal a conserved mechanism that controls appropriate PtdIns3P levels in early-to-late endosome conversion.
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Nordeng, Tommy W., Tone F. Gregers, Thomas Lasker Kongsvik, et al. "The Cytoplasmic Tail of Invariant Chain Regulates Endosome Fusion and Morphology." Molecular Biology of the Cell 13, no. 6 (2002): 1846–56. http://dx.doi.org/10.1091/mbc.01-10-0478.
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The major histocompatibility complex class II associated invariant chain (Ii) has been shown to inhibit endocytic transport and to increase the size of endosomes. We have recently found that this property has a significant impact on antigen processing and presentation. Here, we show in a cell-free endosome fusion assay that expression of Ii can increase fusion after phosphatidylinositol 3-kinase activity is blocked by wortmannin. In live cells wortmannin was also not able to block formation of the Ii-induced enlarged endosomes. The effects of Ii on endosomal transport and morphology depend on elements within the cytoplasmic tail. Data from mutagenesis analysis and nuclear magnetic resonance-based structure calculations of the Ii cytoplasmic tail demonstrate that free negative charges that are not involved in internal salt bridges are essential for both interactions between the tails and for the formation of enlarged endosomes. This correlation indicates that it is interactions between the Ii cytoplasmic tails that are involved in endosome fusion. The combined data from live cells, cell-free assays, and molecular dynamic simulations suggest that Ii molecules on different vesicles can promote endosome docking and fusion and thereby control endosomal traffic of membrane proteins and endosomal content.
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de Wit, Heidi, Yael Lichtenstein, Regis B. Kelly, Hans J. Geuze, Judith Klumperman, and Peter van der Sluijs. "Rab4 Regulates Formation of Synaptic-like Microvesicles from Early Endosomes in PC12 Cells." Molecular Biology of the Cell 12, no. 11 (2001): 3703–15. http://dx.doi.org/10.1091/mbc.12.11.3703.
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Early endosomes in PC12 cells are an important site for the formation of synaptic-like microvesicles and constitutive recycling vesicles. By immunogold electron microscopy, the small GTPase rab4 was localized to early endosomes and numerous small vesicles in the cell periphery and Golgi area of PC12 cells. Overexpression of GTPase-deficient Q67Lrab4 increased the number of early endosome-associated and cytoplasmic vesicles, whereas expression of GDP-bound S22Nrab4 significantly increased the length of early endosomal tubules. In parallel, Q67Lrab4 induced a shift in rab4, VAMP2, and TfR label from early endosomes to peripheral vesicles, whereas S22Nrab4 increased early endosome labeling of all three proteins. These observations were corroborated by early endosome budding assays. Together, our data document a thus far unrecognized role for rab4 in the formation of synaptic-like microvesicles and add to our understanding of the formation of constitutive recycling vesicles from early endosomes.
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Leung, Som-Ming, Wily G. Ruiz, and Gerard Apodaca. "Sorting of Membrane and Fluid at the Apical Pole of Polarized Madin-Darby Canine Kidney Cells." Molecular Biology of the Cell 11, no. 6 (2000): 2131–50. http://dx.doi.org/10.1091/mbc.11.6.2131.
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When fluid-phase markers are internalized from opposite poles of polarized Madin-Darby canine kidney cells, they accumulate in distinct apical and basolateral early endosomes before meeting in late endosomes. Recent evidence suggests that significant mixing of apically and basolaterally internalized membrane proteins occurs in specialized apical endosomal compartments, including the common recycling endosome and the apical recycling endosome (ARE). The relationship between these latter compartments and the fluid-labeled apical early endosome is unknown at present. We report that when the apical recycling marker, membrane-bound immunoglobulin A (a ligand for the polymeric immunoglobulin receptor), and fluid-phase dextran are cointernalized from the apical poles of Madin-Darby canine kidney cells, they enter a shared apical early endosome (≤2.5 min at 37°C) and are then rapidly segregated from one another. The dextran remains in the large supranuclear EEA1-positive early endosomes while recycling polymeric immunoglobulin receptor–bound immunoglobulin A is delivered to a Rab11-positive subapical recycling compartment. This latter step requires an intact microtubule cytoskeleton. Receptor-bound transferrin, a marker of the basolateral recycling pathway, has limited access to the fluid-rich apical early endosome but is excluded from the subapical elements of the Rab11-positive recycling compartment. We propose that the term ARE be used to describe the subapical Rab11-positive compartment and that the ARE is distinct from both the transferrin-rich common recycling endosome and the fluid-rich apical early endosome.
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Wang, Yi, Steven Pennock, Xinmei Chen, and Zhixiang Wang. "Endosomal Signaling of Epidermal Growth Factor Receptor Stimulates Signal Transduction Pathways Leading to Cell Survival." Molecular and Cellular Biology 22, no. 20 (2002): 7279–90. http://dx.doi.org/10.1128/mcb.22.20.7279-7290.2002.
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ABSTRACT In spite of intensified efforts to understand cell signaling from endosomes, there is no direct evidence demonstrating that endosomal signaling is sufficient to activate signal transduction pathways and no evidence to demonstrate that endosomal signaling is able to produce a biological outcome. The lack of breakthrough is due in part to the lack of means to generate endosomal signals without plasma membrane signaling. In this paper, we report the establishment of a system to specifically activate epidermal growth factor (EGF) receptor (EGFR) when it endocytoses into endosomes. We treated cells with EGF in the presence of AG-1478, a specific EGFR tyrosine kinase inhibitor, and monensin, which blocks the recycling of EGFR. This treatment led to the internalization of nonactivated EGF-EGFR complexes into endosomes. The endosome-associated EGFR was then activated by removing AG-1478 and monensin. During this procedure we did not observe any surface EGFR phosphorylation. We also achieved specific activation of endosome-associated EGFR without using monensin. By using this system, we provided original evidence demonstrating that (i) the endosome can serve as a nucleation site for the formation of signaling complexes, (ii) endosomal EGFR signaling is sufficient to activate the major signaling pathways leading to cell proliferation and survival, and (iii) endosomal EGFR signaling is sufficient to suppress apoptosis induced by serum withdrawal.
