nifedipine  (Selleck Chemicals)

 
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    Name:
    Nifedipine
    Description:
    Nifedipine is a dihydropyridine calcium channel blocker used to lower hypertension and to treat angina
    Catalog Number:
    s1808
    Molecular Weight:
    346.33
    Price:
    None
    Category:
    Calcium Channel inhibitor Transmembrane Transporters
    Formula:
    C17H18N2O6
    Buy from Supplier


    Structured Review

    Selleck Chemicals nifedipine
    Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or <t>nifedipine.</t> Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P
    Nifedipine is a dihydropyridine calcium channel blocker used to lower hypertension and to treat angina
    https://www.bioz.com/result/nifedipine/product/Selleck Chemicals
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nifedipine - by Bioz Stars, 2020-09
    94/100 stars

    Images

    1) Product Images from "Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER–mitochondrial dynamics"

    Article Title: Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER–mitochondrial dynamics

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-018-1009-8

    Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P
    Figure Legend Snippet: Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P

    Techniques Used: Labeling, Fluorescence

    2) Product Images from "Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER–mitochondrial dynamics"

    Article Title: Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER–mitochondrial dynamics

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-018-1009-8

    Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P
    Figure Legend Snippet: Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P

    Techniques Used: Labeling, Fluorescence

    3) Product Images from "Modeling Congenital Hyperinsulinism with ABCC8-Deficient Human Embryonic Stem Cells Generated by CRISPR/Cas9"

    Article Title: Modeling Congenital Hyperinsulinism with ABCC8-Deficient Human Embryonic Stem Cells Generated by CRISPR/Cas9

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-03349-w

    ABCC8 -deficient insulin-producing cells exhibited greater insulin secretion and insulin secretion responses to the various stimulations. ( A ) Schematic of directed differentiation from pluripotent stem cells to insulin-producing cells via the small molecule-based method. ( B ) Immunofluorescence for insulin at the final stage of differentiation. ABCC8 -deficient cells demonstrated similar differentiation efficiency as wild-type cells. ( C ) ELISA analysis for insulin content in the supernatant. ABCC8 -deficient cells demonstrated greater insulin secretion than wild-type cells. ( D ) ELISA analysis for C-peptide content in the supernatant. ABCC8 -deficient cells demonstrated greater C-peptide secretion than wild-type cells. ( E ) ELISA analysis for C-peptide levels in the presence of vehicle, diazoxide and glimepiride. ( F ) The fold change of C-peptide content after diazoxide and glimepiride stimulation. Diazoxide and glimepiride decreased and increased C-peptide secretion in wild-type and heterozygous mutated cells, respectively. Neither diazoxide nor glimepiride had an effect on homozygous mutated cells. ( G ) The fold change of C-peptide content after octreotide, nicorandil and nifedipine treatment. Octreotide, nicorandil and nifedipine decreased insulin secretion in wild-type, heterozygous mutated and homozygous mutated cells. ( H ) The fold change of C-peptide content after ouabain, extracellular ATP and calcium chloride treatment.
    Figure Legend Snippet: ABCC8 -deficient insulin-producing cells exhibited greater insulin secretion and insulin secretion responses to the various stimulations. ( A ) Schematic of directed differentiation from pluripotent stem cells to insulin-producing cells via the small molecule-based method. ( B ) Immunofluorescence for insulin at the final stage of differentiation. ABCC8 -deficient cells demonstrated similar differentiation efficiency as wild-type cells. ( C ) ELISA analysis for insulin content in the supernatant. ABCC8 -deficient cells demonstrated greater insulin secretion than wild-type cells. ( D ) ELISA analysis for C-peptide content in the supernatant. ABCC8 -deficient cells demonstrated greater C-peptide secretion than wild-type cells. ( E ) ELISA analysis for C-peptide levels in the presence of vehicle, diazoxide and glimepiride. ( F ) The fold change of C-peptide content after diazoxide and glimepiride stimulation. Diazoxide and glimepiride decreased and increased C-peptide secretion in wild-type and heterozygous mutated cells, respectively. Neither diazoxide nor glimepiride had an effect on homozygous mutated cells. ( G ) The fold change of C-peptide content after octreotide, nicorandil and nifedipine treatment. Octreotide, nicorandil and nifedipine decreased insulin secretion in wild-type, heterozygous mutated and homozygous mutated cells. ( H ) The fold change of C-peptide content after ouabain, extracellular ATP and calcium chloride treatment.

    Techniques Used: Immunofluorescence, Enzyme-linked Immunosorbent Assay

    Related Articles

    Incubation:

    Article Title: Modeling Congenital Hyperinsulinism with ABCC8-Deficient Human Embryonic Stem Cells Generated by CRISPR/Cas9
    Article Snippet: .. Then, the same cells were incubated with KRBH buffer containing 50 μg/mL octreotide acetate (Selleck, dissolved in H2 O), 200 μM nicorandil (Selleck, dissolved in DMSO), or 50 μM nifedipine (Selleck) for 1 h at 37 °C, and the supernatant was collected. ..

