Relevant bibliographies by topics / Intracellular trafficking

Academic literature on the topic 'Intracellular trafficking'

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Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Intracellular trafficking"

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Reinhart, M. P. "Intracellular sterol trafficking." Experientia 46, no. 6 (June 1990): 599–611. http://dx.doi.org/10.1007/bf01939699.

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Stover, Patrick J., and Martha S. Field. "Trafficking of Intracellular Folates." Advances in Nutrition 2, no. 4 (June 28, 2011): 325–31. http://dx.doi.org/10.3945/an.111.000596.

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Borroni, Elena M., Alberto Mantovani, Massimo Locati, and Raffaella Bonecchi. "Chemokine receptors intracellular trafficking." Pharmacology & Therapeutics 127, no. 1 (July 2010): 1–8. http://dx.doi.org/10.1016/j.pharmthera.2010.04.006.

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Li, Xiao-Jiang, and Shi-Hua Li. "HAP1 and intracellular trafficking." Trends in Pharmacological Sciences 26, no. 1 (January 2005): 1–3. http://dx.doi.org/10.1016/j.tips.2004.11.001.

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Hamza, Iqbal. "Intracellular Trafficking of Porphyrins." ACS Chemical Biology 1, no. 10 (November 2006): 627–29. http://dx.doi.org/10.1021/cb600442b.

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Marsh, Mark. "Intracellular trafficking of proteins." Trends in Cell Biology 2, no. 1 (January 1992): 32. http://dx.doi.org/10.1016/0962-8924(92)90143-b.

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Hopkins, Colin R. "Intracellular trafficking of proteins." Trends in Biochemical Sciences 17, no. 8 (August 1992): 324. http://dx.doi.org/10.1016/0968-0004(92)90450-n.

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Davis, Elaine C., and Robert P. Mecham. "Intracellular trafficking of tropoelastin." Matrix Biology 17, no. 4 (August 1998): 245–54. http://dx.doi.org/10.1016/s0945-053x(98)90078-6.

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Jiang, Bingfu, and Eberhard Hildt. "Intracellular Trafficking of HBV Particles." Cells 9, no. 9 (September 2, 2020): 2023. http://dx.doi.org/10.3390/cells9092023.

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The human hepatitis B virus (HBV), that is causative for more than 240 million cases of chronic liver inflammation (hepatitis), is an enveloped virus with a partially double-stranded DNA genome. After virion uptake by receptor-mediated endocytosis, the viral nucleocapsid is transported towards the nuclear pore complex. In the nuclear basket, the nucleocapsid disassembles. The viral genome that is covalently linked to the viral polymerase, which harbors a bipartite NLS, is imported into the nucleus. Here, the partially double-stranded DNA genome is converted in a minichromosome-like structure, the covalently closed circular DNA (cccDNA). The DNA virus HBV replicates via a pregenomic RNA (pgRNA)-intermediate that is reverse transcribed into DNA. HBV-infected cells release apart from the infectious viral parrticle two forms of non-infectious subviral particles (spheres and filaments), which are assembled by the surface proteins but lack any capsid and nucleic acid. In addition, naked capsids are released by HBV replicating cells. Infectious viral particles and filaments are released via multivesicular bodies; spheres are secreted by the classic constitutive secretory pathway. The release of naked capsids is still not fully understood, autophagosomal processes are discussed. This review describes intracellular trafficking pathways involved in virus entry, morphogenesis and release of (sub)viral particles.
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Bassham, Diane C. "Plant autophagy and intracellular trafficking." FEBS Letters 596, no. 17 (September 2022): 2089–92. http://dx.doi.org/10.1002/1873-3468.14466.

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Dissertations / Theses on the topic "Intracellular trafficking"

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Coppola, Stefano, Daniela Pozzi, Giulio Caracciolo, and Thomas Schmidt. "Intracellular trafficking of lipoplexes." Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-182512.

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Guise, Christopher Paul. "The intracellular trafficking of ricin." Thesis, University of Warwick, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392938.

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Liu, Xiao Li. "Nephrin: cellular trafficking and intracellular interactions /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-899-8/.