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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 (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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Stoorvogel, W., V. Oorschot, and H. J. Geuze. "A novel class of clathrin-coated vesicles budding from endosomes." Journal of Cell Biology 132, no. 1 (1996): 21–33. http://dx.doi.org/10.1083/jcb.132.1.21.
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Clathrin-coated vesicles transport selective integral membrane proteins from the plasma membrane to endosomes and from the TGN to endosomes. Recycling of proteins from endosomes to the plasma membrane occurs via unidentified vesicles. To study this pathway, we used a novel technique that allows for the immunoelectron microscopic examination of transferrin receptor-containing endosomes in nonsectioned cells. Endosomes were identified as separate discontinuous tubular-vesicular entities. Each endosome was decorated, mainly on the tubules, with many clathrin-coated buds. Endosome-associated clathrin-coated buds were discerned from plasma membrane-derived clathrin-coated vesicles by three criteria: size (60 nm and 100 nm, respectively), continuity with endosomes, and the lack of labeling for alpha-adaptin. They were also distinguished from TGN-derived clathrin-coated vesicles by their location at the periphery of the cell, size, and the lack of labeling for gamma-adaptin. In the presence of brefeldin A, a large continuous endosomal network was formed. Transferrin receptor recycling as well as the formation of clathrin-coated pits at endosomes was inhibited in the presence of brefeldin A. Together with the localization of transferrin receptors at endosome-associated buds, this indicates that a novel class of clathrin-coated vesicles serves an exit pathway from endosomes. The target organelles for endosome-derived clathrin-coated vesicles remain, however, to be identified.
Dissertations / Theses on the topic "Endosome"
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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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Stimpson, Helen Elizabeth Margaret. "Sorting into the yeast endosome." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615138.
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Legalatladi, Seetsela. "The kinetics of endosome processing." Master's thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27047.
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The present thesis looks at the behaviour of internalised cell surface-derived membrane marker in comparison with the behaviour of endocytosed HRP (horse-radish peroxidase) as a fluid-phase contents marker. The pooling and/or segregation in the endosome was measured by determining co-localization with HRP. Colocalization of the two markers in the endosome is studied by using the ability of HRP to catalyse the crosslinking of membrane marker in endosomes with DAB (3,3'-diaminobenzidine), rendering the membrane marker detergent insoluble. To study the kinetic behaviour of membrane marker, radioactive galactose was covalently bound to cell-surface glycoconjugates on mouse macrophage-cells, P388D₁, as catalysed by galactosyltransferase. This provided a general membrane marker. After endocytosis-derived redistribution of membrane marker between the cell surface and endosomal membrane, a steady state was established with about 16% of the label on internal membranes. The bulk of the label on the cell surface was removable by subsequent treatment with β-galactosidase.
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McKenzie, Jenna Elyse. "The recycling endosome is required for transport of retrograde toxins." Diss., University of Iowa, 2009. https://ir.uiowa.edu/etd/406.
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Shiga toxin and cholera toxin are members of the AB5 family of protein exotoxins. The A subunit is the enzymatic subunit, whereas the pentameric B subunit binds cell surface receptors and carries the A subunit to the endoplasmic reticulum (ER) where it can be released into the cytosol. The B-subunits (STxB or CTxB) mediate toxin traffic along the retrograde pathway from the plasma membrane to the ER via early/recycling endosomes and the Golgi apparatus. It is unknown if STxB requires transport through the Golgi, or if it is just kinetically favorable. It is also unknown if the recycling endosome (RE) plays a role in the retrograde transport of STxB and CTxB. The first goal of this dissertation research was to demonstrate that transport through the Golgi is required for STxB to reach the ER. Using aluminum fluoride treatment, a simple temperature block, and cytoplast studies, I show that Golgi transport is necessary for STxB to reach the ER. The second goal of this dissertation research was to tease apart how STxB and CTxB move through early and recycling endosomes as well as elucidate a mechanism of how STxB exits endosomes en route to the Golgi. The role of the RE in STxB and CTxB transport is unclear. I used transferrin colocalization and temperature block studies to show that STxB and CTxB traffic through the RE. I then used HRP ablation of the RE to show that STxB requires the RE to reach the Golgi. I also examined the role of an RE-specific protein, EHD1, in exit of STxB from the RE. EHD1 has been previously shown to regulate recycling Tfn exit from the RE but its role in STxB transport is unknown. Expression of a dominant negative form of EHD1 arrested STxB at the RE and prevented it from reaching the Golgi. Together, these results suggest that STxB and CTxB transit the RE, STxB requires a functional RE for normal retrograde trafficking, and that STxB exit from the RE is regulated by EHD1.
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Hernández, Pérez Inés. "Kazrin C Controls Endocytic Trafficking and is a Double Regulator of Actin Polymerisation and Microtubule Transport." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/671167.
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Les cèl·lules eucariotes internalitzen i redistribueixen les molècules de la superfície a través de la ruta endocítica. Aquest és un procés clau per a l’adquisició de nutrients i el catabolisme que també controla l’exposició de receptors i complexos d’adhesió cel·lular, entre d’altres. Treballs anteriors del nostre laboratori van identificar la kazrina C com una proteïna que bloquejava l’endocitosi depenent de clatrina (CME) quan es sobreexpressava.
El treball exposat a aquesta tesi confirma el paper de la kazrina en CME, ja que les cèl·lules KO de kazrina generades pel sistema de CRISPR-cas9 no van internalitzar correctament la transferrina (Tfn), un marcador endocític. La kazrina C va co-localitzar amb marcadors d’unions adherents com la N-cadherina a la membrana plasmàtica i en estructures intracel·lulars. De fet, un fraccionament subcel·lular va demostrar la presència de la kazrina als early endosomes (EEs). En concordança amb un paper de la kazrina a EEs, la seva depleció va provocar una acumulació de EEs que contenien N-cadherina, que a més tenien una distribució més perifèrica que a les cèl·lules control. Les cèl·lules KO de kazrina no transportaven Tfn cap al compartiment de reciclatge endocític (ERC) i tenien el conseqüent defecte al reciclatge de Tfn. Tots els fenotips en les cèl·lules KO de kazrina es van recuperar amb la re-expressió de GFP-kazrina C però no amb la de GFP. Aquestes evidències apunten cap a un paper de la kazrina C al reciclatge endosomal i al transport de EEs cap al ERC. En consonància amb aquesta hipòtesi, la depleció de kazrina va causar defectes en processos cel·lulars que depenen del reciclatge a través del ERC, com ara la migració cel·lular i la citoquinesi.
