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The single nucleotide polymorphism A118G alters functional properties of the human mu opioid receptor
Abstract
The most common single nucleotide polymorphism in the coding region of the human mu opioid receptor gene is the A118G variant, an adenine to guanine transition at nucleotide position 118 of the coding sequence of the gene. This polymorphism codes for an asparagine to aspartic acid substitution at amino acid 40 in the amino‐terminus, thereby removing a potential extracellular glycosylation site. Using in vitro cellular expression assays, this variant has been reported to change binding of the endogenous agonist beta‐endorphin and signaling of the receptor following binding of beta‐endorphin. Three clinical studies report that A118G genotype affects opioid antagonist‐mediated increases in cortisol levels. These studies demonstrate a functional role of this variant in responses to endogenous and exogenous opioids. To further characterize function, we expressed the prototype and variant receptors in two types of cells (human 293 embryonic kidney cells and Syrian hamster adenovirus‐12‐induced tumor cells). Stable expression of variant and prototype receptors was characterized by differences in levels of cell surface binding capacity (Bmax), forskolin‐induced cAMP accumulation, as well as agonist‐induced accumulation of cAMP (EC 50) for several agonists, but not for beta‐endorphin. In contrast, transiently expressed variant receptors showed only a minor difference in cell surface binding capacity compared to the prototype, and no differences in cAMP EC 50 values.
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“The A118G variant has enhanced binding and signaling properties, but low expression of mRNA (Zhang et al 2005; Kroslak et al 2007).”
From The behavioral, anatomical and pharmacological parallels between social attachment, love and addiction (2012) · cites this paper as Kroslak et al 2007
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“It must be noted that inconsistent/divergent results regarding ligand affinity and surface expression of the N40D variant have been reported (Kroslak et al., 2007; Oertel et al., 2009).”
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Role of a Functional Human Gene Polymorphism in Stress Responsivity and Addictions
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“Brain region- and sex-specific alterations in DAMGOstimulated [(35) S] GTPgammaS binding in mice with Oprm1 A112G.”
BackgroundInfluentialAdžić, M., Lukić, I., Mitić, M., Glavonic, E., Dragicevic-Curic, N., & Ivković, S. (2023) · Life Sciences · doi:10.1016/j.lfs.2023.121803 · Cited by 22
Evolving Knowledge of Opioid Genetics in Cancer Pain
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“binding affinities for beta-endorphin between wild-type receptor and the MOR coded for by this variant, but did find binding differences for other MOR agonists [46].”
BackgroundMuriel, J., Margarit, C., Planelles, B., Serralta, M. J., Puga, C., Inda, M., Cutillas, E., Morales, D., Horga, J. F., & Peiró, A. M. (2018) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.13735 · Cited by 22
Knapman, A., & Connor, M. A. (2014) · British Journal of Pharmacology · doi:10.1111/bph.12644 · Cited by 22
“Unfortunately, these provocative results were based on very limited quantification of the cellular responses to activation of the N40 and D40 alleles, and no statistical analysis was included.”
BackgroundResultInfluentialHuman Expression Variation in the Mu-Opioid Receptor is Paralleled in Rhesus Macaque
Vallender, E. J., Priddy, C. M., Chen, G., & Miller, G. M. (2008) · Behavior Genetics · doi:10.1007/s10519-008-9207-2 · Cited by 22
“Biochemically, the polymorphism appears to alter beta-endorphin and morphine binding, though in vitro studies have varied widely in their specific results (Bond et al. 1998; Kroslak et al. 2007; Befort et al. 2001; Beyer et al. 2004).”