    Microscopy:

    Article Title: Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER–mitochondrial dynamics
    Article Snippet: .. Briefly, neurons were treated with polybrene for 24 h. For the polybrene treatment with 5 mM EGTA or 50 µM nifedipine (S1808, Selleck), drugs were added simultaneously with polybrene for 12 h. Neurons were observed under a phase-contrast microscope. ..

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  • 94
    Selleck Chemicals nifedipine
    Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or <t>nifedipine.</t> Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P
    Nifedipine, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nifedipine/product/Selleck Chemicals
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nifedipine - by Bioz Stars, 2020-09
    94/100 stars
      Buy from Supplier

    Image Search Results


    Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P

    Journal: Cell Death & Disease

    Article Title: Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER–mitochondrial dynamics

    doi: 10.1038/s41419-018-1009-8

    Figure Lengend Snippet: Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P

    Article Snippet: Briefly, neurons were treated with polybrene for 24 h. For the polybrene treatment with 5 mM EGTA or 50 µM nifedipine (S1808, Selleck), drugs were added simultaneously with polybrene for 12 h. Neurons were observed under a phase-contrast microscope.

    Techniques: Labeling, Fluorescence

    Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P

    Journal: Cell Death & Disease

    Article Title: Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER–mitochondrial dynamics

    doi: 10.1038/s41419-018-1009-8

    Figure Lengend Snippet: Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P

    Article Snippet: Briefly, neurons were treated with polybrene for 24 h. For the polybrene treatment with 5 mM EGTA or 50 µM nifedipine (S1808, Selleck), drugs were added simultaneously with polybrene for 12 h. Neurons were observed under a phase-contrast microscope.

    Techniques: Labeling, Fluorescence

    ABCC8 -deficient insulin-producing cells exhibited greater insulin secretion and insulin secretion responses to the various stimulations. ( A ) Schematic of directed differentiation from pluripotent stem cells to insulin-producing cells via the small molecule-based method. ( B ) Immunofluorescence for insulin at the final stage of differentiation. ABCC8 -deficient cells demonstrated similar differentiation efficiency as wild-type cells. ( C ) ELISA analysis for insulin content in the supernatant. ABCC8 -deficient cells demonstrated greater insulin secretion than wild-type cells. ( D ) ELISA analysis for C-peptide content in the supernatant. ABCC8 -deficient cells demonstrated greater C-peptide secretion than wild-type cells. ( E ) ELISA analysis for C-peptide levels in the presence of vehicle, diazoxide and glimepiride. ( F ) The fold change of C-peptide content after diazoxide and glimepiride stimulation. Diazoxide and glimepiride decreased and increased C-peptide secretion in wild-type and heterozygous mutated cells, respectively. Neither diazoxide nor glimepiride had an effect on homozygous mutated cells. ( G ) The fold change of C-peptide content after octreotide, nicorandil and nifedipine treatment. Octreotide, nicorandil and nifedipine decreased insulin secretion in wild-type, heterozygous mutated and homozygous mutated cells. ( H ) The fold change of C-peptide content after ouabain, extracellular ATP and calcium chloride treatment.

    Journal: Scientific Reports

    Article Title: Modeling Congenital Hyperinsulinism with ABCC8-Deficient Human Embryonic Stem Cells Generated by CRISPR/Cas9

    doi: 10.1038/s41598-017-03349-w

    Figure Lengend Snippet: ABCC8 -deficient insulin-producing cells exhibited greater insulin secretion and insulin secretion responses to the various stimulations. ( A ) Schematic of directed differentiation from pluripotent stem cells to insulin-producing cells via the small molecule-based method. ( B ) Immunofluorescence for insulin at the final stage of differentiation. ABCC8 -deficient cells demonstrated similar differentiation efficiency as wild-type cells. ( C ) ELISA analysis for insulin content in the supernatant. ABCC8 -deficient cells demonstrated greater insulin secretion than wild-type cells. ( D ) ELISA analysis for C-peptide content in the supernatant. ABCC8 -deficient cells demonstrated greater C-peptide secretion than wild-type cells. ( E ) ELISA analysis for C-peptide levels in the presence of vehicle, diazoxide and glimepiride. ( F ) The fold change of C-peptide content after diazoxide and glimepiride stimulation. Diazoxide and glimepiride decreased and increased C-peptide secretion in wild-type and heterozygous mutated cells, respectively. Neither diazoxide nor glimepiride had an effect on homozygous mutated cells. ( G ) The fold change of C-peptide content after octreotide, nicorandil and nifedipine treatment. Octreotide, nicorandil and nifedipine decreased insulin secretion in wild-type, heterozygous mutated and homozygous mutated cells. ( H ) The fold change of C-peptide content after ouabain, extracellular ATP and calcium chloride treatment.

    Article Snippet: Then, the same cells were incubated with KRBH buffer containing 50 μg/mL octreotide acetate (Selleck, dissolved in H2 O), 200 μM nicorandil (Selleck, dissolved in DMSO), or 50 μM nifedipine (Selleck) for 1 h at 37 °C, and the supernatant was collected.

    Techniques: Immunofluorescence, Enzyme-linked Immunosorbent Assay