Gotowe bibliografie tematyczne / Endocytosis

Gotowa bibliografia na temat „Endocytosis”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 30 lipca 2024

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Artykuły w czasopismach na temat "Endocytosis"

1

Bouchard, Beth A., Joseph M. Petty i Benjamin T. Suratt. "Endocytosis of Factor V by Ex Vivo-Derived Mouse Megakaryocytes is Dependent Upon Low Density Lipoprotein Receptor-Related Protein-1." Blood 114, nr 22 (20.11.2009): 4014. http://dx.doi.org/10.1182/blood.v114.22.4014.4014.

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Abstract Abstract 4014 Poster Board III-950 Subsequent to platelet activation at sites of vascular injury, numerous hemostatic proteins are released from platelet α-granules. As platelets possess little, if any, biosynthetic capability, these proteins are either synthesized by megakaryocytes (e.g. vonWillebrand) or endocytosed from the plasma by both megakaryocytes and platelets (e.g. fibrinogen). In contrast, in humans, factor V is endocytosed exclusively by megakaryocytes from the plasma via a specific, receptor-mediated, clathrin-dependent mechanism, requiring two membrane proteins. Factor V initially binds to a specific receptor. This binding event promotes an interaction between a second factor V molecule and low density lipoprotein receptor-related protein-1 (LRP-1), which subsequently mediates the endocytosis of bound factor V. In contrast, in mice, the platelet- and plasma-derived factor V pools appear to be biosynthetically distinct as demonstrated by Ginsburg and colleagues using transgenic animals (Blood 102:2856-61, 2003); however, the ability of mouse megakaryocytes to endocytose factor V was not determined. In the current study, the ability of ex vivo-derived mouse megakaryocytes to endocytose factor V is being assessed. Mouse megakaryocytes were identified by their morphology and expression of CD41. CD41 expression is apparent by Day 3 of culture. By Day 8, > 60% of the cells are positive for CD41 expression. Using a monoclonal anti-human factor V light chain antibody that cross-reacts with mouse factor V by western blotting, factor V was detected by immunohistochemistry in primary, bone marrow-derived mouse megakaryocytes, but not in cultured, ex vivo-derived mouse megakaryocytes (Day 11), when the cells are incubated in the absence of factor V, suggesting that under the conditions of this study ex vivo-derived mouse megakaryocytes are not capable of synthesizing factor V. To assess the ability of mouse megakaryocytes to endocytose factor V, cultures were incubated with fluorescently-labeled human factor V. Human and mouse factor V have an amino acid identity of ∼82% within their light chains, which mediates binding and/or endocytosis of factor V in the human system. Subsequent to incubation of ex vivo-derived mouse megakaryocyte cultures with fluorescently-labeled human factor V, substantial endocytosis was observed both by flow cytometry and fluorescence microcopy. Fluorescence microscopy indicated that these cells also endocytose fluorescently-labeled human fibrinogen, which colocalized substantially with endocytosed factor V. Fluorescence microscopy also demonstrated that while every cell expressed LRP-1 on its cell surface, only some of the cells were capable of endocytosing factor V. Furthermore, preincubation with polyclonal anti-LRP-1 antibodies inhibited 125I-factor V binding and endocytosis by ∼60%. Thus, while factor V binding and endocytosis are dependent, in part, upon the expression of LRP-1, LRP-1 expression by mouse megakaryocytes is not sufficient for factor V endocytosis, similar to observations with human megakaryocytes, and consistent with the notion that a second receptor is required. These combined observations demonstrate that ex vivo-derived mouse megakaryocytes endocytose human factor V and suggest that they may serve as an appropriate model system to study factor V endocytosis. Disclosures: No relevant conflicts of interest to declare.
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Fares, Hanna, i Iva Greenwald. "Genetic Analysis of Endocytosis in Caenorhabditis elegans: Coelomocyte Uptake Defective Mutants". Genetics 159, nr 1 (1.09.2001): 133–45. http://dx.doi.org/10.1093/genetics/159.1.133.

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Abstract The coelomocytes of Caenorhabditis elegans are scavenger cells that continuously and nonspecifically endocytose fluid from the pseudocoelom (body cavity). Green fluorescent protein (GFP) secreted into the pseudocoelom from body wall muscle cells is endocytosed and degraded by coelomocytes. We show that toxin-mediated ablation of coelomocytes results in viable animals that fail to endocytose pseudocoelomic GFP, indicating that endocytosis by coelomocytes is not essential for growth or survival of C. elegans under normal laboratory conditions. We examined known viable endocytosis mutants, and performed RNAi for other known endocytosis genes, for coelomocyte uptake defective (Cup) phenotypes. We also screened for new genes involved in endocytosis by isolating viable mutants with Cup defects; this screen identified 14 different genes, many with multiple alleles. A variety of Cup terminal phenotypes were observed, consistent with defects at various steps in the endocytic pathway. Available molecular information indicates that the Cup mutant screen has identified novel components of the endocytosis machinery that are conserved in mammals but not in Saccharomyces cerevisiae, the only other organism for which large-scale genetic screens for endocytosis mutants have been performed.
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Bouchard, Beth A., Douglas J. Taatjes, Natalie T. Meisler i Paula B. Tracy. "Subsequent to Its Endocytosis by Megakaryocytes, Factor V Is Trafficked to the [Italic]cis[/Italic]-Golgi Network Prior to Its Storage in α-Granules." Blood 108, nr 11 (16.11.2006): 1697. http://dx.doi.org/10.1182/blood.v108.11.1697.1697.

