Gotowa bibliografia na temat „Gárdos channel”
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Artykuły w czasopismach na temat "Gárdos channel"
Petkova-Kirova, Polina, Nicoletta Murciano, Giulia Iacono, Julia Jansen, Greta Simionato, Min Qiao, Carmen Van der Zwaan i in. "The Gárdos Channel and Piezo1 Revisited: Comparison between Reticulocytes and Mature Red Blood Cells". International Journal of Molecular Sciences 25, nr 3 (24.01.2024): 1416. http://dx.doi.org/10.3390/ijms25031416.
Pełny tekst źródłaJansen, Julia, Min Qiao, Laura Hertz, Xijia Wang, Elisa Fermo, Anna Zaninoni, Raffaella Colombatti, Ingolf Bernhardt, Paola Bianchi i Lars Kaestner. "Mechanistic ion channel interactions in red cells of patients with Gárdos channelopathy". Blood Advances 5, nr 17 (1.09.2021): 3303–8. http://dx.doi.org/10.1182/bloodadvances.2020003823.
Pełny tekst źródłaMaher, Anthony D., i Philip W. Kuchel. "The Gárdos channel: a review of the Ca2+-activated K+ channel in human erythrocytes". International Journal of Biochemistry & Cell Biology 35, nr 8 (sierpień 2003): 1182–97. http://dx.doi.org/10.1016/s1357-2725(02)00310-2.
Pełny tekst źródłaBuks, Ralfs, Tracy Dagher, Maria Rotordam, David Monedero Alonso, Sylvie Cochet, Emilie-Fleur Gautier, Philippe Chafey i in. "Altered Ca2+ Homeostasis in Red Blood Cells of Polycythemia Vera Patients Following Disturbed Organelle Sorting during Terminal Erythropoiesis". Cells 11, nr 1 (24.12.2021): 49. http://dx.doi.org/10.3390/cells11010049.
Pełny tekst źródłaMaher, Anthony D., i Philip W. Kuchel. "Erratum to “The Gárdos channel: a review of the Ca2+-activated K+ channel in human erythrocytes” [Int. J. Biochem. Cell Biol. 35 (2003) 1182–1197]". International Journal of Biochemistry & Cell Biology 35, nr 12 (grudzień 2003): 1682. http://dx.doi.org/10.1016/s1357-2725(03)00209-7.
Pełny tekst źródłaMonedero Alonso, David, Laurent Pérès, Aline Hatem, Guillaume Bouyer i Stéphane Egée. "The Chloride Conductance Inhibitor NS3623 Enhances the Activity of a Non-selective Cation Channel in Hyperpolarizing Conditions". Frontiers in Physiology 12 (11.10.2021). http://dx.doi.org/10.3389/fphys.2021.743094.
Pełny tekst źródłaHatem, Aline, Gwendal Poussereau, Martin Gachenot, Laurent Pérès, Guillaume Bouyer i Stéphane Egée. "Dual action of Dooku1 on PIEZO1 channel in human red blood cells". Frontiers in Physiology 14 (10.07.2023). http://dx.doi.org/10.3389/fphys.2023.1222983.
Pełny tekst źródłaHertz, Laura, Daniel Flormann, Lutz Birnbaumer, Christian Wagner, Matthias Laschke i Lars Kaestner. "Evidence of in vivo exogen protein uptake by red blood cells: a putative therapeutic concept". Blood Advances, 9.12.2022. http://dx.doi.org/10.1182/bloodadvances.2022008404.
Pełny tekst źródłaRozprawy doktorskie na temat "Gárdos channel"
Hatem, Aline. "Characterization of cationic conductance in Red Blood Cells; insights from pharmacological and pathophysiological studies". Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS008.
Pełny tekst źródłaOver their lifespan, erythrocytes circulate throughout the body to carry respiratory gases and perform their other functions. Therefore, erythrocytes must deform properly to circulate in all vessels, including the smallest of the capillaries. This ability is governed by a complex membrane-cytoskeleton network combined with a finely tuned surface-volume ratio that allows instantaneous shape changes to enable rapid RBC transit. This highlights how important it is to maintain cell volume to ensure a 120-day journey without the possibility of repair. Cell volume or hydration status is directly influenced by the activity of membrane transporters, pumps, and ion channels. The permeability of erythrocytes, which is dominated by anion movement for physiological reasons, implies that cation movement should be kept as low as possible to avoid any change in cell volume. However, in many pathophysiological conditions, cation permeabilities are known to be deregulated, leading to increased intracellular Ca2+ and Na+ levels. My thesis aimed to better characterize the role of non-selective cation (NSC) channels (PIEZO1, TRPV2), and Gárdos channel in such pathophysiological conditions. Experiments were carried out on healthy erythrocytes as well as on cells from patients suffering from different pathologies like Sickle Cell Disease (SCD), xerocytosis, and stomatocytosis, using electrophysiological methods (MBE and patch-clamp), Ca2+ movements semi-quantification (flow cytometry and live-cell imaging) combined with the measurement of morphometric parameters, and the measurements of intracellular cell volume and other ions contents. In two independent studies using blood from sickle cell patients, we were able to demonstrate from one part the central role of PIEZO1 activation in the enhancement of sickling propensity. In the other part, we demonstrated the increased sensitivity of sickle cells to THC stimulation via TRPV2 activation. Along with these published results, we have contributed to the functional characterization of many PIEZO1 and KCNN4 variants, for which we have designed a series of functional experiments to better describe the genetically identified variants. This part with 5 Gárdos and 10 PIEZO1 variants increases the knowledge about the pathogenicity of the identified mutations, often characterized as variants of uncertain significance (VUS). We were also able to demonstrate that Dooku1, a chemical compound described in the literature as an inhibitor of Yoda1's effects, is in fact, a direct activator of PIEZO1 in erythrocytes, contributing to a more accurate pharmacology of PIEZO1. Furthermore, we conducted a series of experiments in patients treated with Alectinib (a lung cancer treatment), for which frequent anemia associated with cell volume dehydration is observed. Taken together, these studies contribute to the understanding of cation permeabilities under physiological and pathophysiological conditions. Finally, all these results highlight the particularity of RBCs regarding cationic permeability and biophysical membrane properties compared to other cell types and, more importantly when mechanosensitive pathways are involved in such ion movements