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lc3b sepharose  (GE Healthcare)


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    GE Healthcare lc3b sepharose
    Impact of ALS-FTLD mutations on protein-protein interactions of SQSTM1/p62. (A) Effects of the ALS-FTLD mutations on SQSTM1/p62's Keap1-binding function. HEK293Ts were transfected with His-FLAG-SQSTM1/p62 (HFN-SQSTM1) pcDNA3.1 vectors as indicated or empty vector (EV) for 24 h. Levels of endogenous Keap1 (two arrows) and ß-actin as well as transfected HFN-SQSTM1 were determined by western blotting of extracted protein prior to immunoprecipitation (input). Immunoprecipitates (IPs) generated using anti-FLAG beads were blotted for bound HFN-SQSTM1 and co-bound endogenous Keap1. A representative blot of three independent experiments is presented. Boxes highlight the reduced levels of co-precipitating Keap1 with P348L and G351A mutant compared to wild-type sequence. *denotes non-specific bands. (B) The KIR mutations (P348L and G351A) and the K344E mutation do not affect SQSTM1/p62's <t>LC3B-binding</t> function in vitro. Indicated mutations of the full-length GST-SQSTM1/p62 protein were used in LC3B pull-down assays at 37 °C. Bacterial lysates containing the GST-SQSTM1/p62 fusions were incubated with glutathione- (G), control- (C) or <t>LC3B-Sepharose.</t> Bound proteins were detected by western blotting with anti-SQSTM1 antibodies. The L341V mutation serves as a control having previously been shown to cause a loss of LC3B-biding function in pull-down assays .
    Lc3b Sepharose, supplied by GE Healthcare, used in various techniques. Bioz Stars score: 96/100, based on 988 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/lc3b+sepharose/pmc05062946-64-16-14?v=GE+Healthcare
    Average 96 stars, based on 988 article reviews
    lc3b sepharose - by Bioz Stars, 2026-07
    96/100 stars

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    1) Product Images from "ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling"

    Article Title: ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling

    Journal: Molecular and Cellular Neurosciences

    doi: 10.1016/j.mcn.2016.08.004

    Impact of ALS-FTLD mutations on protein-protein interactions of SQSTM1/p62. (A) Effects of the ALS-FTLD mutations on SQSTM1/p62's Keap1-binding function. HEK293Ts were transfected with His-FLAG-SQSTM1/p62 (HFN-SQSTM1) pcDNA3.1 vectors as indicated or empty vector (EV) for 24 h. Levels of endogenous Keap1 (two arrows) and ß-actin as well as transfected HFN-SQSTM1 were determined by western blotting of extracted protein prior to immunoprecipitation (input). Immunoprecipitates (IPs) generated using anti-FLAG beads were blotted for bound HFN-SQSTM1 and co-bound endogenous Keap1. A representative blot of three independent experiments is presented. Boxes highlight the reduced levels of co-precipitating Keap1 with P348L and G351A mutant compared to wild-type sequence. *denotes non-specific bands. (B) The KIR mutations (P348L and G351A) and the K344E mutation do not affect SQSTM1/p62's LC3B-binding function in vitro. Indicated mutations of the full-length GST-SQSTM1/p62 protein were used in LC3B pull-down assays at 37 °C. Bacterial lysates containing the GST-SQSTM1/p62 fusions were incubated with glutathione- (G), control- (C) or LC3B-Sepharose. Bound proteins were detected by western blotting with anti-SQSTM1 antibodies. The L341V mutation serves as a control having previously been shown to cause a loss of LC3B-biding function in pull-down assays .
    Figure Legend Snippet: Impact of ALS-FTLD mutations on protein-protein interactions of SQSTM1/p62. (A) Effects of the ALS-FTLD mutations on SQSTM1/p62's Keap1-binding function. HEK293Ts were transfected with His-FLAG-SQSTM1/p62 (HFN-SQSTM1) pcDNA3.1 vectors as indicated or empty vector (EV) for 24 h. Levels of endogenous Keap1 (two arrows) and ß-actin as well as transfected HFN-SQSTM1 were determined by western blotting of extracted protein prior to immunoprecipitation (input). Immunoprecipitates (IPs) generated using anti-FLAG beads were blotted for bound HFN-SQSTM1 and co-bound endogenous Keap1. A representative blot of three independent experiments is presented. Boxes highlight the reduced levels of co-precipitating Keap1 with P348L and G351A mutant compared to wild-type sequence. *denotes non-specific bands. (B) The KIR mutations (P348L and G351A) and the K344E mutation do not affect SQSTM1/p62's LC3B-binding function in vitro. Indicated mutations of the full-length GST-SQSTM1/p62 protein were used in LC3B pull-down assays at 37 °C. Bacterial lysates containing the GST-SQSTM1/p62 fusions were incubated with glutathione- (G), control- (C) or LC3B-Sepharose. Bound proteins were detected by western blotting with anti-SQSTM1 antibodies. The L341V mutation serves as a control having previously been shown to cause a loss of LC3B-biding function in pull-down assays .

