sirna constructs targeting p22 phox  (Thermo Fisher)


Bioz Verified Symbol Thermo Fisher is a verified supplier
Bioz Manufacturer Symbol Thermo Fisher manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 86
      Buy from Supplier

    Structured Review

    Thermo Fisher sirna constructs targeting p22 phox
    NADPH oxidase- and mitochondria-derived ROS contribute to glucose withdrawal-induced phospho-tyrosine signaling. ( A ) Inhibition of NOX inhibits glucose withdrawal-induced signaling. LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of DMSO or DPI (1 μM). Western blotting demonstrated that NOX activity is required for the induction of phospho-tyrosine signaling. ( B ) Knockdown of the NOX subunit <t>p22</t> <t>phox</t> attenuates phospho-tyrosine signaling following glucose withdrawal. U87 cells were reverse transfected with control, non-targeting <t>siRNA</t> or siRNA against p22 phox , DUOX1 or DUOX2. Forty-eight hours later, cells were starved of glucose and pyruvate for 5 h. Western blotting demonstrated that knockdown of p22 phox but not DUOX1/2 attenuated glucose withdrawal-induced phospho-tyrosine signaling. p22 phox knockdown efficiency was >90% . ( C ) LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of either DMSO or BAPTA-AM (25 μM). Western blotting with an anti-phospho-tyrosine antibody demonstrated that chelation of intracellular Ca 2+ by BAPTA-AM completely abrogated glucose withdrawal-induced phospho-tyrosine signaling. Treatment with extracellular EDTA (25 μM) had no effect. Actin and GRB2 served as equal loading controls. ( D ) ρ 0 derivatives of T98 and U87 cells do not exhibit upregulation of phospho-tyrosine signaling or activation of Src in response to glucose withdrawal. ( E ) Catalase rescues parental but not ρ 0 cells from glucose withdrawal-induced cell death. Cells were starved of glucose and pyruvate with or without catalase (1 kU/ml), and viability was measured by Trypan blue exclusion 24 h later.
    Sirna Constructs Targeting P22 Phox, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sirna constructs targeting p22 phox/product/Thermo Fisher
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sirna constructs targeting p22 phox - by Bioz Stars, 2023-11
    86/100 stars

    Images

    1) Product Images from "Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death"

