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Intracellular protein trafficking is tightly regulated, and improper trafficking might be the fundamental provocateur for human diseases including neurodegeneration. In neurons, protein trafficking to and from the plasma membrane affects synaptic plasticity. Voltage-gated potassium channel 2.1 (Kv2.1) is a predominant delayed rectifier potassium (K+ ) current, and electrical activity patterns of dopamine (DA) neurons within the substantia nigra are generated and modulated by the orchestrated function of different ion channels. The pathological hallmark of Parkinson's disease (PD) is the progressive loss of these DA neurons, resulting in the degeneration of striatal dopaminergic terminals. However, whether trafficking of Kv2.1 channels contributes to PD remains unclear. In this study, we demonstrated that MPTP/MPP+ increases the surface expression of the Kv2.1 channel and causes nigrostriatal degeneration by using a subchronic MPTP mouse model. The inhibition of the Kv2.1 channel by using a specific blocker, guangxitoxin-1E, protected nigrostriatal projections against MPTP/MPP+ insult and thus facilitated the recovery of motor coordination. These findings highlight the importance of trafficking of Kv2.1 channels in the pathogenesis of PD.
Pubmed ID: 29265365 RIS Download
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This unknown targets
View all literature mentionsThis monoclonal targets IgG
View all literature mentionsThis polyclonal targets Rabbit IgG Alexa Fluor
View all literature mentionsThis monoclonal targets β-Actin
View all literature mentionsThis polyclonal targets Caspase 3 active (cleaved) form
View all literature mentionsThis polyclonal targets Potassium Channel, Inward Rectifier GIRK1
View all literature mentionsThis monoclonal targets Kv2.1 K+ channel
View all literature mentionsCell line MN9D is a Hybrid cell line with a species of origin Mus musculus
View all literature mentionsMus musculus with name C57BL/6NJ from IMSR.
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