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Relevant bibliographies by topics / GPCR Signalling Pathways

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Journal articles

Academic literature on the topic 'GPCR Signalling Pathways'

Author: Grafiati

Published: 6 September 2023

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Journal articles on the topic "GPCR Signalling Pathways"

1

Mohamed, Raafat, Reearna Janke, Wanru Guo, et al. "GPCR transactivation signalling in vascular smooth muscle cells: role of NADPH oxidases and reactive oxygen species." Vascular Biology 1, no. 1 (2019): R1—R11. http://dx.doi.org/10.1530/vb-18-0004.

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The discovery and extension of G-protein-coupled receptor (GPCR) transactivation-dependent signalling has enormously broadened the GPCR signalling paradigm. GPCRs can transactivate protein tyrosine kinase receptors (PTKRs) and serine/threonine kinase receptors (S/TKRs), notably the epidermal growth factor receptor (EGFR) and transforming growth factor-β type 1 receptor (TGFBR1), respectively. Initial comprehensive mechanistic studies suggest that these two transactivation pathways are distinct. Currently, there is a focus on GPCR inhibitors as drug targets, and they have proven to be efficacio

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2

Ellisdon, Andrew M., and Michelle L. Halls. "Compartmentalization of GPCR signalling controls unique cellular responses." Biochemical Society Transactions 44, no. 2 (2016): 562–67. http://dx.doi.org/10.1042/bst20150236.

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With >800 members, G protein-coupled receptors (GPCRs) are the largest class of cell-surface signalling proteins, and their activation mediates diverse physiological processes. GPCRs are ubiquitously distributed across all cell types, involved in many diseases and are major drug targets. However, GPCR drug discovery is still characterized by very high attrition rates. New avenues for GPCR drug discovery may be provided by a recent shift away from the traditional view of signal transduction as a simple chain of events initiated from the plasma membrane. It is now apparent that GPCR signallin

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3

Liu, Ying, Yang Yang, Richard Ward, et al. "Biased signalling: the instinctive skill of the cell in the selection of appropriate signalling pathways." Biochemical Journal 470, no. 2 (2015): 155–67. http://dx.doi.org/10.1042/bj20150358.

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GPCRs (G-protein-coupled receptors) are members of a family of proteins which are generally regarded as the largest group of therapeutic drug targets. Ligands of GPCRs do not usually activate all cellular signalling pathways linked to a particular seven-transmembrane receptor in a uniform manner. The fundamental idea behind this concept is that each ligand has its own ability, while interacting with the receptor, to activate different signalling pathways (or a particular set of signalling pathways) and it is this concept which is known as biased signalling. The importance of biased signalling

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4

Bhattacharya, M., A. V. Babwah, and S. S. G. Ferguson. "Small GTP-binding protein-coupled receptors." Biochemical Society Transactions 32, no. 6 (2004): 1040–44. http://dx.doi.org/10.1042/bst0321040.

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Heterotrimeric GPCRs (G-protein-coupled receptors) form the largest group of integral membrane receptor proteins and mediate diverse physiological processes. In addition to signalling via heterotrimeric G-proteins, GPCRs can also signal by interacting with various small G-proteins to regulate downstream effector pathways. The small G-protein superfamily is structurally classified into at least five families: the Ras, Rho/Rac/cdc42, Rab, Sar1/Arf and Ran families. They are monomeric G-proteins with molecular masses over the range 20–30 kDa, which function as molecular switches to control many e

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5

Mary, Sophie, Jean-Alain Fehrentz, Marjorie Damian, et al. "How ligands and signalling proteins affect G-protein-coupled receptors' conformational landscape." Biochemical Society Transactions 41, no. 1 (2013): 144–47. http://dx.doi.org/10.1042/bst20120267.

