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. Author manuscript; available in PMC: 2019 Aug 22.
Published in final edited form as: J Chem Neuroanat. 2016 Nov 9;83-84:10–18. doi: 10.1016/j.jchemneu.2016.10.004

Table 1.

Regulatory inputs and functional responses of demonstrated DAT phosphorylation sites.

In vivo site Increased phosphorylation Outcome Decreased phosphorylation Outcome
PKC domain PKC activators ↓DA uptake Vmax(g,h,l,n) PKC inhibitors ↑DA uptake Vmax(b,l,m)
AMPH, METH ↑DA efflux Vmax(e,i,j) Δ21/22 truncation ↓PKC-induced down-regulation(f,n)
PP1 inhibitors ↑PKC-induced down-regulation(f) Palmitoylation enhancers ↓AMPH-induced efflux(h,i,m)
Palmitoylation inhibitors ↑CFT affinity(k) Botulinum neurotoxin C ↓AMPH-induced down-regulation(a)
Ser7 PKC activators ↓DA uptake Vmax(l) S7A mutation ↑DA uptake Vmax(l)
C580A mutation ↓Cys580 palmitoylation(l) ↓AMPH-induced efflux(j,n,o,p)
Palmitoylation inhibitors ↑CFT affinity(l) ↓PKC-induced down-regulation(f)
↑Cys580 palmitoylation(l)
↓CFT affinity(l)
Thr53 PIN1 inhibitors ↑DA efflux(d) T53A mutation ↓DA uptake Vmax(c,f)
PKC activators ↓AMPH-induced MPP+ efflux(f)
AMPH, METH ↑AMPH-induced DA efflux(c)
PP1/2A inhibitors ↓CFT affinity(c)

Superscripts denote references for studies that link the indicated outcomes to one or more of the conditions that increase or decrease phosphorylation of specified sites:

g

Granas et al., 1995