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anti-Human Mu Opioid Receptor 1 Antibodies:
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Cat (Feline) Polyclonal Mu Opioid Receptor 1 Primary Antibody for IEM, ICC - ABIN617908
Gracy, Svingos, Pickel: Dual ultrastructural localization of mu-opioid receptors and NMDA-type glutamate receptors in the shell of the rat nucleus accumbens. in The Journal of neuroscience : the official journal of the Society for Neuroscience 1997
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Human Polyclonal Mu Opioid Receptor 1 Primary Antibody for IHC - ABIN966719
Wang, Johnson, Persico, Hawkins, Griffin, Uhl: Human mu opiate receptor. cDNA and genomic clones, pharmacologic characterization and chromosomal assignment. in FEBS letters 1994
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Human Polyclonal Mu Opioid Receptor 1 Primary Antibody for IHC, IHC (p) - ABIN441215
Dever, Xu, Fitting, Knapp, Hauser: Differential expression and HIV-1 regulation of μ-opioid receptor splice variants across human central nervous system cell types. in Journal of neurovirology 2012
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Human Polyclonal Mu Opioid Receptor 1 Primary Antibody for IF, IHC - ABIN437976
Nassirpour, Bahima, Lalive, Lüscher, Luján, Slesinger: Morphine- and CaMKII-dependent enhancement of GIRK channel signaling in hippocampal neurons. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2010
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Human Polyclonal Mu Opioid Receptor 1 Primary Antibody for ICC, IHC (fro) - ABIN250447
Vassoler, Wright, Byrnes: Exposure to opiates in female adolescents alters mu opiate receptor expression and increases the rewarding effects of morphine in future offspring. in Neuropharmacology 2016
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Human Polyclonal Mu Opioid Receptor 1 Primary Antibody for IF (p), IHC (p) - ABIN703210
Brewer, Baran, Whitfield, Jensen, Clemens: Dopamine D3 receptor dysfunction prevents anti-nociceptive effects of morphine in the spinal cord. in Frontiers in neural circuits 2014
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Human Polyclonal Mu Opioid Receptor 1 Primary Antibody for IF (p), IHC (p) - ABIN701755
Laureano, Dalle Molle, Alves, Luft, Desai, Ross, Silveira: Intrauterine growth restriction modifies the hedonic response to sweet taste in newborn pups - Role of the accumbal μ-opioid receptors. in Neuroscience 2016
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Polyclonal Mu Opioid Receptor 1 Primary Antibody for WB - ABIN4948303
Rodríguez-Muñoz, de la Torre-Madrid, Gaitán, Sánchez-Blázquez, Garzón: RGS14 prevents morphine from internalizing Mu-opioid receptors in periaqueductal gray neurons. in Cellular signalling 2007
Human Polyclonal Mu Opioid Receptor 1 Primary Antibody for ICC, IF - ABIN250445
Weber, Wang, Ren, Wei, Zhao, Yang, Yuan, Pang, Wang, Wang: The Development of a Macromolecular Analgesic for Arthritic Pain. in Molecular pharmaceutics 2019
cancer pain patients with GG genotype of OPRM1 need a larger dose of oxycodone that patients with AA and AG genotypes
OPRM1 gene polymorphisms could identify the risk of gastrointestinal adverse events in prescription opioid use disorder patients
The OPRM1 A118G AA genotype associated with elevated risk of alcohol-related hospital readmission, more readmissions, and fewer days until first readmission in male patients only. After normalizing patient 2D:4D against control 2D:4D, we found that normalized 2D:4D ratios were lower in male 118G patients than male AA patients, suggesting prenatal androgens interact with OPRM1 to influence alcohol dependence risk.
The results indicated that genetic variation of microopioid receptor 1 (OPRM1) may contribute to interindividual differences in morphine consumption with recommendation grade A for OPRM A118G single nucleotide polymorphism (rs1799971).
Subjects with morbid obesity and binge eating disorder (BED) had widespread reduction in OPRM1 binding compared to control subjects. However, there was no significant difference in brain OPRM1 binding between subjects with morbid obesity and BED.
Of the 63 patients enrolled, 45 (71%) were homozygous genotype A/A (118A group), whereas 18 carried the G variants of OPRM1 (A/G or G/G) (118G group). In the Italian population participating in this study there was a different incidence of pruritus in the postcesarean period in response to intrathecal opioids related to OPRM1 gene polymorphism, but not of postoperative pain.
Genetic variability of the mu-opioid receptor influences intrathecal fentanyl analgesia requirements in laboring women.
Results from the present study suggest that, in patients with hip osteoarthritis, genetic variants in OPRM1 and OPRD1 may contribute to the pain phenotype.
The findings of this study suggested that increased ethanol consumption in male 118GG mice may be due to increased ethanol reward, while increased drinking in female 118GG mice might be due to decreased sensitivity to the sedative/ataxic effects of ethanol.
The results showed that, while both the 118AA and 118GG mice demonstrated robust avoidance of the heroin-paired saccharin cue following daily taste-drug pairings, only the 118AA mice suppressed intake of the heroin-paired saccharin cue when 48h elapsed between each taste-drug pairing
There was no association between OPRM1 SNPs and oral pain sensitivity.
This study showed that The opioid receptor mu 1 (OPRM1) rs1799971 and catechol-O-methyltransferase (COMT) rs4680 as genetic markers for placebo analgesia.