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McKay, Jodi Ho-Jung. "HRas intracellular trafficking and signal transduction." [Ames, Iowa : Iowa State University], 2007.

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Cotta, Doné Stefania. "Nephrin - intracellular trafficking and podocyte maturation /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-411-2/.

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Tonn, Daniela. "Intracellular trafficking of Leishmania major peptidases." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1649/.

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Leishmania resides inside mammalian macrophages, from where it is thought to manipulate the host immune system by releasing virulence factors. The cysteine peptidase CPB has been shown to be secreted by the parasite and act as such a virulence factor. CPB is released through the flagellar pocket while being trafficked to the lysosome. Thus, in this project, the intracellular localisations of eight other L. major peptidases were analysed by fluorescence microscopy, after tagging the enzymes with green fluorescent protein (GFP). The candidate peptidases were chosen by bioinformatics analyses and predictions of N-terminal secretory signal peptides and potential transmembrane domains. The aim was to find a peptidase accumulating in the flagellar pocket of the cell, from where it could be secreted. Five candidate peptidases (a ubiquitin hydrolase, a CaaX prenyl protease, a zinc carboxypeptidase and two rhomboid peptidases) localised to the mitochondrion, which was unexpected. Another, a calpain-like peptidase, localised to the flagellum but not to the flagellar pocket. A serine carboxypeptidase was found very close to the flagellar pocket, possibly in small vesicles budding off or fusing with the pocket membrane, but did not co-localise with a flagellar pocket marker. The bioinformatics predictions differed from the experimental results here and, additionally, using different algorithms to predict protein properties resulted in contradictory predictions in several cases. This suggests that generic protein prediction programmes for mammalian or higher eukaryotic proteins can be unreliable and of limited usefulness for Leishmania proteins. This corroborates the notion that Leishmania may use novel, non-classical secretory pathways rather than or in addition to those characterised for higher eukaryotes. The L. major Bem46-like serine peptidase (LmjF35.4020) of the Clan SC (Family S9) was the only candidate peptidase that localised to the flagellar pocket when labelled with GFP. This was an indication that this enzyme may be released from the cell and could act as a virulence factor. Alternatively, it may be a resident protein of the flagellar pocket. Deleting the Bem46 gene in L. major did not have a measurable effect on promastigote growth or on footpad lesion development in mice inoculated with Bem46-deficient cells, so it does not appear to play a role as a major virulence factor. Apart from the secretion of virulence factors, rapid protein turnover, e.g. in the lysosome, is important for the infectivity of Leishmania. To investigate lysosome structure and function in L. major, a potential LMP (lysosomal membrane protein) was identified by bioinformatics. Thus far, no resident membrane proteins of the Leishmania lysosome are known and identifying such a protein would provide a useful marker for the closer investigation of this important organelle. In this project, the location and role of the LMP protein LmjF30.2670 was investigated using GFP-tagging and fluorescence microscopy. The experiments showed that LMP is not lysosomal in L. major, rather, it could be observed localising to a distinct, elongated and sometimes doughnut-shaped structure in close proximity to the kinetoplast. This structure was not directly associated with the flagellar pocket or the cell membrane, its position in the cell was variable within a certain area alongside the kinetoplast, it appeared to duplicate during cell division and it did not co-localise with the endocytic / lysosomal marker FM4-64. Deletion of the LMP gene did not have any effect on promastigote growth in cell culture and only a small and transient slowing effect on the development of mouse footpad lesions after inoculation with LMP-deficient L. major. Lysosomal membrane proteins can be targeted to the lysosome by the protein carrier complex AP3, which binds to tyrosine or dileucine motifs in cargo proteins. LMP contains two such tyrosine motifs at its C-terminus, but disruption of these by site-directed mutagenesis did not affect LMP localisation, suggesting that its trafficking is AP3-independent, which is in accordance with the non-lysosomal localisation of LMP. Finally, the lysosome-like acidocalcisome organelles have previously been shown to rely on the protein carrier complex AP3 for normal structure and function. In AP3-deficient Leishmania, the acidocalcisomes are defective and, at the same time, parasite virulence is markedly reduced (Besteiro et al., 2008o). To analyse how AP3 is important for acidocalcisome morphology and function, a proton pump of the acidocalcisomal membrane, the V-H+-PPase, was investigated by GFP-labelling and fluorescence microscopy. In wild type L. major the V-H+-PPase could be shown to localise to the acidocalcisomes, whereas in AP3-deficient cells it was not detectable, suggesting that the protein is mislocalised and likely degraded. The V-H+-PPase also contains several tyrosine motifs that may interact with AP3. The two most prominent of these were disrupted by site-directed mutagenesis, but this did not affect the localisation of the V-H+-PPase, suggesting that these two sites are not, or not solely, important for AP3 binding or that the V-H+-PPase is not bound by AP3 directly.
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Wilson, Rona Kirstin. "Intracellular pathways in prion peptide trafficking." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433105.

