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primary antibodies against cdk5  (Proteintech)


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    Structured Review

    Proteintech primary antibodies against cdk5
    Primary Antibodies Against Cdk5, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary antibodies against cdk5/product/Proteintech
    Average 93 stars, based on 33 article reviews
    primary antibodies against cdk5 - by Bioz Stars, 2026-03
    93/100 stars

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    Cyclin dependent kinase 5 <t>(Cdk5)</t> and p35 (CDK5R1) expression in colorectal cancer (CRC) cell lines. ( A ) Western blot analysis of Cdk5 and p35 basal expression in a panel of 10 CRC cell lines. Alpha-tubulin was used as endogenous control. ( B ) Representative western blot images showing the co-immunoprecipitation of Cdk5 and p35/p25 in the indicated cell lines. Co-immunoprecipitation with an immunoglobin G (IgG) antibody was used as a negative control. The results were obtained from at least three independent experiments.
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    Cyclin dependent kinase 5 <t>(Cdk5)</t> and p35 (CDK5R1) expression in colorectal cancer (CRC) cell lines. ( A ) Western blot analysis of Cdk5 and p35 basal expression in a panel of 10 CRC cell lines. Alpha-tubulin was used as endogenous control. ( B ) Representative western blot images showing the co-immunoprecipitation of Cdk5 and p35/p25 in the indicated cell lines. Co-immunoprecipitation with an immunoglobin G (IgG) antibody was used as a negative control. The results were obtained from at least three independent experiments.
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    Cyclin dependent kinase 5 <t>(Cdk5)</t> and p35 (CDK5R1) expression in colorectal cancer (CRC) cell lines. ( A ) Western blot analysis of Cdk5 and p35 basal expression in a panel of 10 CRC cell lines. Alpha-tubulin was used as endogenous control. ( B ) Representative western blot images showing the co-immunoprecipitation of Cdk5 and p35/p25 in the indicated cell lines. Co-immunoprecipitation with an immunoglobin G (IgG) antibody was used as a negative control. The results were obtained from at least three independent experiments.
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    Santa Cruz Biotechnology primary antibodies against phospho-cdk5 (tyr15)
    Dual effect of Sirt1 deficiency in adipose tissue during HFD. Short term vs . chronic effects. A, C : Intraperitoneal glucose tolerance tests (IP-GTT; 1 g/kg) and intraperitoneal insulin tolerance tests (IP-ITT; 0.6 U/kg) during short term HFD feeding (S, 5 wks; n = 10–12 per group) and chronic HFD feeding (C, 15 wks; n = 10–12 per group). B, D : Area under curve (AUC) and basal insulin levels from previous GTTs. Values are expressed as means ± SEM (*P ≤ 0.05, **P ≤ 0.01 and ***P ≤ 0.001 vs . WT at the same time point). E : Hyperinsulinemic-euglycemic clamp study in chronic HFD-fed mice (15 weeks). BW, Body weight. WT and ATKO matched body weights of mice during clamp studies. GIR, glucose infusion rate during hyperinsulinemic-euglycemic clamp. GDR, Glucose disposal rate. IS-GDR, insulin-stimulated glucose disposal rate. Basal-HGP, basal hepatic glucose production rate. HGP-Suppression, percent suppression of HGP. FFA, Free fatty acid suppression. Values are expressed as means ± SEM (*P ≤ 0.05 vs . WT; n = 5/6 mice per group). F : Western blot showing acute insulin-stimulated phosphorylation of AKT in liver, muscle and eWAT from chronic HFD-fed mice. Hsp90 expression was used as loading control. The western blot shown is representative of four independent experiments. G : Densitometry analysis and ratio of <t>phospho-Ser473-Akt/total</t> Akt from F . Values are expressed as means ± SEM (*P ≤ 0.05 **P ≤ 0.001 vs . WT basal. + P ≤ 0.05; ++ P ≤ 0.001 vs . ATKO basal).
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    Santa Cruz Biotechnology primary antibodies against cdk5 ptyr15
    Localization of <t>Cdk5-p</t> Tyr15 in the mouse striatum. (A) Photomontage of parasagittal brain sections stained for <t>Cdk5-pTyr15.</t> (B) Photomicrograph of a striatal section stained for Cdk5-pTyr15. Note that the matrix compartment is enriched in Cdk5-pTyr15 as compared to the striosomes. The asterisk indicates an example of striosomes poor in Cdk5-pTyr15 labeling. (C–C”) Double immunofluorescence staining for Cdk5-pTyr15 (C) and MOR (C') , and merged (C”) . A corresponding striosome is indicated by the asterisks. (D and E) Photomicrographs of striatal neurons immunoreactive for Cdk5-pTyr15. Cdk5-pTyr15 labeling is found in neuronal soma, processes, and nuclei of striatal neurons. Scale bars: (A) , 1 mm; (B) and (C–C”) , 500 μm; (D) , 20 μm; (E) , 5 μm.
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    Image Search Results


    Cyclin dependent kinase 5 (Cdk5) and p35 (CDK5R1) expression in colorectal cancer (CRC) cell lines. ( A ) Western blot analysis of Cdk5 and p35 basal expression in a panel of 10 CRC cell lines. Alpha-tubulin was used as endogenous control. ( B ) Representative western blot images showing the co-immunoprecipitation of Cdk5 and p35/p25 in the indicated cell lines. Co-immunoprecipitation with an immunoglobin G (IgG) antibody was used as a negative control. The results were obtained from at least three independent experiments.

    Journal: Cancers

    Article Title: Tumor Expression of Cyclin-Dependent Kinase 5 (Cdk5) Is a Prognostic Biomarker and Predicts Outcome of Oxaliplatin-Treated Metastatic Colorectal Cancer Patients

    doi: 10.3390/cancers11101540

    Figure Lengend Snippet: Cyclin dependent kinase 5 (Cdk5) and p35 (CDK5R1) expression in colorectal cancer (CRC) cell lines. ( A ) Western blot analysis of Cdk5 and p35 basal expression in a panel of 10 CRC cell lines. Alpha-tubulin was used as endogenous control. ( B ) Representative western blot images showing the co-immunoprecipitation of Cdk5 and p35/p25 in the indicated cell lines. Co-immunoprecipitation with an immunoglobin G (IgG) antibody was used as a negative control. The results were obtained from at least three independent experiments.

