Register or Login
All
  • All
  • Uniprot Id
  • Catalog #
  • Peptide Sequence
COVID19
>   home   >   Products   >   Primary Antibodies   >   Antibody Collections   >   GPCR Antibodies   >   OPRM1 / Mu Opioid Receptor Antibody (Extracellular Domain)   

OPRM1 / Mu Opioid Receptor Antibody (Extracellular Domain)

Rabbit Polyclonal Antibody

     
  • IHC - OPRM1 / Mu Opioid Receptor Antibody (Extracellular Domain) ALS10074
    Human Seminal Vesicle: Formalin-Fixed, Paraffin-Embedded (FFPE)
    detail
  • SPECIFICATION
  • CITATIONS
  • PROTOCOLS
  • BACKGROUND
  • detail
Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
IHC-P
Primary Accession P35372
Reactivity Human, Monkey
Host Rabbit
Clonality Polyclonal
Calculated MW 45kDa
Dilution IHC-P (2.5-5 µg/ml)
Additional Information
Gene ID 4988
Other Names Mu-type opioid receptor, M-OR-1, MOR-1, Mu opiate receptor, Mu opioid receptor, MOP, hMOP, OPRM1, MOR1
Target/Specificity Human OPRM1 / Mu Opioid Receptor. BLAST analysis of the peptide immunogen showed no homology with other human proteins.
Reconstitution & Storage Long term: -70°C; Short term: +4°C
PrecautionsOPRM1 / Mu Opioid Receptor Antibody (Extracellular Domain) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name OPRM1
Synonyms MOR1
Function Receptor for endogenous opioids such as beta-endorphin and endomorphin (PubMed:12589820, PubMed:7891175, PubMed:7905839, PubMed:10529478, PubMed:7957926, PubMed:9689128). Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone (PubMed:12589820, PubMed:7891175, PubMed:7905839, PubMed:7957926, PubMed:10529478, PubMed:9689128, PubMed:10836142, PubMed:19300905). Also activated by enkephalin peptides, such as Met-enkephalin or Met-enkephalin-Arg-Phe, with higher affinity for Met-enkephalin-Arg-Phe (By similarity). 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 (PubMed:7905839). 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 (PubMed:12068084). 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 (By similarity). Also couples to adenylate cyclase stimulatory G alpha proteins (By similarity). The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4 (By similarity). Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta- arrestins is involved in short-term receptor desensitization (By similarity). Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction (By similarity). The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins (By similarity). 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 (By similarity). 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 (By similarity). Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling (By similarity). Endogenous ligands induce rapid desensitization, endocytosis and recycling (By similarity). Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties (By similarity).
Cellular Location Cell membrane; Multi-pass membrane protein. Cell projection, axon {ECO:0000250|UniProtKB:P97266}. Perikaryon {ECO:0000250|UniProtKB:P97266}. Cell projection, dendrite {ECO:0000250|UniProtKB:P97266}. Endosome {ECO:0000250|UniProtKB:P97266}. Note=Is rapidly internalized after agonist binding. {ECO:0000250|UniProtKB:P97266}
Tissue Location Expressed in brain. Isoform 16 and isoform 17 are detected in brain.
Volume 50 µl
Research Areas
Citations (0)
citation

Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.

Submit your citation using an Abcepta antibody to
info@abcepta.com, and receive a free "I Love Antibodies" mug.

Background

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 extend 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 whereas morphine induces only low desensitization and endocytosis. Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties. Involved in neurogenesis. Isoform 12 couples to GNAS and is proposed to be involved in excitatory effects. Isoform 16 and isoform 17 do not bind agonists but may act through oligomerization with binding- competent OPRM1 isoforms and reduce their ligand binding activity.

References

Wang J.-B.,et al.FEBS Lett. 338:217-222(1994).
Bare L.A.,et al.FEBS Lett. 354:213-216(1994).
Mestek A. Jr.,et al.J. Neurosci. 15:2396-2406(1995).
Pan Y.X.,et al.Biochem. Biophys. Res. Commun. 301:1057-1061(2003).
Cadet P.,et al.J. Immunol. 170:5118-5123(2003).

FeedBack
Abcepta welcomes feedback from its customers.

If you have used an Abcepta product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.

If you have any additional inquiries please email technical services at tech@abcepta.com.

$ 467.50
Cat# ALS10074
Size:
Quantity:
Availability: 5 days
Bulk Size

Ordering Information

United States
AlbaniaAustraliaAustriaBelgiumBosnia & HerzegovinaBrazilBulgariaCanadaCentral AmericaChinaCroatiaCyprusCzech RepublicDenmarkEstoniaFinlandFranceGermanyGreeceHong KongHungaryIcelandIndiaIndonesiaIrelandIsraelItalyJapanLatviaLithuaniaLuxembourgMacedoniaMalaysiaMaltaNetherlandsNew ZealandNorwayPakistanPolandPortugalRomaniaSerbiaSingaporeSlovakiaSloveniaSouth AfricaSouth KoreaSpainSwedenSwitzerlandTaiwanTurkeyUnited KingdomUnited StatesVietnamWorldwideOthers
Abcepta, Inc.
(888) 735-7227 / (858) 622-0099
(858) 622-0609
USA Headquarters
(888) 735-7227 / (858) 622-0099 or (858) 875-1900

Shipping Information

Domestic orders (in stock items)
Shipped out the same day. Orders placed after 1 PM (PST) will ship out the next business day.
International orders
Contact your local distributors
Terms & Conditions
"