u18666a Millipore Search Results


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  • 95
    Millipore u18666a
    Npc1 deficiency does not affect the activation of NLRC4 and AIM2 inflammasomes. (A) WT iBMDMs were incubated with or without the presence of increasing concentrations of <t>U18666a</t> (2, 5, and 10 µg/ml) alongside Nlrc4 −/− cells and subsequently infected with S. typhimurium at an MOI of 2 for ∼4 h. Cell lysates were immunoblotted for casp-1 and GAPDH. (B) WT and Npc1 −/− cells were treated with S. typhimurium for 4 h and immunoblotted as in A. (C) Cell supernatants were analyzed for IL-1β. (D) WT cells either treated or not with U18666a (5 µg/ml) and Npc1 −/− cells were transfected with poly(dA:dT) for 4 h before cell lysates were immunoblotted for the antibodies indicated. (E) WT, Asc −/− , and caspase 1/11 −/− cells were exposed or not to U18666a before infection with S. typhimurium as above. Cell lysates were immunoblotted for GSDMD and GAPDH. (F and G) BMDMs were treated with either LPS (500 ng/ml; 4 h) or Pam3 (500 ng/ml; 4 h) in the presence of increasing concentrations of U18666a (1, 2, 5, and 10 µg/ml) followed by ATP (5 mM; 45 min). Cell lysates were immunoblotted for GSDMD and GAPDH.
    U18666a, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 310 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/u18666a/product/Millipore
    Average 95 stars, based on 310 article reviews
    Price from $9.99 to $1999.99
    u18666a - by Bioz Stars, 2020-02
    95/100 stars
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    94
    Merck KGaA u18666a
    Glycoprotein-mediated entry into human and fruit bat cells relies on the same host cell factors. Equal volumes of vesicular stomatitis virus (VSV)-based pseudotypes (VSVpp) harboring the indicated glycoproteins were used to inoculate human (HEK-293T) and fruit bat (EpoNi/22.1, EidNi/41) cell lines pre-incubated with the indicated inhibitors for 3 h. Cells treated with solvent (water or dimethyl sulfoxide) alone served as controls (vehicle control, VC). At 18 h post inoculation, the activity of virus-encoded firefly luciferase as an indicator for transduction efficiency was quantified and normalized against the values of the respective VC (x-fold changes). The results of a representative experiment carried out with quadruplicate samples are shown and were confirmed in an independent experiment, conducted with a separate pseudotype batch. The following inhibitor concentrations were used: Mannan (final concentration: 25 μg/ml), ammonium chloride (NH 4 + ; 50 mM), bafilomycin A1 (50 nM), tetrandrine (2 μM), E-64d (50 μM), MDL28170 (50 μM), camostat mesylate (100 μM), <t>U18666A</t> (20 μM). Error bars indicate SD. An unpaired student’s t-test was used to test statistical significance (* = p
    U18666a, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/u18666a/product/Merck KGaA
    Average 94 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    u18666a - by Bioz Stars, 2020-02
    94/100 stars
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    79
    Millipore compound u18666a
    Compound <t>U18666A</t> inhibits VSV-EboGP infection in canine and feline cells
    Compound U18666a, supplied by Millipore, used in various techniques. Bioz Stars score: 79/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/compound u18666a/product/Millipore
    Average 79 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    compound u18666a - by Bioz Stars, 2020-02
    79/100 stars
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    76
    Millipore cholesterol synthesis inhibitor u18666a
    Compound <t>U18666A</t> inhibits VSV-EboGP infection in canine and feline cells
    Cholesterol Synthesis Inhibitor U18666a, supplied by Millipore, used in various techniques. Bioz Stars score: 76/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cholesterol synthesis inhibitor u18666a/product/Millipore
    Average 76 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    cholesterol synthesis inhibitor u18666a - by Bioz Stars, 2020-02
    76/100 stars
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    Image Search Results


    Npc1 deficiency does not affect the activation of NLRC4 and AIM2 inflammasomes. (A) WT iBMDMs were incubated with or without the presence of increasing concentrations of U18666a (2, 5, and 10 µg/ml) alongside Nlrc4 −/− cells and subsequently infected with S. typhimurium at an MOI of 2 for ∼4 h. Cell lysates were immunoblotted for casp-1 and GAPDH. (B) WT and Npc1 −/− cells were treated with S. typhimurium for 4 h and immunoblotted as in A. (C) Cell supernatants were analyzed for IL-1β. (D) WT cells either treated or not with U18666a (5 µg/ml) and Npc1 −/− cells were transfected with poly(dA:dT) for 4 h before cell lysates were immunoblotted for the antibodies indicated. (E) WT, Asc −/− , and caspase 1/11 −/− cells were exposed or not to U18666a before infection with S. typhimurium as above. Cell lysates were immunoblotted for GSDMD and GAPDH. (F and G) BMDMs were treated with either LPS (500 ng/ml; 4 h) or Pam3 (500 ng/ml; 4 h) in the presence of increasing concentrations of U18666a (1, 2, 5, and 10 µg/ml) followed by ATP (5 mM; 45 min). Cell lysates were immunoblotted for GSDMD and GAPDH.

