lovastatin  (Millipore)


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    Structured Review

    Millipore lovastatin
    Retardation of G 1 -to-S-phase transition in T47DΔMTcycD1 cells, caused by NF-κB inactivation, was rescued by ectopic cyclin D1 expression. (A) Expression of IκBΔN in T47DΔMTcycD1 cells. Cells were transfected with an IκBΔN expression construct or an empty vector, and stable clones were selected with hygromycin (Sigma). Control and IκBΔN-transfected cells were lysed with extraction buffer and analyzed by Western blotting with anti-IκBα antibody. The positions of wild-type (WT) and mutant IκBα are indicated. Lanes 1 and 2, control clones (TC1 and TC2); lanes 3 and 4, IκBΔN-expressing clones (TI3 and TI4). (B) NF-κB-dependent cyclin D1 expression in T47DΔMTcycD1 cells. Western blots of protein extracts prepared from presynchronized TC1 and TI4 cells at the indicated time points after <t>lovastatin</t> removal and mevalonate addition are shown. Cyclin D1 was detected with the monoclonal antibody DCS-6. (C) FACS analysis of progression into S phase of TC1 and TI4 cells at 0, 18, or 22 h after lovastatin removal and mevalonate addition. Ectopic expression of cyclin D1 was induced by the addition of Zn 2+ (+) or was not induced (−), as indicated. Progression through the cell cycle was monitored by detection of the DNA content. TC2 and TI3 cells (data not shown) gave similar results.
    Lovastatin, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lovastatin/product/Millipore
    Average 97 stars, based on 24 article reviews
    Price from $9.99 to $1999.99
    lovastatin - by Bioz Stars, 2020-04
    97/100 stars

    Images

    1) Product Images from "NF-?B Function in Growth Control: Regulation of Cyclin D1 Expression and G0/G1-to-S-Phase Transition"

    Article Title: NF-?B Function in Growth Control: Regulation of Cyclin D1 Expression and G0/G1-to-S-Phase Transition

    Journal: Molecular and Cellular Biology

    doi:

    Retardation of G 1 -to-S-phase transition in T47DΔMTcycD1 cells, caused by NF-κB inactivation, was rescued by ectopic cyclin D1 expression. (A) Expression of IκBΔN in T47DΔMTcycD1 cells. Cells were transfected with an IκBΔN expression construct or an empty vector, and stable clones were selected with hygromycin (Sigma). Control and IκBΔN-transfected cells were lysed with extraction buffer and analyzed by Western blotting with anti-IκBα antibody. The positions of wild-type (WT) and mutant IκBα are indicated. Lanes 1 and 2, control clones (TC1 and TC2); lanes 3 and 4, IκBΔN-expressing clones (TI3 and TI4). (B) NF-κB-dependent cyclin D1 expression in T47DΔMTcycD1 cells. Western blots of protein extracts prepared from presynchronized TC1 and TI4 cells at the indicated time points after lovastatin removal and mevalonate addition are shown. Cyclin D1 was detected with the monoclonal antibody DCS-6. (C) FACS analysis of progression into S phase of TC1 and TI4 cells at 0, 18, or 22 h after lovastatin removal and mevalonate addition. Ectopic expression of cyclin D1 was induced by the addition of Zn 2+ (+) or was not induced (−), as indicated. Progression through the cell cycle was monitored by detection of the DNA content. TC2 and TI3 cells (data not shown) gave similar results.
    Figure Legend Snippet: Retardation of G 1 -to-S-phase transition in T47DΔMTcycD1 cells, caused by NF-κB inactivation, was rescued by ectopic cyclin D1 expression. (A) Expression of IκBΔN in T47DΔMTcycD1 cells. Cells were transfected with an IκBΔN expression construct or an empty vector, and stable clones were selected with hygromycin (Sigma). Control and IκBΔN-transfected cells were lysed with extraction buffer and analyzed by Western blotting with anti-IκBα antibody. The positions of wild-type (WT) and mutant IκBα are indicated. Lanes 1 and 2, control clones (TC1 and TC2); lanes 3 and 4, IκBΔN-expressing clones (TI3 and TI4). (B) NF-κB-dependent cyclin D1 expression in T47DΔMTcycD1 cells. Western blots of protein extracts prepared from presynchronized TC1 and TI4 cells at the indicated time points after lovastatin removal and mevalonate addition are shown. Cyclin D1 was detected with the monoclonal antibody DCS-6. (C) FACS analysis of progression into S phase of TC1 and TI4 cells at 0, 18, or 22 h after lovastatin removal and mevalonate addition. Ectopic expression of cyclin D1 was induced by the addition of Zn 2+ (+) or was not induced (−), as indicated. Progression through the cell cycle was monitored by detection of the DNA content. TC2 and TI3 cells (data not shown) gave similar results.

    Techniques Used: Sublimation, Expressing, Transfection, Construct, Plasmid Preparation, Clone Assay, Western Blot, Mutagenesis, FACS

    2) Product Images from "Hippocampal Dysregulation of Neurofibromin-Dependent Pathways Is Associated with Impaired Spatial Learning in Engrailed 2 Knock-Out Mice"

    Article Title: Hippocampal Dysregulation of Neurofibromin-Dependent Pathways Is Associated with Impaired Spatial Learning in Engrailed 2 Knock-Out Mice

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.2894-13.2014

    Lovastatin rescues ERK phosphorylation but not spatial learning performance in MWM-trained En2 −/− mice. Lovastatin-treated WT and En2 −/− mice were subjected to MWM. Escape latency during training and number of platform crossings in target and opposite quadrants during probe trial are shown in A and B , respectively. Lova, Lovastatin; lovastatin-treated WT, open circles; lovastatin-treated En2 −/− , black squares; T, target quadrant; OP, quadrant opposite to target. * p
    Figure Legend Snippet: Lovastatin rescues ERK phosphorylation but not spatial learning performance in MWM-trained En2 −/− mice. Lovastatin-treated WT and En2 −/− mice were subjected to MWM. Escape latency during training and number of platform crossings in target and opposite quadrants during probe trial are shown in A and B , respectively. Lova, Lovastatin; lovastatin-treated WT, open circles; lovastatin-treated En2 −/− , black squares; T, target quadrant; OP, quadrant opposite to target. * p