ResultGenetic variants associated with thermal pain sensitivity in a paediatric population
Matić, M., van den Bosch, G. E., de Wildt, S. N., Tibboel, D., & van Schaik, R. H. N. (2016) · Pain · doi:10.1097/j.pain.0000000000000664 · Cited by 21
“A study assessing the affinity of endogenous and exogenous opioids for the mu-opioid receptor showed increased b-endorphin affinity and potency in the 118G variant,(7) but this finding could not be replicated by others.(3,5,25) However, results of experimental studies in healthy adult volunteers are in line with our f…”
BackgroundResultCurley, J. P. (2011) · Behavioral Neuroscience · doi:10.1037/a0022939 · Cited by 19
Bruehl, S. P., Chung, O. Y., & Burns, J. W. (2008) · Pain · doi:10.1016/j.pain.2008.05.014 · Cited by 19
“Other work indicates that the variant G allele does not influence exogenous opioid receptor binding [5], but is associated with reduced receptor expression [28,44] and increased exogenous opioid analgesic requirements [16,27,30,37,39].”
BackgroundZhang, T., Xu, J., & Pan, Y. (2020) · Molecular Pharmacology · doi:10.1124/mol.120.119453 · Cited by 18
“A single nucleotide polymorphism, A118G, located at a N-glycosylation site of the humanMOR-1, was shown to alter b-endorphin binding (Bond et al., 1998; Kroslak et al., 2007) and modulate expression of MOR-1 mRNA and protein (Zhang et al.”
BackgroundWeidler, C., Wagels, L., Regenbogen, C., Hofhansel, L., Blendy, J. A., Clemens, B., Montag, C., & Habel, U. (2018) · Neuropharmacology · doi:10.1016/j.neuropharm.2018.12.014 · Cited by 18
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Pharmacogenetically Driven Treatments for Alcoholism
Arias, A. J., & Sewell, R. A. (2012) · CNS Drugs · doi:10.2165/11633180-000000000-00000 · Cited by 16
“Much evidence supports the hypothesis that the G allele is a functional polymorphism with complex physiological effects in humans, despite the fact that it may not contribute to the risk for developing substance dependence, at least for opioid, alcohol or cocaine dependence.([16-18]) A more recent meta-analysis examin…”
Saiz‐Rodríguez, M., Valdez-Acosta, S., Borobia, A. M., Burgueño, M., Gálvez-Múgica, M. Á., Acero, J., Cabaleiro, T., Muñoz-Guerra, M. F., Puerro, M., Llanos, L., et al. (2021) · Clinical Therapeutics · doi:10.1016/j.clinthera.2021.03.005 · Cited by 17
Targeting opioid receptors with pharmacological chaperones
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“The lower expression of the receptor observed in G carriers [9-11], together with the results of studies suggesting increasing consumption rates in G carriers have led to the so-called “opioid receptor deficiency theory”.”
ResultGenotyping Test with Clinical Factors: Better Management of Acute Postoperative Pain?
Hajj, A., Peoc’h, K., Laplanche, J., Jabbour, K., Naccache, N., Zeid, H. A., Yazbeck, P. H., & Khabbaz, L. R. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms16036298 · Cited by 17
“Studies have shown that 118G allele expression in stably transfected cells results in a reduced expression of MOR at the cell surface due to both transcriptional and post-transcriptional effects [10,27], suggesting that this allele may be associated in patients with a reduced expression of the receptor leading to a re…”
BackgroundRhesus monkey tryptophan hydroxylase-2 coding region haplotypes affect mRNA stability
Chen, G.-L., & Miller, G. M. (2008) · Neuroscience · doi:10.1016/j.neuroscience.2008.05.050 · Cited by 17
“…example, a nonsynonymous SNP C77G (P26R) in rhesus monkey mu opioid receptor (OPRM1) functionally parallels a non-identical SNP A118G (N40D) in human OPRM1 and in both cases, the SNP associates with common phenotypes (Kroslak et al., 2007; Bond et al., 1998; Miller et al., 2004; Barr et al., 2007).”
