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phospho dat polyclonal antibody  (PhosphoSolutions)


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    PhosphoSolutions phospho dat polyclonal antibody
    Phospho Dat Polyclonal Antibody, supplied by PhosphoSolutions, used in various techniques. Bioz Stars score: 96/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+dat/Anti-Dopamine+Transporter+(Thr53)+Antibody/pmc13125265-87-14-19
    Average 96 stars, based on 16 article reviews
    phospho dat polyclonal antibody - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    Saline:

    Article Title: Dopamine Dysregulation and Altered Responses to Drugs Affecting Dopaminergic Transmission in a New Dopamine Transporter Knockout (DAT-KO) Rat Model.
    Article Snippet: Under normal conditions, dopamine (DA) clearance after release largely depends on uptake by the DA transporter (DAT).. DAT expression/activity is reduced in some neuropsychiatric and neurological disorders.. Our aim was to characterize the behavioral, neurochemical and electrophysiological effects of eliminating DAT in a novel knockout rat model we generated using CRISPR/Cas9.

    Incubation:

    Article Title: Dopamine Dysregulation and Altered Responses to Drugs Affecting Dopaminergic Transmission in a New Dopamine Transporter Knockout (DAT-KO) Rat Model.
    Article Snippet: Under normal conditions, dopamine (DA) clearance after release largely depends on uptake by the DA transporter (DAT).. DAT expression/activity is reduced in some neuropsychiatric and neurological disorders.. Our aim was to characterize the behavioral, neurochemical and electrophysiological effects of eliminating DAT in a novel knockout rat model we generated using CRISPR/Cas9.

    Blocking Assay:

    Article Title: Dopamine Dysregulation and Altered Responses to Drugs Affecting Dopaminergic Transmission in a New Dopamine Transporter Knockout (DAT-KO) Rat Model.
    Article Snippet: Under normal conditions, dopamine (DA) clearance after release largely depends on uptake by the DA transporter (DAT).. DAT expression/activity is reduced in some neuropsychiatric and neurological disorders.. Our aim was to characterize the behavioral, neurochemical and electrophysiological effects of eliminating DAT in a novel knockout rat model we generated using CRISPR/Cas9.

    other:

    Article Title: Dopamine Dysregulation and Altered Responses to Drugs Affecting Dopaminergic Transmission in a New Dopamine Transporter Knockout (DAT-KO) Rat Model
    Article Snippet: Under normal conditions, dopamine (DA) clearance after release largely depends on uptake by the DA transporter (DAT).. DAT expression/activity is reduced in some neuropsychiatric and neurological disorders.. Our aim was to characterize behavioral, neurochemical and electrophysiological effects of eliminating DAT in a novel knockout rat model we generated using CRISPR/Cas9.