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Abstract Human platelet-derived factor V originates from megakaryocyte endocytosis of its plasma counterpart. Circulating platelets do not endocytose plasma-derived factor V and little, if any, of this hemostatically relevant, and unique, cofactor protein is synthesized by megakaryocytes. Fibrinogen, another α-granule protein, is also endocytosed from plasma, whereas other similarly stored proteins are synthesized by megakaryocytes, e.g. vWF and P-selectin. Using CD34+ex vivo-derived megakaryocytes as a model, mechanisms defining megakaryocyte endocytosis of plasma-derived factor V and its intracellular trafficking to α-granules are being studied. Expression of the well-known megakaryocyte proteins αIIb, β3, vWF, and P-selectin increased in parallel concomitant with the loss of CD34 and increased cellular differentiation. Expression of these proteins was apparent within 4 days of cell culture and was maximal by day 10. In contrast, endocytosis of factor V by cells at earlier stages of megakaryocyte differentiation (day 7) occurred in the absence of αIIb and vWF expression. By day 10 in culture, all cells endocytosing factor V also expressed αIIb and vWF. Fibrinogen endocytosis occurred with the concomitant expression of αIIb/β3. The colocalization of fluorescently-labeled factor V and fibrinogen with various organelle-specific, fluorescent antibodies was determined by confocal microscopy using day 10 or 11 ex vivo-derived megakaryocytes. After a 1 hr endocytosis period, 87.8 ± 7.2% of the factor V colocalized with an antibody to Rab5, an early endosomal marker. Colocalization decreased over time such that only 5% of the Rab5 colocalized with factor V at 4 hrs. Endocytosed factor V also colocalized in a time-dependent manner with an antibody to GM130, a cis-Golgi element, consistent with the hypothesis that endocytosed, plasma-derived factor V is structurally modified to generate the unique platelet-derived molecule. After a 2 hr endocytosis period, 53.2 ± 23.0% of the GM130 specific antibody colocalized with factor V. Colocalization decreased 5-fold by 4 hrs. In contrast, little if any of the GM130 antibody colocalized with endocytosed fibrinogen, while >80% of the cis-Golgi element colocalized with vWF. After 19 hrs, substantial colocalization was also observed between endocytosed factor V and vWF (84.2 ± 3.7%) or P-selectin (54.8 ± 3.5%), which is consistent with their storage in α-granules and confirms flow cytometric analyses. The colocalization of endocytosed factor V and fibrinogen was also determined over time. These proteins colocalized quickly (1 hr) likely due to their uptake into early endosomes as suggested by previous studies in a megakaryocyte-like cell line. Colocalization reached a maximum and plateaued after endocytosis periods ≥ 8 hrs again consistent with their ultimate storage in α-granules. At endocytosis periods < 8 hrs, less factor V colocalized with fibrinogen consistent with the localization of factor V in the cis-Golgi network at these times. In conclusion, these combined observations suggest that following its endocytosis by megakaryocytes, factor V is taken up into early endosomes and trafficked through the Golgi complex prior to its storage in α-granules. Its transport through the Golgi is consistent with previous observations that platelet-derived factor V contains an O-linked glycosylation not found in its plasma counterpart.
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Roweth, Harvey G., Michael Malloy, Jodi A. Forward, Julia Ceglowski, Robert C. Flaumenhaft, Joseph E. Italiano i Elisabeth Battinelli. "The Effects of Antiplatelet Agents on Endocytosis". Blood 134, Supplement_1 (13.11.2019): 1058. http://dx.doi.org/10.1182/blood-2019-131912.