Aquest estudi també va analitzar els mecanismes moleculars de la funció de la kazrina C en el tràfic endocític. Es va demostrar que la kazrina C interacciona amb els motors associats a microtúbuls kinesina-1 i dineïna, i que s’uneix directament a la cadena intermitja lleugera de la dineïna, LIC1. De fet, la kazrina C té un domini coiled-coil similar als dels adaptadors de la dineïna. La kazrina C també té en comú amb aquests adaptadors la localització a la regió pericentriolar, on semblava atrapar EEs. Per tant, proposem que la kazrina C promou el transport de EEs a través de microtúbuls, probablement com un adaptador de EEs i la dineïna. En la mateixa línia, aquest i anteriors estudis del laboratori van mostrar una interacció directa i co-localitzacions parcials de la kazrina C amb components de EEs, com l’adaptador de clatrina AP-1 i les GTPases EHD1/3. A més, la kazrina C va interaccionar amb PI3P i amb la PI3K de classe III, i la seva depleció va causar un augment als nivells endosomals de la sonda de PI3P GFP-FYVE. Finalment, establim una relació entre la kazrina C i un altre element clau del trànsit endocític: la maquinària de polimerització d’actina associada a Arp2/3. Es van observar interaccions directes amb la cortactina i el N-WASP, així com la co-localització de la GFP-kazrina C i la cortactina a la membrana plasmàtica i estructures intracel·lulars. A més, la depleció de la kazrina va provocar una reducció en l’actina ramificada cortical i un augment en l’endosomal.
En conjunt, hem provat una funció de la kazrina C al reciclatge endosomal i proposem que aquesta funció ocorre a través de la regulació del transport a través de microtúbuls, la polimerització d’actina i el metabolisme de PI3P.Las células eucariotas internalizan y redistribuyen las moléculas de su superficie a través de la ruta endocítica. Este es un proceso clave para la adquisición de nutrientes y el catabolismo que también controla la exposición de receptores y complejos de adhesión celular, entre otros. Trabajos anteriores de nuestro laboratorio identificaron la kazrina C como una proteína que bloqueaba la endocitosis dependiente de clatrina (CME) cuando se sobreexpresaba. El trabajo expuesto en esta tesis confirma el papel de la kazrina en la CME, al demostrar que células KO de kazrina generadas por el sistema de CRISPR-cas9 no internalizaban correctamente la transferrina (Tfn), un marcador endocítico. La kazrina C co-localizó con marcadores de uniones adherentes como la N-cadherina en la membrana plasmática y en estructuras intracelulares. De hecho, un fraccionamiento subcelular demostró la presencia de la kazrina en endosomas tempranos (EEs). Además, la depleción de la kazrina provocó una acumulación de EEs con N-cadherina, y estos tenían una distribución más periférica que en las células control, lo cual es coherente con un papel de la kazrina en EEs. Las células KO de kazrina incubadas con Tfn no transportaban el cargo hacia el compartimento de reciclaje endocítico (ERC) y tenían el consiguiente defecto en el reciclaje de Tfn. Todos los fenotipos en las células KO de kazrina se recuperaron con la re-expresión de GFP-kazrina C pero no con la de GFP. Estas evidencias apuntan hacia un papel de la kazrina C en el reciclaje endosomal y el transporte de EEs hacia el ERC. De acuerdo con esta hipótesis, la depleción de la kazrina causó defectos en procesos celulares que dependen del reciclaje a través del ERC, tales como la migración celular y la citoquinesis. Este estudio también analiza los mecanismos moleculares de la función de la kazrina C en el tráfico endocítico. Se demostró que la kazrina C interacciona con los motores asociados a microtúbulos kinesina-1 y dineína, y que se une directamente a la cadena intermedia ligera de la dineína, LIC1. De hecho, la kazrina C tiene un dominio coiled-coil similar a los de los adaptadores de la dineína. La kazrina C tiene también en común con estos adaptadores su localización en la región pericentriolar, donde parecía atrapar EEs. Por lo tanto, proponemos que la kazrina C promueve el transporte de EEs a través de microtúbulos, probablemente como un adaptador de EEs y la dineína. En consonancia, este y anteriores estudios del laboratorio mostraron una interacción directa y co-localizaciones parciales de la kazrina C con componentes de EEs, tales como el adaptador de clatrina AP-1 y las GTPasas EHD1/3. Además, la kazrina C interaccionó con PI3P y con la PI3K de clase III, y su depleción causó un aumento en los niveles endosomales de la sonda de PI3P GFP-FYVE. Por último, hemos establecido una relación entre la kazrina C y otro elemento clave del tráfico endocítico: la maquinaria de polimerización de actina asociada a Arp2/3. Se observaron interacciones directas con la cortactina y el N-WASP, así como la co-localización de la GFP-kazrina C y la cortactina en la membrana plasmática y estructuras intracelulares. La depleción de la kazrina causó una reducción en la actina ramificada cortical y un aumento en la endosomal. En conjunto, probamos una función de la kazrina C en el reciclaje endosomal y proponemos que esta función está mediada por la regulación del transporte a través de microtúbulos, la polimerización de actina y el metabolismo de PI3P.
