Psychiatry related information on NPBWR1

• The localization of GPR7 and GPR8 in some hypothalamic regions of primary importance in the regulation of feeding behavior has provided a springboard for investigation of the role of NPW in the central nervous system [1].

High impact information on NPBWR1

• It binds and activates human GPR7 or GPR8 with median effective concentrations (EC(50)) of 0.23 nM and 15.8 nM, respectively [2].
• Synthetic human NPW binds and activates human GPR7 or GPR8 with EC(50) values of 0.56 nM and 0.51 nM, respectively [2].
• We have purified an endogenous peptide ligand for GPR7 from bovine hypothalamus extracts [2].
• The trap-like relaxin-binding site of the leucine-rich G-protein-coupled receptor 7 [3].
• The structurally related orphan G-protein-coupled receptors GPR7 and GPR8 are expressed in the central nervous system, and their ligands have not been identified [4].

Biological context of NPBWR1

• GPR7 was mapped to chromosome 10q11.2-q21.1 and GPR8 to chromosome 20q13 [5].
• GPR7 mRNA is expressed in discrete regions of the hypothalamus suggesting a role in the regulation of energy homeostasis and neuroendocrine axes [6].
• The absence of a GPR8 gene in the rodent suggests that GPR8 originated from gene duplication of GPR7 after the rodent line diverged from the rabbit, tree shrew, flying lemur, lemur, monkey and human lines [7].
• To determine the molecular structure of the endogenous GPR7 ligand, we purified it from bovine hypothalamic tissue extracts on the basis of cAMP production-inhibitory activity to cells expressing GPR7 [8].

Anatomical context of NPBWR1

• RT-PCR technique revealed the presence of ppNPB, ppNPW, NPBWR1 and NPBWR2-like mRNAs in isolated pancreatic islets of the rat [9].
• These findings indicate that neuropeptide W is the endogenous ligand for both GPR7 and GPR8 and acts as a mediator of the central control of feeding and the neuroendocrine system [4].
• A low level of GPR7 receptor was observed in myelin-forming Schwann cells in both normal human and rat nerve, and in primary rat Schwann cell cultures [10].
• In this study, we investigated whether the GPR7 receptor is expressed in the peripheral nervous system under normal and pathological conditions [10].
• A stable cell line expressing the GPR7 gene was created, but expression levels of the receptor were low [5].

Other interactions of NPBWR1

• [J. Biol. Chem. 277, 34010-34016 (2002)] who observed that iodination of the NPB Tyr(2) resulted in decreased agonistic activity at GPR7 [11].
• Two related G protein-coupled receptors: the distribution of GPR7 in rat brain and the absence of GPR8 in rodents [7].
• The pleated sheet region of the leucine-rich G-protein-coupled receptor 7 supports a relaxin-binding group of amino acids that perfectly matches the binding cassette of relaxin [3].

Analytical, diagnostic and therapeutic context of NPBWR1

• Complementary animal models of immune-inflammatory and ligation-induced nerve injury and neuropathic pain similarly exhibited an increased myelin-associated expression of GPR7 receptor [10].
• In situ hybridization revealed expression of GPR7 in the human pituitary [5].
• 3. Northern blot analysis using human mRNA demonstrated expression of GPR7 mainly in cerebellum and frontal cortex, while GPR8 was located mainly in the frontal cortex [5].
• Using these primers, orthologs of GPR7 and GPR8 were isolated by the PCR from rabbit, tree shrew, and flying lemur, as well as GPR7 in the rat [7].

References