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Journal articles on the topic 'Endocytosis'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Bouchard, Beth A., Joseph M. Petty, and 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, no. 22 (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

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2

Fares, Hanna, and Iva Greenwald. "Genetic Analysis of Endocytosis in Caenorhabditis elegans: Coelomocyte Uptake Defective Mutants." Genetics 159, no. 1 (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 mutant

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3

Bouchard, Beth A., Douglas J. Taatjes, Natalie T. Meisler та 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, № 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 int

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4

Roweth, Harvey G., Michael Malloy, Jodi A. Forward, et al. "The Effects of Antiplatelet Agents on Endocytosis." Blood 134, Supplement_1 (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

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5

Rivera, J., J. M. Mullins, K. Furuichi, and 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, no. 2 (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 ra

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6

Vocelle, Daniel, Olivia M. Chesniak, Amanda P. Malefyt, et al. "Dextran functionalization enhances nanoparticle-mediated siRNA delivery and silencing." TECHNOLOGY 04, no. 01 (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

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7

Eyre, Jeanette, Kyriakos Ioannou, Blair D. Grubb, et al. "Statin-sensitive endocytosis of albumin by glomerular podocytes." American Journal of Physiology-Renal Physiology 292, no. 2 (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

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8

Bouchard, Beth A., Natalie T. Meisler, Michael E. Nesheim, and 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, no. 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+-de

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9

Ivesic, Caroline, Stefanie Krammer, Marianne Koller-Peroutka, et al. "Quantification of Protein Uptake by Endocytosis in Carnivorous Nepenthales." Plants 12, no. 2 (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, fu

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10

Parks, A. L., K. M. Klueg, J. R. Stout, and M. A. Muskavitch. "Ligand endocytosis drives receptor dissociation and activation in the Notch pathway." Development 127, no. 7 (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 me

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11

Furuichi, K., J. Rivera, L. M. Buonocore, and C. Isersky. "Recycling of receptor-bound IgE by rat basophilic leukemia cells." Journal of Immunology 136, no. 3 (1986): 1015–22. http://dx.doi.org/10.4049/jimmunol.136.3.1015.

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Abstract Rat basophilic leukemia (RBL) cells have receptors for immunoglobulin E (IgE). We previously showed that unlike some other ligands, the binding of monomeric rat or mouse IgE to RBL cells does not induce endocytosis. However, aggregation of the cell-bound, monomeric mouse IgE anti-dinitrophenyl (DNP) with DNP-protein conjugates leads to endocytosis of the aggregated mouse IgE and to the co-endocytosis of some unaggregated monomeric rat IgE. In this study we analyzed and compared the fate of co-endocytosed and endocytosed IgE. We found that co-endocytosed rat IgE recycled back to the ce

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12

VEERAMACHANENI, D. N. RAO, and RUPERT P. AMANN. "Endocytosis of Androgen‐Binding Protein, Cluster in, and Transferrin in the Efferent Ducts and Epididymis of the Ram." Journal of Andrology 12, no. 5 (1991): 288–94. http://dx.doi.org/10.1002/j.1939-4640.1991.tb01602.x.

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ABSTRACT: The amount of androgen‐binding protein (ABP) In luminal fluid from the central caput epididymidis of the ram, on a per sperm basis, remains the same as that in rete testis fluid (RTF) entering the ductuli efferentes, although >85% of the testicular protein is absorbed in proximal sites. To determine if ABP is spared from endocytosis in proximal sites and if proteins are differentially and selectively absorbed at specific sites in the excurrent ducts, we studied the endocytosis of ABP, clusterin, transferrin, and a 26/35‐kd dimer isolated from ovine RTF. Each protein was labeled wi

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13

Wang, Zhixiang, Lianfeng Zhang, Tai K. Yeung, and Xinmei Chen. "Endocytosis Deficiency of Epidermal Growth Factor (EGF) Receptor–ErbB2 Heterodimers in Response to EGF Stimulation." Molecular Biology of the Cell 10, no. 5 (1999): 1621–36. http://dx.doi.org/10.1091/mbc.10.5.1621.