    Article Title: Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death

    Journal: Molecular Systems Biology

    doi: 10.1038/msb.2012.20

    NADPH oxidase- and mitochondria-derived ROS contribute to glucose withdrawal-induced phospho-tyrosine signaling. ( A ) Inhibition of NOX inhibits glucose withdrawal-induced signaling. LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of DMSO or DPI (1 μM). Western blotting demonstrated that NOX activity is required for the induction of phospho-tyrosine signaling. ( B ) Knockdown of the NOX subunit p22 phox attenuates phospho-tyrosine signaling following glucose withdrawal. U87 cells were reverse transfected with control, non-targeting siRNA or siRNA against p22 phox , DUOX1 or DUOX2. Forty-eight hours later, cells were starved of glucose and pyruvate for 5 h. Western blotting demonstrated that knockdown of p22 phox but not DUOX1/2 attenuated glucose withdrawal-induced phospho-tyrosine signaling. p22 phox knockdown efficiency was >90% . ( C ) LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of either DMSO or BAPTA-AM (25 μM). Western blotting with an anti-phospho-tyrosine antibody demonstrated that chelation of intracellular Ca 2+ by BAPTA-AM completely abrogated glucose withdrawal-induced phospho-tyrosine signaling. Treatment with extracellular EDTA (25 μM) had no effect. Actin and GRB2 served as equal loading controls. ( D ) ρ 0 derivatives of T98 and U87 cells do not exhibit upregulation of phospho-tyrosine signaling or activation of Src in response to glucose withdrawal. ( E ) Catalase rescues parental but not ρ 0 cells from glucose withdrawal-induced cell death. Cells were starved of glucose and pyruvate with or without catalase (1 kU/ml), and viability was measured by Trypan blue exclusion 24 h later.
    Figure Legend Snippet: NADPH oxidase- and mitochondria-derived ROS contribute to glucose withdrawal-induced phospho-tyrosine signaling. ( A ) Inhibition of NOX inhibits glucose withdrawal-induced signaling. LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of DMSO or DPI (1 μM). Western blotting demonstrated that NOX activity is required for the induction of phospho-tyrosine signaling. ( B ) Knockdown of the NOX subunit p22 phox attenuates phospho-tyrosine signaling following glucose withdrawal. U87 cells were reverse transfected with control, non-targeting siRNA or siRNA against p22 phox , DUOX1 or DUOX2. Forty-eight hours later, cells were starved of glucose and pyruvate for 5 h. Western blotting demonstrated that knockdown of p22 phox but not DUOX1/2 attenuated glucose withdrawal-induced phospho-tyrosine signaling. p22 phox knockdown efficiency was >90% . ( C ) LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of either DMSO or BAPTA-AM (25 μM). Western blotting with an anti-phospho-tyrosine antibody demonstrated that chelation of intracellular Ca 2+ by BAPTA-AM completely abrogated glucose withdrawal-induced phospho-tyrosine signaling. Treatment with extracellular EDTA (25 μM) had no effect. Actin and GRB2 served as equal loading controls. ( D ) ρ 0 derivatives of T98 and U87 cells do not exhibit upregulation of phospho-tyrosine signaling or activation of Src in response to glucose withdrawal. ( E ) Catalase rescues parental but not ρ 0 cells from glucose withdrawal-induced cell death. Cells were starved of glucose and pyruvate with or without catalase (1 kU/ml), and viability was measured by Trypan blue exclusion 24 h later.

    Techniques Used: Derivative Assay, Inhibition, Western Blot, Activity Assay, Transfection, Activation Assay

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • sirna constructs targeting p22 phox  (Thermo Fisher)
    86
    Thermo Fisher sirna constructs targeting p22 phox
    NADPH oxidase- and mitochondria-derived ROS contribute to glucose withdrawal-induced phospho-tyrosine signaling. ( A ) Inhibition of NOX inhibits glucose withdrawal-induced signaling. LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of DMSO or DPI (1 μM). Western blotting demonstrated that NOX activity is required for the induction of phospho-tyrosine signaling. ( B ) Knockdown of the NOX subunit <t>p22</t> <t>phox</t> attenuates phospho-tyrosine signaling following glucose withdrawal. U87 cells were reverse transfected with control, non-targeting <t>siRNA</t> or siRNA against p22 phox , DUOX1 or DUOX2. Forty-eight hours later, cells were starved of glucose and pyruvate for 5 h. Western blotting demonstrated that knockdown of p22 phox but not DUOX1/2 attenuated glucose withdrawal-induced phospho-tyrosine signaling. p22 phox knockdown efficiency was >90% . ( C ) LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of either DMSO or BAPTA-AM (25 μM). Western blotting with an anti-phospho-tyrosine antibody demonstrated that chelation of intracellular Ca 2+ by BAPTA-AM completely abrogated glucose withdrawal-induced phospho-tyrosine signaling. Treatment with extracellular EDTA (25 μM) had no effect. Actin and GRB2 served as equal loading controls. ( D ) ρ 0 derivatives of T98 and U87 cells do not exhibit upregulation of phospho-tyrosine signaling or activation of Src in response to glucose withdrawal. ( E ) Catalase rescues parental but not ρ 0 cells from glucose withdrawal-induced cell death. Cells were starved of glucose and pyruvate with or without catalase (1 kU/ml), and viability was measured by Trypan blue exclusion 24 h later.
    Sirna Constructs Targeting P22 Phox, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sirna constructs targeting p22 phox/product/Thermo Fisher
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sirna constructs targeting p22 phox - by Bioz Stars, 2023-11
    86/100 stars
    		  Buy from Supplier