BackgroundWetmore, L. A., Pascoe, P. J., Shilo‐Benjamini, Y., & Lindsey, J. C. (2016) · American Journal of Veterinary Research · doi:10.2460/ajvr.77.8.828 · Cited by 17
The Role of Opiates in Social Pain and Suicidal Behavior
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Higher frequency of C.3435 of the ABCB1 gene in patients with tramadol dependence disorder
Enabah, D., Baz, H., & Moselhy, H. F. (2014) · The American Journal of Drug and Alcohol Abuse · doi:10.3109/00952990.2014.925468 · Cited by 16
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Pan, Y., & Pasternak, G. W. (2010) · Humana Press eBooks · doi:10.1007/978-1-60761-993-2_6 · Cited by 16
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“The best characterized single nucleotide polymorphism (SNP) in any opioid receptor gene is the A118G transition in the l-opioid receptor, which alters pain perception and the requirement for morphine in pain-relief therapy [4,12,18,43].”
BackgroundTranslational Research on Nicotine Dependence
Falcone, M., Lee, B., Lerman, C. E., & Blendy, J. A. (2015) · Current topics in behavioral neurosciences · doi:10.1007/7854_2015_5005 · Cited by 15
“The G allele has been associated with greater binding affinity for beta-endorphin, but also with reduced receptor expression and reduced signaling in the presence of mu-opioid agonists (Bond et al. 1998; Kroslak et al. 2007; Oertel et al. 2009; Zhang et al. 2005), suggesting an overall profile of reduced receptor func…”
BackgroundA cis‐ eQTL in OPRM 1 is Associated with Subjective Response to Alcohol and Alcohol Use
Otto, J. M., Gizer, I. R., Deak, J. D., Fleming, K. A., & Bartholow, B. D. (2017) · Alcoholism Clinical and Experimental Research · doi:10.1111/acer.13369 · Cited by 15
“, 2012), the amino acid change brought on by the presence of the minor (Asp) G allele has been shown to triple the l-opioid receptor’s binding affinity for b-endorphin and reduce cell-surface receptor binding site availability (Bond et al., 1998; Kroslak et al., 2007), and has also shown association with reduced OPRM1…”
BackgroundConvergent Balancing Selection on the Mu-Opioid Receptor in Primates
Sweeney, C. G., Rando, J. M., Panas, H. N., Miller, G. M., Platt, D. M., & Vallender, E. J. (2017) · Molecular Biology and Evolution · doi:10.1093/molbev/msx105 · Cited by 16
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“The single nucleotide polymorphism, A118G, in the coding region of the mu receptor, removes a potential extracellular glycosylation site, and affects the function of the mu receptor (Kroslak et al .”
BackgroundScarnati, M. S., Boreland, A. J., Joel, M., Hart, R. P., & Pang, Z. P. (2020) · Alcohol · doi:10.1016/j.alcohol.2020.05.004 · Cited by 14
“There have been several studies aimed at understanding the functional consequences of the MOR D40 variant on receptor activation in mouse models, primates, and humans (Bond et al., 1998; Befort et al., 2001; Beyer, Koch, Schröder, Schulz, & Höllt, 2004; Miller et al., 2004; Zhang, Wang, Johnson, Papp, & Sadée, 2005; K…”
BackgroundInsights into the mechanisms underlying opioid use disorder and potential treatment strategies
Cao, D., Li, F. R., Wu, N., & Li, J. (2021) · British Journal of Pharmacology · doi:10.1111/bph.15592 · Cited by 18
Genetic Vulnerability to Opioid AddictionPreprint
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Self-citationFunctional Characteristics of the Naked Mole Rat μ-Opioid Receptor
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“Previous in vitro analysis of MOR mutants revealed no significant changes in morphine-induced cAMP inhibition at high (1 μM) [18] but demonstrated differences at low (1-100 nM) agonist concentrations [19].”
BackgroundResultSubjective Response as a Consideration in the Pharmacogenetics of Alcoholism Treatment
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“In vitro, this variant demonstrates increased binding affinity with β-endorphin [64, 59] and greater inhibition of cAMP accumulation in HEK293 and AV-12 cells [65].”