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Epidermal growth factor (EGF) stimulates the homodimerization of EGF receptor (EGFR) and the heterodimerization of EGFR and ErbB2. The EGFR homodimers are quickly endocytosed after EGF stimulation as a means of down-regulation. However, the results from experiments on the ability of ErbB2 to undergo ligand-induced endocytosis are very controversial. It is unclear how the EGFR–ErbB2 heterodimers might behave. In this research, we showed by subcellular fractionation, immunoprecipitation, Western blotting, indirect immunofluorescence, and microinjection that, in the four breast cancer cell lines

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14

Bi, Yan, Dhriti Mukhopadhyay, Mary Drinane, et al. "Endocytosis of collagen by hepatic stellate cells regulates extracellular matrix dynamics." American Journal of Physiology-Cell Physiology 307, no. 7 (2014): C622—C633. http://dx.doi.org/10.1152/ajpcell.00086.2014.

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Hepatic stellate cells (HSCs) generate matrix, which in turn may also regulate HSCs function during liver fibrosis. We hypothesized that HSCs may endocytose matrix proteins to sense and respond to changes in microenvironment. Primary human HSCs, LX2, or mouse embryonic fibroblasts (MEFs) [wild-type; c-abl−/−; or Yes, Src, and Fyn knockout mice (YSF−/−)] were incubated with fluorescent-labeled collagen or gelatin. Fluorescence-activated cell sorting analysis and confocal microscopy were used for measuring cellular internalization of matrix proteins. Targeted PCR array and quantitative real-time

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15

Rosa, Juliana M., Cristina J. Torregrosa-Hetland, Inés Colmena, Luis M. Gutiérrez, Antonio G. García, and Luis Gandía. "Calcium entry through slow-inactivating L-type calcium channels preferentially triggers endocytosis rather than exocytosis in bovine chromaffin cells." American Journal of Physiology-Cell Physiology 301, no. 1 (2011): C86—C98. http://dx.doi.org/10.1152/ajpcell.00440.2010.

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Calcium (Ca2+)-dependent endocytosis has been linked to preferential Ca2+ entry through the L-type (α1D, CaV1.3) of voltage-dependent Ca2+ channels (VDCCs). Considering that the Ca2+-dependent exocytotic release of neurotransmitters is mostly triggered by Ca2+ entry through N-(α1B, CaV2.2) or PQ-VDCCs (α1A, CaV2.1) and that exocytosis and endocytosis are coupled, the supposition that the different channel subtypes are specialized to control different cell functions is attractive. Here we have explored this hypothesis in primary cultures of bovine adrenal chromaffin cells where PQ channels acco

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16

Smith, Corey, and Erwin Neher. "Multiple Forms of Endocytosis In Bovine Adrenal Chromaffin Cells." Journal of Cell Biology 139, no. 4 (1997): 885–94. http://dx.doi.org/10.1083/jcb.139.4.885.

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We studied endocytosis in chromaffin cells with both perforated patch and whole cell configurations of the patch clamp technique using cell capacitance measurements in combination with amperometric catecholamine detection. We found that chromaffin cells exhibit two relatively rapid, kinetically distinct forms of stimulus-coupled endocytosis. A more prevalent “compensatory” retrieval occurs reproducibly after stimulation, recovering an approximately equivalent amount of membrane as added through the immediately preceding exocytosis. Membrane is retrieved through compensatory endocytosis at an i

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17

Shen, Yingjie, Lizhong Xu, and David A. Foster. "Role for Phospholipase D in Receptor-Mediated Endocytosis." Molecular and Cellular Biology 21, no. 2 (2001): 595–602. http://dx.doi.org/10.1128/mcb.21.2.595-602.2001.

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ABSTRACT In response to epidermal growth factor (EGF), the EGF receptor is endocytosed and degraded. A substantial lag period exists between endocytosis and degradation, suggesting that endocytosis is more than a simple negative feedback. Phospholipase D (PLD), which has been implicated in vesicle formation in the Golgi, is activated in response to EGF and other growth factors. We report here that EGF receptor endocytosis is dependent upon PLD and the PLD1 regulators, protein kinase C α and RalA. EGF-induced receptor degradation is accelerated by overexpression of either wild-type PLD1 or PLD2

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18

Li, Chuang-Ye, Li Liu, Yao-Wang Zhao, et al. "Repair of Tea Polysaccharide Promotes the Endocytosis of Nanocalcium Oxalate Monohydrate by Damaged HK-2 Cells." Oxidative Medicine and Cellular Longevity 2020 (April 27, 2020): 1–12. http://dx.doi.org/10.1155/2020/2198976.

