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ras activation assay biochem kit  (Cytoskeleton Inc)


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    Cytoskeleton Inc ras activation assay biochem kit
    Ras Activation Assay Biochem Kit, supplied by Cytoskeleton Inc, used in various techniques. Bioz Stars score: 95/100, based on 88 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ras+activation+assay+biochem+kit/bio_rxiv__64898__2026__05__29__728724-49-6-13?v=Cytoskeleton+Inc
    Average 95 stars, based on 88 article reviews
    ras activation assay biochem kit - by Bioz Stars, 2026-07
    95/100 stars

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    Functional impacts of ALDH2 mutations on enzyme activity and tumor suppression via <t>RAS-AKT</t> signaling. (A) Schematic of lentiviral overexpression constructs: control (Lenti), wild-type ALDH2 [ALDH2(WT)], E504K mutant, phosphorylation-incapable mutants T261A, S488A, and double mutant T261A/S488A in FaDu and ALDH2 -knockdown Detroit 562 cells. (B-D) Quantification for ALDH activity (fluorometric assay, cell lysates), 4-HNE levels (ELISA, culture medium), and MDA levels (colorimetric assay, cell lysates). (E-G) Cellular phenotypes assessed by soft agar colony formation/MTT assay, transwell migration and invasion, and HUVEC tube formation following treatment with conditioned media from each group. (H , I) Immunoblot analysis and RAS pull-down assays evaluated expression of RAS-AKT-MAPK pathway proteins and active RAS <t>(RAS-GTP).</t> (J) NFκB transcriptional activity measured via Dual-Luciferase ® Reporter Assay following cotransfection with pGL3.21[ luc2P /NF-κB-RE/Hygro] (NFκB reporter) and pRL Renilla control vector (14:1 ratio). Data are presented as mean ± SD. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001
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    Functional impacts of ALDH2 mutations on enzyme activity and tumor suppression via <t>RAS-AKT</t> signaling. (A) Schematic of lentiviral overexpression constructs: control (Lenti), wild-type ALDH2 [ALDH2(WT)], E504K mutant, phosphorylation-incapable mutants T261A, S488A, and double mutant T261A/S488A in FaDu and ALDH2 -knockdown Detroit 562 cells. (B-D) Quantification for ALDH activity (fluorometric assay, cell lysates), 4-HNE levels (ELISA, culture medium), and MDA levels (colorimetric assay, cell lysates). (E-G) Cellular phenotypes assessed by soft agar colony formation/MTT assay, transwell migration and invasion, and HUVEC tube formation following treatment with conditioned media from each group. (H , I) Immunoblot analysis and RAS pull-down assays evaluated expression of RAS-AKT-MAPK pathway proteins and active RAS <t>(RAS-GTP).</t> (J) NFκB transcriptional activity measured via Dual-Luciferase ® Reporter Assay following cotransfection with pGL3.21[ luc2P /NF-κB-RE/Hygro] (NFκB reporter) and pRL Renilla control vector (14:1 ratio). Data are presented as mean ± SD. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001
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    Functional impacts of ALDH2 mutations on enzyme activity and tumor suppression via RAS-AKT signaling. (A) Schematic of lentiviral overexpression constructs: control (Lenti), wild-type ALDH2 [ALDH2(WT)], E504K mutant, phosphorylation-incapable mutants T261A, S488A, and double mutant T261A/S488A in FaDu and ALDH2 -knockdown Detroit 562 cells. (B-D) Quantification for ALDH activity (fluorometric assay, cell lysates), 4-HNE levels (ELISA, culture medium), and MDA levels (colorimetric assay, cell lysates). (E-G) Cellular phenotypes assessed by soft agar colony formation/MTT assay, transwell migration and invasion, and HUVEC tube formation following treatment with conditioned media from each group. (H , I) Immunoblot analysis and RAS pull-down assays evaluated expression of RAS-AKT-MAPK pathway proteins and active RAS (RAS-GTP). (J) NFκB transcriptional activity measured via Dual-Luciferase ® Reporter Assay following cotransfection with pGL3.21[ luc2P /NF-κB-RE/Hygro] (NFκB reporter) and pRL Renilla control vector (14:1 ratio). Data are presented as mean ± SD. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: ALDH2 inhibits head and neck tumorigenesis through RAS signaling suppression, transactivation of TGM2 , and synergy with ALDH6A1

    doi: 10.1007/s00018-025-06027-7

    Figure Lengend Snippet: Functional impacts of ALDH2 mutations on enzyme activity and tumor suppression via RAS-AKT signaling. (A) Schematic of lentiviral overexpression constructs: control (Lenti), wild-type ALDH2 [ALDH2(WT)], E504K mutant, phosphorylation-incapable mutants T261A, S488A, and double mutant T261A/S488A in FaDu and ALDH2 -knockdown Detroit 562 cells. (B-D) Quantification for ALDH activity (fluorometric assay, cell lysates), 4-HNE levels (ELISA, culture medium), and MDA levels (colorimetric assay, cell lysates). (E-G) Cellular phenotypes assessed by soft agar colony formation/MTT assay, transwell migration and invasion, and HUVEC tube formation following treatment with conditioned media from each group. (H , I) Immunoblot analysis and RAS pull-down assays evaluated expression of RAS-AKT-MAPK pathway proteins and active RAS (RAS-GTP). (J) NFκB transcriptional activity measured via Dual-Luciferase ® Reporter Assay following cotransfection with pGL3.21[ luc2P /NF-κB-RE/Hygro] (NFκB reporter) and pRL Renilla control vector (14:1 ratio). Data are presented as mean ± SD. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: Active RAS (RAS-GTP) levels were analyzed using the Ras Pull-down Activation Assay Biochem Kit (Bead Pull-Down Format, #BK008, Cytoskeleton, Denver, CO., USA).

    Techniques: Functional Assay, Activity Assay, Over Expression, Construct, Control, Mutagenesis, Phospho-proteomics, Knockdown, Enzyme-linked Immunosorbent Assay, Colorimetric Assay, MTT Assay, Migration, Western Blot, Expressing, Luciferase, Reporter Assay, Cotransfection, Plasmid Preparation