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Self-citationVariation in OPRM1 and Risk of Suicidal Behavior in Drug‐Dependent Individuals
Arias, A. J., Chan, G., Gelernter, J. E., Farrer, L. A., & Kranzler, H. R. (2011) · American Journal on Addictions · doi:10.1111/j.1521-0391.2011.00195.x · Cited by 12
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“Although several in vitro studies have suggested that this polymorphism has functional consequences (Kroslak et al. 2007), the direction of the effect has been disputed has been disputed.”
BackgroundCollins, D., Zhang, Y., Blendy, J. A., & Kreek, M. J. (2019) · Neuropharmacology · doi:10.1016/j.neuropharm.2019.107864 · Cited by 11
Self-citationAssociations of the A118G OPRM1 polymorphism with sociotropy and interpersonal sensitivity
Suzuki, A., Shirata, T., Noto, K., Matsumoto, Y., Muraosa, H., Abe, M., Goto, K., & Otani, K. (2022) · Brain and Behavior · doi:10.1002/brb3.2674 · Cited by 8
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Pharmacotherapy of Alcohol Dependence: Improving Translation from the Bench to the Clinic
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“OPRM1 A118G has been demonstrated to produce a number of biochemical and molecular alterations (Kroslak et al. 2007).”
BackgroundSelf-citationErratum: The genetics of addiction—a translational perspective
Arpana Agrawal, A., Verweij, K. J. H., Gillespie, N. A., Heath, A. C., Lessov‐Schlaggar, C. N., Martin, N. G., Nelson, E. C., Slutske, W. S., Whitfield, J. B., & Lynskey, M. T. (2012) · Translational Psychiatry · doi:10.1038/tp.2012.129 · Cited by 8
The promise of pharmacogenetics in labor analgesia…tantalizing, but not there yet
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Heroin-induced suppression of saccharin intake in OPRM1 A118G mice
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“In addition, the A118G variant also results in reduced expression of OPRM1 at the cell surface (Kroslak et al., 2007; Zhang et al., 2005) and reduces the accumulation of cAMP in response to morphine, methadone, and DAMGO (Kroslak et al., 2007).”
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“This change can cause altered expression of MOR or its signaling [ 67– 69 ] .”
BackgroundNobile, B., Olié, É., Ramoz, N., Dubois, J., Guillaume, S., Gorwood, P. A. P. M., & Courtet, P. (2021) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s324868 · Cited by 6
“However, more studies are needed to better understand the related biological and behavioural consequences of this change.(26) Some studies in healthy subjects found that the levels of pro-inflammatory cytokines are significantly lower in G allele carriers (correlated with higher score of healthrelated quality of life)…”
BackgroundPharmacogenomics and Personalized Medicine in the Treatment of Human Diseases
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The potential of pharmacogenomics to treat drug addiction.
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“7 Duration of abuse (y) 5 (1-15) 4 (1-16) 0.”
Immune Cell Activation: Stimulation, Costimulation, and Regulation of Cellular Activation
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“[52] showed in HEK293 and AV-12 cells that stable expression of the 118G variant was associated with decreased agonist-mediated cyclic adenosine monophosphate (cAMP) signaling for morphine, methadone, and DAMGO, but not for β-endorphin.”
Erjavec, G. N., Štrac, D. Š., Tudor, L., Konjevod, M., Šagud, M., & Pivac, N. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-32-9721-0_4 · Cited by 5
“This hypothesis was confirmed in several studies [31, 32], but association studies of this SNP in OUD provided opposite findings, suggesting that this association either exists [33] or does not exist [34].”
Kreek, M. J. (2010) · Drug and Alcohol Dependence · doi:10.1016/j.drugalcdep.2010.03.003 · Cited by 5
“Similar to what both the group of Kreek and that of Sadee have found with the human A118G variant, they found that the A112G variant resulted in decreased mu opioid receptor mRNA and cell surface receptor expression (Kroslak et al., 2007; Mague et al., 2009; Zhang et al., 2005).”
