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中文名稱  μ-型阿片受體抗體規(guī)格 

英文名稱  Anti-mu Opioid receptor

別    名 LMOR; MOR 1; mor; MOR1; Mu opiate receptor; mu type opioid receptor; Mu type opioid receptor MOR 1; muOR; Opioid receptor mu 1; Opioid receptor mu; OPRM; OPRM1; OPRM_HUMAN.

產(chǎn)品屬性：

μ-型阿片受體抗體規(guī)格 濃    度  1mg/1ml

規(guī) 格  0.1ml/100μg 0.2ml/200μg

抗體來(lái)源  Rabbit

克隆類型   polyclonal

交叉反應(yīng)   Human, Mouse, Rat, Dog, Pig, Cow, Rabbit, Guinea Pig

產(chǎn)品類型   一抗  

研究領(lǐng)域    免疫學(xué) 神經(jīng)生物學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 轉(zhuǎn)錄調(diào)節(jié)因子 激酶和磷酸酶

蛋白分子量  predicted molecular weight: 45kDa 

性    狀   Lyophilized or Liquid

免 疫 原  KLH conjugated synthetic peptide derived from human mu Opioid receptor

亞    型  IgG

純化方法   affinity purified by Protein A

儲(chǔ) 存 液   0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide

μ-型阿片受體抗體規(guī)格 產(chǎn)品應(yīng)用   WB=1:100-500 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500

（石蠟切片需做抗原修復(fù)） 

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

保存條件  Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. 

Important Note  This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 

產(chǎn)品介紹 Three types of opioid receptors have been cloned: mu, delta, and kappa. Opioid receptors are seven transmembrane G-protein coupled receptors. They share a high degree of homology and are most divergent at the N- and C-termini. Activation of mu opioid receptors leads to a decrease in neuronal excitability. Most actions of exogenous opioids, such as morphine, are mediated through the mu opioid receptor, including analgesia, tolerance and reward. In general, opioids modulate numerous central and peripheral processes including pain perception,neuroendocrine secretion and the immune response. The opioid signal is transduced from receptors through G proteins to various different effectors. Subsequent to G protein activation, several effectors are known to orchestrate the opioid signal. For example, activation of opioid receptors increases phosphatidylinositol turnover, activates K+ channels and reduces adenylyl cyclase and Ca++ channel activities.

Function : 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.

Subunit : Forms homooligomers and heterooligomers with other GPCRs, such as OPRD1, OPRK1, OPRL1, NPFFR2, ADRA2A, SSTR2, CNR1 and CCR5 (probably in dimeric forms). Interacts with PPL; the interaction disrupts agonist-mediated G-protein activation. Interacts (via C-terminus) with DNAJB4 (via C-terminus). Interacts with calmodulin; the interaction inhibits the constitutive activity of OPRM1; it abolishes basal and attenuates agonist-stimulated G-protein coupling. Interacts with FLNA, PLD2, RANBP9 and WLS. Interacts with GPM6A, RTP4, SYP, GNAS, RGS9, RGS17, RGS20, RGS4, PPP1R9B and HINT1 (By similarity).

Subcellular Location : Cell membrane; Multi-pass membrane protein.

Isoform 12: Cytoplasm.

Tissue Specificity : Expressed in brain. Isoform 16 and isoform 17 are detected in brain.

Post-translational modifications : Phosphorylated. Differentially phosphorylated in basal and agonist-induced conditions. Agonist-mediated phosphorylation modulates receptor internalization. Phosphorylated by ADRBK1 in a agonist-dependent manner. Phosphorylation at Tyr-168 requires receptor activation, is dependent on non-receptor protein tyrosine kinase Src and results in a decrease in agonist efficacy by reducing G-protein coupling efficiency. Phosphorylated on tyrosine residues; the phosphorylation is involved in agoinist-induced G-protein-indepenedent receptor down-regulation. Phosphorylation at Ser-377 is involved in G-protein-dependent but not beta-arrestin-dependent activation of the ERK pathway (By similarity).

Ubiquitinated. A basal ubiquitination seems not to be related to degradation. Ubiquitination is increased upon formation of OPRM1:OPRD1 oligomers leading to proteasomal degradation; the ubiquitination is diminished by RTP4 (By similarity).

Similarity : Belongs to the G-protein coupled receptor 1 family.

Database links : UniProtKB/Swiss-Prot: P35372.2

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