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  4. Recombinant Mouse Mu-type opioid receptor (Oprm1), partial

Recombinant Mouse Mu-type opioid receptor (Oprm1), partial

  • 货号：
    CSB-YP016361MO1
  • 规格：
  • 来源：
    Yeast
  • 其他：
  • 货号：
    CSB-EP016361MO1
  • 规格：
  • 来源：
    E.coli
  • 其他：
  • 货号：
    CSB-EP016361MO1-B
  • 规格：
  • 来源：
    E.coli
  • 共轭：
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他：
  • 货号：
    CSB-BP016361MO1
  • 规格：
  • 来源：
    Baculovirus
  • 其他：
  • 货号：
    CSB-MP016361MO1
  • 规格：
  • 来源：
    Mammalian cell
  • 其他：

产品详情

  • 纯度：
    >85% (SDS-PAGE)
  • 基因名：
  • Uniprot No.：
  • 别名：
    Oprm1; Mor; Oprm; Mu-type opioid receptor; M-OR-1; MOR-1
  • 种属：
    Mus musculus (Mouse)
  • 蛋白长度：
    Partial
  • 蛋白标签：
    Tag type will be determined during the manufacturing process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 产品提供形式：
    Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 复溶：
    We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 储存条件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期：
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 货期：
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事项：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet ：
    Please contact us to get it.