Eukaryotic cells internalise and redistribute the molecules from their surface through the endocytic pathway. This process is key to nutrient uptake and catabolism, and controls the surface exposure of signalling receptors and cell adhesion complexes, among others. Previous work in the laboratory identified kazrin C as a protein that blocked Clathrin-Mediated Endocytosis (CME) when overexpressed. The work presented in this thesis further supported the role of kazrin in CME, as kazrin KO cells generated with the CRISPR-cas9 system were defective in the uptake of the endocytic marker Transferrin (Tfn). Kazrin C co-localised with markers of adherence junctions, such as N-cadherin, at the plasma membrane and on intracellular structures. Indeed, subcellular fractionation analysis showed the localisation of kazrin in Early Endosomes (EEs). Consistent with a role of kazrin in EEs, kazrin depletion caused an accumulation of N-cadherin-loaded EEs, which showed a more peripheral distribution as compared to WT cells. Kazrin KO cells loaded with Tfn were unable to transport the cargo towards the Endocytic Recycling Compartment (ERC) and had a concomitant defect in Tfn recycling. All phenotypes on KO cells were recovered by the re-expression of GFP-kazrin C but not GFP. These evidences indicated a role of kazrin C in endosomal recycling and the transport of EEs towards the ERC. In agreement with this hypothesis, kazrin depletion caused defects in cellular processes that strongly depend on recycling through the ERC, such as cell migration and cytokinesis. This study also analysed the molecular mechanisms of kazrin C function in endocytic traffic. Kazrin C was found to interact with the microtubule motors kinesin-1 and dynein, and directly bind to the dynein Light Intermediate Chain LIC1. In fact, kazrin C contains a coiled-coil domain similar to those found in dynein adaptors. Also similar to those, GFP-kazrin C localised to the pericentriolar region, where it seemed to trap EEs. Therefore, we proposed that kazrin C promoted microtubule-dependent transport of EEs, possibly as an EE dynein adaptor. Accordingly, this and previous studies in the laboratory showed direct interactions and partial co-localisations of kazrin C with EE components, such as the AP-1 clathrin adaptor complex and EHD1/3 GTPases. In addition, kazrin C interacted with PI3P and the class III PI3K, and its depletion caused an increase in the endosomal levels of the PI3P probe GFP-FYVE. Finally, we linked kazrin C with another player in endocytic traffic: the Arp2/3-associated machinery for actin polymerisation. Direct interactions were observed with cortactin and N-WASP, as well as co-localisation of GFP-kazrin C with cortactin at the plasma membrane and intracellular structures. Moreover, kazrin depletion caused a reduction in cortical and an increase in endosomal branched actin. Altogether, we proved that kazrin C functions in endosomal recycling and propose that this function is mediated by the regulation of microtubule-dependent transport, actin polymerisation and PI3P metabolism.
Universitat Autònoma de Barcelona. Programa de Doctorat en Bioquímica, Biologia Molecular i Biomedicina
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Schuster, Martin. "Motor cooperation in bi-directional early endosome motility." Thesis, University of Exeter, 2011. http://hdl.handle.net/10036/3169.
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In mammalian cells and fungi, early endosomes form a dynamic compartment that undergoes bi-directional motility along microtubules. Previous work has shown that in the model system Ustilago maydis early endosome motility involves the opposing motor proteins dynein and kinesin-3. Here I performed a detailed analysis of the role of the motors in early endosome motility, using quantitative live cell imaging of kinesin-3, dynein and the endosomal GTPase Rab5a. In the first part of my work, I analysed the role of dynein at MT plus-ends, where the motor forms a strong accumulation that was thought to be involved in capturing early endosomes. I could demonstrate that ~55 dynein motors build up the dynein accumulation. In collaboration with Ms. Congping Lin and Prof. Peter Ashwin (Institute for Mathematics, Exeter), I found theoretical evidence that ~25 dynein motors concentrate and leave the plus-ends stochastically. In addition, dynein motors are captured by an interaction of dynactin and the plus-end binding protein EB1. Together both mechanisms increase the number of motors, which ensures that EEs will be loaded onto dynein before they reach the end of their track. In a second project, I provide evidence that loading of dynein is not restricted to the plus-ends. Instead, dynein leaves the plus-ends and is able to bind to kinesin-3 delivered early endosomes, which changes their transport direction from anterograde to retrograde. Kinesin-3 remains bound to these retrograde EEs. When dynein leaves the organelle, it switches back to anterograde motility. Interestingly, a single dynein wins over three to five kinesin-3 motors. I discuss these findings in the light of current motor cooperation concepts. In a third part, I demonstrated that kinesin-3 has an unexpected role in long-range retrograde endosome motility. In contrast, dynein is only responsible for the distal 10-20 µm. This is possible because most of the hyphal cells contain a symmetric and bi-polar MT array. This MT organization is reminiscent of that in dendrites. Kinesin-3-based retrograde motility is required to mix the organelles and might support long-range communication between both cell poles.
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Cook, N. R. "Reconstitution of TGN to endosome transport in vitro." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597930.
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The trans-Golgi network (TGN) is one of the major intracellular membrane sorting stations in the cell. Here a number of specific proteins are segregated from the pathway of constitutive secretion and transported to a variety of membrane bound organelles. It is thought that newly synthesised lysosomal components are sorted here for delivery to the endocytic pathway. Examples of such proteins are a number of highly glycosylated integral membrane proteins enriched in the limiting membrane of lysosomes. The majority of these proteins are believed to reach this compartment by direct transport from the TGN to endosomes without prior delivery to the cell surface. However the precise membrane trafficking events and the molecular machinery governing this process are currently poorly understood. To get new insight into transport from the TGN to endosomes I focused upon the integral membrane protein lysosomal glycoprotein 120 (lsp120). Tyrosine sulphation has been used in a number of previous studies to specifically label proteins in the TGN. Thus to more closely define the trafficking of lgp120 I created chimeras of this protein incorporating potential tyrosine sulphation motifs and introduced a lumenally oriented modified chicken avidin molecule to enable collection of the synthetic protein in endosomes. Stable expression of this chimera in HeLa cells demonstrated that it was efficiently delivered to lysosomes and this was mediated by the tyrosine based signal in its cytoplasmic tail. The chimera could be specifically labelled with radioactive sulphate and bound biotin with high affinity. This formed the basis of novel assays to measure transport from the TGN to endosomes both in the intact cell and in vitro. In each instance delivery to endosomes was determined by binding of the sulphated chimera to internalised biotinylated immunoglobulin in sealed membrane bound compartments. This new approach indicated that newly synthesised lysosomal membrane proteins are delivered directly to early endosomes.
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Senic-Matuglia, Francesca. "RAB11, une petite GTPase des endosomes de recyclage : étude de trois de ses partenaires et de son rôle dans la mélalogénèse." Paris 11, 2002. http://www.theses.fr/2002PA112220.