    Techniques Used: Mouse Assay

    3) Product Images from "Volatiles Emitted at Different Flowering Stages of Jasminum sambac and Expression of Genes Related to α-Farnesene Biosynthesis"

    Article Title: Volatiles Emitted at Different Flowering Stages of Jasminum sambac and Expression of Genes Related to α-Farnesene Biosynthesis

    Journal: Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry

    doi: 10.3390/molecules22040546

    The percent reduction in emission of selected volatile organic compounds from flowers of J. sambac ‘Bifoliatum’ sprayed with 50 μm/L lovastatin.
    Figure Legend Snippet: The percent reduction in emission of selected volatile organic compounds from flowers of J. sambac ‘Bifoliatum’ sprayed with 50 μm/L lovastatin.

    Techniques Used:

    qRT-PCR analysis of JsHMGS ( A ); JsHMGR ( B ); JsFPPS ( C ); and JsTPS ( D ) expressions in J. sambac ‘Bifoliatum’ flowers immediately after being sprayed with 50 μm/L lovastatin or dimethyl sulfoxide (DMSO) to 6 h, thereafter. The expression levels were normalized based on the expression of the internal control gene actin and corresponding genes expressed at the bud stage. The bars represent standard errors of three replicates ( n = 3).
    Figure Legend Snippet: qRT-PCR analysis of JsHMGS ( A ); JsHMGR ( B ); JsFPPS ( C ); and JsTPS ( D ) expressions in J. sambac ‘Bifoliatum’ flowers immediately after being sprayed with 50 μm/L lovastatin or dimethyl sulfoxide (DMSO) to 6 h, thereafter. The expression levels were normalized based on the expression of the internal control gene actin and corresponding genes expressed at the bud stage. The bars represent standard errors of three replicates ( n = 3).

    Techniques Used: Quantitative RT-PCR, Expressing

    Proposed biosynthesis of α-farnesene in J. sambac ‘Bifoliatum’ where major enzymes include 3-hydroxy-3-methylglutaryl coenzyme A synthase (HMGS), 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR), farnesyl pyrophosphate synthase (FPPS), and terpene synthase (TPS). Lovastatin is an inhibitor to HMGR.
    Figure Legend Snippet: Proposed biosynthesis of α-farnesene in J. sambac ‘Bifoliatum’ where major enzymes include 3-hydroxy-3-methylglutaryl coenzyme A synthase (HMGS), 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR), farnesyl pyrophosphate synthase (FPPS), and terpene synthase (TPS). Lovastatin is an inhibitor to HMGR.

    Techniques Used:

    4) Product Images from "Control of Cyclin D1, p27Kip1, and Cell Cycle Progression in Human Capillary Endothelial Cells by Cell Shape and Cytoskeletal Tension"

    Article Title: Control of Cyclin D1, p27Kip1, and Cell Cycle Progression in Human Capillary Endothelial Cells by Cell Shape and Cytoskeletal Tension

    Journal: Molecular Biology of the Cell

    doi:

    Control of G1 progression by varying cell shape through FN density. (A) Effects of varying FN coating density on DNA synthesis (cumulative BrdU incorporation into nuclei) and pRb hyperphosphorylation as measured in situ by nuclear extractability of hyperphosphorylated pRb (see MATERIALS AND METHODS). Error bars represent SD. (B) Western blots showing the time course of pRb hyperphosphorylation in spread cells on high FN compared with round cells on low FN. Cells were released from the lovastatin block at the time of plating; the slower-migrating band represents the hyperphosphorylated form of pRb. (C) Western blot demonstrating that decreasing the FN coating density inhibits pRb hyperphosphorylation (pRb-pp) when measured 18 h after release of lovastatin arrest in CE cells. (D) Kinetics of entry into S phase in lovastatin-synchronized cells on high FN as measured by pulse labeling with BrdU. (E) Kinetics of entry into S phase was similar in highly extended cells on high FN (3 μg/cm 2 ; ▪) and in moderately spread cells on an intermediate FN density (100 ng/cm 2 ; ○); highly retracted cells on low FN did not enter S phase.
    Figure Legend Snippet: Control of G1 progression by varying cell shape through FN density. (A) Effects of varying FN coating density on DNA synthesis (cumulative BrdU incorporation into nuclei) and pRb hyperphosphorylation as measured in situ by nuclear extractability of hyperphosphorylated pRb (see MATERIALS AND METHODS). Error bars represent SD. (B) Western blots showing the time course of pRb hyperphosphorylation in spread cells on high FN compared with round cells on low FN. Cells were released from the lovastatin block at the time of plating; the slower-migrating band represents the hyperphosphorylated form of pRb. (C) Western blot demonstrating that decreasing the FN coating density inhibits pRb hyperphosphorylation (pRb-pp) when measured 18 h after release of lovastatin arrest in CE cells. (D) Kinetics of entry into S phase in lovastatin-synchronized cells on high FN as measured by pulse labeling with BrdU. (E) Kinetics of entry into S phase was similar in highly extended cells on high FN (3 μg/cm 2 ; ▪) and in moderately spread cells on an intermediate FN density (100 ng/cm 2 ; ○); highly retracted cells on low FN did not enter S phase.