    Journal: The Journal of Cell Biology

    Article Title: Trafficking of cholesterol to the ER is required for NLRP3 inflammasome activation

    doi: 10.1083/jcb.201709057

    Figure Lengend Snippet: Npc1 deficiency does not affect the activation of NLRC4 and AIM2 inflammasomes. (A) WT iBMDMs were incubated with or without the presence of increasing concentrations of U18666a (2, 5, and 10 µg/ml) alongside Nlrc4 −/− cells and subsequently infected with S. typhimurium at an MOI of 2 for ∼4 h. Cell lysates were immunoblotted for casp-1 and GAPDH. (B) WT and Npc1 −/− cells were treated with S. typhimurium for 4 h and immunoblotted as in A. (C) Cell supernatants were analyzed for IL-1β. (D) WT cells either treated or not with U18666a (5 µg/ml) and Npc1 −/− cells were transfected with poly(dA:dT) for 4 h before cell lysates were immunoblotted for the antibodies indicated. (E) WT, Asc −/− , and caspase 1/11 −/− cells were exposed or not to U18666a before infection with S. typhimurium as above. Cell lysates were immunoblotted for GSDMD and GAPDH. (F and G) BMDMs were treated with either LPS (500 ng/ml; 4 h) or Pam3 (500 ng/ml; 4 h) in the presence of increasing concentrations of U18666a (1, 2, 5, and 10 µg/ml) followed by ATP (5 mM; 45 min). Cell lysates were immunoblotted for GSDMD and GAPDH.

    Article Snippet: Experiments with U18666a (662015; EMD Millipore) were optimized in different cell types so as to block lysosomal efflux of cholesterol and achieve absolute lysosomal accumulation.

    Techniques: Activation Assay, Incubation, Infection, Transfection

    Cholesterol supplementation restores inflammasome activation in cells defective in NPC1 function. (A) BMDMs were either left untreated or exposed to LPS and cholesterol–MCD complexes (chol), cholesterol and ATP, or LPS and ATP in the presence or absence of 5 µg/ml U18666a. Where added, cells were incubated with 15 µg/ml cholesterol for 1 h before ATP treatment. Samples were immunoblotted with casp-1, and GAPDH was used as a loading control. (B) Cell supernatants were analyzed for secreted IL-1β by ELISA. Bar graph shows percent IL-1β restoration when cholesterol–MCD was added. (C) IL-1β levels in LPS-primed BMDMs grown in complete DMEM and exposed to alum (1 mg/ml). (D) IL-1β levels in Npc1 −/− cells either left untreated or treated with LPS and cholesterol–MCD for 1 h followed by ATP. (E) BMDMs were either left untreated or exposed to LPS and ATP in the presence or absence of 5 µg/ml U18666a. Where added, cells were incubated with indicated concentrations of cholesterol–MCD for 1 h before ATP treatment. Samples were immunoblotted with the indicated antibodies. GAPDH was used as a loading control. (F) Cell supernatants from above were analyzed for secreted IL-1β by ELISA. Bar graph shows percent IL-1β restoration when cholesterol–MCD was added. Data shown are mean ± SD, and experiments shown are representative of at least three independent experiments. **, P

    Journal: The Journal of Cell Biology

    Article Title: Trafficking of cholesterol to the ER is required for NLRP3 inflammasome activation

    doi: 10.1083/jcb.201709057

    Figure Lengend Snippet: Cholesterol supplementation restores inflammasome activation in cells defective in NPC1 function. (A) BMDMs were either left untreated or exposed to LPS and cholesterol–MCD complexes (chol), cholesterol and ATP, or LPS and ATP in the presence or absence of 5 µg/ml U18666a. Where added, cells were incubated with 15 µg/ml cholesterol for 1 h before ATP treatment. Samples were immunoblotted with casp-1, and GAPDH was used as a loading control. (B) Cell supernatants were analyzed for secreted IL-1β by ELISA. Bar graph shows percent IL-1β restoration when cholesterol–MCD was added. (C) IL-1β levels in LPS-primed BMDMs grown in complete DMEM and exposed to alum (1 mg/ml). (D) IL-1β levels in Npc1 −/− cells either left untreated or treated with LPS and cholesterol–MCD for 1 h followed by ATP. (E) BMDMs were either left untreated or exposed to LPS and ATP in the presence or absence of 5 µg/ml U18666a. Where added, cells were incubated with indicated concentrations of cholesterol–MCD for 1 h before ATP treatment. Samples were immunoblotted with the indicated antibodies. GAPDH was used as a loading control. (F) Cell supernatants from above were analyzed for secreted IL-1β by ELISA. Bar graph shows percent IL-1β restoration when cholesterol–MCD was added. Data shown are mean ± SD, and experiments shown are representative of at least three independent experiments. **, P

    Article Snippet: Experiments with U18666a (662015; EMD Millipore) were optimized in different cell types so as to block lysosomal efflux of cholesterol and achieve absolute lysosomal accumulation.

