Twists and turns on G-protein signalling pathways

1992 ◽  
Vol 2 (10) ◽  
pp. 517-519 ◽  
Author(s):  
Elliott M. Ross
Keyword(s):  
G Protein ◽  
Signalling Pathways ◽  
G Protein Signalling

scholarly journals Plant hormone perception and action: a role for G–protein signal transduction?

1998 ◽  
Vol 353 (1374) ◽  
pp. 1425-1430 ◽  
Author(s):  
Richard Hooley
Keyword(s):  
Signal Transduction ◽  
G Protein ◽  
G Proteins ◽  
Plant Hormone ◽  
Higher Plants ◽  
Signalling Pathways ◽  
Heterotrimeric G Proteins ◽  
Extracellular Signals ◽  
G Protein Signalling ◽  
Auxin Signalling

Plants perceive and respond to a profusion of environmental and endogenous signals that influence their growth and development. The G–protein signalling pathway is a mechanism for transducing extracellular signals that is highly conserved in a range of eukaryotes and prokaryotes. Evidence for the existence of G–protein signalling pathways in higher plants is reviewed, and their potential involvement in plant hormone signal transduction evaluated. A range of biochemical and molecular studies have identified potential components of G–protein signalling in plants, most notably a homologue of the G–protein coupled receptor superfamily ( GCR1 ) and the G α and G β subunits of heterotrimeric G–proteins. G–protein agonists and antagonists are known to influence a variety of signalling events in plants and have been used to implicate heterotrimeric G–proteins in gibberellin and possibly auxin signalling. Antisense suppression of GCR1 in Arabidopsis leads to a phenotype which supports a role for this receptor in cytokinin signalling. These observations suggest that higher plants have at least some of the components of G–protein signalling pathways and that these might be involved in the action of certain plant hormones.

G-protein signalling pathways and the control of cell proliferation

1990 ◽  
Vol 14 ◽  
pp. 10
Author(s):  
J POUYSSEGUR ◽  
C KAHAN ◽  
G LALLEMAIN ◽  
K SEUWEN ◽  
V VOURET ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
G Protein ◽  
Signalling Pathways ◽  
G Protein Signalling

scholarly journals Proteinase-activated receptors (PARs) as targets for antiplatelet therapy

2016 ◽  
Vol 44 (2) ◽  
pp. 606-612 ◽  
Author(s):  
Margaret Cunningham ◽  
Kathryn McIntosh ◽  
Trevor Bushell ◽  
Graeme Sloan ◽  
Robin Plevin
Keyword(s):  
Antiplatelet Therapy ◽  
G Protein ◽  
Inflammatory Diseases ◽  
Signalling Pathways ◽  
Structural Determinants ◽  
Coronary Syndrome ◽  
G Protein Signalling ◽  
Platelet Receptor ◽  
Proteinase Activated Receptors ◽  
Endogenous Proteases

Since the identification of the proteinase-activated receptor (PAR) family as mediators of serine protease activity in the 1990s, there has been tremendous progress in the elucidation of their pathophysiological roles. The development of drugs that target PARs has been the focus of many laboratories for the potential treatment of thrombosis, cancer and other inflammatory diseases. Understanding the mechanisms of PAR activation and G protein signalling pathways evoked in response to the growing list of endogenous proteases has yielded great insight into receptor regulation at the molecular level. This has led to the development of new selective modulators of PAR activity, particularly PAR1. The mixed success of targeting PARs has been best exemplified in the context of inhibiting PAR1 as a new antiplatelet therapy. The development of the competitive PAR1 antagonist, vorapaxar (Zontivity), has clearly shown the value in targeting PAR1 in acute coronary syndrome (ACS); however the severity of associated bleeding with this drug has limited its use in the clinic. Due to the efficacy of thrombin acting via PAR1, strategies to selectively inhibit specific PAR1-mediated G protein signalling pathways or to target the second thrombin platelet receptor, PAR4, are being devised. The rationale behind these alternative approaches is to bias downstream thrombin activity via PARs to allow for inhibition of pro-thrombotic pathways but maintain other pathways that may preserve haemostatic balance and improve bleeding profiles for widespread clinical use. This review summarizes the structural determinants that regulate PARs and the modulators of PAR activity developed to date.

scholarly journals G-protein signalling pathways and oestrogen: a role of balanced maintenance in osteoblasts

1999 ◽  
Vol 1449 (3) ◽  
pp. 284-292 ◽  
Author(s):  
Stelios Papaioannou ◽  
Anthony M. Tumber ◽  
Murray C. Meikle ◽  
Fraser McDonald
Keyword(s):  
G Protein ◽  
Signalling Pathways ◽  
G Protein Signalling

A novel biological role for the phospholipid lysophosphatidylinositol in nociceptive sensitization via activation of diverse G-protein signalling pathways in sensory nerves in vivo

Pain ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 2801-2812 ◽  
Author(s):  
Vijayan Gangadharan ◽  
Deepitha Selvaraj ◽  
Martina Kurejova ◽  
Christian Njoo ◽  
Simon Gritsch ◽  
...  
Keyword(s):  
G Protein ◽  
Sensory Nerves ◽  
Biological Role ◽  
Signalling Pathways ◽  
Nociceptive Sensitization ◽  
G Protein Signalling

Biased signalling: the instinctive skill of the cell in the selection of appropriate signalling pathways

2015 ◽  
Vol 470 (2) ◽  
pp. 155-167 ◽  
Author(s):  
Ying Liu ◽  
Yang Yang ◽  
Richard Ward ◽  
Su An ◽  
Xiao-Xi Guo ◽  
...  
Keyword(s):  
G Protein ◽  
Drug Targets ◽  
Biological Effects ◽  
Signalling Pathways ◽  
Therapeutic Drug ◽  
Biological Responses ◽  
Gpcr Activation ◽  
G Protein Signalling ◽  
Uniform Manner ◽  
And Function

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 is that it may selectively activate biological responses to favour therapeutically beneficial signalling pathways and to avoid adverse effects. There are two levels of biased signalling. First, bias can arise from the ability of GPCRs to couple to a subset of the available G-protein subtypes: Gαs, Gαq/11, Gαi/o or Gα12/13. These subtypes produce the diverse effects of GPCRs by targeting different effectors. Secondly, biased GPCRs may differentially activate G-proteins or β-arrestins. β-Arrestins are ubiquitously expressed and function to terminate or inhibit classic G-protein signalling and initiate distinct β-arrestin-mediated signalling processes. The interplay of G-protein and β-arrestin signalling largely determines the cellular consequences of the administration of GPCR-targeted drugs. In the present review, we highlight the particular functionalities of biased signalling and discuss its biological effects subsequent to GPCR activation. We consider that biased signalling is potentially allowing a choice between signalling through ‘beneficial’ pathways and the avoidance of ‘harmful’ ones.

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