Добірка наукової літератури з теми "GPCR Signalling Pathways"
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Статті в журналах з теми "GPCR Signalling Pathways"
Mohamed, Raafat, Reearna Janke, Wanru Guo, Yingnan Cao, Ying Zhou, Wenhua Zheng, Hossein Babaahmadi-Rezaei, Suowen Xu, Danielle Kamato, and Peter J. Little. "GPCR transactivation signalling in vascular smooth muscle cells: role of NADPH oxidases and reactive oxygen species." Vascular Biology 1, no. 1 (August 14, 2019): R1—R11. http://dx.doi.org/10.1530/vb-18-0004.
Повний текст джерелаEllisdon, Andrew M., and Michelle L. Halls. "Compartmentalization of GPCR signalling controls unique cellular responses." Biochemical Society Transactions 44, no. 2 (April 11, 2016): 562–67. http://dx.doi.org/10.1042/bst20150236.
Повний текст джерелаLiu, Ying, Yang Yang, Richard Ward, Su An, Xiao-Xi Guo, Wei Li, and Tian-Rui Xu. "Biased signalling: the instinctive skill of the cell in the selection of appropriate signalling pathways." Biochemical Journal 470, no. 2 (August 20, 2015): 155–67. http://dx.doi.org/10.1042/bj20150358.
Повний текст джерелаBhattacharya, M., A. V. Babwah, and S. S. G. Ferguson. "Small GTP-binding protein-coupled receptors." Biochemical Society Transactions 32, no. 6 (October 26, 2004): 1040–44. http://dx.doi.org/10.1042/bst0321040.
Повний текст джерелаMary, Sophie, Jean-Alain Fehrentz, Marjorie Damian, Pascal Verdié, Jean Martinez, Jacky Marie, and Jean-Louis Banères. "How ligands and signalling proteins affect G-protein-coupled receptors' conformational landscape." Biochemical Society Transactions 41, no. 1 (January 29, 2013): 144–47. http://dx.doi.org/10.1042/bst20120267.
Повний текст джерелаKamato, Danielle, Mai Gabr, Hirushi Kumarapperuma, Zheng J. Chia, Wenhua Zheng, Suowen Xu, Narin Osman та Peter J. Little. "Gαq Is the Specific Mediator of PAR-1 Transactivation of Kinase Receptors in Vascular Smooth Muscle Cells". International Journal of Molecular Sciences 23, № 22 (20 листопада 2022): 14425. http://dx.doi.org/10.3390/ijms232214425.
Повний текст джерелаGorvin, Caroline M. "Insights into calcium-sensing receptor trafficking and biased signalling by studies of calcium homeostasis." Journal of Molecular Endocrinology 61, no. 1 (July 2018): R1—R12. http://dx.doi.org/10.1530/jme-18-0049.
Повний текст джерелаHart, Stefan, Oliver M. Fischer, Norbert Prenzel, Esther Zwick-Wallasch, Matthias Schneider, Lothar Hennighausen, and Axel Ullrich. "GPCR-induced migration of breast carcinoma cells depends on both EGFR signal transactivation and EGFR-independent pathways." Biological Chemistry 386, no. 9 (September 1, 2005): 845–55. http://dx.doi.org/10.1515/bc.2005.099.
Повний текст джерелаFischer, O. M., S. Hart, A. Gschwind, and A. Ullrich. "EGFR signal transactivation in cancer cells." Biochemical Society Transactions 31, no. 6 (December 1, 2003): 1203–8. http://dx.doi.org/10.1042/bst0311203.
Повний текст джерелаWERRY, Tim D., Graeme F. WILKINSON, and Gary B. WILLARS. "Mechanisms of cross-talk between G-protein-coupled receptors resulting in enhanced release of intracellular Ca2+." Biochemical Journal 374, no. 2 (September 1, 2003): 281–96. http://dx.doi.org/10.1042/bj20030312.