BackgroundResultSelf-citationDaher, M., Costa, F. M. M., & Neves, F. D. A. R. (2013) · Pain Practice · doi:10.1111/papr.12042 · Cited by 4
Neurobiology of Opioid Use Disorder and Comorbid Traumatic Brain Injury
Kosten, T. R., Graham, D. P., & Nielsen, D. A. (2018) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2018.0101 · Cited by 5
Self-citationPharmacogenomics of Pain Management
Janicki, P. K. (2014) · Springer eBooks · doi:10.1007/978-1-4939-1818-8_2 · Cited by 4
Dalton, M. (2013) · White Rose eTheses Online (University of Leeds, The University of Sheffield, University of York) · Cited by 4
Genetic study in patients operated dentally and anesthetized with articaine-epinephrine
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Overview of Genetic Analysis of Human Opioid Receptors
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Genome-wide association study on pharmacological outcomes of musculoskeletal pain in UK Biobank
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“Genetic variants in OPRM1 are thought to in fl uence the opioid response by altering the µ-opioid receptor binding af fi nity of exogenous opioid ligands, such as morphine [12].”
BackgroundWijekumar, P. J., Ranadeva, N. D. K., Jayamaha, A. R., Herath, H. M. N. D. M., Noorden, N., & Fernando, S. (2023) · BMC Research Notes · doi:10.1186/s13104-023-06578-7 · Cited by 2
“To date, OPRM1 gene variants have been identified via PCR amplification of the appropriate gene fragment followed by automated DNA sequencing or PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism) [7, 8].”
MethodKaya-Akyüzlü, D., Özkan-Kotiloğlu, S., Danışman, M., & Bal, C. (2024) · Neuroscience Letters · doi:10.1016/j.neulet.2024.137846 · Cited by 2
Pharmacogenetic Approach to Tramadol Use in the Arab Population
Kwon, C.-H., & Ha, M. W. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25168939 · Cited by 2
Soukho-Kaya, A., Minta, D. K., Diarra, M. T., Konaté, A., Diallo, B., Sidibé, A., Dembélé, M., De, O., Doumbia, A. K., Dao, K., et al. (2012) · PubMed · Cited by 2
Opioid-induced respiratory depression: the role of genetics
Chidambaran, V., & McAuliffe, J. J. (2017) · Expert Review of Precision Medicine and Drug Development · doi:10.1080/23808993.2017.1331704 · Cited by 2
“Brain cells and other cell lines expressing the G variant have shown lower cell-surface receptor-binding site availability for morphine [76,77], less efficient agonistinduced receptor signaling [78], and decreased mRNA expression [79] compared with the A variant.”
BackgroundKreek, M. J., Borg, L., Zhou, Y., & Kravets, I. (2009) · Elsevier eBooks · doi:10.1016/b978-008088783-8.00100-5 · Cited by 2
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Koob, G. F., Arends, M. A., McCracken, M. L., & Moal, M. L. (2023) · Elsevier eBooks · doi:10.1016/b978-0-12-816988-9.00001-1 · Cited by 2
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Фармакогенетика в анестезиологии: на что стоит обратить внимание
Махарин, О. А., Женило, В. М., & Бычков, А. А. (2020) · Annals of critical care · doi:10.21320/1818-474x-2020-2-63-72 · Cited by 1
“В исследованиях, посвященных влиянию полиморфизма А118G на внутриклеточную передачу сигнала, показано, что наличие G-аллеля приводило к уменьшению образования циклического аденозинмонофосфата (цАМФ) при воздействии на μ-опиоидный рецептор экзогенных опиоидов (морфин, метадон), однако при воздействии β-эндорфина образо…”
Daybell, I. S., Wie, C. S., Johnson, B. W., Covington, S. M., Freeman, J., Pew, S., & Maloney, J. A. (2026) · Current Pain and Headache Reports · doi:10.1007/s11916-026-01485-5 · Cited by 1
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Understanding the Agent, Part I: Opioid Biology and Basic Pharmacology
McAnally, H. B. (2017) · Springer eBooks · doi:10.1007/978-3-319-47497-7_2 · Cited by 1
Gillavry, D. W. M., & Ullrich, D. C. (2020) · Military Psychology · doi:10.1080/08995605.2020.1730111 · Cited by 1
“The G allele has been associated with enhanced receptor functioning (Kroslak et al., 2007; Sia et al., 2008) but reduced baseline receptor availability (Kroslak et al.”