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Mukhtar, Mohammed. "Regulation of intracellular trafficking of glucokinase." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419994.

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Henaff, Daniel. "Adenovirus biology : receptors and intracellular trafficking." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20138/document.

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Les adénovirus ont une double nature, soit comme pathogène omniprésent qui peuvent occasionnellement causer des maladies soit comme vecteurs utilisés de transfert de gène. À nos connaissances, les 30 premières minutes depuis la liaison au récepteur jusqu'à l'arrivée au pore nucléaire sont identiques pour le pathogène comme pour le vecteur. L'objectif de ma thèse était de comprendre les mécanismes impliqués dans la liaison au récepteur, l'internalisation, l'échappement et le trafic endosomal vers le MTOC. J'ai d'abord étudié le mécanisme impliqué dans l'hémagglutination des virus à tropisme pour CAR et à tropisme pour SA. J'ai identifié la présence de CAR sur les érythrocytes humains et montré qu'il était le principal responsable de l'agglutination induite par les virus à tropisme pour CAR. De plus, j'ai montré que la présence de CAR sur les érythrocytes pouvait piéger le virus dans le sang et ainsi empêcher l'infection au niveau du foie. Dans un deuxième temps, j'ai participé à la caractérisation du rôle de la protéine VI et la translocation du virus au MTOC. Nous avons montré que Nedd4 était impliqué dans le ciblage du virus au MTOC via l'ubiquitination de la protéine VI. Enfin, j'ai travaillé sur le neurotropisme de CAV-2 et caractérisé sa localisa tion subcellulaire au niveau des synapses. J'ai montré qu'une partie de CAR était localisée dans des radeaux lipidiques à la synapse et que CAV-2 entrait via la voie de recyclage des vésicules synaptiques
Adenoviruses have a dual nature as ubiquitous pathogens that occasionally cause life-threatening disease and their use as gene transfer vectors. To the best of our current knowledge, the first 30 min from binding to nuclear pore docking of both wild-type virus and vector are identical. The goal of my thesis is to understand different mechanisms involved in receptor binding, internalization, endosomal escape and trafficking to the MTOC. First I studied the mechanism involved in hemagglutination of CAR-tropic and SA-tropic viruses. I identified the presence of CAR on human erythrocytes and showed that it was the main responsible for the agglutination mediated by CAR-tropic viruses. Moreover, I show that CAR on erythrocytes can sequester virus in the bloodstream and block liver infection. In a second part I participated to the characterization of the role of the protein VI and the translocation of HAd to the MTOC. We showed that Nedd4 was involved in the targeting of the virus to MTOC through ubiquitination of this protein VI. Finally, I worked on the neurotropism of CAV-2 and characterize its subcellular localization at the synapse. I showed that a part of CAR was localized in lipid raft at the synapse and enter through the synaptic vesicle-recycling pathway
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Hutchinson, James Lawrence. "Salmonella interactions with host intracellular trafficking pathways." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611631.

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Books on the topic "Intracellular trafficking"

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Chang, T. Y., and Dale A. Freeman, eds. Intracellular Cholesterol Trafficking. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3.

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Y, Chang T., and Freeman Dale A, eds. Intracellular cholesterol trafficking. Boston: Kluwer Academic Publishers, 1998.

