Human OPRL1 (Nociceptin receptor) ELISA Kit

Name: Human OPRL1 (Nociceptin receptor) ELISA Kit
SKU: DEIA-FN1056
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

Human

Detection Method

Sandwich ELISA

Intended Use

For quantitative detection of Human OPRL1 (Nociceptin 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

78-5000 pg/mL

Sensitivity

46.9 pg/mL

Standard Curve

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Evidence of efficient stop codon readthrough in four mammalian genes

NUCLEIC ACIDS RESEARCH

Authors: Loughran, Gary; Chou, Ming-Yuan; Ivanov, Ivaylo P.; Jungreis, Irwin; Kellis, Manolis; Kiran, Anmol M.; Baranov, Pavel V.; Atkins, John F.

Abstract

Stop codon readthrough is used extensively by viruses to expand their gene expression. Until recent discoveries in Drosophila, only a very limited number of readthrough cases in chromosomal genes had been reported. Analysis of conserved protein coding signatures that extend beyond annotated stop codons identified potential stop codon readthrough of four mammalian genes. Here we use a modified targeted bioinformatic approach to identify a further three mammalian readthrough candidates. All seven genes were tested experimentally using reporter constructs transfected into HEK-293T cells. Four displayed efficient stop codon readthrough, and these have UGA immediately followed by CUAG. Comparative genomic analysis revealed that in the four readthrough candidates containing UGA-CUAG, this motif is conserved not only in mammals but throughout vertebrates with the first six of the seven nucleotides being universally conserved. The importance of the CUAG motif was confirmed using a systematic mutagenesis approach. One gene, OPRL1, encoding an opiate receptor, displayed extremely efficient levels of readthrough (similar to 31%) in HEK-293T cells. Signals both 5' and 3' of the OPRL1 stop codon contribute to this high level of readthrough. The sequence UGA-CUA alone can support 1.5% readthrough, underlying its importance.

Nociceptin/orphanin FQ receptor gene variation is associated with smoking status in Japanese

PHARMACOGENOMICS

Authors: Kasai, Shinya; Nishizawa, Daisuke; Hasegawa, Junko; Sato, Naomi; Tanioka, Fumihiko; Sugimura, Haruhiko; Ikeda, Kazutaka

Abstract

Aim: The endogenous opioid system has been reportedly implicated in tobacco/nicotine dependence. Materials & methods: We examined the genetic effects of eight SNPs in opioid receptor-related genes on smoking status and smoking-related traits in Japanese. Results: The genotypic and allelic variations of the rs2229205 SNP in the OPRL1 gene were significantly associated with smoking status, but no significant differences were found in the genetic variations of any of the SNPs with regard to smoking-related traits. The rs2229205 SNP did not show high linkage disequilibrium with the other SNPs in the linkage disequilibrium block that contained the SNP. Conclusion: The rs2229205 SNP in the OPRL1 gene may be a genetic factor that contributes to individual differences in the vulnerability to smoking in Japanese individuals.