TPH2 ELISA Kit

Name: TPH2 ELISA Kit
SKU: DEIA-XYA1781
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 TPH2 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor TPH2 protein expression profile in cells. The kit can be used for measuring the relative amounts of TPH2 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on TPH2.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 1 Plates
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-TPH2 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

Increased ethanol consumption despite taste aversion in mice with a human tryptophan hydroxylase 2 loss of function mutation

NEUROSCIENCE LETTERS

Authors: Lemay, Francis; Dore, Francois Y.; Beaulieu, Jean-Martin

Abstract

Polymorphisms in the gene encoding the brain serotonin synthesis enzyme Tph2 have been identified in mental illnesses, with co-morbidity of substance use disorder. However, little is known about the impact of Tph2 gene variants on addiction. Mice expressing a human Tph2 loss of function variant were used to investigate consequences of aversive conditions on ethanol intake. Mice were familiarized either with ethanol or a solution containing both ethanol and the bittering agent quinine. Effect of familiarization to ethanol or an ethanol-quinine solution was then evaluated using a two-bottles preference test in Tph2-KI and control littermates. Mice from both genotypes displayed similar levels of ethanol consumption and quinine avoidance when habituated to ethanol alone. In contrast, addition of quinine to ethanol during the familiarization period resulted in a reduction of avoidance for the quinine-ethanol solution only in mutant mice. These results indicate that loss of function mutation in Tph2 results in greater motivation for ethanol consumption under aversive conditions and may confer enhanced sensitivity to alcohol use disorder. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

Common genetic background in anorexia nervosa and obsessive compulsive disorder: Preliminary results from an association study

JOURNAL OF PSYCHIATRIC RESEARCH

Authors: Mas, Sergi; Teresa Plana, Maria; Castro-Fornieles, Josefina; Gasso, Patricia; Lafuente, Amalia; Moreno, Elena; Martinez, Esteban; Mila, Montserrat; Lazaro, Luisa

Abstract

Several lines of evidence, including psychopathological, neurobiological, pharmacological and epidemiological data, supported the association between Anorexia Nervosa (AN) and Obsessive-Compulsive Disorder (OCD). The aim of the present study is to test the hypothesis of partial common genetic background of both disease, AN and OCD. A total of 116 patients with AN, 74 patients with OCD and 91 controls participated in this study. 213 single-nucleotide polymorphisms (SNPs) in 28 candidate genes were analyzed. Five SNPs achieved 0.004 (the nominal p-value expected by chance), 3 with empirical significant p-values (rs10070190 (CDH9) p = 1 x 10(-3), rs4825476 (GRIA3)p = 4 x 10(-4), and rs1074815 (TPH2) p = 8 x 10(-4)) and 2 additional polymorphisms showing nominal significance (rs2834070 (OLIG2) p = 2 x 10(-3) and rs11783752 (SCL18A1) p = 3 x 10-3), were found to be related to both AN and OCD. In addition, rs3825885 (NTRK3, p = 9 x 10-4) was identified as an AN risk variant, and rs11179027 (TPH2, p = 2 x 10-3) as an OCD marker. The ROC analysis confirmed these results and showed interaction among the significant SNPs. The preliminary results we report here reveal a partial common genetic background in AN and OCD, in agreement with previous clinical findings of common symptomathology between these two diseases and open the field of possible treatments for AN. The interaction observed between the associated polymorphisms, could indicate that there is a biological interaction between the serotonin (TPH2 and SLC18A1) and glutamate (GRIA3) pathways and the factors related to neurogenesis (CDH9, OLIG2 and NTRK3) for the explanation of etiopathophysiology in both diseases. However, the results must be replicated in studies with larger cohorts in order to confirm these associations. (C) 2013 Elsevier Ltd. All rights reserved.