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De Lima, Maria C. Pedroso, Nejat Düzgüneş, and Dick Hoekstra, eds. Trafficking of Intracellular Membranes:. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79547-3.

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J, Steer Clifford, and Hanover John A, eds. Intracellular trafficking of proteins. Cambridge [England]: Cambridge University Press, 1991.

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Peng, Loh Y., ed. Mechanisms of intracellular trafficking and processing of proproteins. Boca Raton, Fla: CRC Press, 1993.

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Pedroso de Lima, Maria C., Düzgüneş Nejat, Hoekstra Dick, and NATO Advanced Study Institute on "Trafficking of Intracellular Membranes: From Molecular Sorting to Membrane Fusion" (1994 : Espinho, Portugal), eds. Trafficking of intracellular membranes: From molecular sorting to membrane fusion. New York: Springer Verlag, 1995.

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Chang, T. Y., and Dale A. Freeman. Intracellular Cholesterol Trafficking. Springer, 2012.

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Intracellular Cholesterol Trafficking. 2000.

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Chang, T. Y., and Dale A. Freeman. Intracellular Cholesterol Trafficking. Springer London, Limited, 2012.

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Maria C. Pedroso De Lima. Trafficking Intracellular Membrane (NATO Asi Series. Subseries H, Cell Biology). Springer-Verlag Telos, 1995.

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Book chapters on the topic "Intracellular trafficking"

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Herrmann, Johannes M., and Anne Spang. "Intracellular Parcel Service: Current Issues in Intracellular Membrane Trafficking." In Membrane Trafficking, 1–12. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2309-0_1.

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Hehl, Adrian B. "Intracellular Protein Trafficking." In Giardia, 219–31. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0198-8_14.

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Chang, Ta-Yuan, Catherine C. Y. Chang, and Oneil Lee. "The Sterol-Specific Regulation of ACAT-1 and SREBPs in Mammalian Cells and in Liver." In Intracellular Cholesterol Trafficking, 1–14. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3_1.

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Phillips, Jane Ellen, and William J. Johnson. "Efflux and Plasma Transport of Biosynthetic Sterols." In Intracellular Cholesterol Trafficking, 147–68. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3_10.

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Stocco, Douglas M., and Jerome F. Strauss. "Intramitochondrial Cholesterol Transfer in Steroidogenic Cells." In Intracellular Cholesterol Trafficking, 169–82. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3_11.

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Tabas, Ira. "Mechanisms and Consequences of Cholesterol Loading in Macrophages." In Intracellular Cholesterol Trafficking, 183–96. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3_12.

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Chanderbhan, R. F., A. T. Kharroubi, A. P. Pastuszyn, L. L. Gallo, and T. J. Scallen. "Direct Evidence for Sterol Carrier Protein-2 (SCP-2) Participation in ACTH Stimulated Steroidogenesis in Isolated Adrenal Cells." In Intracellular Cholesterol Trafficking, 197–212. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3_13.

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Schroeder, Friedhelm, Andrey Frolov, Jonathan K. Schoer, Adalberto M. Gallegos, Barbara P. Atshaves, Neal J. Stolowich, A. Ian Scott, and Ann B. Kier. "Intracellular Sterol Binding Proteins: Cholesterol Transport and Membrane Domains." In Intracellular Cholesterol Trafficking, 213–34. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3_14.

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Seedorf, Udo. "Functional Analysis of Sterol Carrier Protein-2 (SCP2) in the SCP2 Knockout Mouse." In Intracellular Cholesterol Trafficking, 235–52. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3_15.

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Smart, Eric J., and Deneys R. van der Westhuyzen. "Scavenger Receptors, Caveolae, Caveolin, and Cholesterol Trafficking." In Intracellular Cholesterol Trafficking, 253–72. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5113-3_16.

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Conference papers on the topic "Intracellular trafficking"

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Ferrati, Silvia, Rita E. Serda, Andrew Bean, and Mauro Ferrari. "Intracellular Trafficking of Nano-Carriers." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13303.