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Rab 11 est une GTPase principalement associée au compartiment endosomal de recyclage (ERC) où elle joue un rôle d'organisateur de ces membranes. Dans les cellules Mnt1, Rab11 colocalise partiellement avec la forme immature de Pmel17, une protéine de la matrice mélanosomale. La surexpression de Rab11wt et Q70L perturbe la distribution de la forme mature de Pmel17 et induit une diminution de la mélanine intracellulaire. Nous avons démontré que Rab11 joue un rôle dans la maturation de Pmel17, puisque le mutant Q70L induit une accumulation d'une de ses formes précurseurs. De plus, Rab11 interagit avec la queue cytoplasmique de Pmel17. Trois nouveaux partenaires de Rab11 ont été étudié. Le premier correspond à la chaîne Beta3B du complexe adaptateur AP-3. Nous avons démontré que les mélanocytes Mnt1 expriment la sous-unité Beta3B et qu'elle colocalise partiellement avec Rab11. A l'aide d'un essai in vitro, nous avons démontré que Rab11 intervient dans le recrutement du complexe AP3 neuronal sur les membranes du ERC. Nos données suggèrent un rôle de Rab11 dans la maturation de Pmel17 lors de son passage par des compartiments endosomaux de recyclage vers les structures mélanosomales. Au niveau du ERC, l'interaction Rab11/AP-3BetaB pourrait intervenir dans la ségrégation de Pmel17. Le deuxième partenaire correspond à RCP, une protéine interagissant avec Rab11 et Rab4. Nos résultats démontrent que RCP est une nouvelle protéine impliquée dans le recyclage endosomal. Enfin, le dernier partenaire correspond à la protéine Rab3lP, homologue des deux GEF Sec2p et GRAB et interagissant aussi avec Rab3. In vitro, nous avons mis en évidence une activité d'échange qui est pourtant plutôt faible. Néanmoins, in vivo, par des techniques de FRAP, nous avons obtenu des résultats qui confirment une activité GEF de Rab3IP sur Rab11. La surexpression de Rab3IP induit une redistribution intracellulaire du TfR analogue à celle induite par les formes mutantes constitutivement actives de Rab11Rab11 is a small GTPase localized on endosomal recycling compartment (ERC) membranes and implicated in membrane organization and protein recycling to plasma membrane. The molecular mechanisms of membrane traffic leading to melanosome biogenesis are poorly understood. We demonstrate here that active mutated forms of Rab11 reduce the melanin content of melanocytes, while a corresponding Rab4 mutant does not. We show that this is mainly due to the inhibition of the processing and transport of Pmel17, a protein involved in the early stages of melanosome biogenesis. We also provide evidence that Rab11 directly binds to the cytoplasmic tail of Pmel17. Moreover, we found that the neurospecific BetaB subunit of the AP-3 coat complex is associated with Rab11 positive membranes in melanocytic cells and specifically interacts with Rab11. Our results constitute the first evidence that a Rab protein, through specific interactions with tissue-specific coat complex and cargo, regulates sorting from a compartment related to the ERC toward later stages of membrane maturation. Besides these results, were identified by two hybrid screens two novel Rab11 partners. The first, called RCP (Rab coupling protein) is an endosomal membrane-associated protein Interacting both with Rab11 and Rab4. We demonstrated that RCP is implicated in endosomal recycling. The second partner corresponds to Rab3IP, the human orthologue of rat Rabin 3, a previously identified Rab3A interacting protein with sequence homology to two Rab Guanine nucleotide Exchange Factors (Sec2p and GRAB). In vitro results indicate that Rab3lP has a weak exchange activity on Rab11. Furthermore, over-expression of GFP-tagged Rab3IP in HeLa cells induces a phenotype closely related to that generated by Rab11 dominant-positive mutant. Finally, using FRAP experiments, we were able to demonstrate that the fluorescence recovery of GFP-Rab11 after photobleaching of the pericentriolar area is affected in cell co-expressing YFP-Rab3IP
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Barres, Céline. "La galectine-5 associée aux exosomes de réticulocyte de rat : caractérisation et étude fonctionnelle." Montpellier 2, 2009. http://www.theses.fr/2009MON20098.
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Lors de sa maturation en érythrocyte, le réticulocyte sécrète de petites vésicules membranaires appelées exosomes. Les exosomes sont les vésicules intraluménales des endosomes multivésiculaires libérées dans le milieu extracellulaire lors de la fusion de ces compartiments endosomaux avec la membrane plasmique. Cette voie de sécrétion contribue au remodelage de la membrane plasmique durant l'érythropoïèse en éliminant spécifiquement certaines protéines membranaires. Le travail présenté dans cette thèse porte sur la caractérisation et la fonction de la galectine-5 au cours de la maturation du réticulocyte. Cette protéine, faisant partie de la famille des galectines, est spécifique de la lignée érythroïde chez le rat. Nous montrons que la galectine-5, bien que majoritairement cytosolique, est présente à la surface des réticulocytes et des érythrocytes de rat ainsi que dans les compartiments endosomaux du réticulocyte. Nous avons également mis en évidence, (i) la translocation de la galectine-5 du cytosol vers la lumière endosomale conduisant à sa sécrétion en association avec les exosomes, (ii) sa liaison (au moins en partie) à la surface des vésicules, avec l'implication probable dans son tri exosomal de glycoconjugués portant des résidus galactosylés. Finalement, nous démontrons que la présence la galectine-5 à la surface des exosomes module leur capture par des macrophages de rat péritonéaux ou murins J774. Les résultats révèlent que le mécanisme d'internalisation des vésicules est dépendant de la température, de la dynamine, et que cette capture exosomale décroit lors de l'addition de galectine-5, lorsque son domaine de reconnaissance au sucre est disponibleDuring their maturation into erythrocytes, reticulocytes release small membrane vesicles called exosomes. Exosomes are intralumenal vesicles of multivesicular endosomes released in the extracellular medium upon fusion of these endosomal compartments with the plasma membrane. This secretion pathway contributes to reticulocyte plasma membrane remodelling during erythropoiesis by specific clearance of membrane proteins. The study presented in this thesis deals with galectine-5 characteristics and its role during reticulocyte maturation. This protein belongs to the galectin family proteins and is specific of both erythroid lineage and rat species. We show that galectin-5, although mainly cytosolic, is present on the cell surface of rat reticulocytes and erythrocytes but also localizes with endosomal compartments. We also document (i) galectin-5 translocation from the cytosol into the endosomal lumen leading to its secretion in association with exosomes, (ii) its binding (at least in part) onto the vesicle surface, with potential involvement in sorting of galactose-bearing glycoconjugates. Finally, we demonstrate that the presence of galectin-5 on the exosome surface modulates vesicle uptake by rat peritoneal and murine J774 macrophages. Results reveal that the mechanism of internalization is temperature dependent, dynamin dependent, and that exosome uptake is decreased by adding galectin-5 in the absence of haptenic ligand
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Apfeldorfer, Coralie. "Lysosome biogenesis during osteoclastogenesis." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1164801444532-19433.