    Techniques Used: DNA Synthesis, BrdU Incorporation Assay, In Situ, Western Blot, Blocking Assay, Labeling

    Related Articles

    MTT Assay:

    Article Title: Cholesterol dependence of Newcastle Disease Virus entry.
    Article Snippet: .. Reagents and antibodies Methyl-β-cyclodextrin (MβCD), cholesterol, lovastatin, Triton-X-100, OptiPrep, FITC-MALI, monoclonal anti-β-tubulin antibody and 3-(4,5-dimethyl-2-thiazoyl)-2,5-diphenyl tetrazolium bromide (MTT) were from Sigma-Aldrich; Octadecylrhodamine B chloride (R18), Hoechst 33258 and Alexa fluor 488 donkey anti-mouse antibody were from Molecular Probes. .. Polyclonal anti-caveolin-1 (N20) and anti-GAPDH antibodies were from Santa Cruz Biotechnology; FITC-SNA was from Vector Laboratories; polyclonal anti-NDV, monoclonal anti-F (2A6) and HN (7B1) antibodies were generous gifts from Dr. Adolfo García-Sastre (Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, USA).

    Flow Cytometry:

    Article Title: Role of lipid rafts in porcine reproductive and respiratory syndrome virus infection in MARC-145 cells.
    Article Snippet: MARC-145 cells were washed three times with PBS, and left in the absence or the presence of either serum-free DMEM containing varying concentrations of MbCD (Sigma) or filipin complex (Sigma) for 1 h, or serum-free DMEM containing varying concentrations of mevinolin (Sigma) for 48 h at 37°C. .. After treatment, the cells were washed three times with PBS before flow cytometry analysis or PRRSV infection.

    Recombinant:

    Article Title: Cholesterol depletion enhances TGF-β Smad signaling by increasing c-Jun expression through a PKR-dependent mechanism
    Article Snippet: .. Reagents Recombinant TGF-β1 (cat. #100-21C) was from PeproTech (Rocky Hill, NJ) and lovastatin (cat. #438185) from Merck-Calbiochem (Darmstadt, Germany). .. Mevalonate (as dl -mevalonic acid lactone; cat. #M4667), HPβCD (cat. #H107), protease inhibitor cocktail (cat. #P8340), phosphatase inhibitor cocktail 2 and 3 (cat. #P5726 and #P0044, respectively), and actinomycin D (cat. #A9415) were from Sigma-Aldrich (St. Louis, MO).

    Article Title: Control of Cyclin D1, p27Kip1, and Cell Cycle Progression in Human Capillary Endothelial Cells by Cell Shape and Cytoskeletal Tension
    Article Snippet: Primary human pulmonary CE cells were obtained from Clonetics (San Diego, CA) and cultured for three to five passages in EBM medium (Clonetics) supplemented with 10 ng/ml human recombinant epidermal growth factor (EGF), 12 μg/ml bovine brain extract, 1 μg/ml hydrocortisone, and 10% FBS (all from Clonetics). .. Before experimental manipulation, cells were synchronized by treatment with 40 μM lovastatin (Merck, Rahway, NJ) in standard culture medium for 32 h. This cell cycle arrest was released by washing the cells free of lovastatin, trypsinizing, and replating them on FN-coated adhesive substrates in experimental medium containing 4 mM mevalonate (Sigma, St. Louis, MO) prepared from the lactone form ( ).

    Article Title: Cholesterol depletion enhances TGF-β Smad signaling by increasing c-Jun expression through a PKR-dependent mechanism
    Article Snippet: .. Recombinant TGF-β1 (cat. #100-21C) was from PeproTech (Rocky Hill, NJ) and lovastatin (cat. #438185) from Merck-Calbiochem (Darmstadt, Germany). .. Mevalonate (as dl -mevalonic acid lactone; cat. #M4667), HPβCD (cat. #H107), protease inhibitor cocktail (cat. #P8340), phosphatase inhibitor cocktail 2 and 3 (cat. #P5726 and #P0044, respectively), and actinomycin D (cat. #A9415) were from Sigma-Aldrich (St. Louis, MO).

    Modification:

    Article Title: Control of Cyclin D1, p27Kip1, and Cell Cycle Progression in Human Capillary Endothelial Cells by Cell Shape and Cytoskeletal Tension
    Article Snippet: Before experimental manipulation, cells were synchronized by treatment with 40 μM lovastatin (Merck, Rahway, NJ) in standard culture medium for 32 h. This cell cycle arrest was released by washing the cells free of lovastatin, trypsinizing, and replating them on FN-coated adhesive substrates in experimental medium containing 4 mM mevalonate (Sigma, St. Louis, MO) prepared from the lactone form ( ). .. For experiments, the culture medium was modified by lowering the concentration of FBS to 2% and adding 5 ng/ml recombinant basic fibroblast growth factor (bFGF) (Takeda Chemical Industries, Osaka, Japan), 10 μg/ml high-density lipoprotein (Perimmune, Rockville, MD), and 5 μg/ml transferrin (Collaborative Research, Lexington, MA).

    Cell Cycle Assay:

    Article Title: NF-?B Function in Growth Control: Regulation of Cyclin D1 Expression and G0/G1-to-S-Phase Transition
    Article Snippet: Paragraph title: Cell cycle analysis. ... T47DΔMTcycD1 cells were synchronized in early G1 by treatment with lovastatin (20 μM; Calbiochem) for 30 to 36 h and subsequent stimulation by removal of lovastatin and addition of mevalonate (2 mM; Sigma).

    Protease Inhibitor:

    Article Title: Cholesterol depletion enhances TGF-β Smad signaling by increasing c-Jun expression through a PKR-dependent mechanism
    Article Snippet: Reagents Recombinant TGF-β1 (cat. #100-21C) was from PeproTech (Rocky Hill, NJ) and lovastatin (cat. #438185) from Merck-Calbiochem (Darmstadt, Germany). .. Mevalonate (as dl -mevalonic acid lactone; cat. #M4667), HPβCD (cat. #H107), protease inhibitor cocktail (cat. #P8340), phosphatase inhibitor cocktail 2 and 3 (cat. #P5726 and #P0044, respectively), and actinomycin D (cat. #A9415) were from Sigma-Aldrich (St. Louis, MO).

