phenylmethylsulfonyl fluoride Search Results


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  • 99
    Millipore phenylmethylsulfonyl fluouride
    MMP inhibitors prevent the increases in vascular gelatinolytic activity, in ROS concentrations, and in lucigenin chemiluminescence after intraluminal incubation of rabbit aorta with MMP-2. (A) Representative photomicrographs of aortic in situ zymography experiments showing that MMP-2 gelatinolytic activity was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by <t>phenylmethylsulfonyl</t> fluoride (PMSF, 100 µM). The arteries were incubated with the inhibitors together with MMP-2 (16 nM) intraluminally for 30 min. (B) Quantification of aortic gelatinolytic activity measured in experiments described in A. (C) Representative photomicrographs of aortic sections incubated with DHE. Red fluorescence reflects ROS production and shows that incubation with MMP-2 (16 nM) intraluminally for 30 min increased ROS production, and this effect was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by phenylmethylsulfonyl fluoride (PMSF, 100 µM). The experiments were carried out as described in A. (D), Quantification of aortic fluorescence of DHE measured in experiments described in C. (E), Quantification of lucigenin chemiluminescence measured in fresh aortas after intraluminal incubation with MMP-2 (16 nM) or vehicle for 30 min in absence or presence of MMP inhibitors, doxycycline (Doxy 100 µM) or GM6001 (10 µM). Data are shown as the mean ± SEM (n = 4–5/group). * P
    Phenylmethylsulfonyl Fluouride, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1228 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 1228 article reviews
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    99
    Millipore m phenylmethylsulfonyl fluoride pmsf
    MMP inhibitors prevent the increases in vascular gelatinolytic activity, in ROS concentrations, and in lucigenin chemiluminescence after intraluminal incubation of rabbit aorta with MMP-2. (A) Representative photomicrographs of aortic in situ zymography experiments showing that MMP-2 gelatinolytic activity was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by <t>phenylmethylsulfonyl</t> fluoride (PMSF, 100 µM). The arteries were incubated with the inhibitors together with MMP-2 (16 nM) intraluminally for 30 min. (B) Quantification of aortic gelatinolytic activity measured in experiments described in A. (C) Representative photomicrographs of aortic sections incubated with DHE. Red fluorescence reflects ROS production and shows that incubation with MMP-2 (16 nM) intraluminally for 30 min increased ROS production, and this effect was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by phenylmethylsulfonyl fluoride (PMSF, 100 µM). The experiments were carried out as described in A. (D), Quantification of aortic fluorescence of DHE measured in experiments described in C. (E), Quantification of lucigenin chemiluminescence measured in fresh aortas after intraluminal incubation with MMP-2 (16 nM) or vehicle for 30 min in absence or presence of MMP inhibitors, doxycycline (Doxy 100 µM) or GM6001 (10 µM). Data are shown as the mean ± SEM (n = 4–5/group). * P
    M Phenylmethylsulfonyl Fluoride Pmsf, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore phenylmethanesulfonyl fluoride solution
    MMP inhibitors prevent the increases in vascular gelatinolytic activity, in ROS concentrations, and in lucigenin chemiluminescence after intraluminal incubation of rabbit aorta with MMP-2. (A) Representative photomicrographs of aortic in situ zymography experiments showing that MMP-2 gelatinolytic activity was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by <t>phenylmethylsulfonyl</t> fluoride (PMSF, 100 µM). The arteries were incubated with the inhibitors together with MMP-2 (16 nM) intraluminally for 30 min. (B) Quantification of aortic gelatinolytic activity measured in experiments described in A. (C) Representative photomicrographs of aortic sections incubated with DHE. Red fluorescence reflects ROS production and shows that incubation with MMP-2 (16 nM) intraluminally for 30 min increased ROS production, and this effect was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by phenylmethylsulfonyl fluoride (PMSF, 100 µM). The experiments were carried out as described in A. (D), Quantification of aortic fluorescence of DHE measured in experiments described in C. (E), Quantification of lucigenin chemiluminescence measured in fresh aortas after intraluminal incubation with MMP-2 (16 nM) or vehicle for 30 min in absence or presence of MMP inhibitors, doxycycline (Doxy 100 µM) or GM6001 (10 µM). Data are shown as the mean ± SEM (n = 4–5/group). * P
    Phenylmethanesulfonyl Fluoride Solution, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phenylmethanesulfonyl fluoride solution/product/Millipore
    Average 99 stars, based on 29 article reviews
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    phenylmethanesulfonyl fluoride solution - by Bioz Stars, 2020-05
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    99
    Millipore protease inhibitor phenylmethylsulfonyl fluoride
    MMP inhibitors prevent the increases in vascular gelatinolytic activity, in ROS concentrations, and in lucigenin chemiluminescence after intraluminal incubation of rabbit aorta with MMP-2. (A) Representative photomicrographs of aortic in situ zymography experiments showing that MMP-2 gelatinolytic activity was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by <t>phenylmethylsulfonyl</t> fluoride (PMSF, 100 µM). The arteries were incubated with the inhibitors together with MMP-2 (16 nM) intraluminally for 30 min. (B) Quantification of aortic gelatinolytic activity measured in experiments described in A. (C) Representative photomicrographs of aortic sections incubated with DHE. Red fluorescence reflects ROS production and shows that incubation with MMP-2 (16 nM) intraluminally for 30 min increased ROS production, and this effect was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by phenylmethylsulfonyl fluoride (PMSF, 100 µM). The experiments were carried out as described in A. (D), Quantification of aortic fluorescence of DHE measured in experiments described in C. (E), Quantification of lucigenin chemiluminescence measured in fresh aortas after intraluminal incubation with MMP-2 (16 nM) or vehicle for 30 min in absence or presence of MMP inhibitors, doxycycline (Doxy 100 µM) or GM6001 (10 µM). Data are shown as the mean ± SEM (n = 4–5/group). * P
    Protease Inhibitor Phenylmethylsulfonyl Fluoride, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 170 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 170 article reviews
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    Image Search Results