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Lysosomes are acidic, hydrolase-rich vesicles capable of degrading most biological macromolecules. During the past several decades, much has been learned about different aspects of lysosome biogenesis. The selective phosphorylation of mannose residues on lysosomal enzymes, in conjunction with specific receptors for the mannose-6-phosphate recognition marker, has been found to be largely responsible for the targeting of newly synthesized lysosomal enzymes to lyzosomes. It is known that lysosomes receive input from both the endocytotic and biosynthetic pathways. Nevertheless the exact molecular mechanisms responsible for sorting of the biosynthetic imput involved in the lysosome biogenesis is still a matter of debate. Because osteoclast precursors do not secrete their lysosomal enzymes and osteoclasts do, the observation of modifications occuring during osteoclastogenesis is a good model to observe mechanisms responsible for lysosomal enzymes traffic. Osteoclasts are bone-degrading cells. To perform this specific task they have to reorganise the sorting of their lysosomal enzymes to be able to target them toward the bone surface in mature cells. Since few years, the differentiation of osteoclasts in vitro did help to study these cells. Osteoclast morphology has been therefore already well studied, and the nature of their specific membrane domains is now established. Sensing the proximity of a bone-like surface the cell reorganises its cytoskeleton, and creates specific membrane domains: an actin-rich ring-like zone (named actin ring) surrounded by highly ruffled membrane (named the ruffled border) where enzymes are secreted, while subsequent bone degradation products are endocytosed. Endocytosed material is then transported through the cell inside transcytotic vesicles and released at the top of the cell in an area named the functional secretory domain. Several molecular machineries are thought to control these different phenomena. The main purpose of this thesis was to identify the major regulators of lysosomal enzymes secretion and therefore to identify the molecular switches responsible for such a membrane traffic re-organisation.
Books on the topic "Endosome"
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Dikic, Ivan. Endosomes. Springer New York, 2006. http://dx.doi.org/10.1007/978-0-387-39951-5.
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Otegui, Marisa S., ed. Plant Endosomes. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1420-3.
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Otegui, Marisa S., ed. Plant Endosomes. Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0767-1.
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Otegui, Marisa S. Plant endosomes: Methods and protocols. Humana Press, 2014.
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Logan, Niall A., and Paul Vos, eds. Endospore-forming Soil Bacteria. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19577-8.
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Logan, Niall A. Endospore-forming Soil Bacteria. Springer-Verlag Berlin Heidelberg, 2011.
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Grotenhuis, J. A. Endoscope-assisted microneurosurgery: A concise guidebook. Machaon, 1998.
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Neufeld, Jessi. Biomarkers of Alzheimer-Associated Endosomal Dysfunction. [publisher not identified], 2018.
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Kroh, Matthew, and Kevin M. Reavis, eds. The SAGES Manual Operating Through the Endoscope. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24145-6.
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Viguera, José María. La prenda cambiaria: El endoso en garantía. Civitas, 1994.
Book chapters on the topic "Endosome"
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Tooze, J., and M. Hollinshead. "The Tubular Early Endosome." In Molecular Mechanisms of Membrane Traffic. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02928-2_48.
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Podinovskaia, Maria, and Anne Spang. "The Endosomal Network: Mediators and Regulators of Endosome Maturation." In Endocytosis and Signaling. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96704-2_1.
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Vergne, Isabelle, and Vojo Deretic. "In Vitro Phagosome–Endosome Fusion." In Autophagosome and Phagosome. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_19.
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Mayer, R. John, Carron Tipler, Jane Arnold, et al. "Endosome-Lysosomes, Ubiquitin and Neurodegeneration." In Intracellular Protein Catabolism. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0335-0_33.
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Fuchs, R., S. Schmid, I. Mellman, and H. Klapper. "Regulation of ATP-Dependent Endosome Acidification." In Endocytosis. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_17.
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Takeda, Yuichi, and Tomohiko Taguchi. "Retrograde Membrane Traffic and Recycling Endosome." In Glycoscience: Biology and Medicine. Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54836-2_47-1.
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Takeda, Yuichi, and Tomohiko Taguchi. "Retrograde Membrane Traffic and Recycling Endosome." In Glycoscience: Biology and Medicine. Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54841-6_47.
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Thilo, Lutz. "Endosome Processing: Structural, Functional and Kinetic Interrelations." In Botulinum and Tetanus Neurotoxins. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9542-4_18.
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Kaur, Gulpreet, and Aparna Lakkaraju. "Early Endosome Morphology in Health and Disease." In Retinal Degenerative Diseases. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_41.
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Steele-Mortimer, Olivia, Michael J. Clague, Leo Thomas, Jean-Pierre Gorvel, and Jean Gruenberg. "Regulation of Early Endosome Fusion In Vitro." In Molecular Mechanisms of Membrane Traffic. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02928-2_45.
Full textConference papers on the topic "Endosome"
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Freeman, Eric, and Lisa Mauck Weiland. "Endosomal Vaccine Delivery Through the Nastic Model." In ASME 2009 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. ASMEDC, 2009. http://dx.doi.org/10.1115/smasis2009-1338.
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Vaccine enters white blood cells through the process of endocytosis. In this process the cell extends and engulfs the surroundings, including a vaccine when present, for intake; the vaccine is then enclosed in an inclusion known as an endosome. With the foreign species (vaccine) encased, this endosome is then transported to the interior of the cell. While the endosome provides a convenient mode of transport for uptake, it also acts to destroy and break down its contents via a pH driven process before releasing it into the cell. It has been postulated that inducing endosome burst may be an effective way to affect the release of vaccine prior to the onset of degradation. The process of burst will be explored through adaptation of an existing active material (nastic) modeling methodology. The computational methodology employs coupling of transport kinetics to membrane elastic response. The study yields insight into the multi-mechanisms of burst, involved both in the specific case of vaccine delivery and applicable to the more general case of bio inspired materials development.
