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1  rearrangements occurring during forward and reverse transport.
2  uptake to a stimulatory one, and eliminated reverse transport.
3 ceptor activation by DA that is released via reverse transport.
4  promoting nonexocytotic dopamine efflux via reverse transport.
5 m that is independent of DAT trafficking and reverse-transport.
6  dietary oxidative lipid load, including the reverse transport activity of HDL.
7 essing GAT1 greatly reduced both forward and reverse transport and reduced the transport rate in a do
8 anding of molecular mechanisms of macrophage reverse transport and regulators that play important rol
9 es due to alcohol-induced hyperlipolysis are reverse transported and deposited in the liver.
10 depend strongly on transport direction, with reverse transport being faster but less voltage-dependen
11 ed as a consequence of DL-TBOA inhibition of reversed transport by high-affinity, Na-dependent carrie
12 he transporter, N206S exhibited an increased reverse transport capacity.
13             Expressing dynein-adaptor snapin reverses transport defects by competing with hSOD1(G93A)
14 activity, or DIC1B serine-80 phosphorylation reversed transport deficits in PSEN1 knockout neurons.
15 ls, or it can be released from cells through reverse transport, depending on the electrochemical grad
16 mouse model, enhanced cholesterol efflux and reverse transport due to Epsin deficiency was suppressed
17 of vesicular release, non-vesicular leakage, reverse transport, dying cells or glia.
18 -independent release of neurotransmitter via reverse transport independent from normal presynaptic fu
19  aspartate (E404D) prevents both forward and reverse transport induced by K+.
20 hin the microdialysis fiber, suggesting that reversed transport is an important contributor to glutam
21 though it is known that METH releases DA via reverse transport, it is not known how METH increases th
22 However, it is unknown how fast and by which reverse transport mechanism glutamate can be released fr
23 es dopamine (DA) and serotonin release via a reverse transport mechanism.
24 nhibitors even at high concentrations in the reverse transport mode.
25 oes it strongly affect the normal forward or reverse transport modes of NCX1.
26 unctional characteristics of the forward and reverse transport modes of the human Na(+)/glucose trans
27      High density lipoprotein (HDL) mediates reverse transport of cholesterol from atheroma foam cell
28  apolipoprotein (apo) A-I contributes to the reverse transport of cholesterol from the periphery to t
29 lipoproteins and is a key participant in the reverse transport of cholesterol from the periphery to t
30 ified and has been shown to drive persistent reverse transport of DA (i.e. anomalous DA efflux) in tr
31 lous function, characterized as a persistent reverse transport of DA (substrate efflux).
32 s, and was essential for amphetamine-induced reverse transport of DA in neurons but not for DA uptake
33 y to the DAT, thereby enhancing DAT-mediated reverse transport of DA.
34 ompeting with dopamine uptake and increasing reverse transport of dopamine via the transporter.
35 ambient glutamate near synapses by fostering reverse transport of endogenous glutamate.
36  Moreover, the compound does not enhance the reverse transport of glutamate under ionic conditions th
37  increase in proton concentrations slows the reverse transport of glutamate, which may play a neuro-p
38       We developed a novel approach to trace reverse transport of labeled cholesterol specifically fr
39 s identified as being involved in gating the reverse transport of NE (Arg81, Gln314, and Asp473) did
40 e protective effect of HDL may extend to the reverse-transport of oxidised lipid species.
41  OGD-induced glutamate accumulation involves reversed transport of glutamate via glutamate transporte
42 nhance [3H]DA release mediated by either DAT reverse-transport or Ca(2+) channels in dSTR slices.
43                  These results indicate that reversed transport, primarily from glial cells by the EA
44  electrogenicity is distributed over several reverse transport steps, including intracellular Na(+) b
45  1A caused similar reductions in forward and reverse transport that did not involve changes in appare
46 s and driving non-exocytotic release through reverse transport, this psychostimulant also activates p
47   Abnormal DA release is thought to occur by reverse transport through the DA transporter (DAT), and
48 ducing stimulation-independent DA efflux via reverse transport through the DA transporter and by inhi
49 BG washout (p = 0.004) suggesting a role for reverse transport through the uptake-1 carrier.
50 elial cell mitochondria results largely from reverse transport to complex I and through the Q cycle i
51 ndent pathways, but the mechanism underlying reverse transport via endogenously expressed DAT is stil
52 lasm prior to its extrusion from the cell by reverse transport via the DA transporter.
53 expression, internalization, and forward and reverse transport, with phosphorylation sites for these