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    ( A and B ) Representative Western blot ( A ) and quantification ( B ) of glycosylated and nonglycosylated dopamine transporter <t>(DAT)</t> in GBA1 L444P mutant dopaminergic neurons treated with increasing NALL concentrations. ( C and D ) Western blot ( C ) and quantification ( D ) of parkin expression in NALL-treated GBA1 L444P neurons. ( E – J ) Western blots and corresponding quantification of SYNJ1 redistribution from cytosolic (Cyto) to synaptic membrane (SM) fractions following NALL treatment in GBA1 L444P ( E and F ), GBA1 N370S ( G and H ), and parkin mutant ( I and J ) dopaminergic neurons. Synaptophysin (SYP) <t>and</t> <t>GAPDH</t> served as synaptic and cytosolic markers, respectively. ( K ) Scatter plot showing time constants of pHluorin fluorescence recovery following exocytosis in GBA1 L444P neurons. NALL-treated synapses (105.3 ± 5.8 s; n = 59 ROIs) recovered significantly faster than NT (133.2 ± 5.3 s; n = 89 ROIs) (Mann-Whitney test). Lines represent means ± SD. ( L ) Representative traces of pHluorin fluorescence intensity from 50 s before to 300 s after exocytosis in GBA1 L444P mutant neurons. For Western blots, β-III-tubulin and GAPDH served as loading controls ( n = 3 independent experiments). Data are expressed as mean fold-change relative to 0 mM (DMSO) or nontreated (NT) groups. Statistical significance was determined by 1-way ANOVA ( B and D ), Student’s t test ( F , H , and J ), or Mann-Whitney test ( K ). Data represent mean ± SEM, except in K (mean ± SD). * P < 0.05, ** P < 0.01, *** P < 0.005, and **** P < 0.001.
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    ( A and B ) Representative Western blot ( A ) and quantification ( B ) of glycosylated and nonglycosylated dopamine transporter <t>(DAT)</t> in GBA1 L444P mutant dopaminergic neurons treated with increasing NALL concentrations. ( C and D ) Western blot ( C ) and quantification ( D ) of parkin expression in NALL-treated GBA1 L444P neurons. ( E – J ) Western blots and corresponding quantification of SYNJ1 redistribution from cytosolic (Cyto) to synaptic membrane (SM) fractions following NALL treatment in GBA1 L444P ( E and F ), GBA1 N370S ( G and H ), and parkin mutant ( I and J ) dopaminergic neurons. Synaptophysin (SYP) <t>and</t> <t>GAPDH</t> served as synaptic and cytosolic markers, respectively. ( K ) Scatter plot showing time constants of pHluorin fluorescence recovery following exocytosis in GBA1 L444P neurons. NALL-treated synapses (105.3 ± 5.8 s; n = 59 ROIs) recovered significantly faster than NT (133.2 ± 5.3 s; n = 89 ROIs) (Mann-Whitney test). Lines represent means ± SD. ( L ) Representative traces of pHluorin fluorescence intensity from 50 s before to 300 s after exocytosis in GBA1 L444P mutant neurons. For Western blots, β-III-tubulin and GAPDH served as loading controls ( n = 3 independent experiments). Data are expressed as mean fold-change relative to 0 mM (DMSO) or nontreated (NT) groups. Statistical significance was determined by 1-way ANOVA ( B and D ), Student’s t test ( F , H , and J ), or Mann-Whitney test ( K ). Data represent mean ± SEM, except in K (mean ± SD). * P < 0.05, ** P < 0.01, *** P < 0.005, and **** P < 0.001.
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    ( A and B ) Representative Western blot ( A ) and quantification ( B ) of glycosylated and nonglycosylated dopamine transporter <t>(DAT)</t> in GBA1 L444P mutant dopaminergic neurons treated with increasing NALL concentrations. ( C and D ) Western blot ( C ) and quantification ( D ) of parkin expression in NALL-treated GBA1 L444P neurons. ( E – J ) Western blots and corresponding quantification of SYNJ1 redistribution from cytosolic (Cyto) to synaptic membrane (SM) fractions following NALL treatment in GBA1 L444P ( E and F ), GBA1 N370S ( G and H ), and parkin mutant ( I and J ) dopaminergic neurons. Synaptophysin (SYP) <t>and</t> <t>GAPDH</t> served as synaptic and cytosolic markers, respectively. ( K ) Scatter plot showing time constants of pHluorin fluorescence recovery following exocytosis in GBA1 L444P neurons. NALL-treated synapses (105.3 ± 5.8 s; n = 59 ROIs) recovered significantly faster than NT (133.2 ± 5.3 s; n = 89 ROIs) (Mann-Whitney test). Lines represent means ± SD. ( L ) Representative traces of pHluorin fluorescence intensity from 50 s before to 300 s after exocytosis in GBA1 L444P mutant neurons. For Western blots, β-III-tubulin and GAPDH served as loading controls ( n = 3 independent experiments). Data are expressed as mean fold-change relative to 0 mM (DMSO) or nontreated (NT) groups. Statistical significance was determined by 1-way ANOVA ( B and D ), Student’s t test ( F , H , and J ), or Mann-Whitney test ( K ). Data represent mean ± SEM, except in K (mean ± SD). * P < 0.05, ** P < 0.01, *** P < 0.005, and **** P < 0.001.
