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

scholarly journals The dynamic role of regulator of G-protein signalling (RGS) proteins in partial agonism

2014 ◽  
Vol 592 (17) ◽  
pp. 3701-3702
Author(s):  
Joobin Sattar ◽  
Kevin P. Grace ◽  
Guillaume Bastin
Keyword(s):  
G Protein ◽  
Rgs Proteins ◽  
Partial Agonism ◽  
G Protein Signalling

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.

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 Molecular subversion of Cdc42 signalling in cancer

2021 ◽  
Author(s):  
Natasha P. Murphy ◽  
Ana Masara binti Ahmad Mokhtar ◽  
Helen R. Mott ◽  
Darerca Owen
Keyword(s):  
G Protein ◽  
Cell Cycle Progression ◽  
Small Gtpases ◽  
Signalling Pathways ◽  
Cycle Progression ◽  
Small G Protein ◽  
Genomics And Proteomics ◽  
The Subject ◽  
Rho Family

Cdc42 is a member of the Rho family of small GTPases and a master regulator of the actin cytoskeleton, controlling cell motility, polarity and cell cycle progression. This small G protein and its regulators have been the subject of many years of fruitful investigation and the advent of functional genomics and proteomics has opened up new avenues of exploration including how it functions at specific locations in the cell. This has coincided with the introduction of new structural techniques with the ability to study small GTPases in the context of the membrane. The role of Cdc42 in cancer is well established but the molecular details of its action are still being uncovered. Here we review alterations found to Cdc42 itself and to key components of the signal transduction pathways it controls in cancer. Given the challenges encountered with targeting small G proteins directly therapeutically, it is arguably the regulators of Cdc42 and the effector signalling pathways downstream of the small G protein which will be the most tractable targets for therapeutic intervention. These will require interrogation in order to fully understand the global signalling contribution of Cdc42, unlock the potential for mapping new signalling axes and ultimately produce inhibitors of Cdc42 driven signalling.

scholarly journals Dissecting the role of G-protein signalling in primary metabolism in the wheat pathogen Stagonospora nodorum

Microbiology ◽  
2013 ◽  
Vol 159 (Pt_9) ◽  
pp. 1972-1985 ◽  
Author(s):  
Joel P. A. Gummer ◽  
Robert D. Trengove ◽  
Richard P. Oliver ◽  
Peter S. Solomon
Keyword(s):  
G Protein ◽  
Stagonospora Nodorum ◽  
Primary Metabolism ◽  
G Protein Signalling

GRAF1-dependent endocytosis

2009 ◽  
Vol 37 (5) ◽  
pp. 1061-1065 ◽  
Author(s):  
Gary J. Doherty ◽  
Richard Lundmark
Keyword(s):  
G Protein ◽  
Extracellular Fluid ◽  
Endocytic Pathway ◽  
Protein Domain ◽  
Small G Protein ◽  
G Protein Signalling ◽  
Protein Functions ◽  
Membrane Carriers

The role of endocytosis in controlling a multitude of cell biological events is well established. Molecular and mechanistic characterization of endocytosis has predominantly focused on CME (clathrin-mediated endocytosis), although many other endocytic pathways have been described. It was recently shown that the BAR (Bin/amphiphysin/Rvs) and Rho GAP (GTPase-activating protein) domain-containing protein GRAF1 (GTPase regulator associated with focal adhesion kinase-1) is found on prevalent, pleiomorphic endocytic membranes, and is essential for the major, clathrin-independent endocytic pathway that these membranes mediate. This pathway is characterized by its ability to internalize GPI (glycosylphosphatidylinositol)-anchored proteins, bacterial toxins and large amounts of extracellular fluid. These membrane carriers are highly dynamic and associated with the activity of the small G-protein Cdc42 (cell division cycle 42). In the present paper, we review the role of GRAF1 in this CLIC (clathrin-independent carrier)/GEEC (GPI-anchored protein-enriched early endocytic compartment) endocytic pathway and discuss the current understanding regarding how this multidomain protein functions at the interface between membrane sculpting, small G-protein signalling and endocytosis.

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