AB5509
Anti-Opioid Receptor µ Antibody
Chemicon®, from guinea pig
Sinônimo(s):
MOR-1
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About This Item
Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Produtos recomendados
fonte biológica
guinea pig
Nível de qualidade
forma do anticorpo
affinity isolated antibody
tipo de produto de anticorpo
primary antibodies
clone
polyclonal
purificado por
affinity chromatography
reatividade de espécies
primate, rat, mouse
fabricante/nome comercial
Chemicon®
técnica(s)
immunocytochemistry: suitable
immunohistochemistry: suitable
nº de adesão NCBI
nº de adesão UniProt
Condições de expedição
dry ice
modificação pós-traducional do alvo
unmodified
Informações sobre genes
human ... OPRM1(4988)
Especificidade
Mu Opioid receptor.
Imunogênio
Synthetic peptide (Catalog number AG375) from the C-terminus of rat mu Opioid receptor corresponding to residues 384-398 of the rat mu opioid receptor.
Aplicação
Anti-Opioid Receptor μ Antibody-AB5509 is an antibody against Opioid Receptor for use in IC, IH.
Immunohistochemistry: 1:50-500 See Protocol.
Immunocytochemistry: 1:50-500 See Protocol.
Optimal working dilutions must be determined by the end user.
IHC Protocol: Male Sprague-Dawley rats (b.wt. 100-150g) were anesthetized with sodium pentobarbital and perfused via the ascending aorta with: 1) 50 mL of Ca2+-free Tyrode+s solution followed by 2) a paraformaldehyde-picric acid fixative and 3) 10% sucrose in PBS as a cryo-protectant. Tissues were rapidly dissected out and stored overnight in 0.1 M phosphate buffer (pH 7.4) containing 10% sucrose. Slide-mounted tissue sections were incubated with blocking buffer for 1 hour at room temperature. Primary antibody was diluted in blocking buffer to the appropriate working dilution. Blocking buffer was removed and the slides were then incubated at 2-8°C for 18-24 hours with AB5509. After rinsing in PBS 3 times sections were incubated for 60 minutes at room temperature with Cy3-conjugated secondary antibodies. After mounting in a mixture of PBS and glycerol (1:3) containing 0.1% p-phenylenediamine, sections were examined with a Nikon Microphot-SA epifluorescence microscope.
ICC Protocol: Mu opioid receptor transfected cells were processed for indirect immunofluorescence. Media was removed and cells were gently washed 3 times with serum free media. Media was removed and cells were gently washed 3 times with serum free media. Following fixation, cells were processed for indirect immunofluorescence as described above.
Immunocytochemistry: 1:50-500 See Protocol.
Optimal working dilutions must be determined by the end user.
IHC Protocol: Male Sprague-Dawley rats (b.wt. 100-150g) were anesthetized with sodium pentobarbital and perfused via the ascending aorta with: 1) 50 mL of Ca2+-free Tyrode+s solution followed by 2) a paraformaldehyde-picric acid fixative and 3) 10% sucrose in PBS as a cryo-protectant. Tissues were rapidly dissected out and stored overnight in 0.1 M phosphate buffer (pH 7.4) containing 10% sucrose. Slide-mounted tissue sections were incubated with blocking buffer for 1 hour at room temperature. Primary antibody was diluted in blocking buffer to the appropriate working dilution. Blocking buffer was removed and the slides were then incubated at 2-8°C for 18-24 hours with AB5509. After rinsing in PBS 3 times sections were incubated for 60 minutes at room temperature with Cy3-conjugated secondary antibodies. After mounting in a mixture of PBS and glycerol (1:3) containing 0.1% p-phenylenediamine, sections were examined with a Nikon Microphot-SA epifluorescence microscope.
ICC Protocol: Mu opioid receptor transfected cells were processed for indirect immunofluorescence. Media was removed and cells were gently washed 3 times with serum free media. Media was removed and cells were gently washed 3 times with serum free media. Following fixation, cells were processed for indirect immunofluorescence as described above.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neuroinflammation & Pain
Neuroinflammation & Pain
Ligação
Replaces: AB1774
forma física
PBS containing 50% glycerol; Concentration 1.0 mg/ml
Armazenamento e estabilidade
Maintain at -20°C in undiluted for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.
Informações legais
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Exoneração de responsabilidade
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Código de classe de armazenamento
12 - Non Combustible Liquids
Classe de risco de água (WGK)
WGK 2
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
Certificados de análise (COA)
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Activation of spinal alpha-2 adrenoceptors, but not mu-opioid receptors, reduces the intrathecal N-methyl-D-aspartate-induced increase in spinal NR1 subunit phosphorylation and nociceptive behaviors in the rat.
Dae-Hyun Roh,Hyoung-Sig Seo,Seo-Yeon Yoon,Sunok Song,Ho-Jae Han,Alvin J Beitz,Jang-Hern Lee
Anesthesia and Analgesia null
The kappa-opioid receptor is primarily postsynaptic: combined immunohistochemical localization of the receptor and endogenous opioids.
Arvidsson, U, et al.
Proceedings of the National Academy of Sciences of the USA, 92, 5062-5066 (1995)
Morphine potentiates neurodegenerative effects of HIV-1 Tat through actions at ?-opioid receptor-expressing glia.
Zou, S; Fitting, S; Hahn, YK; Welch, SP; El-Hage, N; Hauser, KF; Knapp, PE
Brain null
Yong-Hui Liao et al.
Molecular medicine reports, 17(2), 2803-2810 (2017-12-20)
Chronic pain occurs in ~85-90% of chronic pancreatitis (CP) patients. However, as the pathogenesis of CP pain remains to be fully understood, the current therapies for CP pain remain inadequate. Emerging evidence has suggested that the epigenetic modulations of genes
D Gagnon et al.
Scientific reports, 7, 41432-41432 (2017-01-28)
The loss of nigrostriatal dopamine neurons in Parkinson's disease induces a reduction in the number of dendritic spines on medium spiny neurons (MSNs) of the striatum expressing D1 or D2 dopamine receptor. Consequences on MSNs expressing both receptors (D1/D2 MSNs)
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