Synthetic peptide from the intracellular C-terminal region of human dopamine transporter (CEKDRELVDRGEVRQFTLRHWL).
Application
Anti-Dopamine Transporter Antibody, C-terminus detects level of Dopamine Transporter & has been published & validated for use in IH & WB.
Immunoblotting: 0.1-1.0 μg/mL. The antibody recognizes the ~88 kDa DAT protein in Western blot of human strial samples. Immunohistochemistry using formaldehyde-fixed brain sections. Not recommended for use on rodent. Optimal working dilutions must be determined by the end user.
Physical form
Affinity purified immunoglobulin. Liquid in 100 μL of 10 mM HEPES (pH 7.5), 150 mM NaCl, 100 μg/mL BSA, and 50% glycerol.
Storage and Stability
Maintain at -20 to -80°C in undiluted aliquots for up to six months after date of receipt. Avoid repeated freeze-thaw cycles.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Journal of Parkinson's disease, 1(1), 83-92 (2011-01-01)
We demonstrate that grafted human fetal mesencephalic neurons can survive and extend axons for 22 years in the brain of a patient with Parkinson's disease (PD). In this patient, the overall survival and fiber outgrowth of the grafts were, however
The transporters for dopamine (DAT) and norepinephrine (NET) are members of the Na+- and Cl--dependent neurotransmitter transporter family SLC6. There is a line of evidence that alternative splicing results in several isoforms of neurotransmitter transporters including NET. However, its relevance
Cocaine exerts its stimulant effect by inhibiting dopamine reuptake leading to increased dopamine signaling. This action is thought to reflect binding of cocaine to the dopamine transporter (DAT) to inhibit its function. However, cocaine is a relatively weak inhibitor of
Most inherited neurodegenerative disorders are incurable, and often only palliative treatment is available. Precision medicine has great potential to address this unmet clinical need. We explored this paradigm in dopamine transporter deficiency syndrome (DTDS), caused by biallelic loss-of-function mutations in
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