    Article Title: Cholesterol depletion enhances TGF-β Smad signaling by increasing c-Jun expression through a PKR-dependent mechanism
    Article Snippet: Recombinant TGF-β1 (cat. #100-21C) was from PeproTech (Rocky Hill, NJ) and lovastatin (cat. #438185) from Merck-Calbiochem (Darmstadt, Germany). .. Mevalonate (as dl -mevalonic acid lactone; cat. #M4667), HPβCD (cat. #H107), protease inhibitor cocktail (cat. #P8340), phosphatase inhibitor cocktail 2 and 3 (cat. #P5726 and #P0044, respectively), and actinomycin D (cat. #A9415) were from Sigma-Aldrich (St. Louis, MO).

    Transferring:

    Article Title: Inhibition of Sterol Biosynthesis Reduces Tombusvirus Replication in Yeast and Plants ▿
    Article Snippet: TBSV repRNA was expressed by transferring the culture to SC-LH− medium containing 2% galactose at 29°C. .. To study the effect of lovastatin on TBSV DI-72 repRNA accumulation in yeast, we prepared a stock solution of lovastatin (Sigma) according to reference .

    Transfection:

    Article Title: Influenza A Virus Hemagglutinin and Neuraminidase Mutually Accelerate Their Apical Targeting through Clustering of Lipid Rafts
    Article Snippet: .. For the inhibition of cholesterol synthesis, 293T and MDCK cells were pretreated with 8 μM lovastatin (Merck) for 12 h. After transfection, the cells were incubated in the presence of 8 μM lovastatin for 12 or 24 h. The cells were further treated with 5 or 10 mM methyl-β-cyclodextrin (MβCD) (Sigma) in the presence of 8 μM lovastatin for 1 h. .. Polarized MDCK cells were grown on coverslips in 12-well plates and were either infected with virus or transfected with protein expression plasmids.

    Cell Culture:

    Article Title: Control of Cyclin D1, p27Kip1, and Cell Cycle Progression in Human Capillary Endothelial Cells by Cell Shape and Cytoskeletal Tension
    Article Snippet: Paragraph title: Cell Culture and Reagents ... Before experimental manipulation, cells were synchronized by treatment with 40 μM lovastatin (Merck, Rahway, NJ) in standard culture medium for 32 h. This cell cycle arrest was released by washing the cells free of lovastatin, trypsinizing, and replating them on FN-coated adhesive substrates in experimental medium containing 4 mM mevalonate (Sigma, St. Louis, MO) prepared from the lactone form ( ).

    Mouse Assay:

    Article Title: Hippocampal Dysregulation of Neurofibromin-Dependent Pathways Is Associated with Impaired Spatial Learning in Engrailed 2 Knock-Out Mice
    Article Snippet: .. To test the effect of lovastatin on MWM performance, mice were given subcutaneous injections of 10 mg/kg lovastatin (Mevinolin; Sigma) for 3 d before the first training day and then 6 h before training every day ( ). ..

    Gas Chromatography-Mass Spectrometry:

    Article Title: Volatiles Emitted at Different Flowering Stages of Jasminum sambac and Expression of Genes Related to α-Farnesene Biosynthesis
    Article Snippet: To investigate the effect of exogenous application of lovastatin on gene expression in the MVP pathway, lovastatin (Sigma-Aldrich) was diluted in dimethyl sulphoxide (DMSO) (Sigma-Aldrich) at 50 μm/L and sprayed on living jasmine flowers at the stage 2. .. Control petals or those treated with lovastatin were taken 0, 2, 4, and 6 h after application and analyzed by GC-MS as mentioned above.

    Incubation:

    Article Title: Role of lipid rafts in porcine reproductive and respiratory syndrome virus infection in MARC-145 cells.
    Article Snippet: MARC-145 cells were washed three times with PBS, and left in the absence or the presence of either serum-free DMEM containing varying concentrations of MbCD (Sigma) or filipin complex (Sigma) for 1 h, or serum-free DMEM containing varying concentrations of mevinolin (Sigma) for 48 h at 37°C. .. As mevinolin and filipin complex were dissolved in DMSO (MbCD was dissolved in water), the control cells were also incubated in medium with the same amount of DMSO as used for mevinolin and filipin complex.

    Article Title: Influenza A Virus Hemagglutinin and Neuraminidase Mutually Accelerate Their Apical Targeting through Clustering of Lipid Rafts
    Article Snippet: .. For the inhibition of cholesterol synthesis, 293T and MDCK cells were pretreated with 8 μM lovastatin (Merck) for 12 h. After transfection, the cells were incubated in the presence of 8 μM lovastatin for 12 or 24 h. The cells were further treated with 5 or 10 mM methyl-β-cyclodextrin (MβCD) (Sigma) in the presence of 8 μM lovastatin for 1 h. .. Polarized MDCK cells were grown on coverslips in 12-well plates and were either infected with virus or transfected with protein expression plasmids.

    Inhibition:

    Article Title: Influenza A Virus Hemagglutinin and Neuraminidase Mutually Accelerate Their Apical Targeting through Clustering of Lipid Rafts
    Article Snippet: .. For the inhibition of cholesterol synthesis, 293T and MDCK cells were pretreated with 8 μM lovastatin (Merck) for 12 h. After transfection, the cells were incubated in the presence of 8 μM lovastatin for 12 or 24 h. The cells were further treated with 5 or 10 mM methyl-β-cyclodextrin (MβCD) (Sigma) in the presence of 8 μM lovastatin for 1 h. .. Polarized MDCK cells were grown on coverslips in 12-well plates and were either infected with virus or transfected with protein expression plasmids.