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Endocytosis is a protective mechanism of renal epithelial cells to eliminate retained crystals. This research investigated the endocytosis of 100 nm calcium oxalate monohydrate crystals in human kidney proximal tubular epithelial (HK-2) cells before and after repair by four kinds of tea polysaccharides with molecular weights (MWs) of 10.88 (TPS0), 8.16 (TPS1), 4.82 (TPS2), and 2.31 kDa (TPS3), respectively. When HK-2 cells were repaired by TPSs after oxalic acid injury, the cell viability, wound healing ability, mitochondrial membrane potential, percentage of cells with endocytosed crystals, a

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Kuhn, Dagmar A., Dimitri Vanhecke, Benjamin Michen, et al. "Different endocytotic uptake mechanisms for nanoparticles in epithelial cells and macrophages." Beilstein Journal of Nanotechnology 5 (September 24, 2014): 1625–36. http://dx.doi.org/10.3762/bjnano.5.174.

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Precise knowledge regarding cellular uptake of nanoparticles is of great importance for future biomedical applications. Four different endocytotic uptake mechanisms, that is, phagocytosis, macropinocytosis, clathrin- and caveolin-mediated endocytosis, were investigated using a mouse macrophage (J774A.1) and a human alveolar epithelial type II cell line (A549). In order to deduce the involved pathway in nanoparticle uptake, selected inhibitors specific for one of the endocytotic pathways were optimized regarding concentration and incubation time in combination with fluorescently tagged marker p

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20

Hua, Q., C. B. Knudson, and W. Knudson. "Internalization of hyaluronan by chondrocytes occurs via receptor-mediated endocytosis." Journal of Cell Science 106, no. 1 (1993): 365–75. http://dx.doi.org/10.1242/jcs.106.1.365.

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Several studies have suggested that chondrocytes must have the capacity to internalize and degrade extracellular hyaluronan. In the present study we show direct evidence that hyaluronan is, in fact, endocytosed by chondrocytes and that the endocytosis is mediated via cell surface CD44/hyaluronan receptors. Cultures of bovine articular chondrocytes as well as rat chondrosarcoma chondrocytes were incubated with either fluorescein- or 3H-labeled hyaluronan. Intense binding and accumulation of labeled hyaluronan was visualized by fluorescence microscopy or bright-field/dark-field microscopy follow

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Liu, Ke, Zhaolin Hua, Joshua A. Nepute, and Todd R. Graham. "Yeast P4-ATPases Drs2p and Dnf1p Are Essential Cargos of the NPFXD/Sla1p Endocytic Pathway." Molecular Biology of the Cell 18, no. 2 (2007): 487–500. http://dx.doi.org/10.1091/mbc.e06-07-0592.

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Drs2p family P-type ATPases (P4-ATPases) are required in multiple vesicle-mediated protein transport steps and are proposed to be phospholipid translocases (flippases). The P4-ATPases Drs2p and Dnf1p cycle between the exocytic and endocytic pathways, and here we define endocytosis signals required by these proteins to maintain a steady-state localization to internal organelles. Internalization of Dnf1p from the plasma membrane uses an NPFXD endocytosis signal and its recognition by Sla1p, part of an endocytic coat/adaptor complex with clathrin, Pan1p, Sla2p/End4p, and End3p. Drs2p has multiple

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22

Yao, Wenchao, Dankun Luo, Zhenyi Lv, et al. "The Rabep1-Mediated Endocytosis and Activation of Trypsinogen to Promote Pancreatic Stellate Cell Activation." Biomolecules 12, no. 8 (2022): 1063. http://dx.doi.org/10.3390/biom12081063.