Повний текст джерелаДисертації з теми "GPCR Signalling Pathways"
Archer, Caroline Rose. "Interactions between GPCR- and growth factor-activated signalling pathways in the induction of cardiac hypertrophy." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648427.
Повний текст джерелаMOLTENI, LAURA. "PHARMACOLOGICAL CHARACTERIZATION OF THE INTRACELLULAR SIGNALLING PATHWAY ACTIVATED BY TLQP-21." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/158161.
Повний текст джерелаObesity is a global epidemic for which the current weight loss therapies are relatively ineffective. Many central and peripheral factors are involved in the mechanisms controlling eating behaviour, and the integration of these signals within the hypothalamus results in the generation of specific responses aimed at regulating energy balance. TLQP-21 is a novel neuropeptide that has been implicated in the regulation of energy homeostasis, nociception, gastric function and several other physiologic functions. Although recent studies identified different receptors as the targets for TLQP-21, its molecular mechanisms of action at the cellular level remain largely unknown. Thus, since TLQP-21 is emerging as a novel target for obesity-associated disorders, diabetes, neuropathic pain, and other human pathologies, the purpose of this study was to better investigate the intracellular signalling pathway activated by the peptide-receptor interaction. Here, using intracellular calcium mobilization assay and western blot analysis, we have pharmacologically characterized the intracellular signalling pathway activated by TLQP-21 in ovary, macrophage and microglial cells. TLQP-21 dose-dependently stimulated a rapid and transient intracellular Ca2+ increase in CHO, RAW264.7 and N9 cells, and repeated exposure to the peptide resulted in a reduced response, indicating a possible desensitization mechanism of TLQP-21 receptor. In particular, TLQP-21 stimulation induced an increase of cytoplasmic Ca2+ levels that was sustained by Ca2+ release from the ER, since treatment of the cells with thaspigargin reduced the TLQP-21-mediated increase of intracellular Ca2+. The release of Ca2+ from the ER store is regulated by the activation of PLCs and the subsequent production of IP3 that binds to its receptors on the surface of the ER. In our cellular systems, TLQP-21 activity was reduced by the treatment with the PLC inhibitor U73122 and the IP3R antagonist 2-APB, confirming a PLC-dependent mechanism of action for the peptide. Furthermore, TLQP-21 induced a rapid dephosphorylation of PLCγ1 in CHO cells, suggesting that Ca2+ response to TLQP-21 is mediated by the binding of the peptide to a Gq-coupled receptor that in turn activates PLCβ. Ca2+ release from the ER activated Ca2+ entry from the extracellular environment, as demonstrated by the treatment of the cells with SKF-96365 and YM-58483, two specific inhibitors of the SOCE pathway. In CHO cells, TLQP-21 induced also an increase of PKC phosphorylation and, afterwards, of ERK1/2 phosphorylation. Moreover, the increase of cytosolic Ca2+ concentration following TLQP-21 administration, stimulated the activation of Akt/PKB. Our results suggest that the receptor stimulated by TLQP-21 belongs to the family of the Gq-coupled receptors, that activates membrane-lipid derived second messengers which thereby induce Ca2+ mobilization from the ER followed by a slower store-operated Ca2+ entry from outside the cell. In conclusion, our research provides additional evidences about the molecular mechanisms of action of TLQP-21, and could be useful to open new approaches to improve the treatment of several human disorders, including obesity and diabetes.
Byrne, Eamon. "Molecular mechanisms of Hedgehog signal transduction by the G-protein coupled receptor smoothened." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:38abef20-ae98-4835-919c-73afc21a6252.
Повний текст джерелаJain, Ruchi. "Spatio-temporal Regulation of GPCR mediated MAPK Transactivation in Living Cells." Thesis, 2015. https://etd.iisc.ac.in/handle/2005/4817.
Повний текст джерелаMorgan, Jeremy Andrew McInnes. "Regulation Mechanisms of Peptide Hormones in Neuroendocrine Cancers." Phd thesis, 2016. http://hdl.handle.net/1885/144624.
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