    Image Search Results


    NADPH oxidase- and mitochondria-derived ROS contribute to glucose withdrawal-induced phospho-tyrosine signaling. ( A ) Inhibition of NOX inhibits glucose withdrawal-induced signaling. LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of DMSO or DPI (1 μM). Western blotting demonstrated that NOX activity is required for the induction of phospho-tyrosine signaling. ( B ) Knockdown of the NOX subunit p22 phox attenuates phospho-tyrosine signaling following glucose withdrawal. U87 cells were reverse transfected with control, non-targeting siRNA or siRNA against p22 phox , DUOX1 or DUOX2. Forty-eight hours later, cells were starved of glucose and pyruvate for 5 h. Western blotting demonstrated that knockdown of p22 phox but not DUOX1/2 attenuated glucose withdrawal-induced phospho-tyrosine signaling. p22 phox knockdown efficiency was >90% . ( C ) LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of either DMSO or BAPTA-AM (25 μM). Western blotting with an anti-phospho-tyrosine antibody demonstrated that chelation of intracellular Ca 2+ by BAPTA-AM completely abrogated glucose withdrawal-induced phospho-tyrosine signaling. Treatment with extracellular EDTA (25 μM) had no effect. Actin and GRB2 served as equal loading controls. ( D ) ρ 0 derivatives of T98 and U87 cells do not exhibit upregulation of phospho-tyrosine signaling or activation of Src in response to glucose withdrawal. ( E ) Catalase rescues parental but not ρ 0 cells from glucose withdrawal-induced cell death. Cells were starved of glucose and pyruvate with or without catalase (1 kU/ml), and viability was measured by Trypan blue exclusion 24 h later.

    Journal: Molecular Systems Biology

    Article Title: Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death

    doi: 10.1038/msb.2012.20

    Figure Lengend Snippet: NADPH oxidase- and mitochondria-derived ROS contribute to glucose withdrawal-induced phospho-tyrosine signaling. ( A ) Inhibition of NOX inhibits glucose withdrawal-induced signaling. LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of DMSO or DPI (1 μM). Western blotting demonstrated that NOX activity is required for the induction of phospho-tyrosine signaling. ( B ) Knockdown of the NOX subunit p22 phox attenuates phospho-tyrosine signaling following glucose withdrawal. U87 cells were reverse transfected with control, non-targeting siRNA or siRNA against p22 phox , DUOX1 or DUOX2. Forty-eight hours later, cells were starved of glucose and pyruvate for 5 h. Western blotting demonstrated that knockdown of p22 phox but not DUOX1/2 attenuated glucose withdrawal-induced phospho-tyrosine signaling. p22 phox knockdown efficiency was >90% . ( C ) LN18, T98, and U87 cells were starved of glucose and pyruvate in the presence of either DMSO or BAPTA-AM (25 μM). Western blotting with an anti-phospho-tyrosine antibody demonstrated that chelation of intracellular Ca 2+ by BAPTA-AM completely abrogated glucose withdrawal-induced phospho-tyrosine signaling. Treatment with extracellular EDTA (25 μM) had no effect. Actin and GRB2 served as equal loading controls. ( D ) ρ 0 derivatives of T98 and U87 cells do not exhibit upregulation of phospho-tyrosine signaling or activation of Src in response to glucose withdrawal. ( E ) Catalase rescues parental but not ρ 0 cells from glucose withdrawal-induced cell death. Cells were starved of glucose and pyruvate with or without catalase (1 kU/ml), and viability was measured by Trypan blue exclusion 24 h later.

    Article Snippet: siRNA constructs targeting p22 phox (M-011020) and a non-targeting control siRNA (D-001206) were purchased from Thermo Scientific.

    Techniques: Derivative Assay, Inhibition, Western Blot, Activity Assay, Transfection, Activation Assay