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Background: The pathogenesis of chronic pancreatitis is still unclear. Trypsinogen activation is an active factor in acute pancreatitis that has not been studied in the occurrence of chronic pancreatitis. Methods: Immunofluorescence was used to detect the location and expression of trypsinogen in chronic pancreatitis and normal tissues. Microarray and single-cell RNA-seq (scRNA-seq) were used to screen core genes and pathways in pancreatic stellate cells (PSCs). Western blotting and immunofluorescence were used to verify trypsinogen expression in PSCs after silencing Rabep1. Immunofluorescence

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Li, Tianliang, Kewei Qin, Nan Li, Chaofeng Han, and Xuetao Cao. "An endosomal LAPF is required for macrophage endocytosis and elimination of bacteria." Proceedings of the National Academy of Sciences 116, no. 26 (2019): 12958–63. http://dx.doi.org/10.1073/pnas.1903896116.

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Macrophages can internalize the invading pathogens by raft/caveolae and/or clathrin-dependent endocytosis and elicit an immune response against infection. However, the molecular mechanism for macrophage endocytosis remains elusive. Here we report that LAPF (lysosome-associated and apoptosis-inducing protein containing PH and FYVE domains) is required for caveolae-mediated endocytosis.Lapf-deficient macrophages have impaired capacity to endocytose and eliminate bacteria. Macrophage-specificLapf-deficient mice are more susceptible toEscherichia coli(E. coli) infection with higher bacterial loads

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Pandey, Madhu S., Edward N. Harris, and Paul H. Weigel. "HARE-Mediated Endocytosis of Hyaluronan and Heparin Is Targeted by Different Subsets of Three Endocytic Motifs." International Journal of Cell Biology 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/524707.

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The hyaluronan (HA) receptor for endocytosis (HARE) is a multifunctional recycling clearance receptor for 14 different ligands, including HA and heparin (Hep), which bind to discrete nonoverlapping sites. Four different functional endocytic motifs (M) in the cytoplasmic domain (CD) target coated pit mediated uptake: (YSYFRI2485(M1), FQHF2495(M2), NPLY2519(M3), and DPF2534(M4)). We previously found (Pandey et al. J. Biol. Chem. 283, 21453, 2008) thatM1,M2, andM3mediate endocytosis of HA. Here we assessed the ability of HARE variants with a single-motif deletion or containing only a single motif

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25

Maxfield, Frederick R. "Characterization of endocytosis in intact cells by quantitative fluorescence microscopy." Proceedings, annual meeting, Electron Microscopy Society of America 49 (August 1991): 234–35. http://dx.doi.org/10.1017/s0424820100085472.

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Endocytosis, the process by which extracellular macromolecules are taken into the cell is particularly amenable to quantitative analysis using fluorescence techniques. Fluorescently-labeled proteins and other macromolecules are taken up by cells via receptor-mediated endocytosis or fluid phase pinocytosis. Recently, fluorescent lipid probes have also been synthesized which label the endocytic pathway, allowing observation of lipid membrane traffic.Digital imaging allows the manipulation of images, background and autofluorescence subtractions, and fluorescence intensity measurements of individu

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Hatakeyama, Riko, Masao Kamiya, Terunao Takahara, and Tatsuya Maeda. "Endocytosis of the Aspartic Acid/Glutamic Acid Transporter Dip5 Is Triggered by Substrate-Dependent Recruitment of the Rsp5 Ubiquitin Ligase via the Arrestin-Like Protein Aly2." Molecular and Cellular Biology 30, no. 24 (2010): 5598–607. http://dx.doi.org/10.1128/mcb.00464-10.

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ABSTRACT Endocytosis of nutrient transporters is stimulated under various conditions, such as elevated nutrient availability. In Saccharomyces cerevisiae, endocytosis is triggered by ubiquitination of transporters catalyzed by the E3 ubiquitin ligase Rsp5. However, how the ubiquitination is accelerated under certain conditions remains obscure. Here we demonstrate that closely related proteins Aly2/Art3 and Aly1/Art6, which are poorly characterized members of the arrestin-like protein family, mediate endocytosis of the aspartic acid/glutamic acid transporter Dip5. In aly2Δ cells, Dip5 is stabil

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Emma, F., H. W. Harris, and K. Strange. "Acidification of vasopressin-induced endosomes in toad urinary bladder." American Journal of Physiology-Renal Physiology 267, no. 1 (1994): F106—F113. http://dx.doi.org/10.1152/ajprenal.1994.267.1.f106.

