NMDAR2B ELISA Kit

Name: NMDAR2B ELISA Kit
SKU: DEIA-XYA1333
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

cultured cells

Species Reactivity

Human; Mouse; Rat

Intended Use

The NMDAR2B Colorimetric Cell-Based ELISA Kit allows for the qualitative detection of NMDAR2B and the effects that certain stimulation conditions have on NMDAR2B expression in different cell lines.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 1 Plate.
2. 10x TBS: 24 mL (10x), Clear.
3. Quenching Buffer, 24 mL (1x), Clear.
4. Blocking Buffer, 50 mL (1x), Clear.
5. 10x Wash Buffer, 50 mL (10x), Clear.
6. 100x Anti-NMDAR2B Antibody (Rabbit Polyclonal), 60 μL (100x), Purple.
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal), 60 μL (100x), Green.
8. HRP-Conjugated Anti-Rabbit IgG Antibody, 6 mL (1x), Glass.
9. HRP-Conjugated Anti-Mouse IgG Antibody, 6 mL (1x), Glass.
10. Primary Antibody Diluent, 12 mL (1x), Clear.
11. Ready-to-Use Substrate, 12 mL (1x), Brown.
12. Stop Solution, 12 mL (1x), Clear.
13. Crystal Violet Solution, 6 mL (1x), Glass.
14. SDS Solution, 24 mL (1x), Clear.
15. Adhesive Plate Seals, 4 Seals.

Storage

4°C/6 Months

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Discovery of gene-gene interactions across multiple independent data sets of late onset Alzheimer disease from the Alzheimer Disease Genetics Consortium

NEUROBIOLOGY OF AGING

Authors: Hohman, Timothy J.; Bush, William S.; Jiang, Lan; Brown-Gentry, Kristin D.; Torstenson, Eric S.; Dudek, Scott M.; Mukherjee, Shubhabrata; Naj, Adam; Kunkle, Brian W.; Ritchie, Marylyn D.; Martin, Eden R.; Schellenberg, Gerard D.; Mayeux, Richard; Farrer, Lindsay A.; Pericak-Vance, Margaret A.; Haines, Jonathan L.; Thornton-Wells, Tricia A.

Abstract

Late-onset Alzheimer disease (AD) has a complex genetic etiology, involving locus heterogeneity, polygenic inheritance, and gene-gene interactions; however, the investigation of interactions in recent genome-wide association studies has been limited. We used a biological knowledge-driven approach to evaluate genegene interactions for consistency across 13 data sets from the Alzheimer Disease Genetics Consortium. Fifteen single nucleotide polymorphism (SNP)-SNP pairs within 3 gene-gene combinations were identified: SIRT1 x ABCB1, PSAP x PEBP4, and GRIN2B x ADRA1A. In addition, we extend a previously identified interaction from an endophenotype analysis between RYR3 x CACNA1C. Finally, post hoc gene expression analyses of the implicated SNPs further implicate SIRT1 and ABCB1, and implicate CDH23 which was most recently identified as an AD risk locus in an epigenetic analysis of AD. The observed interactions in this article highlight ways in which genotypic variation related to disease may depend on the genetic context in which it occurs. Further, our results highlight the utility of evaluating genetic interactions to explain additional variance in AD risk and identify novel molecular mechanisms of AD pathogenesis. (C) 2016 Elsevier Inc. All rights reserved.

Calcium/calmodulin-dependent serine protein kinase (CASK), a protein implicated in mental retardation and autism-spectrum disorders, interacts with T-Brain-1 (TBR1) to control extinction of associative memory in male mice

JOURNAL OF PSYCHIATRY & NEUROSCIENCE

Authors: Huang, Tzyy-Nan; Hsueh, Yi-Ping

Abstract

Background: Human genetic studies have indicated that mutations in calcium/calmodulin-dependent serine protein kinase (CASK) result in X-linked mental retardation and autism-spectrum disorders. We aimed to establish a mouse model to study how Cask regulates mental ability. Methods: Because Cask encodes a multidomain scaffold protein, a possible strategy to dissect how CASK regulates mental ability and cognition is to disrupt specific protein-protein interactions of CASK in vivo and then investigate the impact of individual specific protein interactions. Previous in vitro analyses indicated that a rat CASK T724A mutation reduces the interaction between CASK and T-brain-1 (TBR1) in transfected COS cells. Because TBR1 is critical for glutamate receptor, ionotropic, N-methyl-D-aspartate receptor subunit 2B (Grin2b) expression and is a causative gene for autism and intellectual disability, we then generated CASK T740A (corresponding to rat CASK T724A) mutant mice using a gene-targeting approach. Immunoblotting, coimmunoprecipitation, histological methods and behavioural assays (including home cage, open field, auditory and contextual fear conditioning and conditioned taste aversion) were applied to investigate expression of CASK and its related proteins, the protein-protein interactions of CASK, and anatomic and behavioural features of CASK T740A mice. Results: The CASK T740A mutation attenuated the interaction between CASK and TBR1 in the brain. However, CASK T740A mice were generally healthy, without obvious defects in brain morphology. The most dramatic defect among the mutant mice was in extinction of associative memory, though acquisition was normal. Limitations: The functions of other CASK protein interactions cannot be addressed using CASK T740A mice. Conclusion: Disruption of the CASK and TBR1 interaction impairs extinction, suggesting the involvement of CASK in cognitive flexibility.