Browse our anti-Mu Opioid Receptor 1 (OPRM1) Antibodies

Human Opioid Receptor, mu 1 (OPRM1) interaction partners

1. Ligation of the identical phosphopeptide onto the beta2AR, the muscarinic acetylcholine receptor 2 and the mu-opioid receptor reveals that the ability of beta-arrestin1 to enhance agonist binding relative to G protein differs substantially among receptors.

2. DNA methylation analysis in the promoter region of OPRM1 identified twenty-two CpG sites in the OPRM1 promoter region significantly associated with opioid exposure in a Chinese Han population.

3. OPRM1 A118G polymorphism is associated with pain experience in young women with primary dysmenorrhea.

4. findings demonstrated DNA hypermethylation of the R2 region of the OPRM1 promoter in leukocytes of opium use disorder.

5. Genetic variations in the mu-opioid receptor (OPRM1) gene have been related to high sensitivity to rewarding effects of alcohol.

6. Findings suggest no OPRM1-based susceptibility to the number of heavy-drinking peers, adding to the existing mixed findings from correlational studies. Future research on OPRM1-related susceptibility to alcohol-promoting peer environments through meta-analytic synthesis and both experimental and prospective, multiwave designs is needed to resolve these mixed findings.

7. The MDR1 (show TBC1D9 Antibodies)/CYP3A4 (show CYP3A4 Antibodies)/OPRM1 gene polymorphisms influenced the fentanyl consumption and the physiological effects of intravenous analgesia in the Chinese women who received lower segment caesarean section surgeries.

8. Participants with the OPRM1 118G allele evidenced steeper breath alcohol concentration (BrAC) trajectories and greater peak BrAC relative to 118A homozygous participants. Significant indirect associations of OPRM1 with follow-up heavy drinking were observed.

9. Study demonstrated in a cohort of 84 cancer patients that high-dose opioid use correlates with OPRM1 hypermethylation in peripheral leukocytes; and showed that targeted re-expression of mu-opioid receptor on cancer cells inhibits mechanical and thermal hypersensitivity, and prevents opioid tolerance, in a mouse cancer pain model. Epigenetic regulation of OPRM1 contributes to opioid tolerance in cancer patients.

10. In summary, our results suggest that, by genetic association, the mu-opioid receptor interacts with serotonin transporter (show SLC6A4 Antibodies) and serotonin 1A receptor to modulate exercise-induced hypoalgesia in fibromyalgia.

Mouse (Murine) Opioid Receptor, mu 1 (OPRM1) interaction partners

1. Suggest that peripheral and central MOR and central KOR (show OPRK1 Antibodies) may be involved in the modulation of scratching behaviour in imiquimod-treated mice.

2. Results demonstrate that MOR-dependent behavioral effects of BPN including pain sensitivity, locomotor hyperactivity and approach behavior in the NIH test, are modified by genetic variation in the A112G SNP with the A carrier being most responsive to drug effects.

3. The CeA (show CEA Antibodies) was subsequently targeted with bilateral infusions of the MOR antagonist naloxonazine, which significantly reduced sodium appetite in mice. The CeA (show CEA Antibodies) is therefore identified as a key node in the circuit that contributes to sodium appetite. Moreover, endogenous opioids, acting via MOR, within the CeA (show CEA Antibodies) promote this form of appetitive behavior

4. Oprm1 knock-out mice lacking 6TM genetic variants failed to show morphine-induced hyperalgesia.

5. Findings implicate truncated Oprm1 6TM splice variants in analgesic mechanisms and suggest that they may help explain many of the subtle, but important, clinical differences among mu opioids.

6. The data show that somatic MORs in POMC (show POMC Antibodies) neurons couple to multiple effectors that have differential sensitivity to desensitization of the receptor.

7. C termini generated from 3' alternative splicing of the mu opioid receptor gene are pharmacologically distinct.

8. Double mothering normalized the abnormal response to maternal separation in Oprm1-knockout mice, in an animal model of Autism.

9. OPRM1, expressed by primary afferent nociceptors, initiates opiate tolerance and opioid-induced hyperalgesia development.

10. Study reveals dissociable Mu opioid receptors (MOR) functions across mesocorticolimbic networks. Beyond a role in reward processing, operating at the level of local ventral tegmental area neurons, MORs also moderate motivation for appetitive stimuli within forebrain circuits that drive motivated behaviors.

Zebrafish Opioid Receptor, mu 1 (OPRM1) interaction partners

1. MicroRNA miR (show MYLIP Antibodies)-212/132 cluster is actively repressing the expression of mu opioid receptor (Oprm1) by targeting a sequence in the 3' UTR (show UTS2R Antibodies) of its mRNA.

2. demonstrate that zfMOR exhibits a pharmacological profile similar to that of the mammalian MOR.

Cow (Bovine) Opioid Receptor, mu 1 (OPRM1) interaction partners

Rhesus Monkey Opioid Receptor, mu 1 (OPRM1) interaction partners

1. A nonsynonymous SNP in the first exon of the OPRM1 gene (OPRM1 A118G) encodes the ligand-binding domain the receptor and which has been associated with increased alcohol-induced stimulation and euphoria.

2. Coactivation of mu opioid receptors with nociceptin (show PNOC Antibodies) receptors produces synergistic antinociception.

3. Thisstudy adds to the growing literature showing that variation in the mu-opioid receptor gene OPRM1 is associated with social attachment and rejection.

4. OPRM1 gene variation influences hypothalamic-pituitary-adrenal axis function in response to a variety of stressors.

5. findings suggest a role for OPRM1 variation in the expression of attachment behavior, especially as a function of separation from the caregiver