BackgroundRole of Opioid Rotation and Tapering in Managing Opioid-Induced Hyperalgesia
Smith, H. S. (2009) · CRC Press eBooks · doi:10.3109/9781420089004-11 · Cited by 1
Genome-wide association study of nociceptive musculoskeletal pain treatment response in UK BiobankPreprint
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Practical and clinical use of opioids
Bastami, S. (2013) · KTH Publication Database DiVA (KTH Royal Institute of Technology)
Caputi, F. F. (2012) · AMS Dottorato Institutional Doctoral Theses Repository (University of Bologna) · doi:10.6092/unibo/amsdottorato/4558
“However, the 118G variant is associated with reduced OPRM1 mRNA levels in human brains and in decreased receptor levels in cells expressing the same variant (Kroslak et al., 2007).”
BackgroundGenetic Polymorphisms in the µ-Opioid Receptor Gene and Breast Cancer Survival
Bortsov, A. V., Millikan, R. C., Belfer, I., Boortz-Marx, R. L., Arora, H., & McLean, S. A. (2012) · Springer eBooks · doi:10.1007/978-94-007-5678-6_7
Functional Characterization of the OPRM1 A118G Single Nucleotide Polymorphism in Mice
Mague, S. D. (2011) · ScholarlyCommons (University of Pennsylvania)
Björk, K. (2008) · Figshare
Correction: Functional Characteristics of the Naked Mole Rat μ-Opioid Receptor
Busch-Dienstfertig, M., Roth, C. A., & Stein, C. (2014) · PLoS ONE · doi:10.1371/annotation/d86135c4-7a99-43fb-a3ea-445a9e671c51
Peter Riederer “70th birthday” Neurobiological foundations of modern addiction treatment
Jacob, C. (2012) · Journal of Neural Transmission · doi:10.1007/s00702-012-0886-8
Karlsson, C. (2015) · Figshare
Pharmacogenomics and personalised analgesia
Lambert, D. G. (2011) · Trends in Anaesthesia and Critical Care · doi:10.1016/j.tacc.2011.03.003
POST MORTEM STUDIES ON THE HUMAN ALCOHOLIC BRAIN: DNA METHYLATION AND MOLECULAR RESPONSES
Johansson, S. (2008) · Figshare · Cited by 1
Metadata
- Authors
- Kroslak, T., LaForge, K. S., Gianotti, R. J., Ho, A., Nielsen, D. A., & Kreek, M. J.
- Affiliations
- Rockefeller University (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2007-06-03
- Volume
- 103
- Issue
- 1
- Pages
- 77-87
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2039877085
- Cited by
- 213
- References
- 42
- Citations by year
- 2026: 3 · 2024: 3 · 2023: 7 · 2022: 7 · 2021: 4 · 2020: 9 · 2019: 8 · 2018: 9 · 2017: 11 · 2016: 9 · 2015: 16 · 2014: 21 · 2013: 17 · 2012: 23
- FWCI
- 6.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Biotechnology and Biological Sciences Research Council (C17893)
- National Institute on Drug Abuse (R01DA012848, P60 DA 05130, P60DA005130, R01-DA-12848)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- mu-opioid receptor, A118G polymorphism, single nucleotide polymorphisms, cAMP signaling, forskolin, cell surface binding
- MeSH terms
- Cyclic AMP, Analgesics, Opioid, Animals, Binding, Competitive, Cell Line, Cell Membrane, Dose-Response Relationship, Drug, Fibroblasts, Colforsin, Cricetinae, Humans, Kidney, Mesocricetus, Receptors, Opioid, mu, Gene Transfer Techniques, Polymorphism, Single Nucleotide, Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
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