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A multistage delivery system based on biodegradable mesoporous silicon particles loaded with one or multiple second stage nano-particles is likely to be useful for drug delivery. Upon intravenous injection the silicon nano-carriers will travel through the blood stream and migrate to the vessel wall. Vascular endothelial cells have been shown to be promising candidates for drug delivery as they represent both an anchor point and target.[1] It has been shown that human endothelial cells can act as nonprofessional phagocytes internalizing our silicon micron-sized nano-carriers.[2] The complete understanding of the molecular mechanisms required for the internalization of the particles into cells, as well as their fate once internalized, is crucial for the choice and formulation of appropriate second stage particles to be loaded in the silicon carrier. For example, different types of coatings or functionalization for both silicon nano-carriers and nano-particles could favor different trafficking pathways or promote endosomal escape following cellular uptake. In this study the uptake and trafficking of silicon nano-carriers in Human Microvascular Vein Endothelia Cells (HMVECs) was monitored using TEM, confocal microscopy and immunofluorescence.
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John, Ciny, and Michael L. Lu. "Abstract 4287: Intracellular trafficking of androgen receptor splice variant AR8." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4287.

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Shah, V. K., S. Gao, and S. Jelic. "Impaired Intracellular Cholesterol Trafficking Promotes Endothelial Inflammation Observed in Sleep Apnea." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4449.

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Rudkouskaya, Alena, Jason Smith, Xavier Intes, and Margarida Barroso. "Monitoring receptor heterodimerization along intracellular trafficking pathways using anti-HER2 therapeutic antibodies." In Visualizing and Quantifying Drug Distribution in Tissue V, edited by Conor L. Evans and Kin Foong Chan. SPIE, 2021. http://dx.doi.org/10.1117/12.2578402.

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Huss, Anja, Omar Ramírez, Felipe Santibáñez, Andrés Couve, Steffen Härtel, and Jörg Enderlein. "SOFI of GABABneurotransmitter receptors in hippocampal neurons elucidates intracellular receptor trafficking and assembly." In SPIE BiOS, edited by Jörg Enderlein, Ingo Gregor, Zygmunt K. Gryczynski, Rainer Erdmann, and Felix Koberling. SPIE, 2013. http://dx.doi.org/10.1117/12.2006215.

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de Lange Davies, Catharina, Zuzana Garaiova, Nina K. Reitan, Astrid Bjørkøy, Oladayo Folasire, Sigmund Størseth, Kristian Berg, and Sabina P. Strand. "Abstract 5404: DNA-chitosan nanoparticles in gene delivery: Endocytotic pathways and intracellular trafficking." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5404.

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Zhang, Tieqiao, S. Narasimhan Danthi, Jianwu Xie, Dehong Hu, Peter Lu, and King Li. "Live cell imaging of the endocytosis and the intracellular trafficking of multifunctional lipid nanoparticles." In Biomedical Optics 2006, edited by Alexander N. Cartwright and Dan V. Nicolau. SPIE, 2006. http://dx.doi.org/10.1117/12.645398.

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Hatakeyama, Hiroyasu, and Makoto Kanzaki. "Development of dual-color simultaneous single molecule imaging system for analyzing multiple intracellular trafficking activities." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609776.

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He, D., R. Salgia, P. Kogut, J. Solway, V. Natarajan, and Y. Zhao. "Lysophosphatidic Acid Mitigates Lipopolysaccharide-Induced Intracellular Trafficking of c-Met and Airway Epithelial Barrier Dysfunction." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2389.

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Omata, Daiki, Yoichi Negishi, Yoko Endo-Takahashi, Ryo Suzuki, Kazuo Maruyama, Motoyoshi Nomizu, Yukihiko Aramaki, Yoichiro Matsumoto, Lawrence A. Crum, and Gail Reinette ter Haar. "Ultrasound-targeted Bubble Liposome Destruction Enhances AG73-mediated Gene Transfer by Improvement of Intracellular Trafficking." In 10TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND (ISTU 2010). AIP, 2011. http://dx.doi.org/10.1063/1.3607927.

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Reports on the topic "Intracellular trafficking"

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Or, Etti, David Galbraith, and Anne Fennell. Exploring mechanisms involved in grape bud dormancy: Large-scale analysis of expression reprogramming following controlled dormancy induction and dormancy release. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7587232.bard.