    Infection:

    Article Title: Role of lipid rafts in porcine reproductive and respiratory syndrome virus infection in MARC-145 cells.
    Article Snippet: Paragraph title: Cholesterol depletion and replenishment on virus infection ... MARC-145 cells were washed three times with PBS, and left in the absence or the presence of either serum-free DMEM containing varying concentrations of MbCD (Sigma) or filipin complex (Sigma) for 1 h, or serum-free DMEM containing varying concentrations of mevinolin (Sigma) for 48 h at 37°C.

    Expressing:

    Article Title: NF-?B Function in Growth Control: Regulation of Cyclin D1 Expression and G0/G1-to-S-Phase Transition
    Article Snippet: T47DΔMTcycD1 cells were synchronized in early G1 by treatment with lovastatin (20 μM; Calbiochem) for 30 to 36 h and subsequent stimulation by removal of lovastatin and addition of mevalonate (2 mM; Sigma). .. For ectopic cyclin D1 expression, cells were additionally treated with 75 μM ZnSO4 .

    Article Title: Volatiles Emitted at Different Flowering Stages of Jasminum sambac and Expression of Genes Related to α-Farnesene Biosynthesis
    Article Snippet: .. To investigate the effect of exogenous application of lovastatin on gene expression in the MVP pathway, lovastatin (Sigma-Aldrich) was diluted in dimethyl sulphoxide (DMSO) (Sigma-Aldrich) at 50 μm/L and sprayed on living jasmine flowers at the stage 2. ..

    Concentration Assay:

    Article Title: Control of Cyclin D1, p27Kip1, and Cell Cycle Progression in Human Capillary Endothelial Cells by Cell Shape and Cytoskeletal Tension
    Article Snippet: Before experimental manipulation, cells were synchronized by treatment with 40 μM lovastatin (Merck, Rahway, NJ) in standard culture medium for 32 h. This cell cycle arrest was released by washing the cells free of lovastatin, trypsinizing, and replating them on FN-coated adhesive substrates in experimental medium containing 4 mM mevalonate (Sigma, St. Louis, MO) prepared from the lactone form ( ). .. For experiments, the culture medium was modified by lowering the concentration of FBS to 2% and adding 5 ng/ml recombinant basic fibroblast growth factor (bFGF) (Takeda Chemical Industries, Osaka, Japan), 10 μg/ml high-density lipoprotein (Perimmune, Rockville, MD), and 5 μg/ml transferrin (Collaborative Research, Lexington, MA).

    Sampling:

    Article Title: Volatiles Emitted at Different Flowering Stages of Jasminum sambac and Expression of Genes Related to α-Farnesene Biosynthesis
    Article Snippet: To investigate the effect of exogenous application of lovastatin on gene expression in the MVP pathway, lovastatin (Sigma-Aldrich) was diluted in dimethyl sulphoxide (DMSO) (Sigma-Aldrich) at 50 μm/L and sprayed on living jasmine flowers at the stage 2. .. There were three biological replicates per treatment at each sampling time.

    Adsorption:

    Article Title: Role of lipid rafts in porcine reproductive and respiratory syndrome virus infection in MARC-145 cells.
    Article Snippet: Cholesterol depletion and replenishment on virus infection To study the effects of cholesterol depletion on PRRSV infection, MARC-145 cells were washed three times with phosphate-buffered saline (PBS), and then were treated with 0, 1, 2 and 3 mM MbCD for 1 h before viral adsorption or throughout infection period (À1 to 24 h). .. MARC-145 cells were washed three times with PBS, and left in the absence or the presence of either serum-free DMEM containing varying concentrations of MbCD (Sigma) or filipin complex (Sigma) for 1 h, or serum-free DMEM containing varying concentrations of mevinolin (Sigma) for 48 h at 37°C.

    other:

    Article Title: Comparative characteristics of rice wine fermentations using Monascus koji and rice nuruk
    Article Snippet: Other chemicals, including soluble starch, casein, glucose, ethanol, monacolin K, citrinin, 3, 5-dinitrosalicylic acid (DNS), trifluoro acetic acid, phosphoric acid, and acetonitrile, were also purchased from Sigma–Aldrich (St. Louis, USA).

    Plasmid Preparation:

    Article Title: Cholesterol dependence of Newcastle Disease Virus entry.
    Article Snippet: Reagents and antibodies Methyl-β-cyclodextrin (MβCD), cholesterol, lovastatin, Triton-X-100, OptiPrep, FITC-MALI, monoclonal anti-β-tubulin antibody and 3-(4,5-dimethyl-2-thiazoyl)-2,5-diphenyl tetrazolium bromide (MTT) were from Sigma-Aldrich; Octadecylrhodamine B chloride (R18), Hoechst 33258 and Alexa fluor 488 donkey anti-mouse antibody were from Molecular Probes. .. Reagents and antibodies Methyl-β-cyclodextrin (MβCD), cholesterol, lovastatin, Triton-X-100, OptiPrep, FITC-MALI, monoclonal anti-β-tubulin antibody and 3-(4,5-dimethyl-2-thiazoyl)-2,5-diphenyl tetrazolium bromide (MTT) were from Sigma-Aldrich; Octadecylrhodamine B chloride (R18), Hoechst 33258 and Alexa fluor 488 donkey anti-mouse antibody were from Molecular Probes.

