mGluR6 ELISA Kit

Name: mGluR6 ELISA Kit
SKU: DEIA-XYA1209
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

Intended Use

The mGluR6 Colorimetric Cell-Based ELISA Kit allows for the qualitative detection of mGluR6 and the effects that certain stimulation conditions have on mGluR6 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-mGluR6 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

GENE-MAPPING OF NMDA RECEPTORS AND METABOTROPIC GLUTAMATE RECEPTORS IN THE RAT (RATTUS-NORVEGICUS)

GENOMICS

Authors: KURAMOTO, T; MAIHARA, T; MASU, M; NAKANISHI, S; SERIKAWA, T

Abstract

Five N-methyl-D-aspartate receptor subunit genes and six metabotropic glutamate receptor subtype genes have been assigned to particular rat chromosomes by using a rat X mouse somatic cell hybrid clone panel. N-Methyl-D-aspartate receptor subunit genes (gene symbol, GRIN) GRIN1, GRIN2A, GRIN2B, GRIN2C, and GRIN2D have been assigned to chromosomes (Chr) 3, 10, 4, 10, and 1, respectively. Metabotropic glutamate receptor subtype genes (gene symbol, GRM) GRM1, GRM2, GRM3, GRM4, GRM5, and GRM6 have been assigned to Chr 1, 8, 4, 20, 1, and 10, respectively. In addition, GRIN2A and GRM6 loci were successfully localized on Chr 10 linkage maps by linkage analyses. The genetic distances between loci in cM (+/-SD) are as follows: GRIN2A-28.6(+/-7.0)-RR24-23.3(+/-6.4)-MYHSE, from a linkage analysis using the (SHR X WTC)F-1 X WTC cross, and RR24-4.2(+/-2.9)-GR1M64.2(+/-2.9)-MYHSE-2.1(+/-2.1)-ASGR, SHBG-27.1 (+/-6.4)-PPY, from a linkage analysis using the (ZI x TM)F-1 X 21 cross. (C) 1994 Academic Press, Inc.

Allelic variance between GRM6 mutants, Grm6(nob3) and Grm6(nob4) results in differences in retinal ganglion cell visual responses

JOURNAL OF PHYSIOLOGY-LONDON

Authors: Maddox, Dennis M.; Vessey, Kirstan A.; Yarbrough, Gary L.; Invergo, Brandon M.; Cantrell, Donald R.; Inayat, Samsoon; Balannik, Victoria; Hicks, Wanda L.; Hawes, Norman L.; Byers, Shannon; Smith, Richard S.; Hurd, Ron; Howell, Douglas; Gregg, Ronald G.; Chang, Bo; Naggert, Juergen K.; Troy, John B.; Pinto, Lawrence H.; Nishina, Patsy M.; McCall, Maureen A.

Abstract

An electroretinogram (ERG) screen identified a mouse with a normal a-wave but lacking a b-wave, and as such it was designated no b-wave3 (nob3). The nob3 phenotype mapped to chromosome 11 in a region containing the metabotropic glutamate receptor 6 gene (Grm6). Sequence analyses of cDNA identified a splicing error in Grm6, introducing an insertion and an early stop codon into the mRNA of affected mice (designated Grm6(nob3)). Immunohistochemistry of the Grm6(nob3) retina showed that GRM6 was absent. The ERG and visual behaviour abnormalities of Grm6(nob3) mice are similar to Grm6(nob4) animals, and similar deficits were seen in compound heterozygotes (Grm6(nob4/nob3)), indicating that Grm6(nob3) is allelic to Grm6(nob4). Visual responses of Grm6(nob3) retinal ganglion cells (RGCs) to light onset were abnormal. Grm6(nob3) ON RGCs were rarely recorded, but when they were, had ill-defined receptive field (RF) centres and delayed onset latencies. When Grm6(nob3) OFF-centre RGC responses were evoked by full-field stimulation, significantly fewer converted that response to OFF/ON compared to Grm6(nob4) RGCs. Grm6(nob4/nob3) RGC responses verified the conclusion that the two mutants are allelic. We propose that Grm6(nob3) is a new model of human autosomal recessive congenital stationary night blindness. However, an allelic difference between Grm6(nob3) and Grm6(nob4) creates a disparity in inner retinal processing. Because the localization of GRM6 is limited to bipolar cells in the On pathway, the observed difference between RGCs in these mutants is likely to arise from differences in their inputs.