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Tocris dapk1 inhibitor tc dapk6

Increased <t>DAPK1</t> protein expression and activation occur in affected regions of the YAC128 brain and require mHTT cleavage at D586. (A) Cortical (CTX), (B) striatal (STR), or (C) cerebellar (CB) tissues from 1-month-old WT, YAC128 (Y128; line 53), and C6R (line W13) mice were lysed in a stringent buffer and total lysate was assessed by Western blotting for DAPK1, pS308, and β-actin protein levels. Data are normalized to WT ( n = 6–12 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05, ** p < 0.01, *** p < 0.001). (D) Dapk1 mRNA expression in WT and YAC128 brains at 1 month of age was quantified by qPCR. Data are normalized to WT ( n = 6 biological replicates; Student’s t -test). (E) Cortical, striatal, and cerebellar tissues from 1-month-old WT FVB mice were evaluated by Western blot for DAPK1, pS308, and β-actin protein levels. Data are normalized to CTX values ( n = 8 biological replicates, two technical replicates each; Student’s t -test, ### p < 0.001; one-way ANOVA with Bonferroni post hoc analysis, *** p < 0.001).

Dapk1 Inhibitor Tc Dapk6, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease"

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

Journal: Frontiers in Cellular Neuroscience

doi: 10.3389/fncel.2020.590569

Increased DAPK1 protein expression and activation occur in affected regions of the YAC128 brain and require mHTT cleavage at D586. (A) Cortical (CTX), (B) striatal (STR), or (C) cerebellar (CB) tissues from 1-month-old WT, YAC128 (Y128; line 53), and C6R (line W13) mice were lysed in a stringent buffer and total lysate was assessed by Western blotting for DAPK1, pS308, and β-actin protein levels. Data are normalized to WT ( n = 6–12 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05, ** p < 0.01, *** p < 0.001). (D) Dapk1 mRNA expression in WT and YAC128 brains at 1 month of age was quantified by qPCR. Data are normalized to WT ( n = 6 biological replicates; Student’s t -test). (E) Cortical, striatal, and cerebellar tissues from 1-month-old WT FVB mice were evaluated by Western blot for DAPK1, pS308, and β-actin protein levels. Data are normalized to CTX values ( n = 8 biological replicates, two technical replicates each; Student’s t -test, ### p < 0.001; one-way ANOVA with Bonferroni post hoc analysis, *** p < 0.001).

Figure Legend Snippet: Increased DAPK1 protein expression and activation occur in affected regions of the YAC128 brain and require mHTT cleavage at D586. (A) Cortical (CTX), (B) striatal (STR), or (C) cerebellar (CB) tissues from 1-month-old WT, YAC128 (Y128; line 53), and C6R (line W13) mice were lysed in a stringent buffer and total lysate was assessed by Western blotting for DAPK1, pS308, and β-actin protein levels. Data are normalized to WT ( n = 6–12 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05, ** p < 0.01, *** p < 0.001). (D) Dapk1 mRNA expression in WT and YAC128 brains at 1 month of age was quantified by qPCR. Data are normalized to WT ( n = 6 biological replicates; Student’s t -test). (E) Cortical, striatal, and cerebellar tissues from 1-month-old WT FVB mice were evaluated by Western blot for DAPK1, pS308, and β-actin protein levels. Data are normalized to CTX values ( n = 8 biological replicates, two technical replicates each; Student’s t -test, ### p < 0.001; one-way ANOVA with Bonferroni post hoc analysis, *** p < 0.001).

