scholarly journals The regulation of tyrosine kinase signalling pathways by growth factor and G-protein-coupled receptors

1995 ◽  
Vol 309 (2) ◽  
pp. 361-375 ◽  
Author(s):  
K Malarkey ◽  
C M Belham ◽  
A Paul ◽  
A Graham ◽  
A McLees ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tyrosine Kinase ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
Signalling Pathways ◽  
G Protein Coupled

scholarly journals Tethering of the Platelet-derived Growth Factor β Receptor to G-protein-coupled Receptors

2001 ◽  
Vol 276 (30) ◽  
pp. 28578-28585 ◽  
Author(s):  
Forbes Alderton ◽  
Soma Rakhit ◽  
Kok Choi Kong ◽  
Timothy Palmer ◽  
Balwinder Sambi ◽  
...  
Keyword(s):  
Growth Factor ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
Platelet Derived Growth Factor ◽  
Β Receptor ◽  
G Protein Coupled

scholarly journals Atypical Chemokine Receptors in Cardiovascular Disease

2019 ◽  
Vol 119 (04) ◽  
pp. 534-541 ◽  
Author(s):  
Selin Gencer ◽  
Emiel van der Vorst ◽  
Maria Aslani ◽  
Christian Weber ◽  
Yvonne Döring ◽  
...  
Keyword(s):  
G Protein ◽  
Chemokine Receptors ◽  
Cellular Response ◽  
Current Knowledge ◽  
G Protein Coupled Receptors ◽  
Signalling Pathways ◽  
Atherosclerosis Development ◽  
G Protein Coupled ◽  
Precise Role

AbstractInflammation has been well recognized as one of the main drivers of atherosclerosis development and therefore cardiovascular diseases (CVDs). It has been shown that several chemokines, small 8 to 12 kDa cytokines with chemotactic properties, play a crucial role in the pathophysiology of atherosclerosis. Chemokines classically mediate their effects by binding to G-protein-coupled receptors called chemokine receptors. In addition, chemokines can also bind to atypical chemokine receptors (ACKRs). ACKRs fail to induce G-protein-dependent signalling pathways and thus subsequent cellular response, but instead are able to internalize, scavenge or transport chemokines. In this review, we will give an overview of the current knowledge about the involvement of ACKR1–4 in CVDs and especially in atherosclerosis development. In the recent years, several studies have highlighted the importance of ACKRs in CVDs, although there are still several controversies and unexplored aspects that have to be further elucidated. A better understanding of the precise role of these atypical receptors may pave the way towards novel and improved therapeutic strategies.

Regulation of tyrosine kinase cascades by G-protein-coupled receptors

1999 ◽  
Vol 11 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Louis M Luttrell ◽  
Yehia Daaka ◽  
Robert J Lefkowitz
Keyword(s):  
Tyrosine Kinase ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
G Protein Coupled

scholarly journals Role of Protein Kinase C, PI3-kinase and Tyrosine Kinase in Activation of MAP Kinase by Glucose and Agonists of G-protein Coupled Receptors in INS-1 Cells

2001 ◽  
Vol 2 (3) ◽  
pp. 233-244 ◽  
Author(s):  
Dietmar Böcker ◽  
Eugen J. Verspohl
Keyword(s):  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Map Kinase ◽  
G Protein ◽  
Kinase Activity ◽  
Kinase Inhibitor ◽  
Pi3 Kinase ◽  
G Protein Coupled Receptors ◽  
Kinase C ◽  
G Protein Coupled

