| ID | Sequence | Length | GC content |
|---|---|---|---|
| ACCCGCCCCGCCCGCGCGUCGGCCCCCACAGUCGCCUGGGGGUGGCCCG… | 3251 nt | 0.6133 | |
| GAGUCCUGCCCCUCCCUCGACCAGGUGGGGCGGGUCGUGGCGGGGGGCA… | 3376 nt | 0.6060 | |
| ACCCGCCCCGCCCGCGCGUCGGCCCCCACAGUCGCCUGGGGGUGGCCCG… | 3402 nt | 0.6152 | |
| GUACCGUACAGAGUGGAUUUGCAGGGCAGUGGCAUGGAGCCCCUCUUCC… | 2990 nt | 0.6013 | |
| GUACCGUACAGAGUGGAUUUGCAGGGCAGUGGCAUGGAGCCCCUCUUCC… | 3033 nt | 0.6014 | |
| ACCCGCCCCGCCCGCGCGUCGGCCCCCACAGUCGCCUGGGGGUGGCCCG… | 3402 nt | 0.6152 |
The protein encoded by this gene is a member of the 7 transmembrane-spanning G protein-coupled receptor family, and functions as a receptor for the endogenous, opioid-related neuropeptide, nociceptin/orphanin FQ. This receptor-ligand system modulates a variety of biological functions and neurobehavior, including stress responses and anxiety behavior, learning and memory, locomotor activity, and inflammatory and immune responses. A promoter region between this gene and the 5'-adjacent RGS19 (regulator of G-protein signaling 19) gene on the opposite strand functions bi-directionally as a core-promoter for both genes, suggesting co-operative transcriptional regulation of these two functionally related genes. Alternatively spliced transcript variants have been described for this gene. A recent study provided evidence for translational readthrough in this gene, and expression of an additional C-terminally extended isoform via the use of an alternative in-frame translation termination codon. [provided by RefSeq, Dec 2017]
A study in mice demonstrated that spinal nerve ligation induced significant downregulation of the OPRL1 gene in injured dorsal root ganglia, as validated by quantitative real-time PCR [Wu et al. DOI:10.1177/1744806916629048]. A separate review of human, mouse, and rat models established that the expression of the OPRL1 is regulated by DNA methylation and histone modifications, and is altered by chronic exposure to drugs of abuse such as cocaine, MDMA, and alcohol, with specific SNPs associated with vulnerability to substance use disorders [Reid et al. DOI:10.3390/Ijms231911804].