    Article Snippet: After blocking (LICOR Biosciences, Lincoln, NE, USA), membranes were incubated overnight with specific primary antibodies against Cdk5 (Cell Signaling, Danvers, MA, USA, #2506, 1:1000), p35 (Cell Signaling, Danvers, MA, USA, #2680, 1:300), and α-Tubulin (Sigma-Aldrich, St. Louis, MO, USA, #T6074, 1:20,000).

    Techniques: Expressing, Western Blot, Control, Immunoprecipitation, Negative Control

    Effect of Cyclin dependent kinase 5 (Cdk5) siRNA-mediated gene silencing on colorectal cancer (CRC) cells proliferation, migration and invasion. ( A ) Graphic representation of HT29, LoVo, DiFi, and HCT116 time-dependent cell proliferation after Cdk5 gene silencing measured by propidium iodide (PI). ( B , D ) Representative Boyden chamber migration and invasion assays images (4× magnification) and ( C , E ) bar graphs showing (mean ± SD) relative cell migration and invasion after Cdk5 silencing in the indicated cell lines. * p -value < 0.05 relative to control cells siRNA non-target control (siNTC). The results were obtained from at least three independent experiments.

    Journal: Cancers

    Article Title: Tumor Expression of Cyclin-Dependent Kinase 5 (Cdk5) Is a Prognostic Biomarker and Predicts Outcome of Oxaliplatin-Treated Metastatic Colorectal Cancer Patients

    doi: 10.3390/cancers11101540

    Figure Lengend Snippet: Effect of Cyclin dependent kinase 5 (Cdk5) siRNA-mediated gene silencing on colorectal cancer (CRC) cells proliferation, migration and invasion. ( A ) Graphic representation of HT29, LoVo, DiFi, and HCT116 time-dependent cell proliferation after Cdk5 gene silencing measured by propidium iodide (PI). ( B , D ) Representative Boyden chamber migration and invasion assays images (4× magnification) and ( C , E ) bar graphs showing (mean ± SD) relative cell migration and invasion after Cdk5 silencing in the indicated cell lines. * p -value < 0.05 relative to control cells siRNA non-target control (siNTC). The results were obtained from at least three independent experiments.

    Article Snippet: After blocking (LICOR Biosciences, Lincoln, NE, USA), membranes were incubated overnight with specific primary antibodies against Cdk5 (Cell Signaling, Danvers, MA, USA, #2506, 1:1000), p35 (Cell Signaling, Danvers, MA, USA, #2680, 1:300), and α-Tubulin (Sigma-Aldrich, St. Louis, MO, USA, #T6074, 1:20,000).

    Techniques: Migration, Control

    Overview of cohort used in the study.

    Journal: Cancers

    Article Title: Tumor Expression of Cyclin-Dependent Kinase 5 (Cdk5) Is a Prognostic Biomarker and Predicts Outcome of Oxaliplatin-Treated Metastatic Colorectal Cancer Patients

    doi: 10.3390/cancers11101540

    Figure Lengend Snippet: Overview of cohort used in the study.

    Article Snippet: After blocking (LICOR Biosciences, Lincoln, NE, USA), membranes were incubated overnight with specific primary antibodies against Cdk5 (Cell Signaling, Danvers, MA, USA, #2506, 1:1000), p35 (Cell Signaling, Danvers, MA, USA, #2680, 1:300), and α-Tubulin (Sigma-Aldrich, St. Louis, MO, USA, #T6074, 1:20,000).

    Techniques: In Silico, Microarray, Formalin-fixed Paraffin-Embedded, RNA Sequencing

    Cyclin dependent kinase (Cdk5) and p35 expression in colorectal cancer (CRC) tumor samples. Western blot ( A ) and graphic representation ( B , C ) of Cdk5 and p35 protein expression, respectively, in tumoral (T) and normal adjacent (N) tissues of 12 stage IV CRC patients (cohort A). Alpha-tubulin was used as endogenous control. The p -value was according to paired t -test. ( D ) Representative immunohistochemistry images of Cdk5 staining in CRC tumor tissues. The upper panel shows negative staining and lower panel positive staining. Scale bar: 100 μm. ( E ) Graphic representation of Cdk5 and p35 mRNA expression in 98-paired adjacent normal and tumoral tissues from stage II microsatellite stable (MSS) CRC patients (cohort B). ( F ) Graphic representation of Cdk5 mRNA expression in normal and tumoral tissues of 38 I-IV CRC patients. Data were obtained from The Cancer Genome Atlas (TCGA) database (cohort F). ( G ) Graph representing the Cdk5 copy number (CNV) change between normal and tumoral tissues in 67 stage I–IV CRC patients (cohort F). ( H ) Correlation between Cdk5 CNV and Cdk5 gene expression in 429 stage I–IV CRC patients. p-value according to Pearson correlation test (cohort F). ( I ) Correlation between Cdk5 CNV and Cdk5 gene expression in 63 CRC cell lines. The p -value was according to Pearson correlation test. Data from the Broad Institute Cancer Cell Line Encyclopedia.