Techniques Used: Expressing, Activation Assay, Western Blot

$Extrasynaptic GluN2B S1303 phosphorylation and interaction with DAPK1 are elevated in the YAC128 brain. Cortical or striatal tissues were subjected to subcellular fractionation to yield (A,C) synaptic (PSD), (B) cortical extrasynaptic (non-PSD), or (D) striatal “non-synaptic” membrane fractions, which were run by SDS–PAGE and Western blotting for GluN2B expression and S1303 phosphorylation ( n = 6–14 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05, ** p < 0.01). (E) DAPK1 was immunoprecipitated from WT and YAC128 cortical lysates, followed by the detection of co-immunoprecipitated GluN2B by Western blot. All sample blot images in panel (E) are cropped from the same Western blot membrane which contained multiple biological replicates run side-by-side. Data are normalized to WT values ( n = 14 biological replicates, Student’s t -test, * p < 0.05, ** p < 0.01).$
Figure Legend Snippet: Extrasynaptic GluN2B S1303 phosphorylation and interaction with DAPK1 are elevated in the YAC128 brain. Cortical or striatal tissues were subjected to subcellular fractionation to yield (A,C) synaptic (PSD), (B) cortical extrasynaptic (non-PSD), or (D) striatal “non-synaptic” membrane fractions, which were run by SDS–PAGE and Western blotting for GluN2B expression and S1303 phosphorylation ( n = 6–14 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05, ** p < 0.01). (E) DAPK1 was immunoprecipitated from WT and YAC128 cortical lysates, followed by the detection of co-immunoprecipitated GluN2B by Western blot. All sample blot images in panel (E) are cropped from the same Western blot membrane which contained multiple biological replicates run side-by-side. Data are normalized to WT values ( n = 14 biological replicates, Student’s t -test, * p < 0.05, ** p < 0.01).

Techniques Used: Phospho-proteomics, Fractionation, Membrane, SDS Page, Western Blot, Expressing, Immunoprecipitation

$Low-dose memantine normalizes cortical DAPK1 activation and extrasynaptic pS1303 levels in YAC128 mice. Cortical tissues from 1-month-old WT and YAC128 mice treated with low-dose memantine from conception were processed to obtain (A) total or (B) extrasynaptic (non-PSD) membrane protein fractions. Samples were processed for DAPK1 or GluN2B protein expression and phosphorylation levels by Western blot. Data are normalized to WT H 2 O values ( n = 8 biological replicates, two technical replicates each; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, ** p < 0.01; Student’s t -test, # p < 0.05; two-way ANOVA interaction * p < 0.05 for DAPK1 protein level and pS308, two-way ANOVA interaction ** p < 0.01 for pS1303).$
Figure Legend Snippet: Low-dose memantine normalizes cortical DAPK1 activation and extrasynaptic pS1303 levels in YAC128 mice. Cortical tissues from 1-month-old WT and YAC128 mice treated with low-dose memantine from conception were processed to obtain (A) total or (B) extrasynaptic (non-PSD) membrane protein fractions. Samples were processed for DAPK1 or GluN2B protein expression and phosphorylation levels by Western blot. Data are normalized to WT H 2 O values ( n = 8 biological replicates, two technical replicates each; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, ** p < 0.01; Student’s t -test, # p < 0.05; two-way ANOVA interaction * p < 0.05 for DAPK1 protein level and pS308, two-way ANOVA interaction ** p < 0.01 for pS1303).

Techniques Used: Activation Assay, Membrane, Expressing, Phospho-proteomics, Western Blot

