N3033 Search Results


  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 95
    New England Biolabs pbr322 vector
    The DNA-binding properties of β-Casein 197. a ProtParam analysis of predicted binding residues of β-casein 197, predicted binding residues was labeled with a red “+”. b Gel retardation assays. Binding was assayed by the migration of pDNA. Various concentrations of peptides were incubated with 5 µL of 25 µg mL −1 <t>pBR322</t> vector from E. coli at 37 °C for 1 h, and then the reaction mixtures were applied to 0.7% agarose gel electrophoresis. Lane M DNA marker DL 10,000; Lane 1 5 µL pDNA as control; Lanes 2–6 mixture of pDNA and various concentrations of peptides (12.5, 25, 50, 100 and 500 µg mL −1 )
    Pbr322 Vector, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 95/100, based on 62 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pbr322 vector/product/New England Biolabs
    Average 95 stars, based on 62 article reviews
    Price from $9.99 to $1999.99
    pbr322 vector - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    95
    Millipore nitric oxide synthase
    Acetylcholine-mediated vasodilatory responses in isolated mesenteric resistance arteries from HFD fed rats . Vasodilatory responses to acetylcholine (ACh) were measured in the presence and absence of the NOS inhibitor Nω-nitro-L-arginine (LNNA; 100 μM) in small mesenteric arteries ( n = 6-8). Arteries were exposed to LNNA in the lumen and superfusate prior to pre-constriction with phenylephrine to 45-50% resting inner diameter. Vasodilatory responses to acetylcholine (ACh) were also measured in the presence and absence of antioxidants ( n = 5-8). For these studies, arteries were pre-exposed to the ROS scavengers 4,5-Dihydroxy-1,3-benzene-disulfonic acid (tiron; 10 mM) and catalase (1200 U/mL) or EUK-134 (10 μM). Separate arteries were exposed to the nitric oxide <t>synthase</t> inhibitor LNNA (100 μM) or LNNA with the addition of EUK-134 or tiron and catalase. The HFD control data (dotted line) are repeated from figure 2 for comparison. Data are expressed as means ± SEM. * p ≤ 0.05 HFD controls vs. Chow controls; # p ≤ 0.05 vs. HFD controls; † p
    Nitric Oxide Synthase, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 230 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nitric oxide synthase/product/Millipore
    Average 95 stars, based on 230 article reviews
    Price from $9.99 to $1999.99
    nitric oxide synthase - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    Image Search Results


    The DNA-binding properties of β-Casein 197. a ProtParam analysis of predicted binding residues of β-casein 197, predicted binding residues was labeled with a red “+”. b Gel retardation assays. Binding was assayed by the migration of pDNA. Various concentrations of peptides were incubated with 5 µL of 25 µg mL −1 pBR322 vector from E. coli at 37 °C for 1 h, and then the reaction mixtures were applied to 0.7% agarose gel electrophoresis. Lane M DNA marker DL 10,000; Lane 1 5 µL pDNA as control; Lanes 2–6 mixture of pDNA and various concentrations of peptides (12.5, 25, 50, 100 and 500 µg mL −1 )

    Journal: AMB Express

    Article Title: Investigation into the antimicrobial action and mechanism of a novel endogenous peptide β-casein 197 from human milk

    doi: 10.1186/s13568-017-0409-y

    Figure Lengend Snippet: The DNA-binding properties of β-Casein 197. a ProtParam analysis of predicted binding residues of β-casein 197, predicted binding residues was labeled with a red “+”. b Gel retardation assays. Binding was assayed by the migration of pDNA. Various concentrations of peptides were incubated with 5 µL of 25 µg mL −1 pBR322 vector from E. coli at 37 °C for 1 h, and then the reaction mixtures were applied to 0.7% agarose gel electrophoresis. Lane M DNA marker DL 10,000; Lane 1 5 µL pDNA as control; Lanes 2–6 mixture of pDNA and various concentrations of peptides (12.5, 25, 50, 100 and 500 µg mL −1 )

    Article Snippet: DNA binding assay Gel-retardation experiments were performed using 5 µL of a 25 µg mL−1 pBR322 vector from E. coli (BioLabs, New England).