    Journal: Cancers

    Article Title: Tumor Expression of Cyclin-Dependent Kinase 5 (Cdk5) Is a Prognostic Biomarker and Predicts Outcome of Oxaliplatin-Treated Metastatic Colorectal Cancer Patients

    doi: 10.3390/cancers11101540

    Figure Lengend Snippet: Cyclin dependent kinase (Cdk5) and p35 expression in colorectal cancer (CRC) tumor samples. Western blot ( A ) and graphic representation ( B , C ) of Cdk5 and p35 protein expression, respectively, in tumoral (T) and normal adjacent (N) tissues of 12 stage IV CRC patients (cohort A). Alpha-tubulin was used as endogenous control. The p -value was according to paired t -test. ( D ) Representative immunohistochemistry images of Cdk5 staining in CRC tumor tissues. The upper panel shows negative staining and lower panel positive staining. Scale bar: 100 μm. ( E ) Graphic representation of Cdk5 and p35 mRNA expression in 98-paired adjacent normal and tumoral tissues from stage II microsatellite stable (MSS) CRC patients (cohort B). ( F ) Graphic representation of Cdk5 mRNA expression in normal and tumoral tissues of 38 I-IV CRC patients. Data were obtained from The Cancer Genome Atlas (TCGA) database (cohort F). ( G ) Graph representing the Cdk5 copy number (CNV) change between normal and tumoral tissues in 67 stage I–IV CRC patients (cohort F). ( H ) Correlation between Cdk5 CNV and Cdk5 gene expression in 429 stage I–IV CRC patients. p-value according to Pearson correlation test (cohort F). ( I ) Correlation between Cdk5 CNV and Cdk5 gene expression in 63 CRC cell lines. The p -value was according to Pearson correlation test. Data from the Broad Institute Cancer Cell Line Encyclopedia.

    Article Snippet: After blocking (LICOR Biosciences, Lincoln, NE, USA), membranes were incubated overnight with specific primary antibodies against Cdk5 (Cell Signaling, Danvers, MA, USA, #2506, 1:1000), p35 (Cell Signaling, Danvers, MA, USA, #2680, 1:300), and α-Tubulin (Sigma-Aldrich, St. Louis, MO, USA, #T6074, 1:20,000).

    Techniques: Expressing, Western Blot, Control, Immunohistochemistry, Staining, Negative Staining, Gene Expression

    Kaplan–Meyer analysis of disease free survival (DFS) and time to progression (TTP) depending on Cyclin dependent kinase (Cdk5) levels. ( A ) DFS in 98 stage II colorectal cancer (CRC) patients split by the median of Cdk5 expression (cohort B). ( B ) DFS in 37 non-treated stage III CRC patients split by the median of Cdk5 expression (cohort C). ( C ) TTP in 52 stage IV oxaliplatin-treated patients, grouped depending on negative ( n = 18) or positive Cdk5 ( n = 34) immunohistochemistry (IHC) staining (cohort D). ( D ) TTP in 139 stage IV irinotecan-treated patients grouped depending on negative ( n = 73) and positive ( n = 66) Cdk5 IHC staining (cohort E).

    Journal: Cancers

    Article Title: Tumor Expression of Cyclin-Dependent Kinase 5 (Cdk5) Is a Prognostic Biomarker and Predicts Outcome of Oxaliplatin-Treated Metastatic Colorectal Cancer Patients

    doi: 10.3390/cancers11101540

    Figure Lengend Snippet: Kaplan–Meyer analysis of disease free survival (DFS) and time to progression (TTP) depending on Cyclin dependent kinase (Cdk5) levels. ( A ) DFS in 98 stage II colorectal cancer (CRC) patients split by the median of Cdk5 expression (cohort B). ( B ) DFS in 37 non-treated stage III CRC patients split by the median of Cdk5 expression (cohort C). ( C ) TTP in 52 stage IV oxaliplatin-treated patients, grouped depending on negative ( n = 18) or positive Cdk5 ( n = 34) immunohistochemistry (IHC) staining (cohort D). ( D ) TTP in 139 stage IV irinotecan-treated patients grouped depending on negative ( n = 73) and positive ( n = 66) Cdk5 IHC staining (cohort E).

    Article Snippet: After blocking (LICOR Biosciences, Lincoln, NE, USA), membranes were incubated overnight with specific primary antibodies against Cdk5 (Cell Signaling, Danvers, MA, USA, #2506, 1:1000), p35 (Cell Signaling, Danvers, MA, USA, #2680, 1:300), and α-Tubulin (Sigma-Aldrich, St. Louis, MO, USA, #T6074, 1:20,000).

    Techniques: Expressing, Immunohistochemistry

    Kaplan–Meyer analysis of disease free survival (DFS) depending on Cyclin dependent kinase (Cdk5) expression and Kirsten rat sarcoma oncogene ( KRAS) mutational status. ( A ) DFS for 72 stage II colorectal cancer (CRC) patients with wildtype (WT) KRAS and split by the median of Cdk5 expression. ( B ) DFS for 26 stage II CRC patients with mutated KRAS and split by the median of Cdk5 expression (cohort B).

    Journal: Cancers

    Article Title: Tumor Expression of Cyclin-Dependent Kinase 5 (Cdk5) Is a Prognostic Biomarker and Predicts Outcome of Oxaliplatin-Treated Metastatic Colorectal Cancer Patients

    doi: 10.3390/cancers11101540

    Figure Lengend Snippet: Kaplan–Meyer analysis of disease free survival (DFS) depending on Cyclin dependent kinase (Cdk5) expression and Kirsten rat sarcoma oncogene ( KRAS) mutational status. ( A ) DFS for 72 stage II colorectal cancer (CRC) patients with wildtype (WT) KRAS and split by the median of Cdk5 expression. ( B ) DFS for 26 stage II CRC patients with mutated KRAS and split by the median of Cdk5 expression (cohort B).

    Article Snippet: After blocking (LICOR Biosciences, Lincoln, NE, USA), membranes were incubated overnight with specific primary antibodies against Cdk5 (Cell Signaling, Danvers, MA, USA, #2506, 1:1000), p35 (Cell Signaling, Danvers, MA, USA, #2680, 1:300), and α-Tubulin (Sigma-Aldrich, St. Louis, MO, USA, #T6074, 1:20,000).