$DAPK1 inhibition normalizes extrasynaptic GluN2B phosphorylation and DAPK1 protein levels in the YAC128 model. (A) Corticostriatal primary cultures from WT and YAC128 embryos were treated at DIV21 with DMSO (0.1%) or a DAPK1 inhibitor (DKI, 10 μM) for 1 h followed by lysis in a gentle buffer to solubilize non-synaptic protein. Lysates were processed by Western blot to detect GluN2B, pS1303, and DAPK1 levels. Data are normalized to WT DMSO values ( n = 8 biological replicates; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05; Student’s t -test, # p < 0.05). (B) Four-week-old YAC128 mice were treated intranasally with 50 nmol of DAPK1 inhibitor (DKI; TC-DAPK6) or vehicle control (VEH). After 6 h, cortical extrasynaptic fractions were isolated to measure GluN2B, pS1303, and DAPK1 levels ( n = 9 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05). (C) Quantitative measurement of DAPK1-FLAG protein turnover using bio-orthogonal labeling, FLAG immunoprecipitation, CLICK chemistry, and detection of AHA/Streptavidin (Strep)-labeled DAPK1 in transiently transfected COS-7 cells treated with DMSO or 10 μM DKI (TC-DAPK6) for 24 h ( n = 3 for 8 h and 10 h chase time points, n = 7 for all other chase time points; two-way ANOVA ** p < 0.01 for DKI treatment effect; Sidak’s multiple comparisons test, ** p < 0.01).$
Figure Legend Snippet: DAPK1 inhibition normalizes extrasynaptic GluN2B phosphorylation and DAPK1 protein levels in the YAC128 model. (A) Corticostriatal primary cultures from WT and YAC128 embryos were treated at DIV21 with DMSO (0.1%) or a DAPK1 inhibitor (DKI, 10 μM) for 1 h followed by lysis in a gentle buffer to solubilize non-synaptic protein. Lysates were processed by Western blot to detect GluN2B, pS1303, and DAPK1 levels. Data are normalized to WT DMSO values ( n = 8 biological replicates; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05; Student’s t -test, # p < 0.05). (B) Four-week-old YAC128 mice were treated intranasally with 50 nmol of DAPK1 inhibitor (DKI; TC-DAPK6) or vehicle control (VEH). After 6 h, cortical extrasynaptic fractions were isolated to measure GluN2B, pS1303, and DAPK1 levels ( n = 9 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05). (C) Quantitative measurement of DAPK1-FLAG protein turnover using bio-orthogonal labeling, FLAG immunoprecipitation, CLICK chemistry, and detection of AHA/Streptavidin (Strep)-labeled DAPK1 in transiently transfected COS-7 cells treated with DMSO or 10 μM DKI (TC-DAPK6) for 24 h ( n = 3 for 8 h and 10 h chase time points, n = 7 for all other chase time points; two-way ANOVA ** p < 0.01 for DKI treatment effect; Sidak’s multiple comparisons test, ** p < 0.01).

Techniques Used: Inhibition, Phospho-proteomics, Lysis, Gentle, Western Blot, Control, Isolation, Labeling, Immunoprecipitation, Transfection

DAPK1 kinase activity promotes GluN2B surface expression via pS1303. (A) Surface expression (surface/internal YFP fluorescence ratio) and cluster analysis of transfected YFP-GluN2B was performed in 1:1 cortico-striatal co-cultured YAC128 medium spiny neurons (MSNs) treated with DMSO or the DAPK1 inhibitor TC-DAPK6 (DKI; 1 μM for 3 days, 0.01% final DMSO concentration). Absolute values were used for punctae analysis ( n = 24–38 cells from three independent cultures; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, *** p < 0.001). Scale bar = 5 μm. (B) Surface expression of GFP-GluN2B [WT or an S1303A (SA) mutant] in transfected COS-7 cells co-expressing GluN1 and either WT-DAPK1 or a kinase-dead DAPK1 mutant (K42A; KA; n = 23–30 cells from three independent culture passages; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, *** p < 0.001). Scale bar = 15 μm.

Figure Legend Snippet: DAPK1 kinase activity promotes GluN2B surface expression via pS1303. (A) Surface expression (surface/internal YFP fluorescence ratio) and cluster analysis of transfected YFP-GluN2B was performed in 1:1 cortico-striatal co-cultured YAC128 medium spiny neurons (MSNs) treated with DMSO or the DAPK1 inhibitor TC-DAPK6 (DKI; 1 μM for 3 days, 0.01% final DMSO concentration). Absolute values were used for punctae analysis ( n = 24–38 cells from three independent cultures; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, *** p < 0.001). Scale bar = 5 μm. (B) Surface expression of GFP-GluN2B [WT or an S1303A (SA) mutant] in transfected COS-7 cells co-expressing GluN1 and either WT-DAPK1 or a kinase-dead DAPK1 mutant (K42A; KA; n = 23–30 cells from three independent culture passages; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, *** p < 0.001). Scale bar = 15 μm.