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It is well established that water channels (WC) are removed from the apical membrane of vasopressin-sensitive epithelia by endocytosis. The processing and the ultimate fate of endocytosed WC is, however, incompletely understood. In many cells, endosome acidification plays an important role in the processing and sorting of endocytosed proteins. Endosome acidification in the toad urinary bladder was therefore examined in vivo by fluorescence ratio video microscopy after induction of endocytosis by vasopressin removal and transepithelial water flow in the presence of the pH-sensitive fluid phase

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Uhlin-Hansen, L., and M. Yanagishita. "Brefeldin A inhibits the endocytosis of plasma-membrane-associated heparan sulphate proteoglycans of cultured rat ovarian granulosa cells." Biochemical Journal 310, no. 1 (1995): 271–78. http://dx.doi.org/10.1042/bj3100271.

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Rat ovarian granulosa cells were labelled with [35S]sulphate for 0.5-20 h and chased in the presence or absence of 1-2 micrograms/ml of brefeldin A (BFA) for up to 21 h. Heparan [35S]sulphate (HS) proteoglycans from the culture medium, plasma membrane and intracellular fractions were then analysed by gel chromatography. In the absence of BFA, about 85% of the plasma membrane-associated HS proteoglycans were endocytosed and subsequently degraded intracellularly. Recirculation of the HS proteoglycans between the intracellular pool and the cell surface was not observed. Exposing the cells to BFA

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Handagama, PJ, DL Amrani, and MA Shuman. "Endocytosis of fibrinogen into hamster megakaryocyte alpha granules is dependent on a dimeric gamma A configuration." Blood 85, no. 7 (1995): 1790–95. http://dx.doi.org/10.1182/blood.v85.7.1790.bloodjournal8571790.

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Two species of fibrinogen that differ only in the structure of their gamma chains, gamma A and gamma', are present in normal plasma. Fibrinogen stored in platelet alpha granules does not contain gamma' chains. Because platelet fibrinogen was recently shown to be derived exclusively by receptor-mediated endocytosis from plasma and not by endogenous megakaryocyte synthesis, we postulated that the gamma' fibrinogen present in plasma is not endocytosed by megakaryocytes and platelets. We tested this hypothesis by studying endocytosis of peak 1 (containing two gamma A chains) and peak 2 (containing

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Gasingirwa, Marie-Christine, Jacqueline Thirion, Jeannine Mertens-Strijthagen, et al. "Endocytosis of hyaluronidase-1 by the liver." Biochemical Journal 430, no. 2 (2010): 305–13. http://dx.doi.org/10.1042/bj20100711.

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It has been suggested that intracellular Hyal-1 (hyaluronidase-1), which is considered a lysosomal enzyme, originates via endocytosis of the serum enzyme. To test this proposal we have investigated the uptake and intracellular distribution of rhHyal-1 (recombinant human Hyal-1) by mouse liver, making use of centrifugation methods. Experiments were performed on wild-type mice injected with 125I-labelled rhHyal-1 and on Hyal-1−/− mice injected with the unlabelled enzyme, which were killed at various times after injection. Activity of the unlabelled enzyme was determined by zymography. Intracellu

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Schwake, Michael, Thomas Friedrich, and Thomas J. Jentsch. "An Internalization Signal in ClC-5, an Endosomal Cl−Channel Mutated in Dent's Disease." Journal of Biological Chemistry 276, no. 15 (2000): 12049–54. http://dx.doi.org/10.1074/jbc.m010642200.

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The ClC-5 chloride channel resides mainly in vesicles of the endocytotic pathway and contributes to their acidification. Its disruption in mice entails a broad defect in renal endocytosis and causes secondary changes in calciotropic hormone levels. Inactivating mutations in Dent's disease lead to proteinuria and kidney stones. Possibly by recycling, a small fraction of ClC-5 also reaches the plasma membrane. Here we identify a carboxyl-terminal internalization motif in ClC-5. It resembles the PY motif, which is crucial for the endocytosis and degradation of epithelial Na+channels. Mutating thi

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Stephens, Richard S., Farah S. Fawaz, Kathleen A. Kennedy, et al. "Eukaryotic Cell Uptake of Heparin-Coated Microspheres: a Model of Host Cell Invasion by Chlamydia trachomatis." Infection and Immunity 68, no. 3 (2000): 1080–85. http://dx.doi.org/10.1128/iai.68.3.1080-1085.2000.