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The timing of dormancy induction and release is very important to the economic production of table grape. Advances in manipulation of dormancy induction and dormancy release are dependent on the establishment of a comprehensive understanding of biological mechanisms involved in bud dormancy. To gain insight into these mechanisms we initiated the research that had two main objectives: A. Analyzing the expression profiles of large subsets of genes, following controlled dormancy induction and dormancy release, and assessing the role of known metabolic pathways, known regulatory genes and novel sequences involved in these processes B. Comparing expression profiles following the perception of various artificial as well as natural signals known to induce dormancy release, and searching for gene showing similar expression patterns, as candidates for further study of pathways having potential to play a central role in dormancy release. We first created targeted EST collections from V. vinifera and V. riparia mature buds. Clones were randomly selected from cDNA libraries prepared following controlled dormancy release and controlled dormancy induction and from respective controls. The entire collection (7920 vinifera and 1194 riparia clones) was sequenced and subjected to bioinformatics analysis, including clustering, annotations and GO classifications. PCR products from the entire collection were used for printing of cDNA microarrays. Bud tissue in general, and the dormant bud in particular, are under-represented within the grape EST database. Accordingly, 59% of the our vinifera EST collection, composed of 5516 unigenes, are not included within the current Vitis TIGR collection and about 22% of these transcripts bear no resemblance to any known plant transcript, corroborating the current need for our targeted EST collection and the bud specific cDNA array. Analysis of the V. riparia sequences yielded 814 unigenes, of which 140 are unique (keilin et al., manuscript, Appendix B). Results from computational expression profiling of the vinifera collection suggest that oxidative stress, calcium signaling, intracellular vesicle trafficking and anaerobic mode of carbohydrate metabolism play a role in the regulation and execution of grape-bud dormancy release. A comprehensive analysis confirmed the induction of transcription from several calcium–signaling related genes following HC treatment, and detected an inhibiting effect of calcium channel blocker and calcium chelator on HC-induced and chilling-induced bud break. It also detected the existence of HC-induced and calcium dependent protein phosphorylation activity. These data suggest, for the first time, that calcium signaling is involved in the mechanism of dormancy release (Pang et al., in preparation). We compared the effects of heat shock (HS) to those detected in buds following HC application and found that HS lead to earlier and higher bud break. We also demonstrated similar temporary reduction in catalase expression and temporary induction of ascorbate peroxidase, glutathione reductase, thioredoxin and glutathione S transferase expression following both treatments. These findings further support the assumption that temporary oxidative stress is part of the mechanism leading to bud break. The temporary induction of sucrose syntase, pyruvate decarboxylase and alcohol dehydrogenase indicate that temporary respiratory stress is developed and suggest that mitochondrial function may be of central importance for that mechanism. These finding, suggesting triggering of identical mechanisms by HS and HC, justified the comparison of expression profiles of HC and HS treated buds, as a tool for the identification of pathways with a central role in dormancy release (Halaly et al., in preparation). RNA samples from buds treated with HS, HC and water were hybridized with the cDNA arrays in an interconnected loop design. Differentially expressed genes from the were selected using R-language package from Bioconductor project called LIMMA and clones showing a significant change following both HS and HC treatments, compared to control, were selected for further analysis. A total of 1541 clones show significant induction, of which 37% have no hit or unknown function and the rest represent 661 genes with identified function. Similarly, out of 1452 clones showing significant reduction, only 53% of the clones have identified function and they represent 573 genes. The 661 induced genes are involved in 445 different molecular functions. About 90% of those functions were classified to 20 categories based on careful survey of the literature. Among other things, it appears that carbohydrate metabolism and mitochondrial function may be of central importance in the mechanism of dormancy release and studies in this direction are ongoing. Analysis of the reduced function is ongoing (Appendix A). A second set of hybridizations was carried out with RNA samples from buds exposed to short photoperiod, leading to induction of bud dormancy, and long photoperiod treatment, as control. Analysis indicated that 42 genes were significant difference between LD and SD and 11 of these were unique.
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2

Epel, Bernard, and Roger Beachy. Mechanisms of intra- and intercellular targeting and movement of tobacco mosaic virus. United States Department of Agriculture, November 2005. http://dx.doi.org/10.32747/2005.7695874.bard.