Techniques Used: Activity Assay, Expressing, Fluorescence, Transfection, Cell Culture, Concentration Assay, Mutagenesis

DAPK1 inhibition or extrasynaptic NMDAR blockade prevents spine instability in YAC128 MSNs. (A) WT and YAC128 1:3 CS co-cultures were treated from DIV14 to 21 with DMSO (0.01%) or the DAPK1 inhibitor TC-DAPK6 (DKI, 1 μM), and spine analysis was performed on DARPP32+ MSNs. (B) 1:3 co-cultures were treated with either water, memantine (MEM, 3 μM) or (C) ifenprodil (IFEN, 3 μM) from DIV14 to 21 and processed in the same way as for DKI ( n = 24 cells from three independent cultures; Two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, ** p < 0.01, *** p < 0.001). Scale bar = 5 μm.

Figure Legend Snippet: DAPK1 inhibition or extrasynaptic NMDAR blockade prevents spine instability in YAC128 MSNs. (A) WT and YAC128 1:3 CS co-cultures were treated from DIV14 to 21 with DMSO (0.01%) or the DAPK1 inhibitor TC-DAPK6 (DKI, 1 μM), and spine analysis was performed on DARPP32+ MSNs. (B) 1:3 co-cultures were treated with either water, memantine (MEM, 3 μM) or (C) ifenprodil (IFEN, 3 μM) from DIV14 to 21 and processed in the same way as for DKI ( n = 24 cells from three independent cultures; Two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, ** p < 0.01, *** p < 0.001). Scale bar = 5 μm.

Techniques Used: Inhibition

Figure Legend Snippet:

Techniques Used:

Concentration Assay:

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease
Article Snippet: Ifenprodil hemitartrate (Tocris Bioscience; Cat# 0545) and memantine hydrochloride (Tocris Bioscience; Cat# 0773) were dissolved in sterile H 2 O and used at a final treatment concentration of 3 μM. .. The DAPK1 inhibitor TC-DAPK6 (DKI; Tocris Bioscience; Cat# 4301) was dissolved in DMSO and used at a final concentration of 1 μM (0.01% DMSO). ..

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Journal: Frontiers in Cellular Neuroscience

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

doi: 10.3389/fncel.2020.590569

Figure Lengend Snippet: Increased DAPK1 protein expression and activation occur in affected regions of the YAC128 brain and require mHTT cleavage at D586. (A) Cortical (CTX), (B) striatal (STR), or (C) cerebellar (CB) tissues from 1-month-old WT, YAC128 (Y128; line 53), and C6R (line W13) mice were lysed in a stringent buffer and total lysate was assessed by Western blotting for DAPK1, pS308, and β-actin protein levels. Data are normalized to WT ( n = 6–12 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05, ** p < 0.01, *** p < 0.001). (D) Dapk1 mRNA expression in WT and YAC128 brains at 1 month of age was quantified by qPCR. Data are normalized to WT ( n = 6 biological replicates; Student’s t -test). (E) Cortical, striatal, and cerebellar tissues from 1-month-old WT FVB mice were evaluated by Western blot for DAPK1, pS308, and β-actin protein levels. Data are normalized to CTX values ( n = 8 biological replicates, two technical replicates each; Student’s t -test, ### p < 0.001; one-way ANOVA with Bonferroni post hoc analysis, *** p < 0.001).

Article Snippet: The DAPK1 inhibitor TC-DAPK6 (DKI; Tocris Bioscience; Cat# 4301) was dissolved in DMSO and used at a final concentration of 1 μM (0.01% DMSO).

