Id |
Subject |
Object |
Predicate |
Lexical cue |
T181 |
0-126 |
Sentence |
denotes |
GPR32 is primarily expressed in human PMN, monocytes, adipose tissue and vascular endothelial cells (Sansbury and Spite 2016). |
T182 |
127-355 |
Sentence |
denotes |
RvD1 was identified as a potential agonist due to the activation of GPR32, where [3H]-RvD1 binds to human leukocytes and significantly lowers TNF-α-stimulated NF-κB signalling in GPR32 overexpressing cells (Krishnamoorthy et al. |
T183 |
356-362 |
Sentence |
denotes |
2010). |
T184 |
363-499 |
Sentence |
denotes |
Although RvD1 has a higher affinity for GPR32 than FPR2/ALX, its interaction with GPR32 has not been extensively studied (Norling et al. |
T185 |
500-506 |
Sentence |
denotes |
2012). |
T186 |
507-622 |
Sentence |
denotes |
This could be since GPR32 exists as a pseudogene in rodents, which makes animal testing in principle inappropriate. |
T187 |
623-817 |
Sentence |
denotes |
Treatment of inflammatory macrophages expressing GPR32 with RvD1 enhanced the pro-resolving phenotype to increase phagocytosis and decrease the secretion of inflammatory cytokines (Schmid et al. |
T188 |
818-824 |
Sentence |
denotes |
2016). |
T189 |
825-949 |
Sentence |
denotes |
Also, GPR32 was also involved when during the inhibition of the EMT phenomenon of lung cancer cell lines by RvD1 (Lee et al. |
T190 |
950-956 |
Sentence |
denotes |
2013). |
T191 |
957-1096 |
Sentence |
denotes |
Additionally, RvD3, AT-RvD3, and RvD5 have all been shown to activate GPR32 in a recombinant system of β-arrestin recruitment (Dalli et al. |
T192 |
1097-1117 |
Sentence |
denotes |
2013b; Chiang et al. |
T193 |
1118-1124 |
Sentence |
denotes |
2012). |
T194 |
1125-1197 |
Sentence |
denotes |
These facts suggest the potential redundancy of ligands acting on GPCRs. |