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gst tagged pak pbd beads  (Cytoskeleton Inc)


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    Structured Review

    Cytoskeleton Inc gst tagged pak pbd beads
    Gst Tagged Pak Pbd Beads, supplied by Cytoskeleton Inc, used in various techniques. Bioz Stars score: 95/100, based on 64 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/binding+activity/PAK-PBD+beads+-+binds+active+Rac+Cdc42+proteins/pm41638201-290-4-7
    Average 95 stars, based on 64 article reviews
    gst tagged pak pbd beads - by Bioz Stars, 2026-10
    95/100 stars

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    other:

    Article Title: Sphingosine-1-phosphate cross-talks to Notch via a S1PR1-Dll4-MPDZ complex to regulate endothelial barrier function
    Article Snippet: A Flag-tagged EDG1 cDNA (encoding the S1PR1 protein), containing an N-terminal cleavable signal sequence to promote membrane localization, was obtained from Addgene (plasmid #66496).

    Article Title: The TCR-SUB1-DOCK2 axis promotes autoimmunity by driving pathogenic CD4 + T cell tissue infiltration.
    Article Snippet: Article The TCR-SUB1-DOCK2 axis promotes autoimmunity by driving pathogenic CD4+ T cell tissue infiltration Highlights • SUB1 dictates the tissue infiltration of pathogenic CD4+ T cells • Sub1 expression is directly modulated by the TCR-IRF4 pathway • Sub1 deficiency prevents EAE onset by halving DOCK2 levels • SUB1 undergoes LLPS to open chromatin and drive the JUNB-DOCK2 transcriptional cascade Authors Xiaoxue Li, Wenhua Liang, Weifang Wang, Eilon Sherman, Keling Huang, Feng Wang Correspondence wangfeng16@sjtu.edu.cn In brief Blocking pathogenic T cell migration is crucial for treating autoimmune diseases.. Li et al. reveal SUB1 as a gatekeeper of CD4+ T cell infiltration in autoimmunity.. TCR-induced SUB1 drives Rac- dependent cytoskeletal remodeling via DOCK2 transcriptional activation.

    Activation Assay:

    Article Title: Nuclear VAV1 increases GLI1-dependent transcription in pancreatic cancer cells
    Article Snippet: Western blotting for immunoprecipitated proteins was detected using anti-VAV1 (Invitrogen, catalog no.: MA5-31488) and anti-IMPORTIN β1 (Invitrogen, catalog no.: MA3-070). .. To evaluate the activation of RAC1, RAC1-GTP was recovered using the PAK-GST Protein Beads Pull-down Activation Assay kit (Cytoskeleton, catalog no.: PAK02). ..

    Article Title: Nuclear VAV1 increases GLI1-dependent transcription in pancreatic cancer cells.
    Article Snippet: Western blotting for immunoprecipitated proteins were detected using anti-VAV1 (Invitrogen, cat. MA5-31488) and anti-IMPORTIN β1 (Invitrogen, cat. MA3-070). .. To evaluate the activation of RAC1, RAC1-GTP was recovered using the PAK-GST Protein Beads Pull-down Activation Assay kit (Cytoskeleton, cat. PAK02). ..