    Techniques Used: Binding Assay, Transfection, Plasmid Preparation, Western Blot, Immunoprecipitation, Generated, Mutagenesis, Sequencing, In Vitro, Incubation



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    lc3b sepharose  (GE Healthcare)
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    GE Healthcare lc3b sepharose
    Impact of ALS-FTLD mutations on protein-protein interactions of SQSTM1/p62. (A) Effects of the ALS-FTLD mutations on SQSTM1/p62's Keap1-binding function. HEK293Ts were transfected with His-FLAG-SQSTM1/p62 (HFN-SQSTM1) pcDNA3.1 vectors as indicated or empty vector (EV) for 24 h. Levels of endogenous Keap1 (two arrows) and ß-actin as well as transfected HFN-SQSTM1 were determined by western blotting of extracted protein prior to immunoprecipitation (input). Immunoprecipitates (IPs) generated using anti-FLAG beads were blotted for bound HFN-SQSTM1 and co-bound endogenous Keap1. A representative blot of three independent experiments is presented. Boxes highlight the reduced levels of co-precipitating Keap1 with P348L and G351A mutant compared to wild-type sequence. *denotes non-specific bands. (B) The KIR mutations (P348L and G351A) and the K344E mutation do not affect SQSTM1/p62's <t>LC3B-binding</t> function in vitro. Indicated mutations of the full-length GST-SQSTM1/p62 protein were used in LC3B pull-down assays at 37 °C. Bacterial lysates containing the GST-SQSTM1/p62 fusions were incubated with glutathione- (G), control- (C) or <t>LC3B-Sepharose.</t> Bound proteins were detected by western blotting with anti-SQSTM1 antibodies. The L341V mutation serves as a control having previously been shown to cause a loss of LC3B-biding function in pull-down assays .
    Lc3b Sepharose, supplied by GE Healthcare, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/lc3b+sepharose/pmc05062946-64-16-14?v=GE+Healthcare
    Average 96 stars, based on 1 article reviews
    lc3b sepharose - by Bioz Stars, 2026-07
    96/100 stars
    		  Buy from Supplier

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    Impact of ALS-FTLD mutations on protein-protein interactions of SQSTM1/p62. (A) Effects of the ALS-FTLD mutations on SQSTM1/p62's Keap1-binding function. HEK293Ts were transfected with His-FLAG-SQSTM1/p62 (HFN-SQSTM1) pcDNA3.1 vectors as indicated or empty vector (EV) for 24 h. Levels of endogenous Keap1 (two arrows) and ß-actin as well as transfected HFN-SQSTM1 were determined by western blotting of extracted protein prior to immunoprecipitation (input). Immunoprecipitates (IPs) generated using anti-FLAG beads were blotted for bound HFN-SQSTM1 and co-bound endogenous Keap1. A representative blot of three independent experiments is presented. Boxes highlight the reduced levels of co-precipitating Keap1 with P348L and G351A mutant compared to wild-type sequence. *denotes non-specific bands. (B) The KIR mutations (P348L and G351A) and the K344E mutation do not affect SQSTM1/p62's LC3B-binding function in vitro. Indicated mutations of the full-length GST-SQSTM1/p62 protein were used in LC3B pull-down assays at 37 °C. Bacterial lysates containing the GST-SQSTM1/p62 fusions were incubated with glutathione- (G), control- (C) or LC3B-Sepharose. Bound proteins were detected by western blotting with anti-SQSTM1 antibodies. The L341V mutation serves as a control having previously been shown to cause a loss of LC3B-biding function in pull-down assays .

    Journal: Molecular and Cellular Neurosciences

    Article Title: ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling

    doi: 10.1016/j.mcn.2016.08.004

    Figure Lengend Snippet: Impact of ALS-FTLD mutations on protein-protein interactions of SQSTM1/p62. (A) Effects of the ALS-FTLD mutations on SQSTM1/p62's Keap1-binding function. HEK293Ts were transfected with His-FLAG-SQSTM1/p62 (HFN-SQSTM1) pcDNA3.1 vectors as indicated or empty vector (EV) for 24 h. Levels of endogenous Keap1 (two arrows) and ß-actin as well as transfected HFN-SQSTM1 were determined by western blotting of extracted protein prior to immunoprecipitation (input). Immunoprecipitates (IPs) generated using anti-FLAG beads were blotted for bound HFN-SQSTM1 and co-bound endogenous Keap1. A representative blot of three independent experiments is presented. Boxes highlight the reduced levels of co-precipitating Keap1 with P348L and G351A mutant compared to wild-type sequence. *denotes non-specific bands. (B) The KIR mutations (P348L and G351A) and the K344E mutation do not affect SQSTM1/p62's LC3B-binding function in vitro. Indicated mutations of the full-length GST-SQSTM1/p62 protein were used in LC3B pull-down assays at 37 °C. Bacterial lysates containing the GST-SQSTM1/p62 fusions were incubated with glutathione- (G), control- (C) or LC3B-Sepharose. Bound proteins were detected by western blotting with anti-SQSTM1 antibodies. The L341V mutation serves as a control having previously been shown to cause a loss of LC3B-biding function in pull-down assays .

    Article Snippet: One milliliter of each diluted lysate was incubated at 37 °C with excess glutathione-Sepharose (GE Healthcare), LC3B-Sepharose (1 mg/mL LC3B immobilised on CNBr-activated Sepharose 4B) or control-Sepharose (CNBr-activated Sepharose prepared without LC3B).

    Techniques: Binding Assay, Transfection, Plasmid Preparation, Western Blot, Immunoprecipitation, Generated, Mutagenesis, Sequencing, In Vitro, Incubation