产品评价

靶点详情

  • 功能：
    Receptor for endogenous opioids such as beta-endorphin and endomorphin. Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone. Agonist binding to the receptor induces coupling to an inactive GDP-bound heterotrimeric G-protein complex and subsequent exchange of GDP for GTP in the G-protein alpha subunit leading to dissociation of the G-protein complex with the free GTP-bound G-protein alpha and the G-protein beta-gamma dimer activating downstream cellular effectors. The agonist- and cell type-specific activity is predominantly coupled to pertussis toxin-sensitive G(i) and G(o) G alpha proteins, GNAI1, GNAI2, GNAI3 and GNAO1 isoforms Alpha-1 and Alpha-2, and to a lesser extent to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15. They mediate an array of downstream cellular responses, including inhibition of adenylate cyclase activity and both N-type and L-type calcium channels, activation of inward rectifying potassium channels, mitogen-activated protein kinase (MAPK), phospholipase C (PLC), phosphoinositide/protein kinase (PKC), phosphoinositide 3-kinase (PI3K) and regulation of NF-kappa-B. Also couples to adenylate cyclase stimulatory G alpha proteins. The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4. Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization. Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction. The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins. The activation of the ERK pathway occurs either in a G-protein-dependent or a beta-arrestin-dependent manner and is regulated by agonist-specific receptor phosphorylation. Acts as a class A G-protein coupled receptor (GPCR) which dissociates from beta-arrestin at or near the plasma membrane and undergoes rapid recycling. Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling. Endogenous ligands induce rapid desensitization, endocytosis and recycling. Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties. Involved in neurogenesis. Isoform 9 is involved in morphine-induced scratching and seems to cross-activate GRPR in response to morphine.
  • 基因功能参考文献：
    1. 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 PMID: 29899455
    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. PMID: 28188737
    3. 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 PMID: 27849613
    4. Our data demonstrate that the main receptor for morphine predominantly shapes the so-called reward/aversion circuitry, with major influence on negative affect centers. PMID: 27671662
    5. Oprm1 knock-out mice lacking 6TM genetic variants failed to show morphine-induced hyperalgesia. PMID: 28343361
    6. Study shows that mu opioid receptors inhibit GABA function in the ventral periaqueductal gray and dorsal raphe dopaminergic neurons, primarily through inhibition of release. PMID: 26792442
    7. 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. PMID: 27648914
    8. The data show that somatic MORs in POMC neurons couple to multiple effectors that have differential sensitivity to desensitization of the receptor. PMID: 28821664
    9. C termini generated from 3' alternative splicing of the mu opioid receptor gene are pharmacologically distinct. PMID: 28319053
    10. Double mothering normalized the abnormal response to maternal separation in Oprm1-knockout mice, in an animal model of Autism. PMID: 27274875
    11. OPRM1, expressed by primary afferent nociceptors, initiates opiate tolerance and opioid-induced hyperalgesia development. PMID: 28092666
    12. 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. PMID: 28185645
    13. 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 PMID: 27707973
    14. MOR epigenetic regulation requires multiple coordinated signals converging at the MOR promoter, involving mitogen-activated protein kinase (MAPK) activation and mitogen- and stress-activated protein kinase 1. PMID: 28153853
    15. inhibition of mu-opioid receptor expression blocks morphine and DAMGO increases in the translocation of NF-kB p65 protein in microglia.a low dose of morphine, exerting its effects via the mu-opioid receptor, increases the DNA-binding activity of NF-kB via PKCepsilon, while a high dose of morphine triggers a nonopiate receptor response mediated by TLR4 and, interestingly, PKC signalling PMID: 27427408
    16. findings indicate that G9a contributes critically to transcriptional repression of MORs in primary sensory neurons in neuropathic pain. G9a inhibitors may be used to enhance the opioid analgesic effect in the treatment of chronic neuropathic pain. PMID: 26917724
    17. In addition to generating a series of prototypic seven transmembrane domain G protein-coupled receptors, Oprm1 produces a set of truncated splice variants containing only six transmembrane domains through which selected opioids mediate a potent analgesia. PMID: 26976581
    18. Morphine treatment interferes with neuronal differentiation via MOR activation. PMID: 26877219
    19. These investigations represent a reverse translational approach to investigating how the OPRM1 A118G polymorphism alters mesolimbic responses to opioids, which may elucidate mechanisms influencing both opioid and alcohol abuse in human populations PMID: 25881115
    20. Results suggested that the MOPR A118G SNP results in a loss of receptor function in the mouse hippocampus PMID: 25986698
    21. Study demonstrates a functional role for Mu Opioid Splice Variant MOR-1K in a murine model of opioid-induced hyperalgesia. PMID: 26270813
    22. In the colon, monoglyceride lipase deficiency causes increased mu opioid receptor sensitivity. PMID: 26075589
