Dopamine Transporter Antibody [A13P6]

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:1000 IP1:30 IHC1:500

Application
WB, IP, IHC

Reactivity
Mouse, Rat, Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
68 kDa 70-85 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Positive Control	Mouse striatum tissue; Rat striatum tissue; Normal human striatum tissue; Normal human substantia nigra tissue
Negative Control	Mouse kidney tissue; Rat liver tissue; Normal human liver tissue; Mouse liver tissue; Rat spleen tissue; Neuro-2a cells; C6 cells

Datasheet & SDS

Biological Description

Specificity
Dopamine Transporter Antibody [A13P6] detects endogenous levels of total Dopamine Transporter protein.

Clone
A13P6

Synonym(s)
DAT1; SLC6A3; Sodium-dependent dopamine transporter; DA transporter; DAT; Solute carrier family 6 member 3

Background
The dopamine transporter (DAT), encoded by SLC6A3, is a member of the neurotransmitter sodium symporter (NSS) family within the solute carrier 6 (SLC6) group, alongside serotonin and norepinephrine transporters. DAT is comprised of 12 transmembrane helices (TM1–TM12) forming a bowl-shaped structure with extracellular and intracellular gates. The central substrate-binding pocket is created by non-helical regions of TM1, TM3, TM6, and TM8, with key residues such as Asp79, Tyr156, Phe320, and Asp476 stabilizing dopamine through hydrogen bonds and salt bridges. DAT binds two sodium ions (Na1, Na2) and one chloride ion, coupling dopamine uptake with Na+/Cl− symport in a 2Na+:1Cl−:1DA stoichiometry. Cholesterol molecules occupy grooves between TM2–TM7 and TM5–TM7, stabilizing the outward-open conformation during the transport cycle. Dopamine enters the S1 binding site after extracellular sodium binds, leading to closure of the outer gate via salt bridges (A85-D476, Y156-F320) and triggering an inward tilt of TM1 and TM6 for dopamine release into the cytosol. An allosteric S2 site enhances S1 release by facilitating water permeation and hinge bending in TM1/TM6. DAT rapidly clears synaptic dopamine, terminating signaling in dopaminergic pathways of the striatum, nucleus accumbens, and prefrontal cortex, regions critical for reward, motor control, cognition, and motivation. DAT interacts with syntaxin-1A and α-synuclein to regulate trafficking, endocytosis, and surface expression, maintaining dopamine homeostasis. Dysregulated DAT activity is implicated in Parkinson’s disease (dopamine depletion in the substantia nigra), ADHD (impaired prefrontal signaling), and addiction, where cocaine blocks DAT to elevate synaptic dopamine.

Background

The dopamine transporter (DAT), encoded by SLC6A3, is a member of the neurotransmitter sodium symporter (NSS) family within the solute carrier 6 (SLC6) group, alongside serotonin and norepinephrine transporters. DAT is comprised of 12 transmembrane helices (TM1–TM12) forming a bowl-shaped structure with extracellular and intracellular gates. The central substrate-binding pocket is created by non-helical regions of TM1, TM3, TM6, and TM8, with key residues such as Asp79, Tyr156, Phe320, and Asp476 stabilizing dopamine through hydrogen bonds and salt bridges. DAT binds two sodium ions (Na1, Na2) and one chloride ion, coupling dopamine uptake with Na+/Cl− symport in a 2Na+:1Cl−:1DA stoichiometry. Cholesterol molecules occupy grooves between TM2–TM7 and TM5–TM7, stabilizing the outward-open conformation during the transport cycle. Dopamine enters the S1 binding site after extracellular sodium binds, leading to closure of the outer gate via salt bridges (A85-D476, Y156-F320) and triggering an inward tilt of TM1 and TM6 for dopamine release into the cytosol. An allosteric S2 site enhances S1 release by facilitating water permeation and hinge bending in TM1/TM6. DAT rapidly clears synaptic dopamine, terminating signaling in dopaminergic pathways of the striatum, nucleus accumbens, and prefrontal cortex, regions critical for reward, motor control, cognition, and motivation. DAT interacts with syntaxin-1A and α-synuclein to regulate trafficking, endocytosis, and surface expression, maintaining dopamine homeostasis. Dysregulated DAT activity is implicated in Parkinson’s disease (dopamine depletion in the substantia nigra), ADHD (impaired prefrontal signaling), and addiction, where cocaine blocks DAT to elevate synaptic dopamine.

References
https://pubmed.ncbi.nlm.nih.gov/36935752/ https://pubmed.ncbi.nlm.nih.gov/39112705/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%