The Synaptic vesicular amine transporter, also known as the solute carrier family 18 member 2 (SLC18A2), is a protein encoded by the SLC18A2 gene in humans. SLC18A2 is a complete transmembrane protein that transports monoamines, especially neurotransmitters such as dopamine, norepinephrine, serotonin, and histamine, from the cellular cytoplasm to synaptic vesicles. In the striatum pathway and the mid-edge pathway dopamine-releasing neurons, SLC18A2 function is also required for vesicle release from the neurotransmitter GABA. SLC18A2 is thought to possess at least two different binding sites characterized by the binding of tetrabenazine (TBZ) and reserpine to the transporter.
Basic Information of SLC18A2 | |
Protein Name | Synaptic vesicular amine transporter |
Gene Name | SLC18A2 |
Aliases | Monoamine transporter, Solute carrier family 18 member 2, Vesicular amine transporter 2 (VAT2) |
Organism | Homo sapiens (Human) |
UniProt ID | Q05940 |
Transmembrane Times | 12 |
Length (aa) | 514 |
Sequence | MALSELALVRWLQESRRSRKLILFIVFLALLLDNMLLTVVVPIIPSYLYSIKHEKNATEIQTARPVHTASISDSFQSIFSYYDNSTMVTGNATRDLTLHQTATQHMVTNASAVPSDCPSEDKDLLNENVQVGLLFASKATVQLITNPFIGLLTNRIGYPIPIFAGFCIMFVSTIMFAFSSSYAFLLIARSLQGIGSSCSSVAGMGMLASVYTDDEERGNVMGIALGGLAMGVLVGPPFGSVLYEFVGKTAPFLVLAALVLLDGAIQLFVLQPSRVQPESQKGTPLTTLLKDPYILIAAGSICFANMGIAMLEPALPIWMMETMCSRKWQLGVAFLPASISYLIGTNIFGILAHKMGRWLCALLGMIIVGVSILCIPFAKNIYGLIAPNFGVGFAIGMVDSSMMPIMGYLVDLRHVSVYGSVYAIADVAFCMGYAIGPSAGGAIAKAIGFPWLMTIIGIIDILFAPLCFFLRSPPAKEEKMAILMDHNCPIKTKMYTQNNIQSYPIGEDEESESD |
SLC18A2 is involved in the transfer of monoamines to synaptic vesicles and is associated with many neuropsychiatric disorders including major depression. SLC18A2 is a necessary condition for releasing neurotransmitters from axonal terminals of monoamine neurons to the synaptic cleft. If SLC18A2 function is inhibited or destroyed, monoamine neurotransmitters, such as dopamine, cannot be released into the synapse by a typical release mechanism. Cocaine users were significantly reduced in SLC18A2 immune activity. Patients with mood disorders caused by cocaine show significant loss of SLC18A2 immunoactivity; this may reflect damage to dopamine axon terminals in the striatum. These neuronal changes may cause confusing emotional and motivational processes among more addictive users.
Fig.1 The structure of Synaptic vesicular amine transporter.
The results highlight SLC18A2 as a new promising methylation marker for PC diagnosis. In addition, SLC18A2 expression (RNA and protein) showed promising prognostic potential beyond conventional clinicopathological variables. Therefore, the new slc18a2 based molecular test can be applied to personal computers for the detection and identification of high-risk patients in the future.
These data is consistent with the genetic structure of PTSD, which is highly polygenic and is affected by many weakly affected SNPs and may overlap with mood disorders.
These results indicate that SLC18A2 enhances toxicity to METH without increasing the efficacy of the drug.
These findings suggest that the diversity of transcriptional rules is the driving force for haplotype selection in SLC18A2.
Genetic findings from these drugs suggest that hVMAT2 may be a risk factor and target it as a genetic drug for PD.
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