Human NRGN (Neurogranin) ELISA Kit

Name: Human NRGN (Neurogranin) ELISA Kit
SKU: DEIA-FN1031
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 supernatant, cell lysate or tissue lysate,cerebrospinal fluid (CSF), other biological fluid samples.

Species Reactivity

Human

Detection Method

sELISA

Intended Use

In vitro quantitative determination of NRGN concentrations in Serum, plasma, cell culture supernatant, cell lysate or tissue lysate,cerebrospinal fluid (CSF), other biological fluid samples.

Contents of Kit

1. ELISA Microplate(Dismountable), 8×12, Put the rest strips into a sealed foil bag with the desiccant. Stored for 1 month at 2-8°C. Stored for 12 month at -20°C
2. Lyophilized Standard, 2vial, Put the rest standards into a desiccant bag. Stored for 1 month at 2-8°C. Stored for 12 month at -20°C.
3. Cap/Det Ab (Concentrated), 120ul, 2-8°C (Avoid Direct Light)
4. Antibody storage solution, 6ml, 2-8°C (Avoid Direct Light)
5. HRP-Streptavidin (Ready to use, orange), 10ml, 2-8°C (Avoid Direct Light)
6. TMB Substrate, 10ml, 2-8°C (Avoid Direct Light)
7. Sample Dilution Buffer (blue), 20ml, 2-8°C
8. Stop Solution, 5ml, 2-8°C
9. Wash Buffer(25×), 30ml, 2-8°C
10. Plate Sealer, 5 pieces
11. Product Description, 1 copy
Note: The liquid reagent bottle contains slightly more reagent than indicated on the label. Use a micropipette to measure accurately.

Storage

2-8°C (for sealed box), please do not freeze! See kit label for expiry date

Performance Characteristics

Perform the stability test for the sealed kit at 37°C and 2-8°C and get relevant data.

Precision

Intra-assay Precision: samples with low, medium and high concentration are tested 20 times on same plate.
Inter-assay Precision: samples with low, medium and high concentration are tested 20 times on three different plates.

Detection Range

7.813-500pg/ml

Sensitivity

4.688pg/ml

General Description

Neurogranin is a small neuronal protein that binds to calmodulin in the absence of Ca²⁺. Neurogranin is primarily expressed in the brain and is enriched in somato-dendritic compartments of projection neurons in various regions of the brain . Postsynaptically-enriched neurogranin likely influences Ca²⁺ or Ca²⁺/calmodulin-dependent neuronal functions, including synaptic plasticity, by binding to and releasing calmodulin in a Ca²⁺-dependent manner . Genetic variants in the gene encoding neurogranin, NRGN, are linked to several neuropsychiatric diseases, including schizophrenia .

Standard Curve

1. Calculate the mean OD450 value (using the original OD450 value or the corrected OD450 value) of the duplicate readings for each standard, control, and sample. Then, obtain the value of calculation by subtracting the OD450 blank.
2. Create a four parameter logistic curve by plotting the mean absorbance for each standard on the y-axis against the concentration on the x-axis. (Remove the OD450 blank during plotting.) Alternatively, you can use the curve fitting software offered by the microplate reader.
3. Calculate the sample concentration by substituting OD450 value into the standard curve. Note: If the sample is added undiluted, the sample dilution caused by incubation of both the sample and antibody should be considered. In this case, the final concentration should be multiplied by 2 from the calculated value. If the sample is 1/100 diluted before adding the plate wells, the final concentration should be multiplied by 200 from the calculated value. And so on.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Comprehensive promoter level expression quantitative trait loci analysis of the human frontal lobe

GENOME MEDICINE

Authors: Blauwendraat, Cornelis; Francescatto, Margherita; Gibbs, J. Raphael; Jansen, Iris E.; Simon-Sanchez, Javier; Hernandez, Dena G.; Dillman, Allissa A.; Singleton, Andrew B.; Cookson, Mark R.; Rizzu, Patrizia; Heutink, Peter

Abstract

Background: Expression quantitative trait loci (eQTL) analysis is a powerful method to detect correlations between gene expression and genomic variants and is widely used to interpret the biological mechanism underlying identified genome wide association studies (GWAS) risk loci. Numerous eQTL studies have been performed on different cell types and tissues of which the majority has been based on microarray technology. Methods: We present here an eQTL analysis based on cap analysis gene expression sequencing (CAGEseq) data created from human postmortem frontal lobe tissue combined with genotypes obtained through genotyping arrays, exome sequencing, and CAGEseq. Using CAGEseq as an expression profiling technique combined with these different genotyping techniques allows measurement of the molecular effect of variants on individual transcription start sites and increases the resolution of eQTL analysis by also including the non-annotated parts of the genome. Results: We identified 2410 eQTLs and show that non-coding transcripts are more likely to contain an eQTL than coding transcripts, in particular antisense transcripts. We provide evidence for how previously identified GWAS loci for schizophrenia (NRGN), Parkinson's disease, and Alzheimer's disease (PARK16 and MAPT loci) could increase the risk for disease at a molecular level. Furthermore, we demonstrate that CAGEseq improves eQTL analysis because variants obtained from CAGEseq are highly enriched for having a functional effect and thus are an efficient method towards the identification of causal variants. Conclusion: Our data contain both coding and non-coding transcripts and has the added value that we have identified eQTLs for variants directly adjacent to TSS. Future eQTL studies would benefit from combining CAGEseq with RNA sequencing for a more complete interpretation of the transcriptome and increased understanding of eQTL signals.

Postsynaptic damage and microglial activation in AD patients could be linked CXCR4/CXCL12 expression levels

BRAIN RESEARCH

Authors: Sanfilippo, Cristina; Castrogiovanni, Paola; Imbesi, Rosa; Nunnari, Giuseppe; Di Rosa, Michelino

Abstract

Alzheimer's disease (AD) is one of the most common forms of dementia with still unknown pathogenesis. Several cytokines and chemokines are involved in the pathogenesis of AD. Among the chemokines, the CXCR4/CXCL12 complex has been shown to play an important role in the pathogenetic development of AD. We investigated the expression levels of CXCR4 / CXCL12 in fifteen brain regions of healthy non-demented subjects (NDHC) (2139 sample) and AD patients (1170 sample) stratified according to sex and age. Furthermore, we correlated their expressions with the Neurogranin (NRGN) and CHI3L1 levels, two inflamm-aging markers. We highlighted that CXCR4 gene expression levels were age-correlated in the brain of NDHC subjects and that AD nullified this correlation. A similar trend, but diametrically opposite was observed for CXCL12. Its expression was decreased during the aging in both sexes, and in the brains of AD patients, it underwent an inversion of the trend, only and exclusively in females. Brains of AD patients expressed high CXCR4 and CHI3L1, and low CXCL12 and Neurogranin levels compared to NDHC subjects. Both CXCR4 and CXCL12 correlated significantly with CHI3L1 and Neurogranin expression levels, regardless of disease. Furthermore, we showed a selective modulation of CXCL12 and CXCR4 only in specific brain regions. Taken together our results demonstrate that CXCL12 and CXCR4 are linked to Neurogranin and CHI3L1 expression levels and the relationship between postsynaptic damage and microglial activation in AD could be shown using all these genes. Further confirmations are needed to demonstrate the close link between these genes.