Techniques: Expressing, Activation Assay, Western Blot

Journal: Frontiers in Cellular Neuroscience

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

doi: 10.3389/fncel.2020.590569

Figure Lengend Snippet: Extrasynaptic GluN2B S1303 phosphorylation and interaction with DAPK1 are elevated in the YAC128 brain. Cortical or striatal tissues were subjected to subcellular fractionation to yield (A,C) synaptic (PSD), (B) cortical extrasynaptic (non-PSD), or (D) striatal “non-synaptic” membrane fractions, which were run by SDS–PAGE and Western blotting for GluN2B expression and S1303 phosphorylation ( n = 6–14 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05, ** p < 0.01). (E) DAPK1 was immunoprecipitated from WT and YAC128 cortical lysates, followed by the detection of co-immunoprecipitated GluN2B by Western blot. All sample blot images in panel (E) are cropped from the same Western blot membrane which contained multiple biological replicates run side-by-side. Data are normalized to WT values ( n = 14 biological replicates, Student’s t -test, * p < 0.05, ** p < 0.01).

Article Snippet: The DAPK1 inhibitor TC-DAPK6 (DKI; Tocris Bioscience; Cat# 4301) was dissolved in DMSO and used at a final concentration of 1 μM (0.01% DMSO).

Techniques: Phospho-proteomics, Fractionation, Membrane, SDS Page, Western Blot, Expressing, Immunoprecipitation

Journal: Frontiers in Cellular Neuroscience

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

doi: 10.3389/fncel.2020.590569

Figure Lengend Snippet: Low-dose memantine normalizes cortical DAPK1 activation and extrasynaptic pS1303 levels in YAC128 mice. Cortical tissues from 1-month-old WT and YAC128 mice treated with low-dose memantine from conception were processed to obtain (A) total or (B) extrasynaptic (non-PSD) membrane protein fractions. Samples were processed for DAPK1 or GluN2B protein expression and phosphorylation levels by Western blot. Data are normalized to WT H 2 O values ( n = 8 biological replicates, two technical replicates each; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, ** p < 0.01; Student’s t -test, # p < 0.05; two-way ANOVA interaction * p < 0.05 for DAPK1 protein level and pS308, two-way ANOVA interaction ** p < 0.01 for pS1303).

Article Snippet: The DAPK1 inhibitor TC-DAPK6 (DKI; Tocris Bioscience; Cat# 4301) was dissolved in DMSO and used at a final concentration of 1 μM (0.01% DMSO).

Techniques: Activation Assay, Membrane, Expressing, Phospho-proteomics, Western Blot

Journal: Frontiers in Cellular Neuroscience

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

doi: 10.3389/fncel.2020.590569

Figure Lengend Snippet: DAPK1 inhibition normalizes extrasynaptic GluN2B phosphorylation and DAPK1 protein levels in the YAC128 model. (A) Corticostriatal primary cultures from WT and YAC128 embryos were treated at DIV21 with DMSO (0.1%) or a DAPK1 inhibitor (DKI, 10 μM) for 1 h followed by lysis in a gentle buffer to solubilize non-synaptic protein. Lysates were processed by Western blot to detect GluN2B, pS1303, and DAPK1 levels. Data are normalized to WT DMSO values ( n = 8 biological replicates; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05; Student’s t -test, # p < 0.05). (B) Four-week-old YAC128 mice were treated intranasally with 50 nmol of DAPK1 inhibitor (DKI; TC-DAPK6) or vehicle control (VEH). After 6 h, cortical extrasynaptic fractions were isolated to measure GluN2B, pS1303, and DAPK1 levels ( n = 9 biological replicates, two technical replicates each; Student’s t -test, * p < 0.05). (C) Quantitative measurement of DAPK1-FLAG protein turnover using bio-orthogonal labeling, FLAG immunoprecipitation, CLICK chemistry, and detection of AHA/Streptavidin (Strep)-labeled DAPK1 in transiently transfected COS-7 cells treated with DMSO or 10 μM DKI (TC-DAPK6) for 24 h ( n = 3 for 8 h and 10 h chase time points, n = 7 for all other chase time points; two-way ANOVA ** p < 0.01 for DKI treatment effect; Sidak’s multiple comparisons test, ** p < 0.01).