    Techniques: Expressing

    Cyclin dependent kinase 5 (Cdk5) expression in the four consensus molecular subtypes (CMS). ( A ) Dunn and Kruskal–Wallis multiple comparison of Cdk5 expression in CMS in 98 stage II tumors. Note that only six cases were classified as CMS1 as this cohort was restricted to microsatellite stabile (MSS) cases ( B ) ANOVA analysis of Cdk5 expression levels in the CMS in the cancer genome atlas - colorectal adenocarsinoma - rectal adenocarcinoma dataset (TCGA-COAD-READ) including 410 stage I–IV patients. * p -value < 0.05, ** p -value < 0.01, *** p -value < 0.001. ( C ) PFI in the TCGA-COAD CMS1 subgroup including 78 stage I–IV patients; patients were split according to the median of Cdk5 expression (cohort F).

    Journal: Cancers

    Article Title: Tumor Expression of Cyclin-Dependent Kinase 5 (Cdk5) Is a Prognostic Biomarker and Predicts Outcome of Oxaliplatin-Treated Metastatic Colorectal Cancer Patients

    doi: 10.3390/cancers11101540

    Figure Lengend Snippet: Cyclin dependent kinase 5 (Cdk5) expression in the four consensus molecular subtypes (CMS). ( A ) Dunn and Kruskal–Wallis multiple comparison of Cdk5 expression in CMS in 98 stage II tumors. Note that only six cases were classified as CMS1 as this cohort was restricted to microsatellite stabile (MSS) cases ( B ) ANOVA analysis of Cdk5 expression levels in the CMS in the cancer genome atlas - colorectal adenocarsinoma - rectal adenocarcinoma dataset (TCGA-COAD-READ) including 410 stage I–IV patients. * p -value < 0.05, ** p -value < 0.01, *** p -value < 0.001. ( C ) PFI in the TCGA-COAD CMS1 subgroup including 78 stage I–IV patients; patients were split according to the median of Cdk5 expression (cohort F).

    Article Snippet: After blocking (LICOR Biosciences, Lincoln, NE, USA), membranes were incubated overnight with specific primary antibodies against Cdk5 (Cell Signaling, Danvers, MA, USA, #2506, 1:1000), p35 (Cell Signaling, Danvers, MA, USA, #2680, 1:300), and α-Tubulin (Sigma-Aldrich, St. Louis, MO, USA, #T6074, 1:20,000).

    Techniques: Expressing, Comparison

    Dual effect of Sirt1 deficiency in adipose tissue during HFD. Short term vs . chronic effects. A, C : Intraperitoneal glucose tolerance tests (IP-GTT; 1 g/kg) and intraperitoneal insulin tolerance tests (IP-ITT; 0.6 U/kg) during short term HFD feeding (S, 5 wks; n = 10–12 per group) and chronic HFD feeding (C, 15 wks; n = 10–12 per group). B, D : Area under curve (AUC) and basal insulin levels from previous GTTs. Values are expressed as means ± SEM (*P ≤ 0.05, **P ≤ 0.01 and ***P ≤ 0.001 vs . WT at the same time point). E : Hyperinsulinemic-euglycemic clamp study in chronic HFD-fed mice (15 weeks). BW, Body weight. WT and ATKO matched body weights of mice during clamp studies. GIR, glucose infusion rate during hyperinsulinemic-euglycemic clamp. GDR, Glucose disposal rate. IS-GDR, insulin-stimulated glucose disposal rate. Basal-HGP, basal hepatic glucose production rate. HGP-Suppression, percent suppression of HGP. FFA, Free fatty acid suppression. Values are expressed as means ± SEM (*P ≤ 0.05 vs . WT; n = 5/6 mice per group). F : Western blot showing acute insulin-stimulated phosphorylation of AKT in liver, muscle and eWAT from chronic HFD-fed mice. Hsp90 expression was used as loading control. The western blot shown is representative of four independent experiments. G : Densitometry analysis and ratio of phospho-Ser473-Akt/total Akt from F . Values are expressed as means ± SEM (*P ≤ 0.05 **P ≤ 0.001 vs . WT basal. + P ≤ 0.05; ++ P ≤ 0.001 vs . ATKO basal).

    Journal: Molecular Metabolism

    Article Title: Adipocyte SIRT1 knockout promotes PPAR γ activity, adipogenesis and insulin sensitivity in chronic-HFD and obesity

    doi: 10.1016/j.molmet.2015.02.007

    Figure Lengend Snippet: Dual effect of Sirt1 deficiency in adipose tissue during HFD. Short term vs . chronic effects. A, C : Intraperitoneal glucose tolerance tests (IP-GTT; 1 g/kg) and intraperitoneal insulin tolerance tests (IP-ITT; 0.6 U/kg) during short term HFD feeding (S, 5 wks; n = 10–12 per group) and chronic HFD feeding (C, 15 wks; n = 10–12 per group). B, D : Area under curve (AUC) and basal insulin levels from previous GTTs. Values are expressed as means ± SEM (*P ≤ 0.05, **P ≤ 0.01 and ***P ≤ 0.001 vs . WT at the same time point). E : Hyperinsulinemic-euglycemic clamp study in chronic HFD-fed mice (15 weeks). BW, Body weight. WT and ATKO matched body weights of mice during clamp studies. GIR, glucose infusion rate during hyperinsulinemic-euglycemic clamp. GDR, Glucose disposal rate. IS-GDR, insulin-stimulated glucose disposal rate. Basal-HGP, basal hepatic glucose production rate. HGP-Suppression, percent suppression of HGP. FFA, Free fatty acid suppression. Values are expressed as means ± SEM (*P ≤ 0.05 vs . WT; n = 5/6 mice per group). F : Western blot showing acute insulin-stimulated phosphorylation of AKT in liver, muscle and eWAT from chronic HFD-fed mice. Hsp90 expression was used as loading control. The western blot shown is representative of four independent experiments. G : Densitometry analysis and ratio of phospho-Ser473-Akt/total Akt from F . Values are expressed as means ± SEM (*P ≤ 0.05 **P ≤ 0.001 vs . WT basal. + P ≤ 0.05; ++ P ≤ 0.001 vs . ATKO basal).

