|Reactivity||Human, Mouse, Rat|
|Calculated MW||70172 Da|
|Homology||Mouse, human - identical.|
|Other Names||Sodium-dependent serotonin transporter, 5HT transporter, 5HTT, Solute carrier family 6 member 4, Slc6a4|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide ֲ (C)EMRNEDVSEVAKD, corresponding to amino acids residues 388-400 of rat Serotonin Transporter (Accession P31652).ֲ ֲ 4th extracellular loop.|
|Peptide Confirmation||Confirmed by mass-spectrography and amino acid analysis.|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.8 mg/ml.|
|Buffer After Reconstitution||Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.025% NaN3.|
|Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Storage After Reconstitution||The reconstituted solution can be stored at 4ºC for up to 2 weeks. For longer periods, small aliquots should be stored at -20ºC or below. Avoid multiple freezing and thawing. The further dilutions should be made using a carrier protein such as BSA (1%). Centrifuge all antibody preparations before use (10000 × g 5 min).|
|Control Antigen Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Control Antigen Reconstitution||100 ml water.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||1 µg peptide per 1 µg antibody.|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Many physiological, endocrine and behavioral functions are determined and regulated by monoamine signaling1,2. Many brain disorders such as depression, drug abuse, schizophrenia, attention deficit hyperactivity disorder (ADHD) are caused by the malfunction of monoaminergic transmission1-3. The intensity of monoaminergic signaling is determined by the availability of the monoamine, which is in turn determined in part by its uptake from the extracellular milieu via monoamine transporters. These transporters include DAT, SERT, and NET, responsible for uptaking dopamine, serotonin (5-HT) and noradrenaline respectively, and recycling them back for release3-5. DAT, SERT and NET are members of the Na+/Cl- dependent membrane transporter family which also includes other members. These transporters consist of 12 transmembrane domains and intracellular N- and C-termini. Like its counterparts, SERT’s intracellular N- and C-terminal domains are also subject to phosphorylation and protein-protein interactions important for modulating its activity and localization6. SERTs are evidently expressed in serotonergic neurons, and are also expressed in various peripheral tissues including specialized cells of the gut, placenta, lung, blood lymphocytes and platelets6. SERT knockout mice are viable and as a consequence exhibit increased extracellular levels of 5-HT and significantly decreased levels of brain tissue 5-HT due to deficient recycling and re-accumulation of serotonin by SERT7,8. Phenotypes displayed by SERT knockout mice include stress sensitivity, obesity and various behavioral changes9 Abgent is pleased to offer a highly specific antibody directed against an extracellular epitope of rat serotonin transporter. Anti-Serotonin Transporter (SERT) (extracellular) antibody (#AG1204) can be used in western blot analysis, immunohistochemistry, immunocytochemistry and indirect flow cytometry applications and has been designed to recognize SERT from human, mouse and rat samples.
References 1. Carlsson, A. (1987) Annu. Rev. Neurosci. 10, 19. 2. Greengard, P. (2001) Science 294, 1024. 3. Gainetdinov, R.R. and Caron, M.G. (2003) Annu. Rev. Pharmacol. Toxicol. 43, 261. 4. Amara, S.G. and Kuhar, M.J. (1993) Trends Pharmacol. Sci. 14, 43. 5. Miller, G.W. et al. (1999) Trends Pharmacol. Sci. 20, 424. 6. Ramamoorthy, S. et al. (2010) Pharmacol. Ther. Doi. 10.1016. 7. Mathews, T.A. et al. (2004) J. Neurosci. Meth. 140, 169. 8. Kim, D.K. et al. (2005) Neuropharmacology 49, 798. 9. Haenisch, B. and Bönisch, H. (2011) Pharmacol. Ther. 129, 352.
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