Id |
Subject |
Object |
Predicate |
Lexical cue |
T195 |
0-5 |
Sentence |
denotes |
GPR37 |
T196 |
6-176 |
Sentence |
denotes |
GPR37 or Parkin-related endothelin-like receptor (Pael-R) was originally discovered through genomic library screening to find new neuropeptide receptors (Marazziti et al. |
T197 |
177-183 |
Sentence |
denotes |
1997). |
T198 |
184-334 |
Sentence |
denotes |
The GPR37 receptor is primarily expressed in the brain and is associated with neurological disorders such as Parkin’s disease and autism (Lopes et al. |
T199 |
335-341 |
Sentence |
denotes |
2015). |
T200 |
342-495 |
Sentence |
denotes |
Mutations within GPR37 affect various autism spectrum disorders, regulation of dopamine reuptake and oligodendrocyte differentiation (Fujita-Jimbo et al. |
T201 |
496-518 |
Sentence |
denotes |
2012; Marazziti et al. |
T202 |
519-536 |
Sentence |
denotes |
2007; Yang et al. |
T203 |
537-543 |
Sentence |
denotes |
2016). |
T204 |
544-742 |
Sentence |
denotes |
PD1 is considered as a ligand for GPR37 because it induced a significant increase in intracellular calcium in HEK293 cells overexpressing GPR37 and murine peritoneal-derived macrophages (Bang et al. |
T205 |
743-749 |
Sentence |
denotes |
2018). |
T206 |
750-982 |
Sentence |
denotes |
Based on the fact that Gpr37-/- mice exhibited increased apoptosis and infarct size, it has recently been suggested that GPR37 is also involved in cell damage protection and inflammation after ischemic stroke (McCrary et al., 2019). |
T207 |
983-1199 |
Sentence |
denotes |
However, due to its clear role in the central nervous system (CNS), the development of a therapeutic agent targeting GPR37 requires a balance between the effect on the central nervous system and therapeutic benefits. |