    Article Snippet: Proteins from total tissue lysates were prepared as previously described , separated by SDS-PAGE and probed with different primary antibodies against Sirt1, Anti-phospho-Akt (Ser473), total Akt, PPARγ, phospho-CDK5 (Tyr15), CDK5, and Hsp90α/β (Santa Cruz); Acetyl (Lys379) p53, p53 and NF-κB p65 (Cell Signalling); Acetyl (Lys310) NF-κB p65 and FGF21 (Abcam); Anti-phospho- PPARγ (Ser 273) was a kind gift from Dr. Bruce Spiegelman.

    Techniques: Western Blot, Phospho-proteomics, Expressing, Control

    Localization of Cdk5-p Tyr15 in the mouse striatum. (A) Photomontage of parasagittal brain sections stained for Cdk5-pTyr15. (B) Photomicrograph of a striatal section stained for Cdk5-pTyr15. Note that the matrix compartment is enriched in Cdk5-pTyr15 as compared to the striosomes. The asterisk indicates an example of striosomes poor in Cdk5-pTyr15 labeling. (C–C”) Double immunofluorescence staining for Cdk5-pTyr15 (C) and MOR (C') , and merged (C”) . A corresponding striosome is indicated by the asterisks. (D and E) Photomicrographs of striatal neurons immunoreactive for Cdk5-pTyr15. Cdk5-pTyr15 labeling is found in neuronal soma, processes, and nuclei of striatal neurons. Scale bars: (A) , 1 mm; (B) and (C–C”) , 500 μm; (D) , 20 μm; (E) , 5 μm.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Dopamine signaling negatively regulates striatal phosphorylation of Cdk5 at tyrosine 15 in mice

    doi: 10.3389/fncel.2013.00012

    Figure Lengend Snippet: Localization of Cdk5-p Tyr15 in the mouse striatum. (A) Photomontage of parasagittal brain sections stained for Cdk5-pTyr15. (B) Photomicrograph of a striatal section stained for Cdk5-pTyr15. Note that the matrix compartment is enriched in Cdk5-pTyr15 as compared to the striosomes. The asterisk indicates an example of striosomes poor in Cdk5-pTyr15 labeling. (C–C”) Double immunofluorescence staining for Cdk5-pTyr15 (C) and MOR (C') , and merged (C”) . A corresponding striosome is indicated by the asterisks. (D and E) Photomicrographs of striatal neurons immunoreactive for Cdk5-pTyr15. Cdk5-pTyr15 labeling is found in neuronal soma, processes, and nuclei of striatal neurons. Scale bars: (A) , 1 mm; (B) and (C–C”) , 500 μm; (D) , 20 μm; (E) , 5 μm.

    Article Snippet: Primary antibodies against Cdk5-pTyr15 (1:20,000; Santa Cruz), tyrosine hydroxylase (TH, 1:100,000) (Sato et al., ), and DARPP-32-Thr75 (1:20,000; Cell Signaling) (Sako et al., ) were used.

    Techniques: Staining, Labeling, Double Immunofluorescence Staining

    Dopamine receptor stimulation inhibits striatal phosphorylation of Cdk5 at Tyr15. (A) Western blot analysis on the effects of apomorphine on striatal levels of Cdk5-pTyr15. Mice received saline or the indicated amounts of apomorphine 30 min before sacrifice. Values are means ± S.E.M. ( n = 5). * P < 0.005 versus saline-treated mice; two tailed Student's t -test. (B–D) Immunohistochemical assessment of the effects of apomorphine on striatal density of Cdk5-pTyr15 labeling. (B–B”) Frontal sections stained for Cdk5-pTyr15 in the anterior ( B ; 1.3 mm anterior to bregma), middle ( B' ; 1.0 mm anterior to bregma), and posterior ( B” ; 0.1 mm posterior to bregma) levels of the striatum from a saline-treated mouse. (C–C”) Frontal sections stained for Cdk5-pTyr15 in the rostral ( C ; 1.3 mm anterior to bregma), middle ( C' ; 1.0 mm anterior to bregma), and caudal ( C” ; 0.1 mm posterior to bregma) levels of the striatum from an apomorphine-treated mouse. (D) Optical density measurements of striatal Cdk5-pTyr15 labeling in saline- and apomorphine-treated mice. Values are means ± S.E.M. ( n = 5). * P < 0.005 versus saline-treated mice; two-tailed Student's t -test.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Dopamine signaling negatively regulates striatal phosphorylation of Cdk5 at tyrosine 15 in mice

    doi: 10.3389/fncel.2013.00012

    Figure Lengend Snippet: Dopamine receptor stimulation inhibits striatal phosphorylation of Cdk5 at Tyr15. (A) Western blot analysis on the effects of apomorphine on striatal levels of Cdk5-pTyr15. Mice received saline or the indicated amounts of apomorphine 30 min before sacrifice. Values are means ± S.E.M. ( n = 5). * P < 0.005 versus saline-treated mice; two tailed Student's t -test. (B–D) Immunohistochemical assessment of the effects of apomorphine on striatal density of Cdk5-pTyr15 labeling. (B–B”) Frontal sections stained for Cdk5-pTyr15 in the anterior ( B ; 1.3 mm anterior to bregma), middle ( B' ; 1.0 mm anterior to bregma), and posterior ( B” ; 0.1 mm posterior to bregma) levels of the striatum from a saline-treated mouse. (C–C”) Frontal sections stained for Cdk5-pTyr15 in the rostral ( C ; 1.3 mm anterior to bregma), middle ( C' ; 1.0 mm anterior to bregma), and caudal ( C” ; 0.1 mm posterior to bregma) levels of the striatum from an apomorphine-treated mouse. (D) Optical density measurements of striatal Cdk5-pTyr15 labeling in saline- and apomorphine-treated mice. Values are means ± S.E.M. ( n = 5). * P < 0.005 versus saline-treated mice; two-tailed Student's t -test.

    Article Snippet: Primary antibodies against Cdk5-pTyr15 (1:20,000; Santa Cruz), tyrosine hydroxylase (TH, 1:100,000) (Sato et al., ), and DARPP-32-Thr75 (1:20,000; Cell Signaling) (Sako et al., ) were used.