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Dagdug, Leonardo. "Diffusion’s Study of Free Ligands Between Vesicle and Tubules Within the Endosome." In STATISTICAL PHYSICS AND BEYOND: 2nd Mexican Meeting on Mathematical and Experimental Physics. AIP, 2005. http://dx.doi.org/10.1063/1.1900498.
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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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Barra, Jonathan, Iram Nelson, Lauren Elder, Ling Wang, and Margarida M. Barroso. "Abstract 2396: Role of iron transporter DMT1 in endosome-mitochondria interactions and mitochondrial metabolism in breast cancer cells." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2396.
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Wallrabe, Horst, Masilamani Elangovan, Almut Burchard, Ammasi Periasamy, and Margarida Barroso. "FRET microscopy reveals clustered distribution of co-internalized receptor-ligand complexes in the apical recycling endosome of polarized epithelial MDCK cells." In International Symposium on Biomedical Optics, edited by Ammasi Periasamy and Peter T. C. So. SPIE, 2002. http://dx.doi.org/10.1117/12.470677.
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Bhagwani, A. R., B. Harmon, D. Farkas, et al. "Increased Endosome Formation with Deficiency in RNA Recognition Receptors in Pulmonary Arterial Endothelial Cells from Patients with PAH - A P53-Dependent Revolving Door to Altered Endothelial Function in PAH?" In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5395.
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Choi, JungHun, and Robert H. Sturges. "Design and Simulation of a Smart Endoscope: Part II." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-60252.
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In this research, we are developing a noninvasive and safe endoscope for human colonoscopy. To minimize the invasiveness and discomfort, a smart endoscope is composed of a sheath with controllable stiffness that has an exoskeleton structure. A smart endoscope is comprised of an endoscope and a sheath. The stem has more flexibility than a conventional endoscope and the sheath portion maintains controllable flexibility. In principle, this approach could be used for other procedures. The stem of a conventional protoscope has stiffness and it can scratch the inside surface when it pushes into a human colon. It may also deform the colon’s shape. Important parameters used in designing a smart endoscope include the radius of curvature of a sigmoid colon, an appropriate unit diameter for the sheath part, and an ability to lock the units together. An analysis of the cable tensions and external forces is completed for a given configuration based on selected geometric parameters. By applying external forces to the stem of the endoscope, we can solve for the maximum external resisting forces. These are required to maintain the locking ability of the endoscope and the corresponding cable forces.
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Munnae, Jomkwun, Gary McMurray, and Harvey Lipkin. "Static and Kinematic Analysis of a Planar Cable-Driven Flexible Endoscope." In ASME 2009 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/detc2009-87542.
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Flexible endoscopes are mainly used for diagnostics and performing simple therapeutic tasks inside human cavities but are now becoming the key instrument for the incisionless surgery known as natural orifice transluminal endoscopic surgery (NOTES). Since the current endoscope technology gives limited maneuverability, dexterity, and functionality, a number of new endoscope designs have been proposed. Due to miniaturization, conduit, and actuation simplicity, many of the new designs rely on cable-actuating mechanisms similar to the current technology. Basic kinematical and static analyses for this device have not appeared in the literature. In this paper the articulated section of a planar cable-driven endoscope is modeled as a serial robot. The kinematic and static analyses for single-jointed and multi-jointed endoscope structures are performed to relate tip motion to the controlling inputs. Pre-tensioning cables increases the endoscope stiffness and extends its range of operation.
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McLaurin, A. P., and Edwin R. Jones, Jr. "Virtual endoscope." In IS&T/SPIE 1994 International Symposium on Electronic Imaging: Science and Technology, edited by Scott S. Fisher, John O. Merritt, and Mark T. Bolas. SPIE, 1994. http://dx.doi.org/10.1117/12.173900.
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Septier, D., V. Mytskaniuk, R. Habert, et al. "Label-free three photon micro-endoscope." In CLEO: Science and Innovations. Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleo_si.2022.sm3l.5.
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We report the first three photon micro-endoscope enabling imaging of unlabeled biological tissues. It is based on a double clad antiresonant hollow-core fiber which is designed to make the endoscope highly multimodal (2PEF, 3PEF, SHG, THG, CARS).
Reports on the topic "Endosome"
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Kent, Michael S., Bryan Carson, Susan Rempe, et al. Mechanism of fusion of pathogenic enveloped viruses with the endosomal membrane. Office of Scientific and Technical Information (OSTI), 2014. http://dx.doi.org/10.2172/1494634.
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Stone, Gary F., and John Smith. High Resolution Sub-MM Fiberoptic Endoscope Final Report CRADA No. TSB-1447-97. Office of Scientific and Technical Information (OSTI), 2018. http://dx.doi.org/10.2172/1418930.
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Reynolds, Charles M., Karen L. Foley, David B. Ringelberg, and Lawrence B. Perry. Fate of Nonindigenous, Endospore-Forming Bacteria in Soils. Strategies for Laboratory and Field Investigations. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada430422.
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Urzola Mestra, Enrique Carlos. Vulnerabilidad del deudor en el cobro jurídico de un acreedor cooperativa. Ediciones Universidad Cooperativa de Colombia, 2022. http://dx.doi.org/10.16925/gcnc.27.
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En esta nota de clase, se dan a conocer los conceptos básicos y la percepción del autor sobre el endoso a cooperativas de títulos valores, con el propósito de visualizar la problemática del estado de indefensión y vulnerabilidad del deudor frente a cooperativas financieras cuando el estado de necesidad por causas sobrevinientes impide el cumplimiento de la obligación de pagar un título valor que no nace en una cooperativa y es endosado a favor de esta por un tercero, de manera que da los beneficios para el cobro jurídico al nuevo acreedor (la cooperativa), el cual no tiene el acreedor anterior al endoso.
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Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7586538.bard.
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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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Avni, Adi, and Gitta L. Coaker. Proteomic investigation of a tomato receptor like protein recognizing fungal pathogens. United States Department of Agriculture, 2015. http://dx.doi.org/10.32747/2015.7600030.bard.