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    ( A and B ) Representative Western blot ( A ) and quantification ( B ) of glycosylated and nonglycosylated dopamine transporter <t>(DAT)</t> in GBA1 L444P mutant dopaminergic neurons treated with increasing NALL concentrations. ( C and D ) Western blot ( C ) and quantification ( D ) of parkin expression in NALL-treated GBA1 L444P neurons. ( E – J ) Western blots and corresponding quantification of SYNJ1 redistribution from cytosolic (Cyto) to synaptic membrane (SM) fractions following NALL treatment in GBA1 L444P ( E and F ), GBA1 N370S ( G and H ), and parkin mutant ( I and J ) dopaminergic neurons. Synaptophysin (SYP) <t>and</t> <t>GAPDH</t> served as synaptic and cytosolic markers, respectively. ( K ) Scatter plot showing time constants of pHluorin fluorescence recovery following exocytosis in GBA1 L444P neurons. NALL-treated synapses (105.3 ± 5.8 s; n = 59 ROIs) recovered significantly faster than NT (133.2 ± 5.3 s; n = 89 ROIs) (Mann-Whitney test). Lines represent means ± SD. ( L ) Representative traces of pHluorin fluorescence intensity from 50 s before to 300 s after exocytosis in GBA1 L444P mutant neurons. For Western blots, β-III-tubulin and GAPDH served as loading controls ( n = 3 independent experiments). Data are expressed as mean fold-change relative to 0 mM (DMSO) or nontreated (NT) groups. Statistical significance was determined by 1-way ANOVA ( B and D ), Student’s t test ( F , H , and J ), or Mann-Whitney test ( K ). Data represent mean ± SEM, except in K (mean ± SD). * P < 0.05, ** P < 0.01, *** P < 0.005, and **** P < 0.001.
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    ( A and B ) Representative Western blot ( A ) and quantification ( B ) of glycosylated and nonglycosylated dopamine transporter <t>(DAT)</t> in GBA1 L444P mutant dopaminergic neurons treated with increasing NALL concentrations. ( C and D ) Western blot ( C ) and quantification ( D ) of parkin expression in NALL-treated GBA1 L444P neurons. ( E – J ) Western blots and corresponding quantification of SYNJ1 redistribution from cytosolic (Cyto) to synaptic membrane (SM) fractions following NALL treatment in GBA1 L444P ( E and F ), GBA1 N370S ( G and H ), and parkin mutant ( I and J ) dopaminergic neurons. Synaptophysin (SYP) <t>and</t> <t>GAPDH</t> served as synaptic and cytosolic markers, respectively. ( K ) Scatter plot showing time constants of pHluorin fluorescence recovery following exocytosis in GBA1 L444P neurons. NALL-treated synapses (105.3 ± 5.8 s; n = 59 ROIs) recovered significantly faster than NT (133.2 ± 5.3 s; n = 89 ROIs) (Mann-Whitney test). Lines represent means ± SD. ( L ) Representative traces of pHluorin fluorescence intensity from 50 s before to 300 s after exocytosis in GBA1 L444P mutant neurons. For Western blots, β-III-tubulin and GAPDH served as loading controls ( n = 3 independent experiments). Data are expressed as mean fold-change relative to 0 mM (DMSO) or nontreated (NT) groups. Statistical significance was determined by 1-way ANOVA ( B and D ), Student’s t test ( F , H , and J ), or Mann-Whitney test ( K ). Data represent mean ± SEM, except in K (mean ± SD). * P < 0.05, ** P < 0.01, *** P < 0.005, and **** P < 0.001.
    Sc32259, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    ( A and B ) Representative Western blot ( A ) and quantification ( B ) of glycosylated and nonglycosylated dopamine transporter (DAT) in GBA1 L444P mutant dopaminergic neurons treated with increasing NALL concentrations. ( C and D ) Western blot ( C ) and quantification ( D ) of parkin expression in NALL-treated GBA1 L444P neurons. ( E – J ) Western blots and corresponding quantification of SYNJ1 redistribution from cytosolic (Cyto) to synaptic membrane (SM) fractions following NALL treatment in GBA1 L444P ( E and F ), GBA1 N370S ( G and H ), and parkin mutant ( I and J ) dopaminergic neurons. Synaptophysin (SYP) and GAPDH served as synaptic and cytosolic markers, respectively. ( K ) Scatter plot showing time constants of pHluorin fluorescence recovery following exocytosis in GBA1 L444P neurons. NALL-treated synapses (105.3 ± 5.8 s; n = 59 ROIs) recovered significantly faster than NT (133.2 ± 5.3 s; n = 89 ROIs) (Mann-Whitney test). Lines represent means ± SD. ( L ) Representative traces of pHluorin fluorescence intensity from 50 s before to 300 s after exocytosis in GBA1 L444P mutant neurons. For Western blots, β-III-tubulin and GAPDH served as loading controls ( n = 3 independent experiments). Data are expressed as mean fold-change relative to 0 mM (DMSO) or nontreated (NT) groups. Statistical significance was determined by 1-way ANOVA ( B and D ), Student’s t test ( F , H , and J ), or Mann-Whitney test ( K ). Data represent mean ± SEM, except in K (mean ± SD). * P < 0.05, ** P < 0.01, *** P < 0.005, and **** P < 0.001.

