PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22804716-5 2012 DAT was distributed between the synaptosomal membrane (60%) and endosomal vesicles (40%), and in vitro application of the protein kinase C activator phorbol 12-myristate 13-acetate to striatal synaptosomes caused DAT internalization into the vesicle fractions. Tetradecanoylphorbol Acetate 149-180 solute carrier family 6 member 3 Homo sapiens 0-3 30203271-4 2019 The cells differentiated with retinoic acid and 12-o-tetradecanoylphorbol-13-acetate show a significant increase in the expression of tyrosine hydroxylase, vesicular monoamine transporter-2, and dopamine transporter. Tetradecanoylphorbol Acetate 48-84 solute carrier family 6 member 3 Homo sapiens 195-215 28571709-5 2017 Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha. Tetradecanoylphorbol Acetate 43-74 solute carrier family 6 member 3 Homo sapiens 169-172 28571709-5 2017 Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha. Tetradecanoylphorbol Acetate 43-74 solute carrier family 6 member 3 Homo sapiens 331-334 28571709-5 2017 Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha. Tetradecanoylphorbol Acetate 76-79 solute carrier family 6 member 3 Homo sapiens 169-172 28571709-5 2017 Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha. Tetradecanoylphorbol Acetate 76-79 solute carrier family 6 member 3 Homo sapiens 331-334 22804716-5 2012 DAT was distributed between the synaptosomal membrane (60%) and endosomal vesicles (40%), and in vitro application of the protein kinase C activator phorbol 12-myristate 13-acetate to striatal synaptosomes caused DAT internalization into the vesicle fractions. Tetradecanoylphorbol Acetate 149-180 solute carrier family 6 member 3 Homo sapiens 213-216 16109712-2 2005 To gain insight into these mechanisms, human DAT was purified in large amounts using a two-step affinity chromatography procedure from untreated HeLa cells or cells treated with phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 178-209 solute carrier family 6 member 3 Homo sapiens 45-48 19000913-6 2009 Pre-treatment of DAT expressing cells with phorbol-12-myristate-13-acetate, an activator of protein kinase C, attenuated the inhibitory effect of Zn(2+) on uptake in HEK293 cells and increased the stimulatory effect in SK-N-MC cells. Tetradecanoylphorbol Acetate 43-74 solute carrier family 6 member 3 Homo sapiens 17-20 18248623-1 2008 We examined the mechanisms involved in protein kinase C (PKC)-dependent down-regulation of dopamine transporter (DAT) activity and cell surface expression by treating heterologously expressing cells with the clathrin-mediated endocytosis inhibitor concanavalin A (Con A) or the cholesterol depleter/membrane raft disrupter methyl-beta-cyclodextrin (MbetaC) prior to treatment with the PKC activator phorbol 12-myristate, 13-acetate (PMA). Tetradecanoylphorbol Acetate 433-436 solute carrier family 6 member 3 Homo sapiens 113-116 16109712-2 2005 To gain insight into these mechanisms, human DAT was purified in large amounts using a two-step affinity chromatography procedure from untreated HeLa cells or cells treated with phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 211-214 solute carrier family 6 member 3 Homo sapiens 45-48 16109712-3 2005 Mass spectrometric analysis of purified DAT complexes revealed the presence of several proteins, among which ubiquitin was particularly abundant in the PMA-treated sample. Tetradecanoylphorbol Acetate 152-155 solute carrier family 6 member 3 Homo sapiens 40-43 16109712-4 2005 Western blotting of highly purified DAT protein confirmed constitutive ubiquitylation of DAT and a dramatic increase in DAT ubiquitylation in cells treated with PMA. Tetradecanoylphorbol Acetate 161-164 solute carrier family 6 member 3 Homo sapiens 36-39 15111235-3 2004 RA/TPA treated cells exhibited the highest levels of tyrosine hydroxylase and DAT but lower levels of vesicular monoamine transporter. Tetradecanoylphorbol Acetate 3-6 solute carrier family 6 member 3 Homo sapiens 78-81 15111235-5 2004 RA/TPA differentiated cells evidenced high sensitivity to the neurotoxic effects of MPP+ (0.03 to 3.0 mM), and the neurotoxic effects of MPP+ were blocked with the DAT inhibitor 1-(2-[bis(4-fluorophenyl)methoxy]ethyl)-4-(3-phenylpropyl)piperazine (GBR 12909). Tetradecanoylphorbol Acetate 3-6 solute carrier family 6 member 3 Homo sapiens 164-167 11959130-2 2002 Activation of conventional PKCs (cPKCs) and novel PKCs (nPKCs) using 10 nM phorbol 12-myristate 13-acetate (PMA) significantly inhibited DAT-associated transport currents. Tetradecanoylphorbol Acetate 75-106 solute carrier family 6 member 3 Homo sapiens 137-140 11959130-2 2002 Activation of conventional PKCs (cPKCs) and novel PKCs (nPKCs) using 10 nM phorbol 12-myristate 13-acetate (PMA) significantly inhibited DAT-associated transport currents. Tetradecanoylphorbol Acetate 108-111 solute carrier family 6 member 3 Homo sapiens 137-140 9316847-2 1997 When Xenopus oocytes expressing the cloned human dopamine transporter (hDAT) were pretreated with bath-applied phorbol 12-myristate 13-acetate (PMA), a PKC activator, [3H]DA uptake decreased irreversibly in a time- and dose-dependent manner (IC50 = 22 nM; maximal inhibition = 63-85%). Tetradecanoylphorbol Acetate 111-142 solute carrier family 6 member 3 Homo sapiens 49-69 9316847-2 1997 When Xenopus oocytes expressing the cloned human dopamine transporter (hDAT) were pretreated with bath-applied phorbol 12-myristate 13-acetate (PMA), a PKC activator, [3H]DA uptake decreased irreversibly in a time- and dose-dependent manner (IC50 = 22 nM; maximal inhibition = 63-85%). Tetradecanoylphorbol Acetate 144-147 solute carrier family 6 member 3 Homo sapiens 49-69