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ABSTRACT Using polystyrene microspheres coated with heparin or heparan sulfate, it was shown that coated microspheres specifically bound eukaryotic cells and were endocytosed by nonprofessional phagocytic cells. Coated microspheres displayed properties of binding to eukaryotic cells that were similar to those of chlamydiae, and the microspheres were competitively inhibited by chlamydial organisms. Endocytosis of heparin-coated beads resulted in the tyrosine phosphorylation of a similar set of host proteins as did endocytosis of chlamydiae; however, unlike viable chlamydial organisms, which pre

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Subtil, A., A. Hemar, and A. Dautry-Varsat. "Rapid endocytosis of interleukin 2 receptors when clathrin-coated pit endocytosis is inhibited." Journal of Cell Science 107, no. 12 (1994): 3461–68. http://dx.doi.org/10.1242/jcs.107.12.3461.

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The cytokine interleukin 2 (IL2) is produced by activated helper T lymphocytes and modulates the growth and activity of cells expressing high-affinity surface IL2 receptors that transduce its signaling. After ligand binding to receptors on the plasma membrane, receptor-ligand complexes are rapidly endocytosed and IL2 is degraded in acidic compartments. The best known receptor-mediated endocytosis pathway involves clathrin-coated pits. Receptors that carry an internalization signal recognized by adaptors on the cytosolic side of the plasma membrane are clustered into the coated pits and enter c

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Xinhan, Lou, Masafumi Matsushita, Manami Numaza, Akira Taguchi, Keiji Mitsui, and Hiroshi Kanazawa. "Na+/H+ exchanger isoform 6 (NHE6/SLC9A6) is involved in clathrin-dependent endocytosis of transferrin." American Journal of Physiology-Cell Physiology 301, no. 6 (2011): C1431—C1444. http://dx.doi.org/10.1152/ajpcell.00154.2011.

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In mammalian cells, nine conserved isoforms of the Na+/H+ exchanger (NHE) are known to be important for pH regulation of the cytoplasm and organellar lumens. NHE1–5 are localized to the plasma membrane, whereas NHE6–9 are localized to distinct organelles. NHE6 is localized predominantly in endosomal compartments but is also found in the plasma membrane. To investigate the role of NHE6 in endocytosis, we established NHE6-knockdown HeLa cells and analyzed the effect of this knockdown on endocytotic events. The expression level of NHE6 in knockdown cells was decreased to ∼15% of the level seen in

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Nurullin, L. F., N. D. Almazov, and E. M. Volkov. "Participation of Ca<sup>2+</sup>-acceptor proteins in the mechanisms of the exo-endocytic cycle of synaptic vesicles in the motor nerve endings of the somatic musculature of the earthworm <i>Lumbricus terrestris</i>." Rossijskij fiziologičeskij žurnal im. I.M. Sečenova 110, no. 9 (2024): 1430–39. https://doi.org/10.31857/s0869813924090116.

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Using fluorescence microscopy, we studied the participation of Ca2+-acceptor proteins in the processes of the exo-endocytotic cycle of neurotransmitter quantal secretion in the neuromuscular junction of the somatic muscle of the earthworm Lumbricus terrestris. Inhibition of calcineurin, calmodulin and Ca2+/calmodulin dependent protein kinases led to an increase in the process of endocytosis. Blocking the phosphorylation of synaptic proteins enhances the process of endocytosis, causes an increase in the size of the total vesicular pool and accelerates the turnover of synaptic vesicles. It can b

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Beauwens, R., G. te Kronnie, J. Snauwaert, and P. A. in't Veld. "Polycations reduce vasopressin-induced water flow by endocytic removal of water channels." American Journal of Physiology-Cell Physiology 250, no. 5 (1986): C729—C737. http://dx.doi.org/10.1152/ajpcell.1986.250.5.c729.

