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Relevant bibliographies by topics / Internalization inhibitors

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Academic literature on the topic 'Internalization inhibitors'

Author: Grafiati

Published: 19 July 2023

Last updated: 31 July 2025

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Journal articles on the topic "Internalization inhibitors"

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DiCello, Jesse J., Pradeep Rajasekhar, Emily M. Eriksson та ін. "Clathrin and GRK2/3 inhibitors block δ-opioid receptor internalization in myenteric neurons and inhibit neuromuscular transmission in the mouse colon". American Journal of Physiology-Gastrointestinal and Liver Physiology 317, № 2 (2019): G79—G89. http://dx.doi.org/10.1152/ajpgi.00085.2019.

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Endocytosis is a major mechanism through which cellular signaling by G protein-coupled receptors (GPCRs) is terminated. However, recent studies demonstrate that GPCRs are internalized in an active state and continue to signal from within endosomes, resulting in effects on cellular function that are distinct to those arising at the cell surface. Endocytosis inhibitors are commonly used to define the importance of GPCR internalization for physiological and pathophysiological processes. Here, we provide the first detailed examination of the effects of these inhibitors on neurogenic contractions o

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Bigby, M., P. Wang, J. F. Fierro, and M. S. Sy. "Phorbol myristate acetate-induced down-modulation of CD4 is dependent on calmodulin and intracellular calcium." Journal of Immunology 144, no. 8 (1990): 3111–16. http://dx.doi.org/10.4049/jimmunol.144.8.3111.

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Abstract PMA causes rapid down-modulation of CD4 molecules on murine immature thymocytes, human PBL, and CD4-positive human tumor cell lines, but not on murine peripheral lymphocytes. The mechanisms of phorbol ester-induced down modulation of CD4 molecules, however, have not been elucidated. To determine how PMA down-modulates CD4 expression by T lymphocytes, we studied the ability of inhibitors of protein kinase C, calmodulin, actin, and tubulin to block PMA-induced modulation of CD4 in several murine and human cell types. We also tested the ability of intracellular and extracellular calcium

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van Kerkhof, P., and G. J. Strous. "The ubiquitin-proteasome pathway regulates lysosomal degradation of the growth hormone receptor and its ligand." Biochemical Society Transactions 29, no. 4 (2001): 488–93. http://dx.doi.org/10.1042/bst0290488.

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The growth hormone (GH) receptor (GHR) is a mammalian plasma membrane protein whose internalization is mediated by the ubiquitin-proteasome pathway. GH internalization and degradation are inhibited when cells are treated with proteasome inhibitors. Here we show that a GHR truncated at residue 369 can enter the cells in the presence of a proteasome inhibitor, but that the subsequent lysosomal degradation of GH is blocked. Lysosomal inhibitors prolong the half-life of both receptor and ligand. Experiments with antibodies against different receptor tail sections show that degradation of the GHR c

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Luton, F., M. Buferne, J. Davoust, A. M. Schmitt-Verhulst, and C. Boyer. "Evidence for protein tyrosine kinase involvement in ligand-induced TCR/CD3 internalization and surface redistribution." Journal of Immunology 153, no. 1 (1994): 63–72. http://dx.doi.org/10.4049/jimmunol.153.1.63.

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Abstract Triggering of the TCR/CD3 complex can lead to its internalization and modulation from the cell surface. In the present study, we address the question of the dependence of internalization on protein tyrosine kinase (PTK) activation. With use of an activating anti-clonotypic (anti-Ti) mAb on a CTL clone, we have shown that the PTK inhibitors genistein and tyrphostin 25 delayed anti-Ti-induced internalization, but did not affect fluid phase protein uptake or transferrin receptor cycling. Confocal microscopy with use of fluorescent anti-Ti mAb revealed that the inhibition of TCR internali

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Chen, Yang, Shan Wang, Xinan Lu, Haoran Zhang, Yan Fu, and Yongzhang Luo. "Cholesterol sequestration by nystatin enhances the uptake and activity of endostatin in endothelium via regulating distinct endocytic pathways." Blood 117, no. 23 (2011): 6392–403. http://dx.doi.org/10.1182/blood-2010-12-322867.