    Techniques: Phospho-proteomics, Western Blot, Saline, Two Tailed Test, Immunohistochemical staining, Labeling, Staining

    Negative regulation of striatal phosphorylation of Tyr15-Cdk5 through a D2R-mediated mechanism. Western blot analysis was carried out on the striatal extracts from mice that received saline, A-68930 (2 mg/kg), SCH-23390 (0.5 mg/kg), quinpirole (5 mg/kg), or raclopride (1 mg/kg), 30 min before sacrifice. Effects of administration of A-68930 (A) , SCH-23390 (B) , quinpirole (C) , or raclopride (D), on striatal levels of Cdk5-pTyr15 are shown. Values are means ± S.E.M. ( n = 5). * P < 0.005 versus saline-treated mice; two tailed Student's t -test.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Dopamine signaling negatively regulates striatal phosphorylation of Cdk5 at tyrosine 15 in mice

    doi: 10.3389/fncel.2013.00012

    Figure Lengend Snippet: Negative regulation of striatal phosphorylation of Tyr15-Cdk5 through a D2R-mediated mechanism. Western blot analysis was carried out on the striatal extracts from mice that received saline, A-68930 (2 mg/kg), SCH-23390 (0.5 mg/kg), quinpirole (5 mg/kg), or raclopride (1 mg/kg), 30 min before sacrifice. Effects of administration of A-68930 (A) , SCH-23390 (B) , quinpirole (C) , or raclopride (D), on striatal levels of Cdk5-pTyr15 are shown. Values are means ± S.E.M. ( n = 5). * P < 0.005 versus saline-treated mice; two tailed Student's t -test.

    Article Snippet: Primary antibodies against Cdk5-pTyr15 (1:20,000; Santa Cruz), tyrosine hydroxylase (TH, 1:100,000) (Sato et al., ), and DARPP-32-Thr75 (1:20,000; Cell Signaling) (Sako et al., ) were used.

    Techniques: Phospho-proteomics, Western Blot, Saline, Two Tailed Test

    Loss of dopaminergic inputs and increased phosphorylation of Tyr15-Cdk5 in the striatum in MPTP mice. Striatal sections were prepared and subjected to the immunohistochemical study (see “Materials and Methods”). (A–C) Severe loss of TH-immunoreactive afferents in the striatum in MPTP mice. Representative images of striatal sections (0.0–1.0 mm anterior to bregma) immunostained for TH from saline- (A) and MPTP-treated (B) mice. (C) Optical density measurements of striatal TH labeling in saline- and MPTP-treated mice. Values are means ± S.E.M. ( n = 5). * P < 0.001 versus saline-treated mice, two tailed Student's t -test. (D–F) Increased density of striatal Cdk5-pTyr15 labeling in MPTP mice. Representative images of striatal sections (0.0–1.0 mm anterior to bregma) immunostained for Cdk5-pTyr15 from saline- (D) and MPTP-treated (E) mice. (F) Optical density measurements of striatal Cdk5-pTyr15 labeling in saline- and MPTP-treated mice. Values are mean ± S.E.M. ( n = 5). * P < 0.01 versus saline-treated mice, two tailed Student's t -test.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Dopamine signaling negatively regulates striatal phosphorylation of Cdk5 at tyrosine 15 in mice

    doi: 10.3389/fncel.2013.00012

    Figure Lengend Snippet: Loss of dopaminergic inputs and increased phosphorylation of Tyr15-Cdk5 in the striatum in MPTP mice. Striatal sections were prepared and subjected to the immunohistochemical study (see “Materials and Methods”). (A–C) Severe loss of TH-immunoreactive afferents in the striatum in MPTP mice. Representative images of striatal sections (0.0–1.0 mm anterior to bregma) immunostained for TH from saline- (A) and MPTP-treated (B) mice. (C) Optical density measurements of striatal TH labeling in saline- and MPTP-treated mice. Values are means ± S.E.M. ( n = 5). * P < 0.001 versus saline-treated mice, two tailed Student's t -test. (D–F) Increased density of striatal Cdk5-pTyr15 labeling in MPTP mice. Representative images of striatal sections (0.0–1.0 mm anterior to bregma) immunostained for Cdk5-pTyr15 from saline- (D) and MPTP-treated (E) mice. (F) Optical density measurements of striatal Cdk5-pTyr15 labeling in saline- and MPTP-treated mice. Values are mean ± S.E.M. ( n = 5). * P < 0.01 versus saline-treated mice, two tailed Student's t -test.

    Article Snippet: Primary antibodies against Cdk5-pTyr15 (1:20,000; Santa Cruz), tyrosine hydroxylase (TH, 1:100,000) (Sato et al., ), and DARPP-32-Thr75 (1:20,000; Cell Signaling) (Sako et al., ) were used.

    Techniques: Phospho-proteomics, Immunohistochemical staining, Saline, Labeling, Two Tailed Test