Article Snippet: The DAPK1 inhibitor TC-DAPK6 (DKI; Tocris Bioscience; Cat# 4301) was dissolved in DMSO and used at a final concentration of 1 μM (0.01% DMSO).

Techniques: Inhibition, Phospho-proteomics, Lysis, Gentle, Western Blot, Control, Isolation, Labeling, Immunoprecipitation, Transfection

Journal: Frontiers in Cellular Neuroscience

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

doi: 10.3389/fncel.2020.590569

Figure Lengend Snippet: DAPK1 kinase activity promotes GluN2B surface expression via pS1303. (A) Surface expression (surface/internal YFP fluorescence ratio) and cluster analysis of transfected YFP-GluN2B was performed in 1:1 cortico-striatal co-cultured YAC128 medium spiny neurons (MSNs) treated with DMSO or the DAPK1 inhibitor TC-DAPK6 (DKI; 1 μM for 3 days, 0.01% final DMSO concentration). Absolute values were used for punctae analysis ( n = 24–38 cells from three independent cultures; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, *** p < 0.001). Scale bar = 5 μm. (B) Surface expression of GFP-GluN2B [WT or an S1303A (SA) mutant] in transfected COS-7 cells co-expressing GluN1 and either WT-DAPK1 or a kinase-dead DAPK1 mutant (K42A; KA; n = 23–30 cells from three independent culture passages; two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, *** p < 0.001). Scale bar = 15 μm.

Article Snippet: The DAPK1 inhibitor TC-DAPK6 (DKI; Tocris Bioscience; Cat# 4301) was dissolved in DMSO and used at a final concentration of 1 μM (0.01% DMSO).

Techniques: Activity Assay, Expressing, Fluorescence, Transfection, Cell Culture, Concentration Assay, Mutagenesis

Journal: Frontiers in Cellular Neuroscience

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

doi: 10.3389/fncel.2020.590569

Figure Lengend Snippet: DAPK1 inhibition or extrasynaptic NMDAR blockade prevents spine instability in YAC128 MSNs. (A) WT and YAC128 1:3 CS co-cultures were treated from DIV14 to 21 with DMSO (0.01%) or the DAPK1 inhibitor TC-DAPK6 (DKI, 1 μM), and spine analysis was performed on DARPP32+ MSNs. (B) 1:3 co-cultures were treated with either water, memantine (MEM, 3 μM) or (C) ifenprodil (IFEN, 3 μM) from DIV14 to 21 and processed in the same way as for DKI ( n = 24 cells from three independent cultures; Two-way ANOVA with Bonferroni post hoc analysis, * p < 0.05, ** p < 0.01, *** p < 0.001). Scale bar = 5 μm.

Article Snippet: The DAPK1 inhibitor TC-DAPK6 (DKI; Tocris Bioscience; Cat# 4301) was dissolved in DMSO and used at a final concentration of 1 μM (0.01% DMSO).

Techniques: Inhibition

Journal: Frontiers in Cellular Neuroscience

Article Title: DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

doi: 10.3389/fncel.2020.590569

Figure Lengend Snippet:

Article Snippet: The DAPK1 inhibitor TC-DAPK6 (DKI; Tocris Bioscience; Cat# 4301) was dissolved in DMSO and used at a final concentration of 1 μM (0.01% DMSO).

Techniques:

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dapk1 inhibitor tc dapk6 (Tocris)

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1) Product Images from "DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease"

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