|Calculated MW||69255 Da|
|Homology||Rat - identical; human - 14/16 amino acid residues identical.|
|Other Names||Sodium-dependent noradrenaline transporter, Norepinephrine transporter, NET, Solute carrier family 6 member 2, Slc6a2|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptideֲ (C)KLLNASVLGDHTKYSK, corresponding to amino acid residues 189-204 of mouse Noradrenaline Transporter (Accession O55192). 2nd extracellular loop.|
|Peptide Confirmation||Confirmed by 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 µl water.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||1 µg peptide per 1 µg antibody.|
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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 and noradrenaline respectively, and recycling them back for release3-5. While the activity of each transporter is faithful to its neurotransmitter, NET has been shown to clear dopamine in DAT deprived or low DAT regions such as the brain cortex6-8. 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. NET also has a significant extracellular loop between transmembrane regions three and four, which contains various glycosylation sites9. Like its counterparts, NET’s intracellular N- and C-terminal domains are also subject to phosphorylation and protein-protein interactions important for modulating its activity and localization. In addition alternative splicing has also been shown to regulate NET’s expression and function10. NET is specifically expressed on noradrenaline nerve terminals, and is also expressed in the periphery, such as adrenal glands and placenta. NET malfunction is largely associated with attention and mood, as well as various cardiovascular disorders. NET is also a target for psychostimulants such as cocaine and amphetamines which disrupt its function, thereby causing an increase of noradrenaline in synaptic clefts3,9. Abgent is pleased to offer a highly specific antibody directed against an extracellular epitope of mouse noradrenaline transporter. Anti-Noradrenaline Transporter (NET) (extracellular) antibody (#AG1206) can be used for western blot immunohistochemistry and immunocytochemistry applications. It has been designed to recognize NET 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. Moron, J.A. et al. (2002) J. Neurosci. 22, 389. 7. Madras, B.K. et al. (2005) Biol. Psychiatry 57, 1397. 8. Siuta, M.A. et al. (2010) PLoS Biol. 8, e1000393. 9. Ramamoorthy, S. et al. (2010) Pharmacol. Ther. Doi. 10.1016. 10. Kitayama, S. et al. (2001) Neurosci. Lett. 312, 108.
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