A functional polymorphism in the mu opioid receptor OPRM1 (A118G, rs1799971) and interactive effects of maternal overcontrol have been shown to impact sympathetic nervous system activation and stress reactivity associated with the development of Anxiety in school-aged children.
Possession of the OPRM1 minor allele, 118G and lower mother-child language style matching were both associated with greater Separation Anxiety Disorder symptoms.
SNP rs1799971 related to hypnotizability
findings suggest that there may not be an association between OPRM1 rs1799971 genotype and alcohol consumption or sensitivity in individuals of European ancestry.
the present findings on OPRM1 and OPRL1 methylation together with our previous study on OPRK1 and OPRD1, suggest an epigenetic involvement of the opioid system in AD, and a potential diagnostic value of opioid receptor methylation for AD.
ABIN-1 negatively regulates MOR function in vitro and in vivo
Cyclopeptide Dmt-[D-Lys-p-CF3-Phe-Phe-Asp]NH2, a novel G protein-biased agonist of the mu opioid receptor.
Higher methylation levels within the infants at the -18 (11.4% vs 4.4%, P = .0001), -14 (46.1% vs 24.0%, P = .002) and +23 (26.3% vs 12.9%, P = .008) CpG sites were associated with higher rates of infant pharmacologic treatment. Higher levels of methylation within the mothers at the -169 (R = 0.43, P = .008), -152 (R = 0.40, P = .002) and +84 (R = 0.44, P = .006) sites were associated with longer infant length of stay.
Results provide evidence that Oprm1 is involved in hyperalgesia induced by chronic morphine and its metabolite morphine-3-glucuronide.
These findings indicate that inhibition of mu-opioid-receptor-associated V1bR provides an approach for enhancing morphine analgesia without increasing analgesic tolerance
Study showed that MCRT increased colonic contraction via mu- and delta- opioid receptors.
Before behavioral training, mice lacking Oprm1 show perseverative behavior in the Y-maze and severe deficit in social interaction. Behavioral intervention durably relieved social interaction deficit in Oprm1-/- mice.
Phosphorylation-deficient Oprm1 improves analgesia and diminishes tolerance but worsens opioid side effects.
3.5 A resolution cryo-electron microscopy structure of the mu-opioid receptor (muOR) bound to the agonist peptide DAMGO and nucleotide-free Gi; these results shed light on the structural features that contribute to the Gi protein-coupling specificity of the microOR
Suggest that peripheral and central MOR and central KOR may be involved in the modulation of scratching behaviour in imiquimod-treated mice.
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.
The CeA was subsequently targeted with bilateral infusions of the MOR antagonist naloxonazine, which significantly reduced sodium appetite in mice. The CeA is therefore identified as a key node in the circuit that contributes to sodium appetite. Moreover, endogenous opioids, acting via MOR, within the CeA promote this form of appetitive behavior
Our data demonstrate that the main receptor for morphine predominantly shapes the so-called reward/aversion circuitry, with major influence on negative affect centers.
Knockout mice for mu and delta opioid receptor have augmented colon sensitivity in the colonic distension assay.
Oprm1 knock-out mice lacking 6TM genetic variants failed to show morphine-induced hyperalgesia.
Study shows that mu opioid receptors inhibit GABA function in the ventral periaqueductal gray and dorsal raphe dopaminergic neurons, primarily through inhibition of release.
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.
The data show that somatic MORs in POMC neurons couple to multiple effectors that have differential sensitivity to desensitization of the receptor.
C termini generated from 3' alternative splicing of the mu opioid receptor gene are pharmacologically distinct.
Double mothering normalized the abnormal response to maternal separation in Oprm1-knockout mice, in an animal model of Autism.
OPRM1, expressed by primary afferent nociceptors, initiates opiate tolerance and opioid-induced hyperalgesia development.
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.
MOR-T394 mutation or polymorphisms could be a risk factor in developing opioid abuse and addiction and therefore be used as a new biomarker in prediction and prevention of opioid abuse and addiction
MicroRNA miR-212/132 cluster is actively repressing the expression of mu opioid receptor (Oprm1) by targeting a sequence in the 3' UTR of its mRNA.
demonstrate that zfMOR exhibits a pharmacological profile similar to that of the mammalian MOR.
analysis of solubilization of mu-opioid receptors enriched from bovine brain membranes
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.
Coactivation of mu opioid receptors with nociceptin receptors produces synergistic antinociception.
Thisstudy adds to the growing literature showing that variation in the mu-opioid receptor gene OPRM1 is associated with social attachment and rejection.
OPRM1 gene variation influences hypothalamic-pituitary-adrenal axis function in response to a variety of stressors.
findings suggest a role for OPRM1 variation in the expression of attachment behavior, especially as a function of separation from the caregiver
This gene encodes one of three opioid receptors. The mu opioid receptor is the principal target of endogenous opioid peptides and opioid analgesic agents such a s beta-endorphn and enkephalins. The NM_001008503.1:c.118A>G allele had been associated with opioid and alcohol addiction and variations in pain sensitivity but evidence is conflicting. Multiple transcript variants encoding different isoforms have been found for this gene.
micro opioid receptor isoform hMOR-1A2
, mu opiate receptor
, mu opioid receptor hMOR-1a
, mu-type opioid receptor
, MOP receptor
, mu opioid receptor splice variant rMOR-1S
, mu opioid receptor splice variant rMOR-1Z
, opioid receptor B
, opioid receptor, mu 1
, mu opioid receptor
, mu-opioid receptor
, outer membrane protein OprM