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Maximizing food production with minimal negative effects on the environment remains a long-term challenge for sustainable food production. Microbial pathogens cause devastating diseases, minimizing crop losses by controlling plant diseases can contribute significantly to this goal. All plants possess an innate immune system that is activated after recognition of microbial-derived molecules. The fungal protein Eix induces defense responses in tomato and tobacco. Plants recognize Eix through a leucine-rich-repeat receptor- like-protein (LRR-RLP) termed LeEix. Despite the knowledge obtained from studies on tomato, relatively little is known about signaling initiated by RLP-type immune receptors. The focus of this grant proposal is to generate a foundational understanding of how the tomato xylanase receptor LeEix2 signals to confer defense responses. LeEix2 recognition results in pattern triggered immunity (PTI). The grant has two main aims: (1) Isolate the LeEix2 protein complex in an active and resting state; (2) Examine the biological function of the identified proteins in relation to LeEix2 signaling upon perception of the xylanase elicitor Eix. We used two separate approaches to isolate receptor interacting proteins. Transgenic tomato plants expressing LeEix2 fused to the GFP tag were used to identify complex components at a resting and activated state. LeEix2 complexes were purified by mass spectrometry and associated proteins identified by mass spectrometry. We identified novel proteins that interact with LeEix receptor by proteomics analysis. We identified two dynamin related proteins (DRPs), a coiled coil – nucleotide binding site leucine rich repeat (SlNRC4a) protein. In the second approach we used the split ubiquitin yeast two hybrid (Y2H) screen system to identified receptor-like protein kinase At5g24010-like (SlRLK-like) (Solyc01g094920.2.1) as an interactor of LeEIX2. We examined the role of SlNRC4a in plant immunity. Co-immunoprecipitation demonstrates that SlNRC4a is able to associate with different PRRs. Physiological assays with specific elicitors revealed that SlNRC4a generally alters PRR-mediated responses. SlNRC4a overexpression enhances defense responses while silencing SlNRC4 reduces plant immunity. We propose that SlNRC4a acts as a non-canonical positive regulator of immunity mediated by diverse PRRs. Thus, SlNRC4a could link both intracellular and extracellular immune perception. SlDRP2A localizes at the plasma membrane. Overexpression of SlDRP2A increases the sub-population of LeEIX2 inVHAa1 endosomes, and enhances LeEIX2- and FLS2-mediated defense. The effect of SlDRP2A on induction of plant immunity highlights the importance of endomembrane components and endocytosis in signal propagation during plant immune . The interaction of LeEIX2 with SlRLK-like was verified using co- immunoprecipitation and a bimolecular fluorescence complementation assay. The defence responses induced by EIX were markedly reduced when SlRLK-like was over-expressed, and mutation of slrlk-likeusing CRISPR/Cas9 increased EIX- induced ethylene production and SlACSgene expression in tomato. Co-expression of SlRLK-like with different RLPs and RLKs led to their degradation, apparently through an endoplasmic reticulum-associated degradation process. We provided new knowledge and expertise relevant to expression of specific be exploited to enhance immunity in crops enabling the development of novel environmentally friendly disease control strategies.
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Palmer, Guy, Varda Shkap, Wendy Brown, and Thea Molad. Control of bovine anaplasmosis: cytokine enhancement of vaccine efficacy. United States Department of Agriculture, 2007. http://dx.doi.org/10.32747/2007.7695879.bard.
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Anaplasmosis an arthropod-born disease of cattle caused by the rickettsia Anaplasma marginale and is an impediment to efficient production of healthy livestock in both Israel and the United States. Currently the only effective vaccines are derived from the blood of infected cattle. The risk of widespread transmission of both known and newly emergent pathogens has prevented licensure of live blood-based vaccines in the U.S. and is a major concern for their continued use in Israel. Consequently development of a safe, effective vaccine is a high priority. In this collaborative project we focused on two approaches to vaccine development. The first focused o n improving antigen delivery to livestock and specifically examined how DNA vaccines could be improved to enhance priming and expansion of the immune response. This research resulted in development and testing of two novel vaccine delivery systems--one that targeted antigen spread among dendritic cells (the key cell in priming immune responses and a follow-on construct that also specifically targeted antigen to the endosomal-lysosomal compartment the processing organelle within the dendritic cell that directs vaccine antigen to the MHC class ll-CD4* T cell priming pathway). The optimized construct targeting vaccine antigen to the dendritic cell MHC class II pathway was tested for ability to prime A. marginale specific immune responses in outbred cattle. The results demonstrated both statistically significant effects of priming with a single immunization, continued expansion of the primary immune response including development of high affinity lgG antibodies and rapid recall of the memory response following antigen challenge. This portion of the study represented a significant advance in vaccine delivery for livestock. Importantly the impact of these studies is not limited to A. marginale a s the targeting motifs are optimized for cattle and can be adapted to other cattle vaccinations by inserting a relevant pathogen-specific antigen. The second approach (which represented an addition to the project for which approval was requested as part of the first annual report) was a comparative approach between A . marginale and the Israel A . centrale vaccines train. This addition was requested as studies on Major Surface Protein( MSP)- 2 have shown that this antigen is highly antigenically variable and presented solely as a "static vaccine" antigen does not give cross-strain immunity. In contrast A. . centrale is an effective vaccine which Kimron Veterinary institute has used in the field in Israel for over 50 years. Taking advantage of this expertise, a broad comparison of wild type A. marginale and vaccine strain was initiated. These studies revealed three primary findings: i) use of the vaccine is associated with superinfection, but absence of clinical disease upon superinfection with A. marginale; ii) the A. centrale vaccine strain is not only less virulent but transmission in competent in Dermacentor spp. ticks; and iii) some but not all MSPs are conserved in basic orthologous structure but there are significant polymorphisms among the strains. These studies clearly indicated that there are statistically significant differences in biology (virulence and transmission) and provide a clear path for mapping of biology with the genomes. Based on these findings, we initiated complete genome sequencing of the Israel vaccine strain (although not currently funded by BARD) and plant to proceed with a comparative genomics approach using already sequenced wild-type A. marginale. These findings and ongoing collaborative research tie together filed vaccine experience with new genomic data, providing a new approach to vaccine development against a complex pathogen.
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Health hazard evaluation report: HETA-2006-0298-3090, evaluation of worker exposures to peracetic acid-based sterilant during endoscope reprocessing, Kaleida Health-Buffalo General Hospital, Buffalo, New York. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2009. http://dx.doi.org/10.26616/nioshheta200602983090.
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