    23. This study resolves distinct ligand-directed mechanisms of JNK activation by mu opioid agonists and understanding ligand-directed signaling at MOR may improve opioid therapeutics. PMID: 26056051
    24. Study showed that the acquisition and escalation of heroin self-administration is greater in a mouse model of the OPRM1 A118G polymorphism PMID: 25336208
    25. In the forebrain, mu-opioid receptors are mainly detected in separate neurons. In contrast, neuronal co-localization is detected in subcortical networks. PMID: 24623156
    26. In mu opioid receptor knockout mice, a sex difference was seen in alcohol consumption following social deprivation. PMID: 25363463
    27. MOR-1-dependent alterations in the survival of new neurons in the DG, and not MOR-1-dependent changes in proliferation of progenitor cells in the DG, is important for spatial learning. PMID: 25086317
    28. solution-state NMR to examine the process of muOR activation using a purified receptor (mouse sequence) preparation in an amphiphile membrane-like environment PMID: 26245377
    29. 2.1 A X-ray crystal structure of the murine muOR bound to the morphinan agonist BU72 and a G protein mimetic camelid antibody fragment PMID: 26245379
    30. a truncated 6TM splice variant, mMOR-1G, can rescue IBNtxA analgesia in a mu-opioid receptor-deficient mouse that lacks all Oprm1 splice variants, ablating mu-opioid activity in these animals PMID: 26011641
    31. Deletion of the CB2 r gene increased preference for and vulnerability to ethanol consumption, at least in part, by increased ethanol-induced sensitivity of the TH and mu-opioid receptor gene expressions in mesolimbic neurons. PMID: 23855434
    32. The results of this study indicated that mu-opioid receptor have a differential role in cue-induced reinstatement of cocaine-seeking behavior. PMID: 24943644
    33. In mice with the Oprm1 A112G SNP, G allele is associated with an increase in home-cage dominance and increased motivation for nonaggressive social interactions. PMID: 25716856
    34. Data show that the crystallographic structures of the mouse mu-opioid receptor (MOPr) and human kappa-opioid receptor (KOPr) indicate putative interfacial interactions. PMID: 24651466
    35. Study describes MOR expression in several compartments of the medial habenula-interpeduncular nucleus circuitry; high MOR density in the pathway suggests that these receptors are in a unique position to mediate analgesic, autonomic and reward responses PMID: 25086313
    36. findings suggest specific localization of beta-arrestin2 in the myenteric plexus within MOR1-expressing neurons and provide a relation for direct intracellular crosstalk between activation and beta-arrestin2 signaling in the myenteric neurons. PMID: 25083714
    37. Data provide first evidence that disrupted Oprm1 signaling is sufficient to trigger a comprehensive autistic syndrome, maybe through blunted social reward processes, and this mouse model opens promising avenues for therapeutic innovation PMID: 24619243
    38. Results show Mice homozygous for the G112 allele (G/G)Single nucleotide polymorphism in Oprm1 protein displayed lower morphine-induced antinociception than mice homozygous for the A112 allele (A/A), in a sex specific manner PMID: 22862850
    39. Our study suggests that MOR and DOR are involved in the interactions between cocaine and both deltorphins analogs. PMID: 23965295
    40. the role of mu opioid, D and D dopamine ventral hippocampal (CA) receptors upon cholestasis-induced anxiolytic-like behaviors PMID: 23876451
    41. Transmission through mu opioid receptors mediates hedonic responses to palatable stimuli and contributes to normal and pathological eating. PMID: 23568577
    42. Data indicate 3-methoxythiophen-2-yl)methyl]({2-[(9R)-9-(pyridin-2-yl)-6-oxaspiro-[4.5]decan-9-yl]ethyl})amine (TRV130) as a selective, and G protein biased mu opioid receptor agonist. PMID: 24063433
    43. Deletion of a cis (trans)-element in the 5'-UTR of MOR results in loss of gene expression. PMID: 23353576
    44. The truncated single transmembrane variants can dimerize with the full-length 7-TM mu-opioid receptor (MOR-1) in the endoplasmic reticulum, leading to increased expression of MOR-1 at the protein level. PMID: 23760268
    45. Demonstrated this assay to be an effective method for assessing ligand signaling at mu-opioid receptor. PMID: 23015017
    46. In the ventral tegmental area, natural food reward and ghrelin administration activate mu opioid receptors. PMID: 23220294
    47. Upregulation of mu opioid receptor in periaqueductal gray is related to C-C chemokine receptor (CCR)5 deficiency. PMID: 23147416
    48. MOR constitutive activity initiates both analgesic signaling and a compensatory opponent process that generates endogenous opioid dependence PMID: 24052307
    49. These data provide evidence for the involvement of endogenous opioids and mu-opioid receptors in xylazine-induced central antinociception PMID: 23485547
    50. Data suggest that MOPR and NOPR (nociceptin/orphanin FQ receptor) in spinal cord independently drive antinociception; MOPR/NOPR ligands attenuate neuropathic/inflammatory pain and have high antinociceptive potency with low tolerance development. PMID: 23652222

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  • 亚细胞定位：
    Cell membrane; Multi-pass membrane protein. Cell projection, axon. Perikaryon. Cell projection, dendrite. Endosome.
  • 蛋白家族：
    G-protein coupled receptor 1 family
  • 数据库链接：

    KEGG: mmu:18390

    STRING: 10090.ENSMUSP00000101236

    UniGene: Mm.438000