    Techniques: Activation Assay, Incubation, Enzyme-linked Immunosorbent Assay

    Lysosomal sterol accumulation dampens inflammasome activation. (A) BMDMs were incubated with U18666a in the presence or absence of LPS followed by measurement of total cholesterol. (B) BMDMs were either left untreated or exposed to 5 µg/ml U18666a before treating them with LPS (500 ng/ml; 4 h) and ATP (5 mM; 45 min). Cell lysates were immunoblotted for casp-1 antibody, and GAPDH was used as loading control. (C) IL-1β release from cells treated as above. (D) BMDMs were either left untreated or exposed to increasing concentrations of U18666a (1, 2, 5, and 10 µg/ml) before stimulating them with LPS and ATP. (E and F) Cell lysates were immunoblotted for the antibodies indicated, and cell supernatants were analyzed for IL-1β (E) or IL-18 (F) by ELISA. (G) Microscopy images of cells treated as above in B or with Pam3 (500 ng/ml; 4 h) followed by ATP. Arrows show characteristic pyroptotic cell death. Bars, 20 µm. (H and I) LDH release in supernatants from cells treated as in G. (J and K) LPS-primed BMDMs treated with indicated concentrations of Baf A1 (J) or CQ (K) followed by ATP. Data shown are mean ± SD, and experiments shown are representative of at least three independent experiments. *, P

    Journal: The Journal of Cell Biology

    Article Title: Trafficking of cholesterol to the ER is required for NLRP3 inflammasome activation

    doi: 10.1083/jcb.201709057

    Figure Lengend Snippet: Lysosomal sterol accumulation dampens inflammasome activation. (A) BMDMs were incubated with U18666a in the presence or absence of LPS followed by measurement of total cholesterol. (B) BMDMs were either left untreated or exposed to 5 µg/ml U18666a before treating them with LPS (500 ng/ml; 4 h) and ATP (5 mM; 45 min). Cell lysates were immunoblotted for casp-1 antibody, and GAPDH was used as loading control. (C) IL-1β release from cells treated as above. (D) BMDMs were either left untreated or exposed to increasing concentrations of U18666a (1, 2, 5, and 10 µg/ml) before stimulating them with LPS and ATP. (E and F) Cell lysates were immunoblotted for the antibodies indicated, and cell supernatants were analyzed for IL-1β (E) or IL-18 (F) by ELISA. (G) Microscopy images of cells treated as above in B or with Pam3 (500 ng/ml; 4 h) followed by ATP. Arrows show characteristic pyroptotic cell death. Bars, 20 µm. (H and I) LDH release in supernatants from cells treated as in G. (J and K) LPS-primed BMDMs treated with indicated concentrations of Baf A1 (J) or CQ (K) followed by ATP. Data shown are mean ± SD, and experiments shown are representative of at least three independent experiments. *, P

    Article Snippet: Experiments with U18666a (662015; EMD Millipore) were optimized in different cell types so as to block lysosomal efflux of cholesterol and achieve absolute lysosomal accumulation.

    Techniques: Activation Assay, Incubation, Enzyme-linked Immunosorbent Assay, Microscopy

    ER cholesterol depletion blunts ASC-dependent inflammasome assembly. (A) WT (control), U18666a-treated, and Npc1 −/− cells were exposed to LPS + ATP followed by labeling with anti-ASC antibody and DAPI staining. (B) Quantitative analysis of percentage of cells with ASC specks in samples treated as above. Each dot represents an individual field with at least n = 40 cells. (C and D) LPS-primed BMDMs exposed to ATP (C) or poly(dA:dT)-transfected BMDMs (D) were exposed or not to lovastatin (40 µM; 1 h) followed by labeling with anti-ASC antibody and DAPI staining. (E) Quantitative analysis of percentage of cells with ASC specks in samples treated as above. Each dot represents an individual field with at least n = 30 cells. Data shown are mean ± SEM, and experiments shown are representative of at least three independent experiments. Arrowheads show ASC specks. Bars, 5 µm. ****, P

