Relevant bibliographies by topics / System xc - antiporter

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'System xc - antiporter'

Author: Grafiati
Published: 3 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "System xc - antiporter"

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Dhaval, V. Patel Mukesh Nandave Prashant S. Kharkar. "PHARMACOPHORE MODELLING FOR THE DISCOVERY OF SYSTEM XC- ANTIPORTER INHIBITORS." INDO AMERICAN JOURNAL OF PHARMACEUTICAL RESEARCH 07, no. 09 (2017): 532–36. https://doi.org/10.5281/zenodo.1036492.

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Cancer is one of the major disorders with increasing rates of morbidity and mortality. Recent drug discovery of anti cancer drug has identified several molecular targets and tried to achieve a goal of therapeutic effecative and safe molecule. Amongst these, system xc- antiporter is a novel promising target to control cancer progression. This antiporter is found to be over expressed in majority of cancer cells and functions by transporting amino acids, cystine and glutamate, in opposite directions. System xc- antiporter uptakes one molecule of cystine with the release of one molecule of glutama
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Martis, Renita M., Luis J. Knight, Paul J. Donaldson, and Julie C. Lim. "Identification, Expression, and Roles of the Cystine/Glutamate Antiporter in Ocular Tissues." Oxidative Medicine and Cellular Longevity 2020 (June 18, 2020): 1–10. http://dx.doi.org/10.1155/2020/4594606.

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The cystine/glutamate antiporter (system xc-) is composed of a heavy chain subunit 4F2hc linked by a disulphide bond to a light chain xCT, which exchanges extracellular cystine, the disulphide form of the amino acid cysteine, for intracellular glutamate. In vitro research in the brain, kidney, and liver have shown this antiporter to play a role in minimising oxidative stress by providing a source of intracellular cysteine for the synthesis of the antioxidant glutathione. In vivo studies using the xCT knockout mouse revealed that the plasma cystine/cysteine redox couple was tilted to a more oxi
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Hung, Chung-Chieh, Chieh-Hsin Lin, and Hsien-Yuan Lane. "Cystine/Glutamate Antiporter in Schizophrenia: From Molecular Mechanism to Novel Biomarker and Treatment." International Journal of Molecular Sciences 22, no. 18 (2021): 9718. http://dx.doi.org/10.3390/ijms22189718.

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Glutamate, a crucial excitatory neurotransmitter, plays a major role in the modulation of schizophrenia’s pathogenesis. New drug developments for schizophrenia have been prompted by the hypoglutamatergic hypothesis of schizophrenia. The cystine/glutamate antiporter system xc− is related to glutamate-release regulation. Patients with schizophrenia were recently discovered to exhibit downregulation of xc− subunits—the solute carrier (SLC) family 3 member 2 and the SLC family 7 member 11. We searched for relevant studies from 1980, when Bannai and Kitamura first identified the protein subunit sys
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de Baat, Axel, Daniel T. Meier, Adriano Fontana, Marianne Böni-Schnetzler, and Marc Y. Donath. "Cystine/Glutamate antiporter system xc- deficiency impairs macrophage glutathione metabolism and cytokine production." PLOS ONE 18, no. 10 (2023): e0291950. http://dx.doi.org/10.1371/journal.pone.0291950.

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System xc-, encoded by Slc7a11, is an antiporter responsible for exporting glutamate while importing cystine, which is essential for protein synthesis and the formation of thiol peptides, such as glutathione. Glutathione acts as a co-factor for enzymes responsible for scavenging reactive oxygen species. Upon exposure to bacterial products, macrophages exhibit a rapid upregulation of system xc-. This study investigates the impact of Slc7a11 deficiency on the functionality of peritoneal and bone marrow-derived macrophages. Our findings reveal that the absence of Slc7a11 results in significantly
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Domercq, M., B. Szczupak, J. Gejo, et al. "PET imaging with [18F]FSPG evidences the role of system xc- on brain inflammation following cerebral ischemia in rats." Theranostics 6, no. 11 (2016): 1753–67. https://doi.org/10.7150/thno.15616.

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In vivo Positron Emission Tomography (PET) imaging of the cystine-glutamate antiporter (system xc-) activity with [18F]FSPG is meant to be an attractive tool for the diagnosis and therapy evaluation of brain diseases. However, the role of system xc- in cerebral ischemia and its involvement in inflammatory reaction has been scarcely explored. In this work, we report the longitudinal investigation of the neuroinflammatory process following transient middle cerebral artery occlusion (MCAO) in rats using PET with [18F]FSPG and the translocator protein (TSPO) ligand [18F]DPA-714. In the ischemic te
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Wang, Weimin, Michael Green, Jae Eun Choi, et al. "CD8+ T cells regulate tumor ferroptosis by targeting the system xc− during cancer immunotherapy." Journal of Immunology 202, no. 1_Supplement (2019): 137.11. http://dx.doi.org/10.4049/jimmunol.202.supp.137.11.