    Effects of L-dopa on striatal phosphorylation of Cdk5 and DARPP-32 in MPTP mice. Saline- or MPTP-treated mice received vehicle or L-dopa 30 min before sacrifice. Striatal tissue extracts and sections were prepared and subjected to western blotting and immunohistochemical staining (see “Materials and Methods”). (A) Western blot analysis of striatal levels of Cdk5-pTyr15 and Cdk5 in mice treated with saline + vehicle, saline + L-dopa, MPTP + vehicle, or MPTP + L-dopa. Values are means ± S.E.M. ( n = 5–6). * P < 0.001 versus mice treated with saline + vehicle, saline + L-dopa, or MPTP + L-dopa; One-Way ANOVA [ F (3.18) = 31.06] followed by Bonferroni–Dunn test. (B) Immunohistochemical study on striatal labeling for Cdk5-pTyr15 in mice treated with saline + vehicle, saline + L-dopa, MPTP + vehicle, or MPTP + L-dopa. Representative images of the striatal sections (0.0–1.0 mm anterior to bregma) stained for Cdk5-pTyr15 from each group are shown. Densitometric analysis was made on a striatal section from each mouse in a group of saline + vehicle, saline + L-dopa, MPTP + vehicle or MPTP + L-dopa. Values are means ± S.E.M. ( n = 5). * P < 0.005 versus mice treated with saline + vehicle, saline + L-dopa, or MPTP + L-dopa; One-Way ANOVA [ F (3.16) = 26.84] followed by Fisher's PLSD test. (C) Western blot analysis of striatal levels of DARPP-32-pThr75, DARPP-32-pThr34, and DARPP-32 in mice treated with saline + vehicle, saline + L-dopa, MPTP + vehicle, or MPTP + L-dopa. Values are means ± S.E.M. ( n = 4–7). * P < 0.01 versus mice treated with saline + vehicle, saline + L-dopa, or MPTP + L-dopa; One-Way ANOVA [ F (3.18) = 6.96] followed by Bonferroni–Dunn test. (D) Immunohistochemical study on striatal labeling for DARPP-32-pThr75 in mice treated with saline + vehicle ( n = 5), saline + L-dopa ( n = 5), MPTP + vehicle ( n = 5), or MPTP + L-dopa ( n = 5). Representative images of the striatal sections (0.0–1.0 mm anterior to bregma) stained for DARPP-32-pThr75 from each group are shown. Densitometric analyses were made on a striatal section from each mouse in a group of saline + vehicle, saline + L-dopa, MPTP + vehicle or MPTP + L-dopa. Values are means ± S.E.M ( n = 5). * P < 0.005 versus mice treated with saline + vehicle, saline + L-dopa, or MPTP + L-dopa; One-Way ANOVA [ F (3.16) = 19.62] followed by Fisher's PLSD test.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Dopamine signaling negatively regulates striatal phosphorylation of Cdk5 at tyrosine 15 in mice

    doi: 10.3389/fncel.2013.00012

    Figure Lengend Snippet: Effects of L-dopa on striatal phosphorylation of Cdk5 and DARPP-32 in MPTP mice. Saline- or MPTP-treated mice received vehicle or L-dopa 30 min before sacrifice. Striatal tissue extracts and sections were prepared and subjected to western blotting and immunohistochemical staining (see “Materials and Methods”). (A) Western blot analysis of striatal levels of Cdk5-pTyr15 and Cdk5 in mice treated with saline + vehicle, saline + L-dopa, MPTP + vehicle, or MPTP + L-dopa. Values are means ± S.E.M. ( n = 5–6). * P < 0.001 versus mice treated with saline + vehicle, saline + L-dopa, or MPTP + L-dopa; One-Way ANOVA [ F (3.18) = 31.06] followed by Bonferroni–Dunn test. (B) Immunohistochemical study on striatal labeling for Cdk5-pTyr15 in mice treated with saline + vehicle, saline + L-dopa, MPTP + vehicle, or MPTP + L-dopa. Representative images of the striatal sections (0.0–1.0 mm anterior to bregma) stained for Cdk5-pTyr15 from each group are shown. Densitometric analysis was made on a striatal section from each mouse in a group of saline + vehicle, saline + L-dopa, MPTP + vehicle or MPTP + L-dopa. Values are means ± S.E.M. ( n = 5). * P < 0.005 versus mice treated with saline + vehicle, saline + L-dopa, or MPTP + L-dopa; One-Way ANOVA [ F (3.16) = 26.84] followed by Fisher's PLSD test. (C) Western blot analysis of striatal levels of DARPP-32-pThr75, DARPP-32-pThr34, and DARPP-32 in mice treated with saline + vehicle, saline + L-dopa, MPTP + vehicle, or MPTP + L-dopa. Values are means ± S.E.M. ( n = 4–7). * P < 0.01 versus mice treated with saline + vehicle, saline + L-dopa, or MPTP + L-dopa; One-Way ANOVA [ F (3.18) = 6.96] followed by Bonferroni–Dunn test. (D) Immunohistochemical study on striatal labeling for DARPP-32-pThr75 in mice treated with saline + vehicle ( n = 5), saline + L-dopa ( n = 5), MPTP + vehicle ( n = 5), or MPTP + L-dopa ( n = 5). Representative images of the striatal sections (0.0–1.0 mm anterior to bregma) stained for DARPP-32-pThr75 from each group are shown. Densitometric analyses were made on a striatal section from each mouse in a group of saline + vehicle, saline + L-dopa, MPTP + vehicle or MPTP + L-dopa. Values are means ± S.E.M ( n = 5). * P < 0.005 versus mice treated with saline + vehicle, saline + L-dopa, or MPTP + L-dopa; One-Way ANOVA [ F (3.16) = 19.62] followed by Fisher's PLSD test.

    Article Snippet: Primary antibodies against Cdk5-pTyr15 (1:20,000; Santa Cruz), tyrosine hydroxylase (TH, 1:100,000) (Sato et al., ), and DARPP-32-Thr75 (1:20,000; Cell Signaling) (Sako et al., ) were used.

    Techniques: Phospho-proteomics, Saline, Western Blot, Immunohistochemical staining, Staining, Labeling

