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MABN669

Sigma-Aldrich

Anti-Dopamine Transporter Antibody, clone mAb16

clone mAB16, from mouse

Synonym(s):

Sodium-dependent dopamine transporter, DA transporter, DAT, Solute carrier family 6 member 3

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

mAB16, monoclonal

species reactivity

mouse, rat

technique(s)

western blot: suitable

isotype

IgG1

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

General description

The transmembrane dopamine transporter (DAT) is located on the presynaptic nerve terminal and is responsible for terminating dopaminergic transmission by transporting dopamine from the synaptic cleft into the dopaminergic neuron (reuptake). Dopaminergic pathways have been strongly implicated in reward and addiction, motivation, alcoholism, ADHD and degenerative motor diseases such as Parkinson′s, Huntington′s and Chorea. EMD Millipore’s Anti-Dopamine Transporter antibody has been validated in western blotting for mouse and rat specimens.

Specificity

This antibody recognizes the cytoplasmic domain of Dopamine Transporter.

Immunogen

Epitope: Cytoplasmic domain
Linear peptide corresponding to the cytoplasmic domain of rat Dopamine Transporter.

Application

Anti-Dopamine Transporter Antibody, clone mAb16 is a highly specific mouse monoclonal antibody & that targets Dopamine Transporter & has been tested in western blotting.
Research Category
Neuroscience
Research Sub Category
Developmental Signaling
Western Blotting Analysis: A representative lot from an independent laboratory detected Dopamine Transporter in rat striatal membrane tissue lysate.

Quality

Evaluated by Western Blotting in mouse brain tissue lysate.

Western Blotting Analysis: 1.0 µg/mL of this antibody detected Dopamine Transporter in 10 µg of mouse brain tissue lysate.

Target description

~ 68 kDa observed

Physical form

Format: Purified
Protein G Purified
Purified mouse monoclonal IgG1 in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Analysis Note

Control
Mouse brain tissue lysate

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Jon D Gaffaney et al.
Neurochemistry international, 73, 16-26 (2013-11-26)
Ligand-induced changes in the conformation of extracellular loop (EL) 2 in the rat (r) dopamine transporter (DAT) were examined using limited proteolysis with endoproteinase Asp-N and detection of cleavage products by epitope-specific immunoblotting. The principle N-terminal fragment produced by Asp-N
Durairaj Ragu Varman et al.
Behavioural brain research, 408, 113267-113267 (2021-04-02)
Dopamine (DA) transporter (DAT) is dynamically regulated by several protein kinases and the Thr53 phosphorylation of DAT (pT53-DAT) is documented in heterologous cell models and in rat brain. However, the role of endogenous pT53-DAT in living animals has never been
Katrina L Paumier et al.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 40(4), 874-883 (2014-10-01)
In addition to alleviating depression, long-term adaptive changes induced by antidepressants may regulate neural plasticity in the diseased brain, providing symptomatic and disease-modifying effects in Parkinson's disease. The present study investigated whether chronic treatment with a frequently prescribed tricyclic antidepressant

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