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Abstract Specific internalization of endostatin into endothelial cells has been proved to be important for its biologic functions. However, the mechanism of endostatin internalization still remains elusive. In this study, we report for the first time that both caveolae/lipid rafts and clathrin-coated pits are involved in endostatin internalization. Inhibition of either the caveolae pathway or the clathrin pathway with the use of chemical inhibitors, small interfering RNAs, or dominant-negative mutants alters endostatin internalization in vitro. Intriguingly, cholesterol sequestration by nystat

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Lazari, Maria de Fatima M., Xuebo Liu, Kazuto Nakamura, Jeffrey L. Benovic, and Mario Ascoli. "Role of G Protein-Coupled Receptor Kinases on the Agonist-Induced Phosphorylation and Internalization of the Follitropin Receptor." Molecular Endocrinology 13, no. 6 (1999): 866–78. http://dx.doi.org/10.1210/mend.13.6.0289.

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Abstract The experiments presented herein were designed to identify members of the G protein-coupled receptor kinase (GRK) family that participate in the agonist-induced phosphorylation and internalization of the rat FSH receptor (rFSHR). Western blots of human kidney 293 cells (the cell line used in transfection experiments) and MSC-1 cells (a cell line derived from Sertoli cells that displays many of the differentiated functions of their normal counterparts) reveal the presence of GRK2 and GRK6 in both cell lines as well as GRK4 in MSC-1 cells. Cotransfection of 293 cells with the rFSHR and

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Almeida, Raul A., John R. Dunlap, and Stephen P. Oliver. "Binding of Host Factors Influences Internalization and Intracellular Trafficking ofStreptococcus uberisin Bovine Mammary Epithelial Cells." Veterinary Medicine International 2010 (2010): 1–8. http://dx.doi.org/10.4061/2010/319192.

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We showed that internalization ofStreptococcus uberisinto bovine mammary epithelial cells occurred through receptor- (RME) and caveolae-mediated endocytosis (CME). We reported also that treatment ofS. uberiswith host proteins including lactoferrin (LF) enhanced its internalization into host cells. Since the underlying mechanism(s) involved in such enhancement was unknown we investigated if preincubation ofS. uberiswith host proteins drives internalization of this pathogen into host cells through CME. Thus, experiments involving coculture of collagen-, fibronectin-, and LF-pretreatedS. uberiswi

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Van Hamme, Evelien, Hannah L. Dewerchin, Els Cornelissen, Bruno Verhasselt, and Hans J. Nauwynck. "Clathrin- and caveolae-independent entry of feline infectious peritonitis virus in monocytes depends on dynamin." Journal of General Virology 89, no. 9 (2008): 2147–56. http://dx.doi.org/10.1099/vir.0.2008/001602-0.

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Feline infectious peritonitis virus (FIPV), a coronavirus that causes a lethal chronic disease in cats, enters feline monocytes via endocytosis. In this study, the pathway of internalization is characterized by evaluating the effect of chemical inhibitors and/or expression of dominant-negative (DN) proteins on the percentage of internalized virions per cell and infection. Further, co-localization studies were performed to determine the involvement of certain cellular internalization proteins. FIPV is not internalized through a clathrin-mediated pathway, as chlorpromazine, amantadine and DN eps

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Pan, Weiling, Yongxian Zhang, Fangfei Qi, et al. "Abstract 2039: Cellular characterization of small molecule PD-L1 inhibitors reveal their novel mechanisms of action." Cancer Research 84, no. 6_Supplement (2024): 2039. http://dx.doi.org/10.1158/1538-7445.am2024-2039.