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    a , Immunoblots showing cleaved Notch1 (c-Notch1) and total Notch1 in MVECs treated with S1P for 1-hour ± γ-secretase inhibitor DAPT; quantification below (mean ± SEM). b , Fluorescent micrographs of YFP-Notch1 reporter intensity after S1P treatment; quantification below. Scale bar, 50 μm. c-d , Fold change in HES1 and HEY1 gene expression levels in (c) MVECs after S1P ± DAPT treatment, and in (d) mouse tissues after intravenous injection of S1P ± DAPT. e , Evans blue dye leakage in mouse dermis 1-hour post-injection with DMSO, S1P, or S1P + DAPT. Scale bar, 5 mm. f-i , Quantified dye leakage in (f) dermis, (g) lung, (h) liver, and (i) kidney, measured via absorbance. j , Heat maps of dextran dye diffusion in engineered microvessels ± S1P. Scale bar, 50 μm. k-l , Diffusive permeability in microvessels lined with (k) DAPT-vs. DMSO-treated or (l) NOTCH1 KO vs. SCR KO MVECs (mean ± SD). m , Micrographs of VE-cadherin (magenta), actin (green), and nuclei (blue) staining in microvessels. Scale bar, 50 μm. n-o , Mean corrected intensities of junctional (n) VE-cadherin and (o) actin from (m). p , <t>Rac1</t> activity (PBD pull-down). Active/total Rac1 quantification below. q , Schematic of canonical Notch signaling. r , HES1 / HEY1 gene expression levels in dominant negative-MAML-GFP (DN-MAML-GFP) normalized to GFP expressing cells. s , Permeability in DN-MAML-GFP vs GFP-lined microvessels ± S1P. t , Schematic of Notch cortical pathway mediated by its transmembrane domain (TMD). u , Permeability in TMD-RFP vs RFP-lined microvessels ± S1P. v , Permeability in TMD-RFP vs RFP-lined microvessels ± clinical S1P receptor degrader fingolimod.
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    a , Immunoblots showing cleaved Notch1 (c-Notch1) and total Notch1 in MVECs treated with S1P for 1-hour ± γ-secretase inhibitor DAPT; quantification below (mean ± SEM). b , Fluorescent micrographs of YFP-Notch1 reporter intensity after S1P treatment; quantification below. Scale bar, 50 μm. c-d , Fold change in HES1 and HEY1 gene expression levels in (c) MVECs after S1P ± DAPT treatment, and in (d) mouse tissues after intravenous injection of S1P ± DAPT. e , Evans blue dye leakage in mouse dermis 1-hour post-injection with DMSO, S1P, or S1P + DAPT. Scale bar, 5 mm. f-i , Quantified dye leakage in (f) dermis, (g) lung, (h) liver, and (i) kidney, measured via absorbance. j , Heat maps of dextran dye diffusion in engineered microvessels ± S1P. Scale bar, 50 μm. k-l , Diffusive permeability in microvessels lined with (k) DAPT-vs. DMSO-treated or (l) NOTCH1 KO vs. SCR KO MVECs (mean ± SD). m , Micrographs of VE-cadherin (magenta), actin (green), and nuclei (blue) staining in microvessels. Scale bar, 50 μm. n-o , Mean corrected intensities of junctional (n) VE-cadherin and (o) actin from (m). p , Rac1 activity (PBD pull-down). Active/total Rac1 quantification below. q , Schematic of canonical Notch signaling. r , HES1 / HEY1 gene expression levels in dominant negative-MAML-GFP (DN-MAML-GFP) normalized to GFP expressing cells. s , Permeability in DN-MAML-GFP vs GFP-lined microvessels ± S1P. t , Schematic of Notch cortical pathway mediated by its transmembrane domain (TMD). u , Permeability in TMD-RFP vs RFP-lined microvessels ± S1P. v , Permeability in TMD-RFP vs RFP-lined microvessels ± clinical S1P receptor degrader fingolimod.

    Journal: bioRxiv

    Article Title: Sphingosine-1-phosphate cross-talks to Notch via a S1PR1-Dll4-MPDZ complex to regulate endothelial barrier function

    doi: 10.64898/2026.05.20.726610

    Figure Lengend Snippet: a , Immunoblots showing cleaved Notch1 (c-Notch1) and total Notch1 in MVECs treated with S1P for 1-hour ± γ-secretase inhibitor DAPT; quantification below (mean ± SEM). b , Fluorescent micrographs of YFP-Notch1 reporter intensity after S1P treatment; quantification below. Scale bar, 50 μm. c-d , Fold change in HES1 and HEY1 gene expression levels in (c) MVECs after S1P ± DAPT treatment, and in (d) mouse tissues after intravenous injection of S1P ± DAPT. e , Evans blue dye leakage in mouse dermis 1-hour post-injection with DMSO, S1P, or S1P + DAPT. Scale bar, 5 mm. f-i , Quantified dye leakage in (f) dermis, (g) lung, (h) liver, and (i) kidney, measured via absorbance. j , Heat maps of dextran dye diffusion in engineered microvessels ± S1P. Scale bar, 50 μm. k-l , Diffusive permeability in microvessels lined with (k) DAPT-vs. DMSO-treated or (l) NOTCH1 KO vs. SCR KO MVECs (mean ± SD). m , Micrographs of VE-cadherin (magenta), actin (green), and nuclei (blue) staining in microvessels. Scale bar, 50 μm. n-o , Mean corrected intensities of junctional (n) VE-cadherin and (o) actin from (m). p , Rac1 activity (PBD pull-down). Active/total Rac1 quantification below. q , Schematic of canonical Notch signaling. r , HES1 / HEY1 gene expression levels in dominant negative-MAML-GFP (DN-MAML-GFP) normalized to GFP expressing cells. s , Permeability in DN-MAML-GFP vs GFP-lined microvessels ± S1P. t , Schematic of Notch cortical pathway mediated by its transmembrane domain (TMD). u , Permeability in TMD-RFP vs RFP-lined microvessels ± S1P. v , Permeability in TMD-RFP vs RFP-lined microvessels ± clinical S1P receptor degrader fingolimod.

    Article Snippet: PAK-PBD beads to bind active Rac1 (PAK-02) were purchased from Cytoskeleton and reconstituted according to the manufacturer’s instructions.

    Techniques: Western Blot, Gene Expression, Injection, Diffusion-based Assay, Permeability, Staining, Activity Assay, Dominant Negative Mutation, Expressing