MAP (mitogen-activated protein) kinase (also called Erk 1/2) plays a crucial role in cell proliferation and differentiation. Its impact on secretory events is less well established. The interplay of protein kinase C (PKC), PI3-kinase nd cellular tyrosine kinase with MAP kinase activity using inhibitors and compounds such as glucose, phorbol 12-myristate 13-acetate (PMA) and agonists of G-protein coupled receptors like gastrin releasing peptide (GRP), oxytocin (OT) and glucose-dependent insulinotropic peptide (GIP) was investigated in INS-1 cells, an insulin secreting cell line. MAP kinase activity was determined by using a peptide derived from the EGF receptor as a MAP kinase substrate and [P32]ATP. Glucose as well as GRP, OT and GIP exhibited a time-dependent increase in MAP kinase activity with a maximum at time point 2.5 min. All further experiments were performed using 2.5 min incubations. The flavone PD 098059 is known to bind to the inactive forms of MEK1 (MAPK/ERK-Kinase) thus preventing activation by upstream activators. 20 μM PD 098059 (IC50=51 μM) inhibited MAP kinase stimulated by either glucose, GRP, OT, GIP or PMA. Inhibiton (“downregulation”) of PKC by a long term (22h) pretreatment with 1 μM PMA did not influence MAP kinase activity when augmented by either of the above mentioned compound. To investigate whether PI3-kinase and cellular tyrosine kinase are involved in G-protein mediated effects on MAP kinase, inhibitors were used: 100 nM wortmannin (PI3-kinase inhibitor) reduced the effects of GRP, OT and GIP but not that of PMA; 100 μM genistein (tyrosine kinase inhibitor) inhibited the stimulatory effect of either above mentioned compound on MAP kinase activation. Inhibition of MAP kinase by 20 μM PD 098059 did not influence insulin secretion modulated by either compound (glucose, GRP, OT or GIP). [H3]Thymidine incorporation, however, was severely inhibited by PD 098059. Thus MAP kinase is important for INS-1 cell proliferation but not for its insulin secretory response with respect to major initiators and modulators of insulin release. The data indicate that MAP kinase is active and under the control of MAP kinase. PKC is upstream of a genisteinsensitive tyrosine kinase and probably downstream of a PI3-kinase in INS-1 cells.

scholarly journals Lysophospholipids in the limelight

2002 ◽  
Vol 158 (2) ◽  
pp. 197-199 ◽  
Author(s):  
Wouter H. Moolenaar
Keyword(s):  
Growth Factor ◽  
Cell Motility ◽  
Tumor Progression ◽  
G Protein ◽  
Lysophosphatidic Acid ◽  
Cell Types ◽  
G Protein Coupled Receptors ◽  
Serum Phospholipid ◽  
A Cell ◽  
G Protein Coupled

Lysophosphatidic acid (LPA) is a serum phospholipid that evokes growth factor–like responses in many cell types through the activation of its G protein–coupled receptors. Although much is known about LPA signaling, it has remained unclear where and how bioactive LPA is produced. Umezu-Goto et al. (2002)(this issue, page 227) have purified a serum lysophospholipase D that generates LPA from lysophosphatidylcholine and found it to be identical to autotaxin, a cell motility–stimulating ectophosphodiesterase implicated in tumor progression. This result is surprising, as there was previously no indication that autotaxin could act as a phospholipase.

How ligands and signalling proteins affect G-protein-coupled receptors' conformational landscape

2013 ◽  
Vol 41 (1) ◽  
pp. 144-147 ◽  
Author(s):  
Sophie Mary ◽  
Jean-Alain Fehrentz ◽  
Marjorie Damian ◽  
Pascal Verdié ◽  
Jean Martinez ◽  
...  
Keyword(s):  
G Protein ◽  
G Protein Coupled Receptors ◽  
Effector Proteins ◽  
New Drugs ◽  
Signalling Pathways ◽  
Ghrelin Receptor ◽  
Multiple Data ◽  
Conformational Landscape ◽  
G Protein Coupled ◽  
Receptor Conformation

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 conformational landscape of GPCRs in different manners, as we show with the isolated ghrelin receptor. Such modulation of the GPCR conformational landscape by pharmacologically distinct ligands and effector proteins has major implications for the design of new drugs that activate specific signalling pathways.

scholarly journals Crosstalk between G protein-coupled receptors (GPCRs) and tyrosine kinase receptor (TXR) in the heart after morphine withdrawal

2013 ◽  
Vol 4 ◽  
Author(s):  
Pilar Almela ◽  
Juan-Antonio García-Carmona ◽  
Elena Martínez-Laorden ◽  
María-Victoria Milanés ◽  
María-Luisa Laorden
Keyword(s):  
Tyrosine Kinase ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
Morphine Withdrawal ◽  
Tyrosine Kinase Receptor ◽  
G Protein Coupled
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