    Journal: The Journal of Clinical Investigation

    Article Title: N-acetyl- l -leucine lowers α -synuclein levels and improves synaptic function in Parkinson’s disease models

    doi: 10.1172/JCI196137

    Figure Lengend Snippet: ( A and B ) Representative Western blot ( A ) and quantification ( B ) of glycosylated and nonglycosylated dopamine transporter (DAT) in GBA1 L444P mutant dopaminergic neurons treated with increasing NALL concentrations. ( C and D ) Western blot ( C ) and quantification ( D ) of parkin expression in NALL-treated GBA1 L444P neurons. ( E – J ) Western blots and corresponding quantification of SYNJ1 redistribution from cytosolic (Cyto) to synaptic membrane (SM) fractions following NALL treatment in GBA1 L444P ( E and F ), GBA1 N370S ( G and H ), and parkin mutant ( I and J ) dopaminergic neurons. Synaptophysin (SYP) and GAPDH served as synaptic and cytosolic markers, respectively. ( K ) Scatter plot showing time constants of pHluorin fluorescence recovery following exocytosis in GBA1 L444P neurons. NALL-treated synapses (105.3 ± 5.8 s; n = 59 ROIs) recovered significantly faster than NT (133.2 ± 5.3 s; n = 89 ROIs) (Mann-Whitney test). Lines represent means ± SD. ( L ) Representative traces of pHluorin fluorescence intensity from 50 s before to 300 s after exocytosis in GBA1 L444P mutant neurons. For Western blots, β-III-tubulin and GAPDH served as loading controls ( n = 3 independent experiments). Data are expressed as mean fold-change relative to 0 mM (DMSO) or nontreated (NT) groups. Statistical significance was determined by 1-way ANOVA ( B and D ), Student’s t test ( F , H , and J ), or Mann-Whitney test ( K ). Data represent mean ± SEM, except in K (mean ± SD). * P < 0.05, ** P < 0.01, *** P < 0.005, and **** P < 0.001.

    Article Snippet: Antibodies used for immunoblotting include anti-pS129-syn antibody (Cell Signaling Technology: 23706S), anti-SYP antibody (MilliporeSigma: ab9272), anti-α-syn antibody (Santa Cruz Biotechnology: sc-7011-R), anti-β-III-tubulin antibody (BioLegend: 801202), anti-SYNJ1 antibody (LsBio: 65169), anti-parkin antibody (Santa Cruz Biotechnology: sc-32282), anti-HTRA1 (R&D Systems: MAB2916), anti-HTRA1 (Proteintech: 55011-1-AP), anti-caspase 3 (Cell Signaling Technology: 9662), anti-cleaved caspase-3 (Cell Signaling Technology: 9661S), anti-DAT antibody (Santa Cruz Biotechnology: sc-32259), anti-GAPDH antibody (MilliporeSigma: MAB374), Goat Anti-Rat IgG (H+L) (Peroxidase AffiniPure: 112-035-062), Goat Anti-Rabbit IgG (H+L) (Peroxidase-AffiniPure: 111-035-144), and Goat Anti-Mouse IgG (H+L) (Peroxidase-AffiniPure: 115-035-146).

    Techniques: Western Blot, Mutagenesis, Expressing, Membrane, Fluorescence, MANN-WHITNEY