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Abstract Introductions: Immune checkpoint inhibitors, including PD-1/L1, are key regulators of immune response and promising targets in cancer immunotherapy. Like anti-PD-1/L1 antibodies, small molecule PD-L1 inhibitors that have been discovered by us and others could also efficiently block PD-1 and PD-L1 interaction and exhibit anti-tumor efficacy in preclinical and clinically settings. In this study, we explore the cellular mechanism of small molecule PD-L1 inhibitors, unveiling their novel mechanisms of action in the regulation of PD-L1 and its functions. Materials and Methods: The cellular

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Goretzki, L., and B. M. Mueller. "Receptor-mediated endocytosis of urokinase-type plasminogen activator is regulated by cAMP-dependent protein kinase." Journal of Cell Science 110, no. 12 (1997): 1395–402. http://dx.doi.org/10.1242/jcs.110.12.1395.

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Internalization of the urokinase-type plasminogen activator (uPA) requires two receptors, the uPA receptor (uPAR) and the low density lipoprotein receptor-related protein (LRP)/alpha2-macroglobulin (alpha2M) receptor. Here, we address whether protein kinases are involved in the internalization of uPA by human melanoma cells. Initially, we found that the internalization of uPA was significantly inhibited by the serine/threonine protein kinase inhibitors staurosporine, K-252a and H-89, but not by the tyrosine kinase inhibitors, genistein and lavendustin A. Internalization of uPA was also inhibit

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Dissertations / Theses on the topic "Internalization inhibitors"

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Qian, Yanrong. "Internalization of Extracellular ATP in Cancer Cells and Development of New Generations of Anticancer Glucose Transport Inhibitors." Ohio University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1416411921.

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Alvear-Perez, Rodrigo. "Voies de signalisation activées lors de la stimulation du récepteur de l'apéline, responsables de l'effet hypotenseur de l'apéline." Electronic Thesis or Diss., Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB021.

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L'apéline est un neuropeptide vasoactif qui joue un rôle crucial dans le maintien de l'équilibre hydrique et des fonctions cardiovasculaires. Des études réalisées au laboratoire sur les effets de l'apéline-17 (K17F) et du fragment d'apéline K16P, correspondant à K17F delétée de la phénylalanine (Phe) à son extrémité C-terminale, ont montré que la présence de cette Phe est nécessaire pour que l'apéline puisse d'une part, induire l'internalisation du récepteur de l'apéline, et d'autre part, provoquer une baisse de la pression artérielle. Par la suite, nous avons identifié dans les cellules CHO,

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Paradis, Justine. "Rôles non-canoniques des arrestines dans la signalisation et l’endocytose des récepteurs couplés aux protéines G." Thèse, 2017. http://hdl.handle.net/1866/20229.

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Book chapters on the topic "Internalization inhibitors"

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Jiang, Fei, Naiguo Xing, Taiyong Lv, Zhanliang Sun, and Yan Zhao. "Effects of Eluting Volumes to Isolation Efficiencies in Manual Synthesis of Ga-68 Labelled FAPI-04." In Springer Proceedings in Physics. Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-1023-6_25.

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AbstractAmong different FAPIs (fibroblast activation protein inhibitors) developed for PET imaging, 68Ga-FAPI-04 has demonstrated the most impressive properties with low nanomolar affinity to FAP, near-complete internalization of radioactivity bound to FAP, and rapid blood clearance. The application of 68Ga-FAPI-04 has been extended to 28 different kinds of clinical cancer detection. The manual synthesis of 68Ga-FAPI-04 is like other 68Ga-labeling peptides, such as PSMA-11 and DOTATATE. However, because the radiochemical conversion (RCC) is about 90%, it is required to conduct a purification a

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Conference papers on the topic "Internalization inhibitors"

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Barrott, Jared J., Aaron P. Smith, Takuya Osada, et al. "Abstract C86: Tethered Hsp90 inhibitors carrying optical or radioiodinated probes reveal selective internalization of ectopic Hsp90 in malignant breast tumor cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c86.

