Rat Oprm1 (Mu-type opioid receptor) ELISA Kit

Name: Rat Oprm1 (Mu-type opioid receptor) ELISA Kit
SKU: DEIA-FN1057
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

serum, plasma, cell culture supernatants, tissue homogenate

Species Reactivity

Rat

Detection Method

Sandwich ELISA

Intended Use

For quantitative detection of Rat Oprm1 (Mu-type opioid receptor) in serum, plasma, tissue homogenates and other biological fluids.

Contents of Kit

1. 96-well strip plate (Dismountable), 1 plate
2. Lyophilized Standard, 2 vials
3. Sample/Standard dilution buffer, 20 mL
4. Biotin-detection antibody (Concentrated), 120 uL
5. Antibody dilution buffer, 10 mL
6. HRP-Streptavidin Conjugate(SABC), 120 uL
7. SABC dilution buffer, 10 mL
8. TMB substrate, 10 mL
9. Stop solution, 10 mL
10. Wash buffer (25X), 30 mL
11. Plate Sealer, 5 pieces
12. Product Manual, 1 copy

Storage

Store the unopened product at 2 - 8 °C. Do not use past expiration date.

Precision

Intra-Assay: CV<8%
Inter-Assay: CV<10%

Detection Range

31.2-2000 pg/mL

Sensitivity

18.75 pg/mL

Standard Curve

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

A review of opioid addiction genetics

CURRENT OPINION IN PSYCHOLOGY

Authors: Crist, Richard C.; Reiner, Benjamin C.; Berrettini, Wade H.

Abstract

Opioid use disorder (OUD) affects millions of people worldwide and the risk of developing the disorder has a significant genetic component according to twin and family studies. Identification of the genetic variants underlying this inherited risk has focused on two different methods: candidate gene studies and genome-wide association studies (GWAS). The most studied candidate genes have included the mu-opioid receptor (OPRM1), the delta-opioid receptor (OPRD1), the dopamine D2 receptor (DRD2), and brain-derived neurotrophic factor (BDNF). Variants in these genes have been associated with relatively small, but reproducible, effects on OUD risk. More recently, GWAS have identified potential associations with variants in KCNG2, KCNC1, CNIH3, APBB2, and RGMA. In total the genetic associations identified so far explain only a small portion of OUD risk. GWAS of OUD is still in the early stages when compared to studies of other psychiatric disorders, such as schizophrenia, which have found many relevant variants with small effect sizes only after large meta-analyses. Substantial increases in cohort sizes will likely be necessary in the OUD field to achieve similar results. In addition, it will be important for future studies of OUD to incorporate rare variants, epigenetics, and gene x environment interactions into models in order to better explain the observed heritability.

beta-Adrenergic receptor gene expression in HIV-associated neurocognitive impairment and encephalitis: implications for MOR-1K subcellular localization

JOURNAL OF NEUROVIROLOGY

Authors: Dever, Seth M.; Rodriguez, Myosotys; El-Hage, Nazira

Abstract

We previously reported that mRNA expression of the unique alternatively spliced OPRM1 isoform mu-opioid receptor-1K (MOR-1K), which exhibits excitatory cellular signaling, is elevated in HIV-infected individuals with combined neurocognitive impairment (NCI) and HIV encephalitis (HIVE). It has recently been shown that the beta(2)-adrenergic receptor (beta(2)-AR) chaperones MOR-1K, normally localized intracellularly, to the cell surface. Here, we found mRNA expression of the adrenoceptor beta 2 (ADRB2) gene is also elevated in NCI-HIVE individuals, as well as that beta(2)-AR protein expression is elevated in HIV-1-infected primary human astrocytes treated with morphine, and discuss the implications for MOR-1K subcellular localization in this condition.