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Several polycations added to the luminal solution were found to inhibit the vasopressin (ADH)-induced water flow in toad urinary bladder but not the ADH-induced increase in sodium transport or in urea permeability. Ultrastructural studies were conducted to evaluate the uptake of cationized ferritin. It was found that endocytosis of cationized ferritin by luminal cells was strikingly enhanced on exposure to ADH; this increased endocytosis was concomitant with inhibition of transepithelial ADH-induced water flow. Various maneuvers preventing endocytosis were also found to counteract the polycati

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McGary, C. T., R. H. Raja, and P. H. Weigel. "Endocytosis of hyaluronic acid by rat liver endothelial cells. Evidence for receptor recycling." Biochemical Journal 257, no. 3 (1989): 875–84. http://dx.doi.org/10.1042/bj2570875.

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Hyaluronic acid (HA) is cleared from the blood by liver endothelial cells through receptor-mediated endocytosis [Eriksson, Fraser, Laurent, Pertoft & Smedsrod (1983) Exp. Cell Res. 144, 223-238]. We have measured the capacity of cultured rat liver endothelial cells to endocytose and degrade 125I-HA (Mr approximately 44,000) at 37 degrees C. Endocytosis was linear for 3 h and then reached a plateau. The rate of endocytosis was concentration-dependent and reached a maximum of 250 molecules/s per cell. Endocytosis of 125I-HA was inhibited more than 92% by a 150-fold excess of non-radiolabelle

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Koller-Peroutka, Marianne, Stefanie Krammer, Anselm Pavlik, Manfred Edlinger, Ingeborg Lang, and Wolfram Adlassnig. "Endocytosis and Digestion in Carnivorous Pitcher Plants of the Family Sarraceniaceae." Plants 8, no. 10 (2019): 367. http://dx.doi.org/10.3390/plants8100367.

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Highly evolved carnivorous plants secrete digestive enzymes for degradation of trapped animals and absorb whole macromolecules from their prey by means of endocytosis. (1) Background: In the pitcher-plant family Sarraceniaceae, the production of enzymes is dubious and no evidence for endocytosis is known so far. (2) Methods: Heliamphora nutans, Darlingtonia californica, and nine taxa of Sarracenia are tested for cuticular pores, and for protease and endocytosis of the fluorescent protein analogue FITC-BSA, after 10–48 h of stimulation. (3) Results: Cuticular pores as a prerequisite for enzyme

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Gekle, M., S. Mildenberger, R. Freudinger, and S. Silbernagl. "Endosomal alkalinization reduces Jmax and Km of albumin receptor-mediated endocytosis in OK cells." American Journal of Physiology-Renal Physiology 268, no. 5 (1995): F899—F906. http://dx.doi.org/10.1152/ajprenal.1995.268.5.f899.

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In this study, we investigated the effects of endosomal alkalinization on kinetics of endocytotic uptake in intact proximal tubule-derived opossum kidney cells. We used fluorescein isothiocyanate (FITC)-labeled albumin and FITC-dextran as endocytotic substrates for receptor-mediated endocytosis and fluid-phase endocytosis, respectively. The pH in endosomes labeled with either FITC-albumin or FITC-dextran rose in the presence of the vacuolar-type ATPase inhibitor, bafilomycin A1, and in the presence of NH4Cl. Cytoplasmic pH, decreased in the presence of bafilomycin A1, but was not significantly

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Céfaï, Daniel, Helga Schneider, Oranart Matangkasombut, Hyun Kang, Joshua Brody, and Christopher E. Rudd. "CD28 Receptor Endocytosis Is Targeted by Mutations That Disrupt Phosphatidylinositol 3-Kinase Binding and Costimulation." Journal of Immunology 160, no. 5 (1998): 2223–30. http://dx.doi.org/10.4049/jimmunol.160.5.2223.

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Abstract Although the lipid kinase phosphatidylinositol 3-kinase (PI-3K) binds at high levels to the cytoplasmic tail of CD28, controversy exists regarding its role in CD28 costimulation. Potentially, the kinase could be linked to a signaling cascade or be needed indirectly in events such as receptor endocytosis. Indeed, little is known regarding both the fate of CD28 following receptor ligation and the events that control the process. In this study, we help to resolve this issue by providing evidence that PI-3K plays a role in regulating CD28 endocytosis. We show that ∼25 to 35% of wild-type

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Shi, Yuanyuan, Chen Wang, Xiaoshuang Zhou, et al. "Downregulation of PTEN promotes podocyte endocytosis of lipids aggravating obesity-related glomerulopathy." American Journal of Physiology-Renal Physiology 318, no. 3 (2020): F589—F599. http://dx.doi.org/10.1152/ajprenal.00392.2019.