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Abstract Cytotoxic T cells recognize specific antigens expressed on tumor cells and mediate tumor cell apoptosis mainly through perforin–granzyme-mediated and FAS-mediated pathways. Ferroptosis is a recently discovered form of cell death that differs from apoptosis and results from iron-dependent lipid peroxide accumulation. The potential contribution of CD8+ T cell-mediated cytotoxic activity and immunotherapy to tumor ferroptosis remains unknown. Here, we find that immunotherapy-activated CD8+ T cells sensitize tumor cell ferroptosis. Mechanistically, IFNγ released from CD8+ T cells downregu
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Yoon, Sang Jun, and Gina M. DeNicola. "IL1RAP Pulls a Double Shift in the Cysteine Factory." Cancer Discovery 11, no. 11 (2021): 2679–81. http://dx.doi.org/10.1158/2159-8290.cd-21-1053.

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Abstract Summary: Anoikis is a critical barrier to cancer cell metastasis. In this issue of Cancer Discovery, Zhang and colleagues identify that IL1 receptor accessory protein suppresses anoikis in Ewing sarcoma by promoting both the activity of the system Xc− cystine/glutamate antiporter and cystathionine γ-lyase (CTH) transcription to sustain cysteine levels for reactive oxygen species detoxification. See related article by Zhang et al., p. 2884.
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Gallagher, Martin. "The System xc- Cystine/Glutamate Antiporter: An Exciting Target for Antiepileptogenic Therapy?" Epilepsy Currents 20, no. 1 (2020): 39–42. http://dx.doi.org/10.1177/1535759719891983.

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9

Rebalka, Irena A., Andrew W. Cao, Linda L. May, Mark A. Tarnopolsky, and Thomas J. Hawke. "Statin administration activates system xC− in skeletal muscle: a potential mechanism explaining statin-induced muscle pain." American Journal of Physiology-Cell Physiology 317, no. 5 (2019): C894—C899. http://dx.doi.org/10.1152/ajpcell.00308.2019.

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Statins are a cholesterol-lowering drug class that significantly reduce cardiovascular disease risk. Despite their safety and effectiveness, musculoskeletal side-effects, particularly myalgia, are prominent and the most common reason for discontinuance. The cause of statin-induced myalgia is unknown, so defining the underlying mechanism(s) and potential therapeutic strategies is of clinical importance. Here we tested the hypothesis that statin administration activates skeletal muscle system xC−, a cystine/glutamate antiporter, to increase intracellular cysteine and therefore glutathione synthe
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Zhang, Lei, Wen Liu, Fangyan Liu, et al. "IMCA Induces Ferroptosis Mediated by SLC7A11 through the AMPK/mTOR Pathway in Colorectal Cancer." Oxidative Medicine and Cellular Longevity 2020 (April 4, 2020): 1–14. http://dx.doi.org/10.1155/2020/1675613.

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Ferroptosis, implicated in several diseases, is a new form of programmed and nonapoptotic cell death triggered by iron-dependent lipid peroxidation after inactivation of the cystine/glutamate antiporter system xc–, which is composed of solute carrier family 7 membrane 11 (SLC7A11) and solute carrier family 3 membrane 2 (SLC3A2). Therefore, inducing ferroptosis through inhibiting the cystine/glutamate antiporter system xc– may be an effective way to treat cancer. In previous screening tests, we found that the benzopyran derivative 2-imino-6-methoxy-2H-chromene-3-carbothioamide (IMCA) significan
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Dissertations / Theses on the topic "System xc - antiporter"

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Slosky, Lauren M. "Targeting the Cystine/Glutamate Antiporter System xc⁻ in Cancer-Induced Bone Pain." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/594941.

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Many common cancers, including breast, prostate and lung cancers, have a propensity to metastasize to bone. Although these cancers go undetected in their native tissues, bone metastases often produce excruciating pain, the etiology of which is poorly understood. Cancer-induced bone pain (CIBP) is not well-controlled with existing medications, severely compromising patient quality of life. While CIBP is multifaceted, increased level of the excitatory neurotransmitter glutamate in the bone-tumor microenvironment may contribute to the pain state. Here, we demonstrate for the first time a relation
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Von, Vagerow Michael [Verfasser]. "Die Induktion des Glutamat/Cystin-Antiporters System xc- durch therapeutische Konzentrationen des Stimmungsstabilisators Lithium / Michael Von Vagerow." Ulm : Universität Ulm, 2021. http://d-nb.info/1226855415/34.

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Klaus, Richard Carl Philipp [Verfasser]. "Charakterisierung der TNF-α-vermittelten Hochregulation des Glutamat-Cystin-Antiporters System xc- in Astrozyten und Fibroblasten / Richard Carl Philipp Klaus". Ulm : Universität Ulm, 2020. http://d-nb.info/1215188838/34.

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Book chapters on the topic "System xc - antiporter"

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Favale, Gregorio, Vincenza Capone, Daniela Carannante, et al. "Role of Ferroptosis in AML Pathophysiology and Therapeutic Strategies." In Cell Death Regulation in Pathology [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1011347.

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Ferroptosis, an iron-dependent form of regulated cell death marked by lipid peroxidation, is critically implicated in the pathology of acute myeloid leukemia (AML). The dysregulation of iron metabolism and ferroptotic regulators, such as GPX4, the cystine/glutamate antiporter System Xc−, and several iron homeostasis proteins, contributes to leukemic cell survival and therapy resistance. These disruptions not only facilitate the survival and proliferation of leukemic cells but also enable them to evade traditional apoptotic pathways, thereby increasing resistance to standard therapeutic interve
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