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PC165L

Sigma-Aldrich

Anti-Opioid μ Receptor (384-398) Rabbit pAb

lyophilized, Calbiochem®

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

form

lyophilized

does not contain

preservative

species reactivity

rat

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze

isotype

IgG

shipped in

ambient

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

General description

Rabbit polyclonal antibody supplied as lyophilized, undiluted serum. Recognizes the ~44-45 kDa opioid µ receptor protein.
Recognizes the ~44-45 kDa opiod μ receptor in caudate putamen and the dorsal horn of the spinal cord.
This Anti-Opioid µ Receptor (384-398) Rabbit pAb is validated for use in Frozen Sections, Immunoblotting, IF, IP for the detection of Opioid µ Receptor (384-398).

Immunogen

Rat
a synthetic peptide corresponding to amino acids 384-398 of rat opioid µ receptor

Application

Frozen Sections (1:500-1:1000, Cy3 technique; 1:3000-1:6000, HRP)

Immunoblotting (1:2000-1:2500; see application references)

Immunofluorescence (1:100-1:200)

Immunoprecipitation (see comments)

Warning

Toxicity: Highly Toxic (H)

Physical form

Undiluted serum.

Reconstitution

Reconstitute the lyophilized antibody with 100 µl sterile distilled H₂O. Resulting reconstituted solution contains ≤0.1% sodium azide. Be careful to reconstitute the entire contents of the vial; during shipment and handling portions of the lyophilized pellet may have become dislodged and may not be in the bottom of the vial. Following reconstitution, aliquot and freeze (-20°C).

Analysis Note

Positive Control
Rat caudate putamen or spinal cord (dorsal horn)

Other Notes

The specificity was determined by immunolabeling of transfected cells, immunoblotting analysis, and immunoisolation studies. Antibody specificity was examined in the rat caudate putamen and dorsal horn of the spinal cord. Staining is completely eliminated by pre-treatment of antibody with immunogen peptide at a concentration of 10 µg/ml. This antibody has also been reported to work for immunopercipitation. Antibody should be titrated for optimal results in individual systems.
Zaki, P.A., et al. 1996. Annu. Rev. Pharmacol. Toxicol.36, 379.
Arvidsson, U., et al. 1995. J. Neurosci.15, 3328.
Kieffer, B.L. 1995. Cell. Mol. Neurobiol.15, 615-635.
Childers, S.R. 1991. Life Sci.48, 1991.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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Heng Xu et al.
The Journal of pharmacology and experimental therapeutics, 315(1), 248-255 (2005-07-01)
A growing body of literature indicates that chronic morphine exposure alters the expression and function of cytoskeletal proteins in addition to the well established interactions between mu opioid receptors and G proteins. In the present study, we hypothesized that chronic
Belén Gago et al.
Journal of neuroscience research, 91(12), 1533-1540 (2013-09-17)
The peptides dynorphin and enkephalin modulate many physiological processes, such as motor activity and the control of mood and motivation. Their expression in the caudate putamen (CPu) is regulated by dopamine and opioid receptors. The current work was designed to
Heng Xu et al.
Synapse (New York, N.Y.), 61(3), 166-175 (2006-12-08)
Previous studies established that Tyr-D-Ala-Gly-N-Me-Phe-Gly-ol (DAMGO) and (2S,4aR,6aR,7R,9S,10aS,10bR)-9-(Benzoyloxy)-2-(3-furanyl)dodecahydro-6a,10b-dimethyl-4,10-dioxo-2H-naphtho-[2,1-c]pyran-7-carboxylic acid methyl ester (herkinorin) are fully efficacious mu-agonists. Herkinorin (HERK), unlike DAMGO, does not recruit beta-arrestin and promote mu-receptor internalization, even in cells that over express beta-arrestin. We hypothesized that chronic HERK
Alicia Rivera et al.
Cells, 11(1) (2022-01-12)
Long-term exposition to morphine elicits structural and synaptic plasticity in reward-related regions of the brain, playing a critical role in addiction. However, morphine-induced neuroadaptations in the dorsal striatum have been poorly studied despite its key function in drug-related habit learning.

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