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  • 99
    Millipore lovastatin
    Statins diminish UCN-01–induced ERK1/2 activation and enhance Akt inactivation while reciprocally promoting JNK activation . (A) U937 cells (upper panels) were exposed for 18 hours to 100 nM UCN-01 (UCN) with or without 20 μM <t>lovastatin</t>
    Lovastatin, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lovastatin/product/Millipore
    Average 99 stars, based on 24 article reviews
    Price from $9.99 to $1999.99
    lovastatin - by Bioz Stars, 2020-04
    99/100 stars
      Buy from Supplier

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    Statins diminish UCN-01–induced ERK1/2 activation and enhance Akt inactivation while reciprocally promoting JNK activation . (A) U937 cells (upper panels) were exposed for 18 hours to 100 nM UCN-01 (UCN) with or without 20 μM lovastatin

    Journal:

    Article Title: Statins synergistically potentiate 7-hydroxystaurosporine (UCN-01) lethality in human leukemia and myeloma cells by disrupting Ras farnesylation and activation

    doi: 10.1182/blood-2006-09-047076

    Figure Lengend Snippet: Statins diminish UCN-01–induced ERK1/2 activation and enhance Akt inactivation while reciprocally promoting JNK activation . (A) U937 cells (upper panels) were exposed for 18 hours to 100 nM UCN-01 (UCN) with or without 20 μM lovastatin

    Article Snippet: Lovastatin (Calbiochem, San Diego, CA) and fluvastatin (LKT, St. Paul, MN) were dissolved in DMSO and stored at −80°C.

    Techniques: Activation Assay

    Expression of constitutively activated Ras (Q61L) prevents lovastatin from interrupting UCN-01–mediated ERK1/2 activation and significantly attenuates apoptosis induced by the regimen . (A) U266 cells were stably transfected with constructs encoding

    Journal:

    Article Title: Statins synergistically potentiate 7-hydroxystaurosporine (UCN-01) lethality in human leukemia and myeloma cells by disrupting Ras farnesylation and activation

    doi: 10.1182/blood-2006-09-047076

    Figure Lengend Snippet: Expression of constitutively activated Ras (Q61L) prevents lovastatin from interrupting UCN-01–mediated ERK1/2 activation and significantly attenuates apoptosis induced by the regimen . (A) U266 cells were stably transfected with constructs encoding

    Article Snippet: Lovastatin (Calbiochem, San Diego, CA) and fluvastatin (LKT, St. Paul, MN) were dissolved in DMSO and stored at −80°C.

    Techniques: Expressing, Activation Assay, Stable Transfection, Transfection, Construct

    Statins, administered alone or in combination with UCN-01, induce perturbations in protein prenylation . (A) U937 cells (left panels) were exposed for 18 hours to 100 nM UCN-01 (UCN) with or without 20 μM lovastatin (LV), 40 μM fluvastatin

    Journal:

    Article Title: Statins synergistically potentiate 7-hydroxystaurosporine (UCN-01) lethality in human leukemia and myeloma cells by disrupting Ras farnesylation and activation

    doi: 10.1182/blood-2006-09-047076

    Figure Lengend Snippet: Statins, administered alone or in combination with UCN-01, induce perturbations in protein prenylation . (A) U937 cells (left panels) were exposed for 18 hours to 100 nM UCN-01 (UCN) with or without 20 μM lovastatin (LV), 40 μM fluvastatin

    Article Snippet: Lovastatin (Calbiochem, San Diego, CA) and fluvastatin (LKT, St. Paul, MN) were dissolved in DMSO and stored at −80°C.

    Techniques:

    Statin-mediated disruption of farnesylation but not geranylation contributes to potentiation of UCN-01–induced apoptosis . (A) U937 cells were incubated for 18 hours with 100 nM UCN-01 (UCN) + 20 μM lovastatin (LV) in either the presence

    Journal:

    Article Title: Statins synergistically potentiate 7-hydroxystaurosporine (UCN-01) lethality in human leukemia and myeloma cells by disrupting Ras farnesylation and activation

    doi: 10.1182/blood-2006-09-047076

    Figure Lengend Snippet: Statin-mediated disruption of farnesylation but not geranylation contributes to potentiation of UCN-01–induced apoptosis . (A) U937 cells were incubated for 18 hours with 100 nM UCN-01 (UCN) + 20 μM lovastatin (LV) in either the presence

    Article Snippet: Lovastatin (Calbiochem, San Diego, CA) and fluvastatin (LKT, St. Paul, MN) were dissolved in DMSO and stored at −80°C.

    Techniques: Incubation

    Statins interact synergistically with UCN-01 to induce apoptosis in human malignant hematopoietic cells . (A) Human myelomonoyctic leukemia U937 cells were exposed for 18 hours to 100 nM UCN-01 (UCN) with or without 20 μM lovastatin (LV), 40 μM

    Journal:

    Article Title: Statins synergistically potentiate 7-hydroxystaurosporine (UCN-01) lethality in human leukemia and myeloma cells by disrupting Ras farnesylation and activation

    doi: 10.1182/blood-2006-09-047076

    Figure Lengend Snippet: Statins interact synergistically with UCN-01 to induce apoptosis in human malignant hematopoietic cells . (A) Human myelomonoyctic leukemia U937 cells were exposed for 18 hours to 100 nM UCN-01 (UCN) with or without 20 μM lovastatin (LV), 40 μM

    Article Snippet: Lovastatin (Calbiochem, San Diego, CA) and fluvastatin (LKT, St. Paul, MN) were dissolved in DMSO and stored at −80°C.

    Techniques:

    Statins inhibit the ERK MAP kinase pathway in YT-INDY cells. YT-INDY cells were incubated with various concentration of statins, followed by Western blotting for ERK and phospho-ERK. Control cells were treated with the solvents in which the drugs were dissolved. All compounds were added to the cells at the start of the experiment. Each experiment was performed at least four times. a The results demonstrate that lovastatin, simvastatin, atorvastatin, mevastatin and fluvastatin could inhibit ERK MAP kinase pathway activation at relatively low drug concentrations, whereas no inhibition of the pathway was observed with pravastatin. This was likely due to the hydrophilic nature of the drug preventing it from crossing the YT-INDY cell membrane. b Using the five statins that inhibited the ERK MAP kinase pathway, the ability of mevalonate (1 mM or 0.5 mM) to restore the pathway was determined. Our results showed that 1 mM mevalonate was capable of restoring all statin-mediated inhibition of the ERK MAP pathway and 0.5 mM was sufficient to restore activity for all statins except lovastatin