    Effects of imatinib on striatal phosphorylation of Cdk5 and DARPP-32 in MPTP mice. Saline- or MPTP-treated received vehicle or imatinib 30 min before sacrifice. Striatal tissue extracts and sections were prepared and subjected to western blotting and immunohistochemical staining (see “Materials and Methods”). (A) Western blot analysis of striatal levels of Cdk5-pTyr15 and Cdk5 in mice treated with saline + vehicle, saline + imatinib, MPTP + vehicle, or MPTP + imatinib. Values are mean ± S.E.M. ( n = 4–5). * P < 0.05 versus mice treated with saline + vehicle, saline + imatinib, or MPTP + imatinib; One-Way ANOVA [ F (3.14) = 9.28] followed by Bonferroni–Dunn test. (B) Immunohistochemical study on striatal labeling for Cdk5-pTyr15 in mice treated with saline + vehicle, saline + imatinib, MPTP + vehicle or MPTP + imatinib. Representative images of the striatal sections (0.0–1.0 mm anterior to bregma) stained for Cdk5-pTyr15 from each group are shown. Densitometric analyses were made on a striatal section from each mouse in a group of saline + vehicle, saline + imatinib, MPTP + vehicle or MPTP + imatinib. Values are means ± S.E.M. ( n = 5). * P < 0.01 versus mice treated with saline + vehicle, saline + imatinib, or MPTP + imatinib; One-Way ANOVA [ F (3.16) = 9.82] followed by Fisher's PLSD test. (C) Western blot analysis of striatal levels of DARPP-32-pThr75, DARPP-32-pThr34, and total DARPP-32 in mice treated with saline + vehicle, saline + imatinib, MPTP + vehicle, or MPTP + imatinib. Values are means ± S.E.M. ( n = 4–5). * P < 0.05 versus mice treated with saline + vehicle, saline + imatinib, or MPTP + imatinib; One-Way ANOVA [ F (3.13) = 4.13] followed by Bonferroni–Dunn test. (D) Immunohistochemical study on striatal labeling for DARPP-32-pThr75 in mice treated with saline + vehicle, saline + imatinib, MPTP + vehicle or MPTP + imatinib. Representative images of the striatal sections (0.0–1.0 mm anterior to bregma) stained for DARPP-32-pThr75 from each group are shown. Densitometric analyses were made on a striatal section from each mouse in a group of saline + vehicle, saline + imatinib, MPTP + vehicle or MPTP + imatinib. Values are means ± S.E.M. ( n = 5). * P < 0.05 versus mice treated with saline + vehicle, saline + imatinib, or MPTP + imatinib; One-Way ANOVA [ F (3.16) = 5.12] followed by Fisher's PLSD test.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Dopamine signaling negatively regulates striatal phosphorylation of Cdk5 at tyrosine 15 in mice

    doi: 10.3389/fncel.2013.00012

    Figure Lengend Snippet: Effects of imatinib on striatal phosphorylation of Cdk5 and DARPP-32 in MPTP mice. Saline- or MPTP-treated received vehicle or imatinib 30 min before sacrifice. Striatal tissue extracts and sections were prepared and subjected to western blotting and immunohistochemical staining (see “Materials and Methods”). (A) Western blot analysis of striatal levels of Cdk5-pTyr15 and Cdk5 in mice treated with saline + vehicle, saline + imatinib, MPTP + vehicle, or MPTP + imatinib. Values are mean ± S.E.M. ( n = 4–5). * P < 0.05 versus mice treated with saline + vehicle, saline + imatinib, or MPTP + imatinib; One-Way ANOVA [ F (3.14) = 9.28] followed by Bonferroni–Dunn test. (B) Immunohistochemical study on striatal labeling for Cdk5-pTyr15 in mice treated with saline + vehicle, saline + imatinib, MPTP + vehicle or MPTP + imatinib. Representative images of the striatal sections (0.0–1.0 mm anterior to bregma) stained for Cdk5-pTyr15 from each group are shown. Densitometric analyses were made on a striatal section from each mouse in a group of saline + vehicle, saline + imatinib, MPTP + vehicle or MPTP + imatinib. Values are means ± S.E.M. ( n = 5). * P < 0.01 versus mice treated with saline + vehicle, saline + imatinib, or MPTP + imatinib; One-Way ANOVA [ F (3.16) = 9.82] followed by Fisher's PLSD test. (C) Western blot analysis of striatal levels of DARPP-32-pThr75, DARPP-32-pThr34, and total DARPP-32 in mice treated with saline + vehicle, saline + imatinib, MPTP + vehicle, or MPTP + imatinib. Values are means ± S.E.M. ( n = 4–5). * P < 0.05 versus mice treated with saline + vehicle, saline + imatinib, or MPTP + imatinib; One-Way ANOVA [ F (3.13) = 4.13] followed by Bonferroni–Dunn test. (D) Immunohistochemical study on striatal labeling for DARPP-32-pThr75 in mice treated with saline + vehicle, saline + imatinib, MPTP + vehicle or MPTP + imatinib. Representative images of the striatal sections (0.0–1.0 mm anterior to bregma) stained for DARPP-32-pThr75 from each group are shown. Densitometric analyses were made on a striatal section from each mouse in a group of saline + vehicle, saline + imatinib, MPTP + vehicle or MPTP + imatinib. Values are means ± S.E.M. ( n = 5). * P < 0.05 versus mice treated with saline + vehicle, saline + imatinib, or MPTP + imatinib; One-Way ANOVA [ F (3.16) = 5.12] followed by Fisher's PLSD test.

    Article Snippet: Primary antibodies against Cdk5-pTyr15 (1:20,000; Santa Cruz), tyrosine hydroxylase (TH, 1:100,000) (Sato et al., ), and DARPP-32-Thr75 (1:20,000; Cell Signaling) (Sako et al., ) were used.

    Techniques: Phospho-proteomics, Saline, Western Blot, Immunohistochemical staining, Staining, Labeling

    Hypothesized model of striatal Cdk5/DARPP-32 signal regulations. Depicted are postsynaptic dopamine/PKA/Thr34-DARPP-32 and glutamate/Cdk5/Thr75-DARPP-32 signaling cascades. c-Abl is the known kinase to phosphorylate Cdk5 at Tyr15.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Dopamine signaling negatively regulates striatal phosphorylation of Cdk5 at tyrosine 15 in mice

    doi: 10.3389/fncel.2013.00012

    Figure Lengend Snippet: Hypothesized model of striatal Cdk5/DARPP-32 signal regulations. Depicted are postsynaptic dopamine/PKA/Thr34-DARPP-32 and glutamate/Cdk5/Thr75-DARPP-32 signaling cascades. c-Abl is the known kinase to phosphorylate Cdk5 at Tyr15.

    Article Snippet: Primary antibodies against Cdk5-pTyr15 (1:20,000; Santa Cruz), tyrosine hydroxylase (TH, 1:100,000) (Sato et al., ), and DARPP-32-Thr75 (1:20,000; Cell Signaling) (Sako et al., ) were used.

    Techniques: