# |
PMID |
Sentence |
1 |
20838378
|
Indeed we demonstrate that LPI is able to induce calcium mobilization and activation of Akt and extracellular signal-regulated kinase (ERK)1/2 in these cells and that both pharmacological blockade of GPR55 and its downregulation using specific small interfering RNA strongly inhibits these processes.
|
2 |
20838378
|
We further identify an autocrine loop by which LPI is synthesized by cytosolic phospholipase A2, pumped out of the cell by the ATP-binding cassette transporter ABCC1/MRP1, and is then able to initialize cascades downstream of GPR55.
|
3 |
20838378
|
Indeed we demonstrate that LPI is able to induce calcium mobilization and activation of Akt and extracellular signal-regulated kinase (ERK)1/2 in these cells and that both pharmacological blockade of GPR55 and its downregulation using specific small interfering RNA strongly inhibits these processes.
|
4 |
20838378
|
We further identify an autocrine loop by which LPI is synthesized by cytosolic phospholipase A2, pumped out of the cell by the ATP-binding cassette transporter ABCC1/MRP1, and is then able to initialize cascades downstream of GPR55.
|
5 |
21220919
|
Endogenous endocannabinoids bind to cannabinoid receptors; namely CB1, CB2, TRPV1 and GPR55, to activate intracellular pathways that control many cellular functions.
|
6 |
21220919
|
Characterisation of HK2 cells demonstrated that mRNA and protein for CB1, CB2, TRPV1 and GPR55 occurs in these cells.
|
7 |
21220919
|
In general, treatment with CB1 antagonist AM-251, reduces hypertrophy while treatment with CB2 (AM-630) and TRPV1 (SB-366791) antagonists increases hypertrophy.
|
8 |
21220919
|
Endogenous endocannabinoids bind to cannabinoid receptors; namely CB1, CB2, TRPV1 and GPR55, to activate intracellular pathways that control many cellular functions.
|
9 |
21220919
|
Characterisation of HK2 cells demonstrated that mRNA and protein for CB1, CB2, TRPV1 and GPR55 occurs in these cells.
|
10 |
21220919
|
In general, treatment with CB1 antagonist AM-251, reduces hypertrophy while treatment with CB2 (AM-630) and TRPV1 (SB-366791) antagonists increases hypertrophy.
|
11 |
21885477
|
We found high Gpr55 mRNA content in pancreatic islets and considerable protein distribution in insulin-secreting β-cells.
|
12 |
21885477
|
Activation of GPR55 by the agonist O-1602 increased calcium transients (P<0.01) and insulin secretion (P<0.001) stimulated by glucose.
|
13 |
21885477
|
Indeed, acute in vivo experiments showed that GPR55 activation increases glucose tolerance (P<0.05) and plasma insulin levels (P<0.05), suggesting an in vivo physiological relevance of GPR55 systemic stimulation.
|
14 |
21885477
|
Taken together, these results reveal the expression of GPR55 receptors in the endocrine pancreas as well as its function at stimulus-secretion coupling of insulin secretion, suggesting a role in glucose homeostasis.
|
15 |
21885477
|
We found high Gpr55 mRNA content in pancreatic islets and considerable protein distribution in insulin-secreting β-cells.
|
16 |
21885477
|
Activation of GPR55 by the agonist O-1602 increased calcium transients (P<0.01) and insulin secretion (P<0.001) stimulated by glucose.
|
17 |
21885477
|
Indeed, acute in vivo experiments showed that GPR55 activation increases glucose tolerance (P<0.05) and plasma insulin levels (P<0.05), suggesting an in vivo physiological relevance of GPR55 systemic stimulation.
|
18 |
21885477
|
Taken together, these results reveal the expression of GPR55 receptors in the endocrine pancreas as well as its function at stimulus-secretion coupling of insulin secretion, suggesting a role in glucose homeostasis.
|
19 |
21885477
|
We found high Gpr55 mRNA content in pancreatic islets and considerable protein distribution in insulin-secreting β-cells.
|
20 |
21885477
|
Activation of GPR55 by the agonist O-1602 increased calcium transients (P<0.01) and insulin secretion (P<0.001) stimulated by glucose.
|
21 |
21885477
|
Indeed, acute in vivo experiments showed that GPR55 activation increases glucose tolerance (P<0.05) and plasma insulin levels (P<0.05), suggesting an in vivo physiological relevance of GPR55 systemic stimulation.
|
22 |
21885477
|
Taken together, these results reveal the expression of GPR55 receptors in the endocrine pancreas as well as its function at stimulus-secretion coupling of insulin secretion, suggesting a role in glucose homeostasis.
|
23 |
21885477
|
We found high Gpr55 mRNA content in pancreatic islets and considerable protein distribution in insulin-secreting β-cells.
|
24 |
21885477
|
Activation of GPR55 by the agonist O-1602 increased calcium transients (P<0.01) and insulin secretion (P<0.001) stimulated by glucose.
|
25 |
21885477
|
Indeed, acute in vivo experiments showed that GPR55 activation increases glucose tolerance (P<0.05) and plasma insulin levels (P<0.05), suggesting an in vivo physiological relevance of GPR55 systemic stimulation.
|
26 |
21885477
|
Taken together, these results reveal the expression of GPR55 receptors in the endocrine pancreas as well as its function at stimulus-secretion coupling of insulin secretion, suggesting a role in glucose homeostasis.
|
27 |
23679955
|
Antagonists for the orphan G-protein-coupled receptor GPR55 based on a coumarin scaffold.
|
28 |
23679955
|
The orphan G-protein-coupled receptor GPR55, which is activated by 1-lysophosphatidylinositol and interacts with cannabinoid (CB) receptor ligands, has been proposed as a new potential drug target for the treatment of diabetes, Parkinson's disease, neuropathic pain, and cancer.
|
29 |
23679955
|
Selectivity versus the related receptors CB1, CB2, and GPR18 was assessed.
|
30 |
23679955
|
Antagonists for the orphan G-protein-coupled receptor GPR55 based on a coumarin scaffold.
|
31 |
23679955
|
The orphan G-protein-coupled receptor GPR55, which is activated by 1-lysophosphatidylinositol and interacts with cannabinoid (CB) receptor ligands, has been proposed as a new potential drug target for the treatment of diabetes, Parkinson's disease, neuropathic pain, and cancer.
|
32 |
23679955
|
Selectivity versus the related receptors CB1, CB2, and GPR18 was assessed.
|