    Journal: Biomarker Research

    Article Title: Combination statin and chemotherapy inhibits proliferation and cytotoxicity of an aggressive natural killer cell leukemia

    doi: 10.1186/s40364-018-0140-0

    Figure Lengend Snippet: Statins inhibit the ERK MAP kinase pathway in YT-INDY cells. YT-INDY cells were incubated with various concentration of statins, followed by Western blotting for ERK and phospho-ERK. Control cells were treated with the solvents in which the drugs were dissolved. All compounds were added to the cells at the start of the experiment. Each experiment was performed at least four times. a The results demonstrate that lovastatin, simvastatin, atorvastatin, mevastatin and fluvastatin could inhibit ERK MAP kinase pathway activation at relatively low drug concentrations, whereas no inhibition of the pathway was observed with pravastatin. This was likely due to the hydrophilic nature of the drug preventing it from crossing the YT-INDY cell membrane. b Using the five statins that inhibited the ERK MAP kinase pathway, the ability of mevalonate (1 mM or 0.5 mM) to restore the pathway was determined. Our results showed that 1 mM mevalonate was capable of restoring all statin-mediated inhibition of the ERK MAP pathway and 0.5 mM was sufficient to restore activity for all statins except lovastatin

    Article Snippet: The statin drugs used in the research include atorvastatin (Toronto Research Chemicals Inc., Toronto, Canada), fluvastatin (Selleck Chemicals, Houston, TX, USA), lovastatin (EMD Millipore, Billerica, MA, USA), mevastatin (EMD Millipore, Billerica, MA, USA), pravastatin (EMD Millipore, Billerica, MA, USA) and simvastatin (EMD Millipore, Billerica, MA, USA).

    Techniques: Incubation, Concentration Assay, Western Blot, Activation Assay, Inhibition, Activity Assay

    Apoptotic staining. Monolayers were stained with propidium iodide and fluorescein-labelled annexin V after 18 days of culture. Propidium (red) stains the nuclei of necrotic cells only. Green stain labels both apoptotic and necrotic cells. Therefore, apoptotic cells are single-stained (green), and necrotic cells are double-stained. Viable cells are not visible on these images. C, non-induced control; D, dexa; L1, 1 μM lovastatin; L5, 5 μM lovastatin; S1, 1 μM simvastatin; S5, 5 μM simvastatin.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Statin-induced calcification in human mesenchymal stem cells is cell death related

    doi: 10.1111/j.1582-4934.2008.00545.x

    Figure Lengend Snippet: Apoptotic staining. Monolayers were stained with propidium iodide and fluorescein-labelled annexin V after 18 days of culture. Propidium (red) stains the nuclei of necrotic cells only. Green stain labels both apoptotic and necrotic cells. Therefore, apoptotic cells are single-stained (green), and necrotic cells are double-stained. Viable cells are not visible on these images. C, non-induced control; D, dexa; L1, 1 μM lovastatin; L5, 5 μM lovastatin; S1, 1 μM simvastatin; S5, 5 μM simvastatin.

    Article Snippet: Lovastatin, simvastatin and pravastatin (all synthetic, from Calbiochem, San Diego, CA, USA) were stored as 1000× stock solutions at −20° C. Pravastatin was reconstituted in Milli-Q water, lovastatin and simvastatin in DMSO.

    Techniques: Staining

    Ca-45 incorporation rates. (A) Dose-dependent increase of Ca-45 incorporation by statins at day 18. C, non-induced control; D, dexa; L, lovastatin; S, simvastatin. The numbers next to letters represent concentrations in μM. 1 donor, the error bars show S.D. of triplicates (experimental error). (B) Calcium incorporation rates relative to non-induced control after 25 days, on a logarithmic scale (3–9 donors, triplicates). C, non-induced control; D, dexa; L1, 1 μM lovastatin; L5, 5 μM lovastatin; S1, 1 μM simvastatin; S5, 5 μM simvastatin. The box contains 50% of the data points. Outliers are noted by circles. * P ≤ 0.05, ** P ≤ 0.01 compared with non-induced control.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Statin-induced calcification in human mesenchymal stem cells is cell death related

    doi: 10.1111/j.1582-4934.2008.00545.x

    Figure Lengend Snippet: Ca-45 incorporation rates. (A) Dose-dependent increase of Ca-45 incorporation by statins at day 18. C, non-induced control; D, dexa; L, lovastatin; S, simvastatin. The numbers next to letters represent concentrations in μM. 1 donor, the error bars show S.D. of triplicates (experimental error). (B) Calcium incorporation rates relative to non-induced control after 25 days, on a logarithmic scale (3–9 donors, triplicates). C, non-induced control; D, dexa; L1, 1 μM lovastatin; L5, 5 μM lovastatin; S1, 1 μM simvastatin; S5, 5 μM simvastatin. The box contains 50% of the data points. Outliers are noted by circles. * P ≤ 0.05, ** P ≤ 0.01 compared with non-induced control.

    Article Snippet: Lovastatin, simvastatin and pravastatin (all synthetic, from Calbiochem, San Diego, CA, USA) were stored as 1000× stock solutions at −20° C. Pravastatin was reconstituted in Milli-Q water, lovastatin and simvastatin in DMSO.

