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rabbit polyclonal vasp antibody  (Proteintech)


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    Structured Review

    Proteintech rabbit polyclonal vasp antibody
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
    Rabbit Polyclonal Vasp Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Integrated bioinformatics and experimental validation identify ATF3 as a key gene in secondary brain damage after intracerebral hemorrhage"

    Article Title: Integrated bioinformatics and experimental validation identify ATF3 as a key gene in secondary brain damage after intracerebral hemorrhage

    Journal: PLOS One

    doi: 10.1371/journal.pone.0328530

    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the VASP promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
    Figure Legend Snippet: (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the VASP promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).

    Techniques Used: Binding Assay, Microarray, Western Blot, Over Expression, Plasmid Preparation, Control, shRNA, Knockdown, Transduction, Luciferase, Reporter Assay, Activity Assay, Mutagenesis, Construct



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    Proteintech rabbit polyclonal vasp antibody
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    Cell Signaling Technology Inc rabbit polyclonal anti phospho ser 157 vasp
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    Cell Signaling Technology Inc rabbit polyclonal anti phospho ser239 vasp antibodies
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    Cell Signaling Technology Inc rabbit polyclonal anti phospho ser 239 vasp antibodies
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    Cell Signaling Technology Inc rabbit polyclonal anti phospho ser157 vasp
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    Santa Cruz Biotechnology rabbit polyclonal antibody anti-vasp-phospho-ser 239
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    Cell Signaling Technology Inc 2018 rabbit polyclonal vasp phospho s157 cell signaling
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    Cell Signaling Technology Inc 2018 rabbit polyclonal vasp phospho s239 cell signaling
    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the <t>VASP</t> promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).
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    Image Search Results


    (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the VASP promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).

    Journal: PLOS One

    Article Title: Integrated bioinformatics and experimental validation identify ATF3 as a key gene in secondary brain damage after intracerebral hemorrhage

    doi: 10.1371/journal.pone.0328530

    Figure Lengend Snippet: (A) Evolutionary-conserved ATF3 binding motif identified by JASPAR (Matrix ID MA0606.1) within the VASP promoter (−1.5 kb upstream of TSS). Position frequency matrix conservation score >85% across mammals. (B) Reanalysis of GSE24265 microarray data showing VASP upregulation (linear models for microarray data [LIMMA], adj.p = 0.017). (C) ATF3 gain-of-function model: Western blot of HT-22 cells 48 h post-lentiviral ATF3 overexpression (pLVX-EF1α vector). Blots: Rabbit anti-ATF3 (CST 33593, 1:1,000), mouse anti-VASP (BD 611175, 1:500), β-actin control (Sigma A2228, 1:5,000). (D/E) Densitometric quantification of ATF3 (D) and VASP (E) protein levels (n = 3 biological replicates; unpaired t-test, **p = 0.0007 vs. EV control). (F) ATF3 loss-of-function: shRNA-mediated knockdown in HT-22 cells. Blots: 72 h post-transduction; scramble shRNA control (Addgene #1864). (G/H) The quantification of ATF3 (G) and VASP (H) suppression (n = 3; two-way ANOVA, **p < 0.0001 vs. scramble). (I) Dual-luciferase reporter assay of VASP promoter activity. Left: Wild-type vs. ΔATF3-binding mutant constructs. Right: Firefly/Renilla ratio (n = 6; **p = 0.0004, ordinary one-way ANOVA).

    Article Snippet: For immunostaining, cells were incubated with either a mouse monoclonal ATF3 antibody (Abcam, ab254268) or a rabbit polyclonal VASP antibody (Proteintech, 13472-1-AP, China) as primary antibodies.

    Techniques: Binding Assay, Microarray, Western Blot, Over Expression, Plasmid Preparation, Control, shRNA, Knockdown, Transduction, Luciferase, Reporter Assay, Activity Assay, Mutagenesis, Construct