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Almost every platelet-derived protein originates from either megakaryocytes (MKs), or the endocytosis of factors within blood circulation. These endocytosed factors can be locally released upon platelet activation to regulate hemostasis, or to promote the growth and neovascularization of solid tumors. Although platelet endocytosis has long been recognized, our mechanistic understanding remains largely confined to receptor-mediated endocytosis of fibrinogen via integrin αIIbβ3. Whether antiplatelet therapy and/or different disease states influence platelet endocytosis remain understudied areas of investigation. In this project, we examined how various antiplatelet agents affect the endocytosis of vascular endothelial growth factor (VEGF) and endostatin, which are broad pro-angiogenic and anti-angiogenic regulators, respectively. For our initial experiments, human platelets in platelet-rich plasma were exposed to either recombinant VEGF or endostatin for 1 hour, then washed to remove residual/unbound protein. Platelets were then lysed and changes in VEGF or endostatin concentration determined by ELISA. Using this approach, we demonstrated that platelets endocytose VEGF and endostatin in a concentration-dependent manner. We next established that following platelet activation, lysate concentrations of endocytosed VEGF and endostatin decreased and supernatant concentrations increased. This finding implies that endocytosed VEGF and endostatin are packaged into platelet alpha granules and are released following their activation, which we aim to confirm by measuring co-localization with endosomal and alpha granule markers. We have also developed two assays to track endocytosis into platelets, one where proteins are conjugated to pH-sensitive dyes that increase their fluorescence upon endosomal compartmentalization, and another utilizing fluorophore-targeting antibodies to quench eternal fluorescence of labeled factors. We next assessed if antiplatelet agents modulated endocytosis into platelets. We found that pre-treating platelets with aspirin, vorapaxar or ticagrelor resulted in dose-dependent inhibition of VEGF and fibrinogen but not endostatin endocytosis. This finding suggests that antiplatelet agents selectively inhibit the uptake of pro-angiogenic regulators, a statement we aim to support by measuring the endocytosis of additional angiogenic proteins. Our observations also affirm previous studies, claiming that fibrinogen and VEGF are differentially packaged into a subset of alpha granules distinct from endostatin. Experiments are ongoing to measure platelet levels of VEGF and endostatin in human subjects before and after aspirin intervention, to assess if our findings hold physiological relevance. The fact that several antiplatelet agents impaired VEGF endocytosis suggests a common inhibitory mechanism linked to suppressing basal levels of platelet activation. We tested this hypothesis by either simulating platelets with low-dose adenosine diphosphate or by chelating intracellular calcium to prevent basal activation. Neither of these processes influenced VEGF or endostatin endocytosis, suggesting that the process is not associated with basal platelet activation. We are currently investigating if antiplatelet agents alter the activity of small GTPases Arf6 and Dynamin-2, which have been shown to regulate receptor-mediated endocytosis of fibrinogen by platelets. Future experiments will aim to elucidate the mechanism by which antiplatelet agents inhibit protein uptake. It has previously been shown that platelets endocytose tumor-derived factors and RNA that may promote disease progression or act as biomarkers for liquid biopsies. We are currently studying if the daily administration of aspirin prevents the endocytosis of tumor-derived factors in a mouse model of tumor generation. In summary, our data show platelets endocytose and release key angiogenic regulators, a process which can be blocked through pre-treatment with various antiplatelet agents. Given the important role of platelets to tumor neovascularization, preventing the endocytosis of pro-angiogenic mediators could represent a novel mechanism that contributes to the inhibitory effects of antiplatelet agents on tumor growth and metastasis. Disclosures Flaumenhaft: Relay Therapeutics: Consultancy; PlateletDiagnostics: Consultancy, Other: Founder. Italiano:Platelet Biogenesis: Employment, Equity Ownership; Ionis Research Funding: Research Funding.
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Rivera, J., J. M. Mullins, K. Furuichi i C. Isersky. "Endocytosis of aggregated immunoglobulin G by rat basophilic leukemia cells; rate, extent, and effects on the endocytosis of immunoglobulin E." Journal of Immunology 136, nr 2 (15.01.1986): 623–27. http://dx.doi.org/10.4049/jimmunol.136.2.623.

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Abstract Rat basophilic leukemia (RBL) cells have distinct receptors for IgE and IgG. We assessed the endocytosis of chemically and immunochemically cross-linked mouse-IgG and its influence on the simultaneous endocytosis of IgE. We found that at 37 degrees C, aggregates of IgG and IgE were endocytosed at about the same rate with one-half of the maximal endocytosis occurring in 5 to 13 min, and the efficiency of endocytosis for both ligands ranging from 40 to 70%. We also found that endocytosis of cross-linked IgE and IgG occurred simultaneously and neither ligand significantly affected the rate or extent of endocytosis of the other. The cells accumulated the cross-linked IgG, and then released it to the extracellular environment, at a rate (less than 3%/hr) slower than the released endocytosed IgE (greater than 10%/hr). Using an assay that discriminates between unbound and receptor-bound oligomeric IgG, we found that oligomeric IgG is endocytosed with its receptor, and that the bulk of the ligand remains bound to its receptor for greater than 120 min after endocytosis. The differences in the rate of release of endocytosed IgG vs IgE suggests that the intracellular fate or pathway of these two oligomeric ligands may differ.
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Vocelle, Daniel, Olivia M. Chesniak, Amanda P. Malefyt, Georgina Comiskey, Kwasi Adu-Berchie, Milton R. Smith, Christina Chan i S. Patrick Walton. "Dextran functionalization enhances nanoparticle-mediated siRNA delivery and silencing". TECHNOLOGY 04, nr 01 (marzec 2016): 42–54. http://dx.doi.org/10.1142/s2339547816400100.

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Understanding the endocytosis and intracellular trafficking of short interfering RNA (siRNA) delivery vehicle complexes remains a critical bottleneck in designing siRNA delivery vehicles for highly active RNA interference (RNAi)-based therapeutics. In this study, we show that dextran functionalization of silica nanoparticles enhanced uptake and intracellular delivery of siRNAs in cultured cells. Using pharmacological inhibitors for endocytotic pathways, we determined that our complexes are endocytosed via a previously unreported mechanism for siRNA delivery in which dextran initiates scavenger receptor-mediated endocytosis through a clathrin/caveolin-independent process. Our findings suggest that siRNA delivery efficiency could be enhanced by incorporating dextran into existing delivery platforms to activate scavenger receptor activity across a variety of target cell types.
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Eyre, Jeanette, Kyriakos Ioannou, Blair D. Grubb, Moin A. Saleem, Peter W. Mathieson, Nigel J. Brunskill, Erik I. Christensen i Peter S. Topham. "Statin-sensitive endocytosis of albumin by glomerular podocytes". American Journal of Physiology-Renal Physiology 292, nr 2 (luty 2007): F674—F681. http://dx.doi.org/10.1152/ajprenal.00272.2006.

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Glomerular podocytes are critical regulators of glomerular permeability via the slit diaphragm and may play a role in cleaning the glomerular filter. Whether podocytes are able to endocytose proteins is uncertain. We studied protein endocytosis in conditionally immortalized mouse and human podocytes using FITC-albumin by direct quantitative assay and by fluorescence microscopy and electron microscopy in mouse podocytes. Furthermore, in vivo uptake was studied in human, rat, and mouse podocytes. Both mouse and human podocytes displayed specific one-site binding for FITC-albumin with Kd of 0.91 or 0.44 mg/ml and Bmax of 3.15 or 0.81 μg/mg cell protein, respectively. In addition, they showed avid endocytosis of FITC-albumin with Km of 9.48 or 4.5 mg/ml and Vmax of 474.3 or 97.4 μg·mg cell protein−1·h−1, respectively. Immunoglobulin and transferrin were inefficient competitors of this process, indicating some specificity for albumin. Accumulation of endocytosed albumin could be demonstrated in intracellular vesicles by fluorescence confocal microscopy and electron microscopy. Endocytosis was sensitive to pretreatment with simvastatin. In vivo accumulation of albumin was found in all three species but was most pronounced in the rat. We conclude that podocytes are able to endocytose protein in a statin-sensitive manner. This function is likely to be highly significant in health and disease. In addition, protein endocytosis by podocytes may represent a useful, measurable phenotypic characteristic against which potentially injurious or beneficial interventions can be assessed.
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Bouchard, Beth A., Natalie T. Meisler, Michael E. Nesheim i Paula B. Tracy. "Uptake of Factor V by Megakaryocytes Requires a Specific Factor V Receptor Linked to a Low-Density Lipoprotein Receptor-Related Protein." Blood 106, nr 11 (16.11.2005): 688. http://dx.doi.org/10.1182/blood.v106.11.688.688.

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Abstract Factor V is endocytosed by megakaryocytes from plasma to form the platelet-derived factor V/Va pool via a receptor-mediated, clathrin-dependent mechanism. However, the megakaryocyte receptor that mediates the binding and subsequent endocytosis of plasma-derived factor V is unknown. Because of its known ability to interact with proteins involved in coagulation and fibrinolysis, the role of low-density lipoprotein receptor-related protein (LRP) or an LRP-like molecule was examined in factor V endocytosis by the megakaryocyte-like cell line CMK. As endocytosis by such proteins is Ca2+-dependent, binding and endocytosis of factor V ± added Ca2+ were examined. While endocytosis of factor V was absolutely dependent upon the presence of Ca2+, binding of factor V to megakaryocytes was unaffected by its absence allowing for the quantification of 125I-factor V binding in the absence of factor V endocytosis. The time-dependent, specific 125I-factor V binding to megakaryocytes reached a steady-state within 20–25 min and displayed a sigmoidal character. The steady state binding of a plasma concentration of 125I-factor V could be displaced 56.4 ± 7.8% by the addition of a 150-fold molar excess of the LRP ligand, receptor associated protein (RAP). In contrast, nearly all of the 125I-factor V bound could be displaced following the addition of a 50-fold molar excess of factor V alone or by the addition of both factor V and RAP. These observations suggest that factor V binds to two binding sites on megakaryocytes, which consist of a specific factor V receptor and LRP (or an LRP-like molecule). This notion of a two-receptor system was confirmed in steady state, concentration-dependent binding analyses of 125I-factor V in the presence or absence of RAP. Binding of factor V was saturable at a concentration ~15–20 times higher than the plasma concentration of factor V, which is consistent with observations that the platelet-derived factor V concentration is dependent upon and parallels the plasma-derived factor V concentration. Similar to the observations described above, concentration-dependent binding was also inhibited 40–50% by the presence of excess RAP. The binding curves in the presence or absence of RAP remained sigmoidal and were fit with confidence (r ≥ 0.95) to a two-receptor binding model. In support of these observations, AlexaFluor488-labeled factor V and AlexaFluor633-labeled RAP co-localized within the same cells subsequent to their endocytosis by megakaryocytes as demonstrated by confocal microscopy. Flow cytometric analyses of the same cell population confirmed these observations: All of the cells that endocytosed factor V also endocytosed RAP. Based upon the combined observations we propose a binding model where factor V endocytosis is mediated by a two-receptor system consisting of a specific factor V receptor and an LRP co-receptor closely linked on the cell surface. In this model, factor V binds to its specific receptor in a Ca2+-independent manner. Bound factor V is then transferred to LRP (or an LRP-like molecule) to allow for the binding of a second factor V molecule to the unoccupied site on the factor V receptor. Factor V bound to LRP is then endocytosed in Ca2+- and clathrin-dependent manners. As our flow cytometric analyses indicate that all of the cells bind and endocytose RAP, we hypothesize that it is the presence or absence of the specific factor V receptor that defines the megakaryocytes’ ability to endocytose factor V from plasma.
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Ivesic, Caroline, Stefanie Krammer, Marianne Koller-Peroutka, Aicha Laarouchi, Daniela Gruber, Ingeborg Lang, Irene K. Lichtscheidl i Wolfram Adlassnig. "Quantification of Protein Uptake by Endocytosis in Carnivorous Nepenthales". Plants 12, nr 2 (11.01.2023): 341. http://dx.doi.org/10.3390/plants12020341.

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Carnivorous plants adsorb prey-derived nutrients partly by endocytosis. This study quantifies endocytosis in Drosophyllum lusitanicum, Drosera capensis, Drosera roseana, Dionaea muscipula and Nepenthes × ventrata. Traps were exposed to 1% fluorescent-labeled albumin (FITC-BSA), and uptake was quantified repeatedly for 64 h. Formation of vesicles started after ≤1 h in adhesive traps, but only after 16 h in species with temporary stomach (D. muscipula and N. × ventrata). In general, there are similarities in the observed species, especially in the beginning stages of endocytosis. Nonetheless, further intracellular processing of endocytotic vesicles seems to be widely different between species. Endocytotic vesicle size increased significantly over time in all species except in D. capensis. Fluorescence intensity of the endocytotic vesicles increased in all species except D. muscipula. After 64 h, estimates for FITC-BSA absorption per gland ranged from 5.9 ± 6.3 ng in D. roseana to 47.8 ± 44.3 ng in N. × ventrata, demonstrating that endocytosis substantially contributes to the adsorption of prey-derived nutrients.
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Parks, A. L., K. M. Klueg, J. R. Stout i M. A. Muskavitch. "Ligand endocytosis drives receptor dissociation and activation in the Notch pathway". Development 127, nr 7 (1.04.2000): 1373–85. http://dx.doi.org/10.1242/dev.127.7.1373.

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Endocytosis of the ligand delta; is required for activation of the receptor Notch during Drosophila development. The Notch extracellular domain (NotchECD) dissociates from the Notch intracellular domain (NotchICD) and is trans-endocytosed into delta;-expressing cells in wild-type imaginal discs. Reduction of dynamin-mediated endocytosis in developing eye and wing imaginal discs reduces Notch dissociation and Notch signalling. Furthermore, dynamin-mediated delta endocytosis is required for Notch trans-endocytosis in Drosophila cultured cell lines. Endocytosis-defective delta proteins fail to mediate trans-endocytosis of Notch in cultured cells, and exhibit aberrant subcellular trafficking and reduced signalling capacity in Drosophila. We suggest that endocytosis into delta-expressing cells of NotchECD bound to delta plays a critical role during activation of the Notch receptor and is required to achieve processing and dissociation of the Notch protein.
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Rozprawy doktorskie na temat "Endocytosis"

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Haglund, Kaisa. "Ubiquitination and Receptor Endocytosis". Doctoral thesis, Uppsala University, Ludwig Institute for Cancer Research, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4259.

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Protein ubiquitination is an evolutionary conserved mechanism that controls a wide variety of cellular functions. Polyubiquitinated proteins are generally degraded in the proteasome, whereas monoubiquitination controls various other cellular processes, including endocytosis and endosomal sorting.

Termination of signaling by activated receptor tyrosine kinases (RTKs) largely occurs via their endocytosis and subsequent lysosomal degradation, processes accompanied by receptor ubiquitination. Cbl family proteins are major ubiquitin ligases that promote RTK ubiquitination and downregulation. We showed that epidermal growth factor (EGF) and platelet derived growth factor (PDGF) receptors are monoubiquitinated at multiple sites following their ligand-induced activation and that a single ubiquitin is sufficient for both receptor internalization and degradation. Cbl also controls EGF receptor (EGFR) downregulation by binding to CIN85, which recruits endophilins to EGFR/Cbl complexes. In the complex with activated EGFRs, Cbl directs monoubiquitination of CIN85, and the entire complex is targeted for degradation in the lysosome. We propose that multiple monoubiquitination of activated receptors and associated protein complexes ensures proper receptor sorting towards the lysosome. Importantly, the functions of Cbl are also negatively controlled in order to maintain cellular homestasis. Sprouty2 blocks EGFR downregulation by sequestering Cbl from activated EGFRs. We showed that Sprouty2 also associates with CIN85 and that this binding is required for efficient inhibition of EGFR ubiquitination and endocytosis.

Cbl is also implicated in other aspects of RTK signaling, including organization of the actin cytoskeleton. We found that growth factor receptor signals promote lamellipodia formation in neuronal cells via a complex containing Cbl, the adaptor protein ArgBP2 and Pyk2. The lamellipodia formation required intact lipid rafts and the recruitment of Crk and PI(3)K to tyrosine phosphorylated Cbl.

In conclusion, our findings contribute to a better understanding of monoubiquitin signals in downregulation of RTKs and point at a role of Cbl in the regulation of cytoskeleton dynamics.

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Webster, Paul. "Endocytosis by African trypanosomes". Thesis, Brunel University, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280722.

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Kalkman, Edward R. I. C. "Endocytosis in filamentous fungi". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/1970.

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Endocytosis is little understood in filamentous fungi. For some time it has been controversial as to whether endocytosis occurs in filamentous fungi. A comparative genomics analysis between Saccharomyces cerevisiae and 10 genomes of filamentous fungal species showed that filamentous fungi possess complex endocytic machineries. The use of the endocytic marker dye FM4-64, and various vesicle trafficking inhibitors revealed many similarities between endocytosis in the filamentous fungus Neurospora crassa, and endocytosis in budding yeast and mammalian cells. Actin polymerization was found to be crucial for endocytosis in N. crassa, and the microtubule cytoskeleton seemed to be necessary for long distance movement of putative early endosomes. Brefeldin A (BFA) blocked vesicular transport to the Spitzenkörper. Three putative endocytic proteins (WASP, clathrin light chain and Rab5) were labelled with fluorescent proteins in N. crassa. WASP-GFP was found to localise to motile, punctate structures in the plasma membrane just behind the hyphal apex in growing hyphae. This localisation changed to the hyphal apex when growth was temporarily arrested, indicating a possible role in endocytosis and polarized growth. Clathrin light chain-GFP was found to be concentrated in a region just behind the Spitzenkörper, which is consistent with there being a high concentration of clathrinmediated endocytosis in this region. Clathrin light chain-GFP also labelled putative Golgi and this labelling was found to be BFA sensitive, whereas BFA did not have a detectable effect on FM4-64 internalisation and organelle staining. GFP-Rab5 labelled putative early endosomes and decorated microtubules. Knock-outs of putative endocytic proteins in N. crassa, generated as part of the Neurospora genome consortium gene knock-out project, were analysed for defects in endocytosis. 14 out of 17 gene knock-outs were found to be ascospore lethal. The Rab5 knock-out was viable, but did not show a detectable effect on the endocytic internalisation of FM4-64 or its pattern of staining. However, it did exhibit a defect in sexual crossing.
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Gagliardi, M. "Endocytosis and wingless signalling". Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1353109/.

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Wingless (Drosophila Wnt-1) is secreted glycoprotein that triggers an evolutionary conserved signal transduction pathway. The role of endocytosis in Wnt/Wingless signaling is not clearly understood and highly debated. In my thesis I explore the role that endocytosis/endocytic trafficking has on Wingless signalling activation and termination. In the canonical pathway Wingless binds to a member of the Frizzled family of seven-pass transmembrane receptor (Frizzled1 or Frizzled2) and to Arrow. Formation of this trimeric complex leads to the inactivation of the Armadillo degradation complex and translocation of Armadillo into the nucleus where it contributes to the activation of target genes. I show that internalization of the ligand-receptor complex is not required for signalling activation. I also show that Wingless has different effects on the trafficking route of its receptors: it induces the degradation of Frizzled2 and the recycling of Arrow. To identify post translational modifications that regulate Arrow trafficking I conducted an RNAi screen in Drosophila S2R+ cells for de-ubiquitylating enzymes (DUBs) and ubiquitin conjugating enzymes (E2) that modulate signalling. To carry out this screen, improvements on the current TOPFlash Wnt/Wingless signalling reporter were made. I also directly assessed the role of endocytic trafficking on signalling using a chemical inhibitor of endocytosis, Dynasore. I find that Dynasore inhibits signalling by causing a strong decrease in Armadillo levels. Future experiments will determine whether it is the stability or the rate of production of Armadillo that is affected.
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Rehman, Michael. "Analysis of endocytosis at eisosomes". Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-135951.

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Jha, Ankita. "Quantitative control of GPCR organization and signaling by endocytosis in epithelial morphogenesis". Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0393/document.

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Au cours de la gastrulation de l’embryon de Drosophile, l’activation apicale du cytosquelette d’acto-myosine orchestre la constriction apicale dans le mésoderme en invagination ainsi que l’intercalation cellulaire dans l’ectoderme en extension. Un contrôle quantitatif de l’activité des GPCRs et, par conséquent, de l’activation de Rho1 est à l’origine des différences de déformation des cellules du mésoderme et de l’ectoderme mais ces mécanismes demeurent incompris. L’activité du GPCR Smog se concentre respectivement en deux compartiments distincts à la surface de la membrane plasmique (PM) et dans ses invaginations (PMI). Au moyen de la FCS, nous avons étudié la surface de la PM et pu montrer que Smog oligomérise en homo-clusters en réponse à son activation par le ligand Fog. L’endocytose de Smog est facilitée par la kinase Gprk2 et sa protéine adaptatrice la β-Arrestine-2 qui retire Smog actif de la PM. Lorsque que la concentration de Fog est élevée ou que l’endocytose est réduite, Smog s’organise en homo-clusters et s’accumule au niveau des PMI qui agissent comme des centres d’activation de Rho1. Une concentration plus importante d’homo-clusters de Smog et un nombre plus important PMI dans le mésoderme par comparaison avec l’ectoderme. Répartition dynamique de Smog actif à la surface de la PM ou dans ses invaginations impacte directement sur la signalisation Rho1. Les PMI accumulent de hauts niveaux de Rho1-GTP suggérant qu’elles forment des centres de signalisation. La concentration de Fog et l’endocytose de Smog sont des processus régulateurs couplés qui contrôlent la différence quantitative d’activation de Rho1 dans le mésoderme et l’ectoderme de la Drosophile
During Drosophila gastrulation, apical activation of the actomyosin networks drives apical constriction in the invaginating mesoderm and cell-cell intercalation in the extending ectoderm. Here, we show that cell-surface G-protein coupled receptor, Smog activates G-proteins, Rho1 and Rho-kinase that is required for apical constriction and cell-cell intercalation. Quantitative control over GPCR activity and thereby Rho1 activation underlies differences in deformation of the mesoderm and ectoderm cells but the mechanisms remain elusive. We show that GPCR-Smog activity is concentrated on two different apical plasma membrane compartments i.e. the surface and the plasma membrane invaginations. Using FCS, we probe the surface of the plasma membrane (PM) and show that Smog homo-clusters in response to its activating ligand Fog. Endocytosis of Smog is facilitated by the kinase Gprk2 and the adaptor protein β-Arrestin-2 that clears active Smog from the surface of PM. When Fog concentration is high or endocytosis is low, Smog arranges in homo-clusters and accumulates in plasma membrane invaginations (PMI), that are hubs for Rho1 activation. Lastly, we find high Smog homo-cluster concentrations and numerous apical PMIs in the mesoderm compared to the ectoderm. We identify that dynamic partitioning of active Smog on the surface of the PM or PMI directly impact on Rho1 signaling. PMIs accumulate high Rho1-GTP suggesting they form signaling centers. Fog concentration and Smog endocytosis form coupled regulatory processes that regulate quantitative differential Rho1/MyoII activation in the Drosophila mesoderm and ectoderm
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Shurety, Wenda. "Apical endocytosis in Caco-2 cells". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242912.

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Karagiannis, Sophia. "The process of endocytosis of CD23". Thesis, King's College London (University of London), 1995. https://kclpure.kcl.ac.uk/portal/en/theses/the-process-of-endocytosis-of-cd23(553202e7-a9c8-444e-b0a5-f7561d1e6297).html.

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Nichols, II James Tucker. "DSL-ligand endocytosis and notch signaling". Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1692099791&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Wilbur, Jeremy D. "Conformational switches regulate clathrin mediated endocytosis". Diss., Search in ProQuest Dissertations & Theses. UC Only, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3324583.

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Książki na temat "Endocytosis"

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Pastan, Ira, i Mark C. Willingham, red. Endocytosis. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-6904-6.

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Courtoy, Pierre J., red. Endocytosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5.

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H, Pastan Ira, i Willingham Mark C, red. Endocytosis. New York: Plenum Press, 1985.

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Mark, Marsh, red. Endocytosis. Oxford [England]: Oxford University Press, 2001.

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Šamaj, Jozef, František Baluška i Diedrik Menzel, red. Plant Endocytosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/b103851.

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Šamaj, Jozef, red. Endocytosis in Plants. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-32463-5.

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Lamaze, Christophe, i Ian Prior, red. Endocytosis and Signaling. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96704-2.

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Swan, Laura E., red. Clathrin-Mediated Endocytosis. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8719-1.

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Ivanov, Andrei I., red. Exocytosis and Endocytosis. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-178-9.

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Ivanov, Andrei I., red. Exocytosis and Endocytosis. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0944-5.

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Części książek na temat "Endocytosis"

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De Brabander, M., R. Nuydens i H. Geerts. "Dynamic Cytomatrix-Membrane Interactions Investigated with Nanovid Microscopy". W Endocytosis, 3–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_1.

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Storrie, B., i Y. Deng. "Protein Exchange Within the Lysosome and Pre-Lysosome Compartment: A Mechanism for Maintaining Organelle Functionality?" W Endocytosis, 85–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_10.

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Murphy, Robert F., Mario Roederer, David M. Sipe, Cynthia Corley Cain i Russell B. Wilson. "Endosomal pH Regulation and the Maturation Model for Lysosome Biogenesis". W Endocytosis, 91–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_11.

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Pypaert, Marc, i Graham Warren. "Effect of ATPγS on the Formation of Coated Vesicles in Broken Hela Cells". W Endocytosis, 99–104. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_12.

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Schmid, Sandra L., Laura L. Carter i Elizabeth Smythe. "ATP is Required for Receptor-Mediated Endocytosis Both in Vivo and in Vitro". W Endocytosis, 105–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_13.

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Gruenberg, Jean, Jean-Pierre Gorvel i Morgane Bomsel. "Regulation of Endocytic Membrane Traffic". W Endocytosis, 113–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_14.

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Luzio, J. Paul, i Barbara M. Mullock. "The Interaction of Late Endosomes with Lysosomes in a Cell-Free System". W Endocytosis, 123–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_15.

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Howell, Kathryn. "Roundtable on Cell-Free Systems". W Endocytosis, 131–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_16.

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Fuchs, R., S. Schmid, I. Mellman i H. Klapper. "Regulation of ATP-Dependent Endosome Acidification". W Endocytosis, 135–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_17.

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Desbuquois, Bernard, François Authier, Jean-Pierre Clot, Michel Janicot i Françoise Fouque. "Degradation of Insulin and Glucagon in Isolated Liver Endosomes: Functional Relationships with ATP-Dependent Endosomal Acidification and Partial Characterization of Degradation Products". W Endocytosis, 141–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_18.

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Streszczenia konferencji na temat "Endocytosis"

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Guan, Yingxue, Aili Zhang i Lisa X. Xu. "Theoretical Study of Cellular Uptake of QD Nanoparticles". W ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53361.

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Cellular uptake kinetics of nanoparticles is one of the key issues determining the design and application of the particles. It is widely accepted that the nanoparticles getting into the cells mainly by endocytosis[1], a process which is found to be inhibited distinctly when temperature is below 4 °C. In fact, some nanoparticles could enter cells at lower temperatures or when the endocytosis was blocked[2–4]. Models describing the intrusion of the nanoparticles into cells only take the endocytosis process into consideration5. Meanwhile, other than the factors as concentration, size, electrical charge, temperature is also an important parameter affecting the uptake process, as binding with the receptors on the cell membranes[6] and endocytosis of nanoparticles[2, 3, 7] and etc. are all energy related. Thus, in this paper, the influence of temperature on the cellular uptake of QDs is studied experimentally, and a two-step mass transfer model describing the cellular internalization of the nanoparticles is developed by taking the temperature effect into consideration.
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Ciobanu, Gabriel. "On the power of endocytosis and exocytosis". W 2008 3rd International Conference on Bio-Inspired Computing: Theories and Applications (BIC-TA 2008). IEEE, 2008. http://dx.doi.org/10.1109/bicta.2008.4656694.

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Nuzzo, G. "Fractional diffusion of membrane receptors in endocytosis pathway". W AIMETA 2022. Materials Research Forum LLC, 2023. http://dx.doi.org/10.21741/9781644902431-50.

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Abstract. In this paper the diffusion model representing the motion of membrane receptors with respect to virus endocytosis is considered in the context of applied mechanics. The unexpected behaviour of the receptor density that moves from higher concentrations in the unbound phase to lower concentration at the right of the virus surface is accounted for introducing a mechanical drift term in the governing equation so that the difference of concentrations, higher in the bounded phase and lower in the unbounded phase is accounted for in the receptor motion. Additionally, a non-gaussian model of diffusion has been introduced in terms of fractional generalization of the Fick law.
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Massaeli, Hamid, Divya Viswanathan, Dhanya Pillai i Nasrin Mesaeli. "Regulation Of Caveolin-dependent Endocytosis By Endoplasmic Reticulum Chaperones". W Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp1034.

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Grøvdal, Lene M., Lasse Henriksen, Michael V. Grandal, Stine LJ Knudsen i Bo van Deurs. "Abstract 264: EGFR endocytosis after binding of different ligands". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-264.

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Kyung- Hwa Yoo. "Capacitance-based real time monitoring of receptor-mediated endocytosis". W 2010 Conference on Precision Electromagnetic Measurements (CPEM 2010). IEEE, 2010. http://dx.doi.org/10.1109/cpem.2010.5544238.

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Dufour, A., V. Meas-Yedid, A. Grassart i J. C. Olivo-Marin. "Automated quantification of cell endocytosis using active contours and wavelets". W 2008 19th International Conference on Pattern Recognition (ICPR). IEEE, 2008. http://dx.doi.org/10.1109/icpr.2008.4761748.

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Khan, Imran, i Patricia S. Steeg. "Abstract 1047: Role of endocytosis in NM23 mediated motility suppression". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1047.

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Baek, Jongho, Jieqiong Lou, Simao Coelho, Yean Jin Lim, Silvia Seidlitz, Philip R. Nicovich, Christian Wunder, Ludger Johannes i Katharina Gaus. "Imaging galectin-3 dependent endocytosis with lattice light-sheet microscopy". W International Conference on Biophotonics V, redaktorzy David D. Sampson, Dennis L. Matthews, Jürgen Popp, Halina Rubinsztein-Dunlop i Brian C. Wilson. SPIE, 2017. http://dx.doi.org/10.1117/12.2275706.

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Hiroaki Suzuki, Thomas Pucadyil, Rajesh Ramachandran, Shoji Takeuchi i Sandra L. Schmid. "Supported lipid bilayer array to study clathrin mediated endocytosis in vitro". W 2007 IEEE 20th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2007. http://dx.doi.org/10.1109/memsys.2007.4433076.

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Raporty organizacyjne na temat "Endocytosis"

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Ceresa, Brian, i Sandra L. Schmid. EGF-Receptor Signaling in Endocytosis Deficient Cells. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2001. http://dx.doi.org/10.21236/ada396679.

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Ceresa, Brian, i Sandra Schmid. EGF-Receptor Signaling in Endocytosis Deficient Cells. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2000. http://dx.doi.org/10.21236/ada383645.

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Schmid, Sandra L., i Christophe Lamaze. Characterization of Ligand-Induced Endocytosis of EGF Receptors. Fort Belvoir, VA: Defense Technical Information Center, maj 1995. http://dx.doi.org/10.21236/ada300531.

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Schmid, Sandra L., i Christophe LAmaze. Characterization of Ligand-Induced Endocytosis of EGF - Receptors. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 1996. http://dx.doi.org/10.21236/ada314743.

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Lee, Anthony, i Mark A. Lemmon. Study of the Regulation of ErbB Signaling by Receptor-Mediated Endocytosis. Fort Belvoir, VA: Defense Technical Information Center, maj 2002. http://dx.doi.org/10.21236/ada406114.

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Lee, Anthony. Study of the Regulation of erbB Signaling by Receptor-Mediated Endocytosis. Fort Belvoir, VA: Defense Technical Information Center, maj 2001. http://dx.doi.org/10.21236/ada406140.

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Lee, Anthony, i Mark A. Lemmon. Study of the Regulation of erbB Signaling by Receptor-mediated Endocytosis. Fort Belvoir, VA: Defense Technical Information Center, maj 2000. http://dx.doi.org/10.21236/ada383058.

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El Bejjani, Rachid M. Effect of MUC1 Expression on EGFR Endocytosis and Degradation in Human Breast Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2009. http://dx.doi.org/10.21236/ada504024.

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El Bejjani, Rachid M. Effect of MUC1 Expression on EGFR Endocytosis and Degradation in Human Breast Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2007. http://dx.doi.org/10.21236/ada470580.

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Brittingham, Katherine C., Gordon Ruthel, Rekha G. Panchal, Claudette L. Fuller i Wilson J. Ribot. Dendritic Cells Endocytose Bacillus Anthracis Spores: Implications for Anthrax Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, luty 2005. http://dx.doi.org/10.21236/ada434591.

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