Theoretical and Natural Science
- The Open Access Proceedings Series for Conferences
Series Vol. 6 , 03 August 2023
* Author to whom correspondence should be addressed.
G protein-coupled receptor can be written in GPCR, it has a big great family and this species include 800 human genes, it become the important part of human body. Although each species has their own unique skills, it can make different kind of medicine that can save human’s life. And then there's the G-protein-coupled receptor mechanism. The GPCR desensitization regulator - arrestin was further analyzed, and researchers discovered that GPCRs could be activated not only through the G-protein-dependent pathway but also through the non-G-protein-dependent pathway, known as the -inhibitor pathway, to control the ingestion and desensitization throughout vivo and even start a new wave of signal transduction. The development of G-protein-coupled receptor drugs followed. GPCR is strongly associated to pathological conditions and has an essential function in cell signal transmission. More than 40% of the medicines on the market today target GPCR, which is the reached a high point family of pharmacological targets. The intracellular effector proteins (G proteins, etc.) that are activated by the GPCR play an important role in the regulation of its physiological function.
G protein-coupled receptor (GPCR), medicines, signal transduction, pharmacological targets, intracellular effector proteins
1. Leemann, S. and Kleinlogel, S., “Functional optimization of light-activatable Opto-GPCRs: Illuminating the importance of the proximal C-terminus in G-protein specificity,” Front Cell Dev Biol. Papers 11, 1053022 (2023).
2. Zhang, H., Ren, X., Yang, Z. and Lai, J., “Vitamin A Concentration in Human Milk: A Meta-Analysis,” Nutrients Papaers 14(22), 4844 (2022).
3. Sims, C., Birkett, M. A. and Withall, D. M., “Enantiomeric Discrimination in Insects: The Role of OBPs and ORs,” Insects Papers 13(4), 368 (2022).
4. Talbot, F., Luckman, S. M. and Farooqi, I. S., “A rare human variant that disrupts GPR10 signalling causes weight gain in mice,” Nat Commun. Papers 14(1), 1450 (2023).
5. Yuzaki, M. and Aricescu, A. R., “A GluD coming-of-age story,” Trends Neurosci. Papaers 40(3), 138–150 (2017).
6. Kubatova, N., Schmidt, T., Schwieters, C. D. and Clore, G. M., “Quantitative analysis of sterol-modulated monomer-dimer equilibrium of the β1-adrenergic receptor by DEER spectroscopy,” Proc Natl Acad Sci USA. Paper 120(7), e2221036120 (2023).
7. Lu, J. and Wu, W., “Cholinergic modulation of the immune system - A novel therapeutic target for myocardial inflammation,” Int Immunopharmacol 93, 107391 (2021).
8. Ramanujam, R. and Naqvi, N. I., “PdeH, a High-Affinity cAMP Phosphodiesterase, Is a Key Regulator of Asexual and Pathogenic Differentiation in Magnaporthe oryzae,” PLoS Pathog. Papaers 6(5), e1000897 (2010).
9. Umar, S. A., Dong, B., Nihal, M. and Chang, H., “Frizzled receptors in melanomagenesis: From molecular interactions to target identification,” Front Oncol. Papers 12, 1096134 (2022).
10. Kriebel, C. N., Becker-Baldus, J. and Glaubitz, C., “Solid-State NMR Spectroscopy on Microbial Rhodopsins,” Methods Mol Biol. Papers 2501, 181–206 (2022).
11. Pandey, S., “Plant receptor-like kinase signaling through heterotrimeric G-proteins,” J Exp Bot. Papaers 71(5), 1742–1751 (2020).
12. Hashemi, S. F. and Khorramdelazad, H., “The cryptic role of CXCL17/CXCR8 axis in the pathogenesis of cancers: a review of the latest evidence,” J Cell Commun Signal. Papaers (2022).
13. Otte, M. L., Lama Tamang, R., Papapanagiotou, J., Ahmad, R., Dhawan, P. and Singh, A. B., “Mucosal healing and inflammatory bowel disease: Therapeutic implications and new targets,” World J Gastroenterol. Papers 29(7), 1157–1172 (2023).
14. Stone, T. W., Clanchy, F. I. L., Huang, Y.-S., Chiang, N.-Y., Darlington, L. G. and Williams, R. O., “An integrated cytokine and kynurenine network as the basis of neuroimmune communication,” Frontiers in Neuroscience Papers 16 (2022).
15. Henderson, S. R., Horsley, H., Frankel, P., Khosravi, M., Goble, T., Carter, S., Antonelou, M., Evans, R. D. R., Zhang, X., Chu, T.-Y., Lin, H.-H., Gordon, S. and Salama, A. D., “Proteinase 3 promotes formation of multinucleated giant cells and granuloma-like structures in patients with granulomatosis with polyangiitis,” Ann Rheum Dis, Papers annrheumdis-2021-221800 (2023).
16. De Giovanni, M., Chen, H., Li, X. and Cyster, J. G., “GPR35 and mediators from platelets and mast cells in neutrophil migration and inflammation,” Immunol Rev. Papers (2023).
17. Mackiewicz, T., Włodarczyk, J., Zielińska, M., Włodarczyk, M., Durczyński, A., Hogendorf, P., Dziki, Ł. and Fichna, J., “Increased GPR35 expression in human colorectal and pancreatic cancer samples: A preliminary clinical validation of a new biomarker,” Adv Clin Exp Med. Papers (2023).
18. Karayay, B., Olze, H. and Szczepek, A. J., “Degranulation of Murine Resident Cochlear Mast Cells: A Possible Factor Contributing to Cisplatin-Induced Ototoxicity and Neurotoxicity,” Int J Mol Sci. Papers 24(5), 4620 (2023).
19. Guleria, P., Srinivasan, R., Rana, C. and Agarwal, S., “Molecular Landscape of Pediatric Thyroid Cancer: A Review,” Diagnostics (Basel) Papers 12(12), 3136 (2022).
20. Xu, G., Li, T. and Huang, Y., “The Effects of Intraoperative Hypothermia on Postoperative Cognitive Function in the Rat Hippocampus and Its Possible Mechanisms,” Brain Sci. Papers 12(1), 96 (2022).
21. Gu, X., Zhang, Y. Z., O’Malley, J. J., De Preter, C. C., Penzo, M. and Hoon, M. A., “Neurons in the caudal ventrolateral medulla mediate descending pain control,” Nat Neurosci. Papers (2023).
22. McIntire, W. E., “A model for how Gβγ couples Gα to GPCR,” J Gen Physiol. Papers 154(5), e202112982 (2022).
23. Yang, W. and Xia, S.-H., “Mechanisms of regulation and function of G-protein-coupled receptor kinases,” World J. Gastroenterol. Papaers 12(48), 7753–7757 (2006).
24. Offermanns, S., “G-proteins as transducers in transmembrane signalling,” Prog. Biophys. Mol. Biol. Papaers 83(2), 101–130 (2003).
25. Martyniak, A. and Tomasik, P. J., “A New Perspective on the Renin-Angiotensin System,” 1, Diagnostics Papaers 13(1), 16 (2023).
The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.
This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License. Authors who publish this series agree to the following terms:
1. Authors retain copyright and grant the series right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgment of the work's authorship and initial publication in this series.
2. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the series's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgment of its initial publication in this series.
3. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See Open Access Instruction).