    Techniques: Binding Assay, Labeling, Electrophoretic Mobility Shift Assay, Migration, Incubation, Plasmid Preparation, Agarose Gel Electrophoresis, Marker

    Acetylcholine-mediated vasodilatory responses in isolated mesenteric resistance arteries from HFD fed rats . Vasodilatory responses to acetylcholine (ACh) were measured in the presence and absence of the NOS inhibitor Nω-nitro-L-arginine (LNNA; 100 μM) in small mesenteric arteries ( n = 6-8). Arteries were exposed to LNNA in the lumen and superfusate prior to pre-constriction with phenylephrine to 45-50% resting inner diameter. Vasodilatory responses to acetylcholine (ACh) were also measured in the presence and absence of antioxidants ( n = 5-8). For these studies, arteries were pre-exposed to the ROS scavengers 4,5-Dihydroxy-1,3-benzene-disulfonic acid (tiron; 10 mM) and catalase (1200 U/mL) or EUK-134 (10 μM). Separate arteries were exposed to the nitric oxide synthase inhibitor LNNA (100 μM) or LNNA with the addition of EUK-134 or tiron and catalase. The HFD control data (dotted line) are repeated from figure 2 for comparison. Data are expressed as means ± SEM. * p ≤ 0.05 HFD controls vs. Chow controls; # p ≤ 0.05 vs. HFD controls; † p

    Journal: Nutrition & Metabolism

    Article Title: Comparison of mechanisms involved in impaired vascular reactivity between high sucrose and high fat diets in rats

    doi: 10.1186/1743-7075-7-48

    Figure Lengend Snippet: Acetylcholine-mediated vasodilatory responses in isolated mesenteric resistance arteries from HFD fed rats . Vasodilatory responses to acetylcholine (ACh) were measured in the presence and absence of the NOS inhibitor Nω-nitro-L-arginine (LNNA; 100 μM) in small mesenteric arteries ( n = 6-8). Arteries were exposed to LNNA in the lumen and superfusate prior to pre-constriction with phenylephrine to 45-50% resting inner diameter. Vasodilatory responses to acetylcholine (ACh) were also measured in the presence and absence of antioxidants ( n = 5-8). For these studies, arteries were pre-exposed to the ROS scavengers 4,5-Dihydroxy-1,3-benzene-disulfonic acid (tiron; 10 mM) and catalase (1200 U/mL) or EUK-134 (10 μM). Separate arteries were exposed to the nitric oxide synthase inhibitor LNNA (100 μM) or LNNA with the addition of EUK-134 or tiron and catalase. The HFD control data (dotted line) are repeated from figure 2 for comparison. Data are expressed as means ± SEM. * p ≤ 0.05 HFD controls vs. Chow controls; # p ≤ 0.05 vs. HFD controls; † p

    Article Snippet: Inhibition of nitric oxide synthase, using 100 μM Nω-nitro-L-arginine (LNNA; Sigma), was performed to determine the role of NO in ACh-induced vasodilation.

    Techniques: Isolation

    Immunostaining of endothelial nitric oxide synthase (eNOS) in mesenteric artery homogenates from Chow (C), HSD (HS), and HFD (HF) fed rats . Densitized values of the immunoblot were normalized to β-actin protein concentration and are expressed as a ratio (mean ± SEM). Inset: representative blot of eNOS and β-actin in isolated rat mesenteric arteries from rats in all three treatment groups. n = 5-6 per group. Data are not significantly different.

    Journal: Nutrition & Metabolism

    Article Title: Comparison of mechanisms involved in impaired vascular reactivity between high sucrose and high fat diets in rats

    doi: 10.1186/1743-7075-7-48

    Figure Lengend Snippet: Immunostaining of endothelial nitric oxide synthase (eNOS) in mesenteric artery homogenates from Chow (C), HSD (HS), and HFD (HF) fed rats . Densitized values of the immunoblot were normalized to β-actin protein concentration and are expressed as a ratio (mean ± SEM). Inset: representative blot of eNOS and β-actin in isolated rat mesenteric arteries from rats in all three treatment groups. n = 5-6 per group. Data are not significantly different.

    Article Snippet: Inhibition of nitric oxide synthase, using 100 μM Nω-nitro-L-arginine (LNNA; Sigma), was performed to determine the role of NO in ACh-induced vasodilation.

    Techniques: Immunostaining, Protein Concentration, Isolation

    Acetylcholine-mediated vasodilatory responses in isolated mesenteric resistance arteries from Chow fed rats . Vasodilatory responses to acetylcholine (ACh) were measured in the presence and absence of the NOS inhibitor Nω-nitro-L-arginine (LNNA; 100 μM) in small mesenteric arteries ( n = 6-8). Arteries were exposed to LNNA in the lumen and superfusate prior to pre-constriction with phenylephrine to 45-50% resting inner diameter. Vasodilatory responses to acetylcholine (ACh) were also measured in the presence and absence of antioxidants ( n = 4-5). For these studies, arteries were pre-constricted as previously described. Treated arteries were pre-exposed to the ROS scavengers 4,5-Dihydroxy-1,3-benzene-disulfonic acid (tiron; 10 mM) and catalase (1200 U/mL) or EUK-134 (10 μM). Separate arteries were exposed to the nitric oxide synthase inhibitor LNNA (100 μM) or LNNA with the addition of EUK-134 or tiron and catalase. The Chow control data (dotted line) are repeated from figure 2 for comparison. Data are expressed as means ± SEM. * p ≤ 0.05 vs. controls; † p