    MMP inhibitors prevent the increases in vascular gelatinolytic activity, in ROS concentrations, and in lucigenin chemiluminescence after intraluminal incubation of rabbit aorta with MMP-2. (A) Representative photomicrographs of aortic in situ zymography experiments showing that MMP-2 gelatinolytic activity was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by phenylmethylsulfonyl fluoride (PMSF, 100 µM). The arteries were incubated with the inhibitors together with MMP-2 (16 nM) intraluminally for 30 min. (B) Quantification of aortic gelatinolytic activity measured in experiments described in A. (C) Representative photomicrographs of aortic sections incubated with DHE. Red fluorescence reflects ROS production and shows that incubation with MMP-2 (16 nM) intraluminally for 30 min increased ROS production, and this effect was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by phenylmethylsulfonyl fluoride (PMSF, 100 µM). The experiments were carried out as described in A. (D), Quantification of aortic fluorescence of DHE measured in experiments described in C. (E), Quantification of lucigenin chemiluminescence measured in fresh aortas after intraluminal incubation with MMP-2 (16 nM) or vehicle for 30 min in absence or presence of MMP inhibitors, doxycycline (Doxy 100 µM) or GM6001 (10 µM). Data are shown as the mean ± SEM (n = 4–5/group). * P

    Journal: Redox Biology

    Article Title: Matrix metalloproteinase-2-induced epidermal growth factor receptor transactivation impairs redox balance in vascular smooth muscle cells and facilitates vascular contraction

    doi: 10.1016/j.redox.2018.07.005

    Figure Lengend Snippet: MMP inhibitors prevent the increases in vascular gelatinolytic activity, in ROS concentrations, and in lucigenin chemiluminescence after intraluminal incubation of rabbit aorta with MMP-2. (A) Representative photomicrographs of aortic in situ zymography experiments showing that MMP-2 gelatinolytic activity was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by phenylmethylsulfonyl fluoride (PMSF, 100 µM). The arteries were incubated with the inhibitors together with MMP-2 (16 nM) intraluminally for 30 min. (B) Quantification of aortic gelatinolytic activity measured in experiments described in A. (C) Representative photomicrographs of aortic sections incubated with DHE. Red fluorescence reflects ROS production and shows that incubation with MMP-2 (16 nM) intraluminally for 30 min increased ROS production, and this effect was totally inhibited by phenanthroline (Phe, 100 µM) or doxycycline (Doxy, 100 µM), but not by phenylmethylsulfonyl fluoride (PMSF, 100 µM). The experiments were carried out as described in A. (D), Quantification of aortic fluorescence of DHE measured in experiments described in C. (E), Quantification of lucigenin chemiluminescence measured in fresh aortas after intraluminal incubation with MMP-2 (16 nM) or vehicle for 30 min in absence or presence of MMP inhibitors, doxycycline (Doxy 100 µM) or GM6001 (10 µM). Data are shown as the mean ± SEM (n = 4–5/group). * P

    Article Snippet: Tyrphostin AG 1478, Phenylephrine, Apocynin, Peg-Catalase (PG-Cat), Dihydroethidium (DHE), phenanthroline, Phenylmethylsulfonyl fluoride were purchased from Sigma Chemical Co. (St. Louis, MO, USA).

    Techniques: Activity Assay, Incubation, In Situ, Zymography, Fluorescence

    Biochemical properties of HCA. ( A ) Activity–pH relationship curve; ( B ) activity–temperature relationship curve; ( C ) effects of Ca 2+ on the fibrinogen clotting activity; ( D ) effect of PMSF on the clotting time of fibrinogen solution after the addition of HCA. The values shown are the mean values ± SEM (n=3). Abbreviations: HCA, hemocoagulase agkistrodon; PMSF, phenylmethanesulfonyl fluoride; SEM, standard error of mean.

    Journal: Drug Design, Development and Therapy

    Article Title: Effects of hemocoagulase agkistrodon on the coagulation factors and its procoagulant activities

    doi: 10.2147/DDDT.S159210

    Figure Lengend Snippet: Biochemical properties of HCA. ( A ) Activity–pH relationship curve; ( B ) activity–temperature relationship curve; ( C ) effects of Ca 2+ on the fibrinogen clotting activity; ( D ) effect of PMSF on the clotting time of fibrinogen solution after the addition of HCA. The values shown are the mean values ± SEM (n=3). Abbreviations: HCA, hemocoagulase agkistrodon; PMSF, phenylmethanesulfonyl fluoride; SEM, standard error of mean.

    Article Snippet: HCA (Beijing, Konruns Pharmaceutical Co., Ltd.); DEAE-Sepharose Fast Flow and Sephadex-G25 were obtained from Amersham Biosciences (Uppsala, Sweden); peroxidase-conjugated goat anti-rabbit IgG was purchased from BoaoBioTech (Beijing, People’s Republic of China); human fibrinogen, FPA, FPB, phenylmethanesulfonyl fluoride (PMSF), egg-yolk L-α-phosphatidylcholine, and bovine brain L-α-phosphatidylserine were from Sigma-Aldrich Co. (St Louis, MO, USA); human prothrombin (FII), thrombin, active factor V (FVa), FVII/VIIa, factor IX (FIX)/IXa, and FX/Xa were purchased from Hematologic Technologies (Burlington, VT, USA); the chromogenic substrate H-D-Phe-Pip-Arg-pNa•2HCl (S2238) was from Hyphen BioMed (Neuville-Sur-Oise, France); rabbit anti-HCA polyclonal antibodies were prepared in our laboratory as described in Supplementary materials (section “The preparation of polyclonal antibody”) and its ELISA titer was above 1:1,000,00.

    Techniques: High Content Screening, Activity Assay, Coagulation