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Abstract:
To cause disease, plant viruses must replicate and spread locally and systemically within the host. Cell-to-cell virus spread is mediated by virus-encoded movement proteins (MPs), which modify the structure and function of plasmodesmata (Pd), trans-wall co-axial membranous tunnels that interconnect the cytoplasm of neighboring cells. Tobacco mosaic virus (TMV) employ a single MP for cell- cell spread and for which CP is not required. The PIs, Beachy (USA) and Epel (Israel) and co-workers, developed new tools and approaches for study of the mechanism of spread of TMV that lead to a partial identification and molecular characterization of the cellular machinery involved in the trafficking process. Original research objectives: Based on our data and those of others, we proposed a working model of plant viral spread. Our model stated that MPᵀᴹⱽ, an integral ER membrane protein with its C-terminus exposed to the cytoplasm (Reichel and Beachy, 1998), alters the Pd SEL, causes the Pd cytoplasmic annulus to dilate (Wolf et al., 1989), allowing ER to glide through Pd and that this gliding is cytoskeleton mediated. The model claimed that in absence of MP, the ER in Pd (the desmotubule) is stationary, i.e. does not move through the Pd. Based on this model we designed a series of experiments to test the following questions: -Does MP potentiate ER movement through the Pd? - In the presence of MP, is there communication between adjacent cells via ER lumen? -Does MP potentiate the movement of cytoskeletal elements cell to cell? -Is MP required for cell-to-cell movement of ER membranes between cells in sink tissue? -Is the binding in situ of MP to RNA specific to vRNA sequences or is it nonspecific as measured in vitro? And if specific: -What sequences of RNA are involved in binding to MP? And finally, what host proteins are associated with MP during intracellular targeting to various subcellular targets and what if any post-translational modifications occur to MP, other than phosphorylation (Kawakami et al., 1999)? Major conclusions, solutions and achievements. A new quantitative tool was developed to measure the "coefficient of conductivity" of Pd to cytoplasmic soluble proteins. Employing this tool, we measured changes in Pd conductivity in epidermal cells of sink and source leaves of wild-type and transgenic Nicotiana benthamiana (N. benthamiana) plants expressing MPᵀᴹⱽ incubated both in dark and light and at 16 and 25 ᵒC (Liarzi and Epel, 2005 (appendix 1). To test our model we measured the effect of the presence of MP on cell-to-cell spread of a cytoplasmic fluorescent probe, of two ER intrinsic membrane protein-probes and two ER lumen protein-probes fused to GFP. The effect of a mutant virus that is incapable of cell-to-cell spread on the spread of these probes was also determined. Our data shows that MP reduces SEL for cytoplasmic molecules, dilates the desmotubule allowing cell-cell diffusion of proteins via the desmotubule lumen and reduces the rate of spread of the ER membrane probes. Replicase was shown to enhance cell-cell spread. The data are not in support of the proposed model and have led us to propose a new model for virus cell-cell spread: this model proposes that MP, an integral ER membrane protein, forms a MP:vRNAER complex and that this ER-membrane complex diffuses in the lipid milieu of the ER into the desmotubule (the ER within the Pd), and spreads cell to cell by simple diffusion in the ER/desmotubule membrane; the driving force for spread is the chemical potential gradient between an infected cell and contingent non-infected neighbors. Our data also suggests that the virus replicase has a function in altering the Pd conductivity. Transgenic plant lines that express the MP gene of the Cg tobamovirus fused to YFP under the control the ecdysone receptor and methoxyfenocide ligand were generated by the Beachy group and the expression pattern and the timing and targeting patterns were determined. A vector expressing this MPs was also developed for use by the Epel lab . The transgenic lines are being used to identify and isolate host genes that are required for cell-to-cell movement of TMV/tobamoviruses. This line is now being grown and to be employed in proteomic studies which will commence November 2005. T-DNA insertion mutagenesis is being developed to identify and isolate host genes required for cell-to-cell movement of TMV.
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