    Techniques:

    Effect of statins on cell number. (A) Dose-dependent decrease in cell number at day 18. C, non-induced control; D, dexa; L, lovastatin; S, simvastatin. The numbers next to letters represent concentrations in μM. 1 donor, the error bars show S.D. of triplicates (experimental error). (B) Relative metabolic activity determined by MTT assay at different time-points. All values are compared to day 0. The grey error bars represent standard deviation of triplicate samples from 2 donors. † P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Statin-induced calcification in human mesenchymal stem cells is cell death related

    doi: 10.1111/j.1582-4934.2008.00545.x

    Figure Lengend Snippet: Effect of statins on cell number. (A) Dose-dependent decrease in cell number at day 18. C, non-induced control; D, dexa; L, lovastatin; S, simvastatin. The numbers next to letters represent concentrations in μM. 1 donor, the error bars show S.D. of triplicates (experimental error). (B) Relative metabolic activity determined by MTT assay at different time-points. All values are compared to day 0. The grey error bars represent standard deviation of triplicate samples from 2 donors. † P

    Article Snippet: Lovastatin, simvastatin and pravastatin (all synthetic, from Calbiochem, San Diego, CA, USA) were stored as 1000× stock solutions at −20° C. Pravastatin was reconstituted in Milli-Q water, lovastatin and simvastatin in DMSO.

    Techniques: Activity Assay, MTT Assay, Standard Deviation

    Alkaline phosphatase. (A) Dose-dependent suppression of ALP activity by statins at day 18. C, non-induced control; D, dexa; L, lovastatin; S, simvastatin. The numbers next to letters represent concentrations in μM. 1 donor, the error bars show S.D. of triplicates (experimental error). (B) ALP activity was measured with a para-nitrophenylphosphate assay at day 11. The amount of product was normalized to DNA, and compared with the activity of the non-induced control. C, non-induced control; D, dexa; L1, 1 μM lovastatin; L5, 5 μM lovastatin; S1, 1 μM simvastatin; S5, 5 μM simvastatin. The error bars represent ±1 S.D. The data are triplicates from 1 to 6 donors ( n = 1 in case of S1). * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Statin-induced calcification in human mesenchymal stem cells is cell death related

    doi: 10.1111/j.1582-4934.2008.00545.x

    Figure Lengend Snippet: Alkaline phosphatase. (A) Dose-dependent suppression of ALP activity by statins at day 18. C, non-induced control; D, dexa; L, lovastatin; S, simvastatin. The numbers next to letters represent concentrations in μM. 1 donor, the error bars show S.D. of triplicates (experimental error). (B) ALP activity was measured with a para-nitrophenylphosphate assay at day 11. The amount of product was normalized to DNA, and compared with the activity of the non-induced control. C, non-induced control; D, dexa; L1, 1 μM lovastatin; L5, 5 μM lovastatin; S1, 1 μM simvastatin; S5, 5 μM simvastatin. The error bars represent ±1 S.D. The data are triplicates from 1 to 6 donors ( n = 1 in case of S1). * P

    Article Snippet: Lovastatin, simvastatin and pravastatin (all synthetic, from Calbiochem, San Diego, CA, USA) were stored as 1000× stock solutions at −20° C. Pravastatin was reconstituted in Milli-Q water, lovastatin and simvastatin in DMSO.

    Techniques: ALP Assay, Activity Assay

    BMP-2 expression. Relative amount of BMP-2 mRNA in different treatment groups at three time-points (distinguished by greyscale shading). C, non-induced control; D, dexa; L1, 1 μM lovastatin; L5, 5 μM lovastatin; S1, 1 μM simvastatin; S5, 5 μM simvastatin. Each bar represents a mean value of 2–6 experiments ( n = 2–6). All values are relative to day 4 non-induced control of the respective experiment, and are plotted on a logarithmic scale. The error bars span 1 S.D.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Statin-induced calcification in human mesenchymal stem cells is cell death related

    doi: 10.1111/j.1582-4934.2008.00545.x

    Figure Lengend Snippet: BMP-2 expression. Relative amount of BMP-2 mRNA in different treatment groups at three time-points (distinguished by greyscale shading). C, non-induced control; D, dexa; L1, 1 μM lovastatin; L5, 5 μM lovastatin; S1, 1 μM simvastatin; S5, 5 μM simvastatin. Each bar represents a mean value of 2–6 experiments ( n = 2–6). All values are relative to day 4 non-induced control of the respective experiment, and are plotted on a logarithmic scale. The error bars span 1 S.D.

    Article Snippet: Lovastatin, simvastatin and pravastatin (all synthetic, from Calbiochem, San Diego, CA, USA) were stored as 1000× stock solutions at −20° C. Pravastatin was reconstituted in Milli-Q water, lovastatin and simvastatin in DMSO.

    Techniques: Expressing

    Antiviral activity of other statins against EBOV. (A) Huh7 cells were infected with Ebola virus (EBOV) at an MOI of 0.05. After infection, cells were washed and then treated with various concentrations of lovastatin, fluvastatin, simvastatin, atorvastatin, rosuvastatin, and pitavastatin or DMSO (control). Culture supernatants were harvested 72 hpi, and viral titers were quantified by 50% tissue culture infective dose (TCID 50 ) determination. (B) Viability (percentage) of Huh7 cells treated with lovastatin, fluvastatin, simvastatin, atorvastatin, rosuvastatin, and pitavastatin or DMSO (control) was determined after 72 h of treatment. Values were normalized to DMSO-treated controls.

    Journal: mBio

    Article Title: Statins Suppress Ebola Virus Infectivity by Interfering with Glycoprotein Processing

    doi: 10.1128/mBio.00660-18

    Figure Lengend Snippet: Antiviral activity of other statins against EBOV. (A) Huh7 cells were infected with Ebola virus (EBOV) at an MOI of 0.05. After infection, cells were washed and then treated with various concentrations of lovastatin, fluvastatin, simvastatin, atorvastatin, rosuvastatin, and pitavastatin or DMSO (control). Culture supernatants were harvested 72 hpi, and viral titers were quantified by 50% tissue culture infective dose (TCID 50 ) determination. (B) Viability (percentage) of Huh7 cells treated with lovastatin, fluvastatin, simvastatin, atorvastatin, rosuvastatin, and pitavastatin or DMSO (control) was determined after 72 h of treatment. Values were normalized to DMSO-treated controls.

    Article Snippet: Lovastatin was from Calbiochem (Billerica, MA).

    Techniques: Activity Assay, Infection