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With the increasing prevalence of obesity in adults worldwide, the incidence of obesity-related glomerulopathy (ORG) has increased yearly, becoming one of the leading causes of end-stage renal disease. Studies have demonstrated significant correlations between hyperlipidemia and impaired renal function in patients with ORG, indicating that hyperlipidemia causes damage in kidney cells. In podocytes, the endocytosis of lipids triggers an intracellular oxidative stress response that disrupts cellular integrity, resulting in proteinuria and glomerular sclerosis. However, the specific molecular mec

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Lowther, Katie M., Viacheslav O. Nikolaev, and Lisa M. Mehlmann. "Endocytosis in the mouse oocyte and its contribution to cAMP signaling during meiotic arrest." REPRODUCTION 141, no. 6 (2011): 737–47. http://dx.doi.org/10.1530/rep-10-0461.

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Mammalian oocytes are arrested at prophase I of meiosis until a preovulatory surge of LH stimulates them to resume meiosis. Prior to the LH surge, high levels of cAMP within the oocyte maintain meiotic arrest; this cAMP is generated in the oocyte through the activity of the constitutively active, Gs-coupled receptor, G-protein-coupled receptor 3 (GPR3) or GPR12. Activated GPRs are typically targeted for desensitization through receptor-mediated endocytosis, but a continuously high level of cAMP is needed for meiotic arrest. The aim of this study was to examine whether receptor-mediated endocyt

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Becuwe, Michel, Neide Vieira, David Lara, et al. "A molecular switch on an arrestin-like protein relays glucose signaling to transporter endocytosis." Journal of Cell Biology 196, no. 2 (2012): 247–59. http://dx.doi.org/10.1083/jcb.201109113.

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Endocytosis regulates the plasma membrane protein landscape in response to environmental cues. In yeast, the endocytosis of transporters depends on their ubiquitylation by the Nedd4-like ubiquitin ligase Rsp5, but how extracellular signals trigger this ubiquitylation is unknown. Various carbon source transporters are known to be ubiquitylated and endocytosed when glucose-starved cells are exposed to glucose. We show that this required the conserved arrestin-related protein Rod1/Art4, which was activated in response to glucose addition. Indeed, Rod1 was a direct target of the glucose signaling

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DEAN, ROGER T. "Endocytosis." Biochemical Society Transactions 14, no. 2 (1986): 512. http://dx.doi.org/10.1042/bst0140512.

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Traub, Linton M. "Endocytosis." Cell 107, no. 3 (2001): 272–74. http://dx.doi.org/10.1016/s0092-8674(01)00554-2.

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Hurley, James H., and Beverly Wendland. "Endocytosis." Cell 111, no. 2 (2002): 143–46. http://dx.doi.org/10.1016/s0092-8674(02)01044-9.

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Walker, J. H. "Endocytosis." Biochemical Education 14, no. 4 (1986): 198. http://dx.doi.org/10.1016/0307-4412(86)90236-0.

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Hubbard, A. L. "Endocytosis." Current Opinion in Cell Biology 1, no. 4 (1989): 675–83. http://dx.doi.org/10.1016/0955-0674(89)90033-1.

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Mukherjee, S., R. N. Ghosh, and F. R. Maxfield. "Endocytosis." Physiological Reviews 77, no. 3 (1997): 759–803. http://dx.doi.org/10.1152/physrev.1997.77.3.759.

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Mammalian cells take up extracellular material by a variety of different mechanisms that are collectively termed endocytosis. Endocytic mechanisms serve many important cellular functions including the uptake of extracellular nutrients, regulation of cell-surface receptor expression, maintenance of cell polarity, and antigen presentation. Endocytic pathways are also utilized by viruses, toxins, and symbiotic microorganisms to gain entry into cells. One of the best-characterized endocytic mechanisms is receptor-mediated endocytosis via clathrin-coated pits. This type of endocytosis constitutes t

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Boyle, John A. "Endocytosis." Biochemistry and Molecular Biology Education 30, no. 2 (2002): 139. http://dx.doi.org/10.1002/bmb.2002.494030020025.

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