    Journal: Nutrition & Metabolism

    Article Title: Comparison of mechanisms involved in impaired vascular reactivity between high sucrose and high fat diets in rats

    doi: 10.1186/1743-7075-7-48

    Figure Lengend Snippet: Acetylcholine-mediated vasodilatory responses in isolated mesenteric resistance arteries from Chow fed rats . Vasodilatory responses to acetylcholine (ACh) were measured in the presence and absence of the NOS inhibitor Nω-nitro-L-arginine (LNNA; 100 μM) in small mesenteric arteries ( n = 6-8). Arteries were exposed to LNNA in the lumen and superfusate prior to pre-constriction with phenylephrine to 45-50% resting inner diameter. Vasodilatory responses to acetylcholine (ACh) were also measured in the presence and absence of antioxidants ( n = 4-5). For these studies, arteries were pre-constricted as previously described. Treated arteries were pre-exposed to the ROS scavengers 4,5-Dihydroxy-1,3-benzene-disulfonic acid (tiron; 10 mM) and catalase (1200 U/mL) or EUK-134 (10 μM). Separate arteries were exposed to the nitric oxide synthase inhibitor LNNA (100 μM) or LNNA with the addition of EUK-134 or tiron and catalase. The Chow control data (dotted line) are repeated from figure 2 for comparison. Data are expressed as means ± SEM. * p ≤ 0.05 vs. controls; † p

    Article Snippet: Inhibition of nitric oxide synthase, using 100 μM Nω-nitro-L-arginine (LNNA; Sigma), was performed to determine the role of NO in ACh-induced vasodilation.

    Techniques: Isolation

    Acetylcholine-mediated vasodilatory responses in isolated mesenteric resistance arteries from HSD fed rats . Vasodilatory responses to acetylcholine (ACh) were measured in the presence and absence of the NOS inhibitor Nω-nitro-L-arginine (LNNA; 100 μM) in small mesenteric arteries ( n = 6-8). Arteries were exposed to LNNA in the lumen and superfusate prior to pre-constriction with phenylephrine to 45-50% resting inner diameter. Vasodilatory responses to acetylcholine (ACh) were also measured in the presence and absence of antioxidants HSD ( n = 4-9). For these studies, arteries were pre-exposed to the ROS scavengers 4,5-Dihydroxy-1,3-benzene-disulfonic acid (tiron; 10 mM) and catalase (1200 U/mL) or EUK-134 (10 μM). Separate arteries were exposed to the nitric oxide synthase inhibitor LNNA (100 μM) or LNNA with the addition of EUK-134 or tiron and catalase. The HSD control data (dotted line) are repeated from figure 2 for comparison.Data are expressed as means ± SEM. * p ≤ 0.05 HSD controls vs. Chow controls; # p ≤ 0.05 vs. HSD controls; † p

    Journal: Nutrition & Metabolism

    Article Title: Comparison of mechanisms involved in impaired vascular reactivity between high sucrose and high fat diets in rats

    doi: 10.1186/1743-7075-7-48

    Figure Lengend Snippet: Acetylcholine-mediated vasodilatory responses in isolated mesenteric resistance arteries from HSD fed rats . Vasodilatory responses to acetylcholine (ACh) were measured in the presence and absence of the NOS inhibitor Nω-nitro-L-arginine (LNNA; 100 μM) in small mesenteric arteries ( n = 6-8). Arteries were exposed to LNNA in the lumen and superfusate prior to pre-constriction with phenylephrine to 45-50% resting inner diameter. Vasodilatory responses to acetylcholine (ACh) were also measured in the presence and absence of antioxidants HSD ( n = 4-9). For these studies, arteries were pre-exposed to the ROS scavengers 4,5-Dihydroxy-1,3-benzene-disulfonic acid (tiron; 10 mM) and catalase (1200 U/mL) or EUK-134 (10 μM). Separate arteries were exposed to the nitric oxide synthase inhibitor LNNA (100 μM) or LNNA with the addition of EUK-134 or tiron and catalase. The HSD control data (dotted line) are repeated from figure 2 for comparison.Data are expressed as means ± SEM. * p ≤ 0.05 HSD controls vs. Chow controls; # p ≤ 0.05 vs. HSD controls; † p

    Article Snippet: Inhibition of nitric oxide synthase, using 100 μM Nω-nitro-L-arginine (LNNA; Sigma), was performed to determine the role of NO in ACh-induced vasodilation.

    Techniques: Isolation