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The dynamic character of GPCRs (G-protein-coupled receptors) is essential to their function. However, the details of how ligands and signalling proteins stabilize a receptor conformation to trigger the activation of a given signalling pathway remain largely unexplored. Multiple data, including recent results obtained with the purified ghrelin receptor, suggest a model where ligand efficacy and functional selectivity are directly related to different receptor conformations. Importantly, distinct effector proteins (G-proteins and arrestins) as well as ligands are likely to affect the conformatio

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6

Kamato, Danielle, Mai Gabr, Hirushi Kumarapperuma та ін. "Gαq Is the Specific Mediator of PAR-1 Transactivation of Kinase Receptors in Vascular Smooth Muscle Cells". International Journal of Molecular Sciences 23, № 22 (2022): 14425. http://dx.doi.org/10.3390/ijms232214425.

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Aims: G protein-coupled receptor (GPCR) transactivation of kinase receptors greatly expands the actions attributable to GPCRs. Thrombin, via its cognate GPCR, protease-activated receptor (PAR)-1, transactivates tyrosine and serine/threonine kinase receptors, specifically the epidermal growth factor receptor and transforming growth factor-β receptor, respectively. PAR-1 transactivation-dependent signalling leads to the modification of lipid-binding proteoglycans involved in the retention of lipids and the development of atherosclerosis. The mechanisms of GPCR transactivation of kinase receptors

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7

Gorvin, Caroline M. "Insights into calcium-sensing receptor trafficking and biased signalling by studies of calcium homeostasis." Journal of Molecular Endocrinology 61, no. 1 (2018): R1—R12. http://dx.doi.org/10.1530/jme-18-0049.

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The calcium-sensing receptor (CASR) is a class C G-protein-coupled receptor (GPCR) that detects extracellular calcium concentrations, and modulates parathyroid hormone secretion and urinary calcium excretion to maintain calcium homeostasis. The CASR utilises multiple heterotrimeric G-proteins to mediate signalling effects including activation of intracellular calcium release; mitogen-activated protein kinase (MAPK) pathways; membrane ruffling; and inhibition of cAMP production. By studying germline mutations in the CASR and proteins within its signalling pathway that cause hyper- and hypocalca

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8

Hart, Stefan, Oliver M. Fischer, Norbert Prenzel, et al. "GPCR-induced migration of breast carcinoma cells depends on both EGFR signal transactivation and EGFR-independent pathways." Biological Chemistry 386, no. 9 (2005): 845–55. http://dx.doi.org/10.1515/bc.2005.099.

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Abstract The epidermal growth factor receptor (EGFR) plays a key role in the regulation of important cellular processes under normal and pathophysiological conditions such as cancer. In human mammary carcinomas the EGFR is involved in regulating cell growth, survival, migration and metastasis and its activation correlates with the lack of response in hormone therapy. Here, we demonstrate in oestrogen receptor-positive and -negative human breast cancer cells and primary mammary epithelial cells a cross-communication between G protein-coupled receptors (GPCRs) and the EGFR. We present evidence t

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9

Fischer, O. M., S. Hart, A. Gschwind, and A. Ullrich. "EGFR signal transactivation in cancer cells." Biochemical Society Transactions 31, no. 6 (2003): 1203–8. http://dx.doi.org/10.1042/bst0311203.

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The EGFR (epidermal growth factor receptor) plays a key role in the regulation of essential normal cellular processes and in the pathophysiology of hyperproliferative diseases such as cancer. Recent investigations have demonstrated that GPCRs (G-protein-coupled receptors) are able to utilize the EGFR as a downstream signalling partner in the generation of mitogenic signals. This cross-talk mechanism combines the broad diversity of GPCRs with the signalling capacities of the EGFR and has emerged as a general concept in a multitude of cell types. The molecular mechanisms of EGFR signal transacti

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10

WERRY, 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 (2003): 281–96. http://dx.doi.org/10.1042/bj20030312.

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Alteration in [Ca2+]i (the intracellular concentration of Ca2+) is a key regulator of many cellular processes. To allow precise regulation of [Ca2+]i and a diversity of signalling by this ion, cells possess many mechanisms by which they are able to control [Ca2+]i both globally and at the subcellular level. Among these are many members of the superfamily of GPCRs (G-protein-coupled receptors), which are characterized by the presence of seven transmembrane domains. Typically, those receptors able to activate PLC (phospholipase C) enzymes cause release of Ca2+ from intracellular stores and influ

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