    Journal: The Journal of Cell Biology

    Article Title: Trafficking of cholesterol to the ER is required for NLRP3 inflammasome activation

    doi: 10.1083/jcb.201709057

    Figure Lengend Snippet: ER cholesterol depletion blunts ASC-dependent inflammasome assembly. (A) WT (control), U18666a-treated, and Npc1 −/− cells were exposed to LPS + ATP followed by labeling with anti-ASC antibody and DAPI staining. (B) Quantitative analysis of percentage of cells with ASC specks in samples treated as above. Each dot represents an individual field with at least n = 40 cells. (C and D) LPS-primed BMDMs exposed to ATP (C) or poly(dA:dT)-transfected BMDMs (D) were exposed or not to lovastatin (40 µM; 1 h) followed by labeling with anti-ASC antibody and DAPI staining. (E) Quantitative analysis of percentage of cells with ASC specks in samples treated as above. Each dot represents an individual field with at least n = 30 cells. Data shown are mean ± SEM, and experiments shown are representative of at least three independent experiments. Arrowheads show ASC specks. Bars, 5 µm. ****, P

    Article Snippet: Experiments with U18666a (662015; EMD Millipore) were optimized in different cell types so as to block lysosomal efflux of cholesterol and achieve absolute lysosomal accumulation.

    Techniques: Labeling, Staining, Transfection

    Glycoprotein-mediated entry into human and fruit bat cells relies on the same host cell factors. Equal volumes of vesicular stomatitis virus (VSV)-based pseudotypes (VSVpp) harboring the indicated glycoproteins were used to inoculate human (HEK-293T) and fruit bat (EpoNi/22.1, EidNi/41) cell lines pre-incubated with the indicated inhibitors for 3 h. Cells treated with solvent (water or dimethyl sulfoxide) alone served as controls (vehicle control, VC). At 18 h post inoculation, the activity of virus-encoded firefly luciferase as an indicator for transduction efficiency was quantified and normalized against the values of the respective VC (x-fold changes). The results of a representative experiment carried out with quadruplicate samples are shown and were confirmed in an independent experiment, conducted with a separate pseudotype batch. The following inhibitor concentrations were used: Mannan (final concentration: 25 μg/ml), ammonium chloride (NH 4 + ; 50 mM), bafilomycin A1 (50 nM), tetrandrine (2 μM), E-64d (50 μM), MDL28170 (50 μM), camostat mesylate (100 μM), U18666A (20 μM). Error bars indicate SD. An unpaired student’s t-test was used to test statistical significance (* = p

    Journal: PLoS ONE

    Article Title: The Glycoproteins of All Filovirus Species Use the Same Host Factors for Entry into Bat and Human Cells but Entry Efficiency Is Species Dependent

    doi: 10.1371/journal.pone.0149651

    Figure Lengend Snippet: Glycoprotein-mediated entry into human and fruit bat cells relies on the same host cell factors. Equal volumes of vesicular stomatitis virus (VSV)-based pseudotypes (VSVpp) harboring the indicated glycoproteins were used to inoculate human (HEK-293T) and fruit bat (EpoNi/22.1, EidNi/41) cell lines pre-incubated with the indicated inhibitors for 3 h. Cells treated with solvent (water or dimethyl sulfoxide) alone served as controls (vehicle control, VC). At 18 h post inoculation, the activity of virus-encoded firefly luciferase as an indicator for transduction efficiency was quantified and normalized against the values of the respective VC (x-fold changes). The results of a representative experiment carried out with quadruplicate samples are shown and were confirmed in an independent experiment, conducted with a separate pseudotype batch. The following inhibitor concentrations were used: Mannan (final concentration: 25 μg/ml), ammonium chloride (NH 4 + ; 50 mM), bafilomycin A1 (50 nM), tetrandrine (2 μM), E-64d (50 μM), MDL28170 (50 μM), camostat mesylate (100 μM), U18666A (20 μM). Error bars indicate SD. An unpaired student’s t-test was used to test statistical significance (* = p

    Article Snippet: Treatment of cell lines with chemical substances and inhibitors The impact of the following compounds on filovirus GP-driven entry was studied (for detailed information please refer to ): Mannan, ammonium chloride, bafilomycin A1, E-64d, camostat mesylate (all Sigma-Aldrich), tetrandrine, MDL28170 (both Abcam) and U18666A (Merck Millipore).

    Techniques: Incubation, Activity Assay, Luciferase, Transduction, Concentration Assay

    Compound U18666A inhibits VSV-EboGP infection in canine and feline cells

    Journal: Veterinary microbiology

    Article Title: Ebola Virus Mediated Infectivity is Restricted in Canine and Feline Cells

    doi: 10.1016/j.vetmic.2015.11.011

    Figure Lengend Snippet: Compound U18666A inhibits VSV-EboGP infection in canine and feline cells

    Article Snippet: Compound U18666A was purchased from EMD Millipore (662015-10mg) and a 100mM stock solution was prepared in dH2 O and stored at −20°C.

    Techniques: Infection