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Yalcin, Huseyin, Hissa Al-Thani, and Samar Shurbaji. "Development and In Vivo Testing of Smart Nanoparticles for Enhanced Anti-Cancer Activity and Reduced Cardiotoxicity Associated with Tyrosine Kinase Inhibitors." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0088.

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Tyrosine kinase inhibitors (TKIs) are new generation of anti-cancer drugs with very high efficiency against cancer cells. However, TKIs are associated with severe cardiotoxicity limiting their clinical benefits. One TKI that has been developed recently but not explored much is Ponatinib. The use of nanoparticles as a better therapeutic agent to deliver anti-cancer drugs and reduce their cardiotoxicity has been recently considered. In this study, PLGA-PEG-PLGA nanoparticles were synthesized to deliver Ponatinib while reducing its cardiotoxicity for treatment of chronic myeloid leukemia. Shape,

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Hutchinson, TE, S. Kuchibhotla, J. Zhang, ER Block та JM Patel. "Peptide Mediated Caveolar PKC-α Phosphorylation Inhibits Its Internalization in Lung Endothelial Cells." У American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6123.

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Allen, Fred D., Clara F. Asnes, Alan Wells, Elliot L. Elson, and Douglas A. Lauffenburger. "Alternative Pathways of Epidermal Growth Factor Receptor Mediated Contractile Force in NR6 Fibroblasts." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0403.

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Abstract We investigated the contractile force response to epidermal growth factor (EGF) stimulation in 3T3-derived NR6 fibroblast cells in order to determine significant pathways of biochemical signaling that mediate the response. We examined the force generating specificity of the EGF receptor (EGFR) signaling mechanism by using mutant NR6 fibroblasts expressing variations of the EGFR construct. The wild-type (WT) cell presented the complete internalizing EGFR signaling construct while the c’973 cell presented an internalization-defective EGFR construct, and the M721 cell presented a kinase-

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Hettmann, Thore, Matthias Schneider, Selam Ogbagabriel, et al. "Abstract LB-306: U3-1287 (AMG 888), a fully human anti-HER3 mAb, inhibits HER3 activation and induces HER3 internalization and degradation." In 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-lb-306.

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Wortinger, Mark A., Wei Zeng, Wei Jennifer Yang, et al. "Abstract 695: LA480, a c-Met antibody with neutralization and internalization properties, inhibits HGF-dependent and HGF-independent c-Met pathway activation and tumor growth." In 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.am10-695.

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de Agostini, A., J. Marcum, and R. Rosenberg. "THE BINDING OF ANTITHROMBIN TO CAPILLARY ENDOTHELIAL CELLS GROWN IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643343.

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Cloned endothelial cells from rat epididymal fat pads synthesize anticoagulantly active heparan sulfate proteoglycans containing the disaccharide, GlcA→ AMN-3,6-O-SO3, which is a marker for the antithrombin-binding domain of heparin. To demonstrate that antithrombin (AT) binds to cell surface heparan sulfate, a binding assay employing 125I-AT and cell monolayers has been developed. Post-confluent endothelial cells (7 days) were incubated with radiolabeled AT for 1 h at 4° and washed with PBS. Bound radioactivity was quantitated after solubilizing whole cells. Under these conditions, ∼1% (2174±

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Dupuy, E., P. S. Rohrlich, and G. Tobelem. "HEPARIN STIMULATES FIBROBLAST GROWTH INDUCED BY PDGF." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643750.

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Heparin binds to smooth muscle cells and endothelial cells. It inhibits the proliferation of the smooth muscle cells and modulates the growth of endothelial cells. Fibroblasts which represent an other cell type belonging to the vascular wall could also have their growth modified by heparin. We have at first, demonstrated that 125I unfractionated heparin bigds to cultured human skin fibroblasts with a Kd of 1.16 10 M.A low molecular weight heparin fraction (PK 10169) competed (50 %)with I unfractionated heparin, but at aless extent than cold unfractionated heparin(90%).As it has been reported w

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