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Santa Cruz Biotechnology monophosphorothioate rp camps
Fig. 3. The ability of C-type natriuretic peptide (CNP), in the presence or absence of the protein kinase A inhibitor <t>Rp-cAMPS</t> (1 mM), protein kinase G inhibitor Rp-8CPT- cGMPS (1 mM) and potassium channel blocker charybdotoxin (0.1 mM), to cause relaxation of the rat internal anal sphincter. The values are expressed as percent of papaverine (100 mM)-induced relaxation. The results given are from at least three experiments. The vertical bars represent standard error of the mean. * Represents significant difference from CNP (100 nM) alone (p < 0.05).
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Fig. 3. The ability of C-type natriuretic peptide (CNP), in the presence or absence of the protein kinase A inhibitor <t>Rp-cAMPS</t> (1 mM), protein kinase G inhibitor Rp-8CPT- cGMPS (1 mM) and potassium channel blocker charybdotoxin (0.1 mM), to cause relaxation of the rat internal anal sphincter. The values are expressed as percent of papaverine (100 mM)-induced relaxation. The results given are from at least three experiments. The vertical bars represent standard error of the mean. * Represents significant difference from CNP (100 nM) alone (p < 0.05).
Rpcamps, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Tocris camps rp triethylammonium salt
Fig. 3. The ability of C-type natriuretic peptide (CNP), in the presence or absence of the protein kinase A inhibitor <t>Rp-cAMPS</t> (1 mM), protein kinase G inhibitor Rp-8CPT- cGMPS (1 mM) and potassium channel blocker charybdotoxin (0.1 mM), to cause relaxation of the rat internal anal sphincter. The values are expressed as percent of papaverine (100 mM)-induced relaxation. The results given are from at least three experiments. The vertical bars represent standard error of the mean. * Represents significant difference from CNP (100 nM) alone (p < 0.05).
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Santa Cruz Biotechnology sp 8 br camps
Fig. 3. The ability of C-type natriuretic peptide (CNP), in the presence or absence of the protein kinase A inhibitor <t>Rp-cAMPS</t> (1 mM), protein kinase G inhibitor Rp-8CPT- cGMPS (1 mM) and potassium channel blocker charybdotoxin (0.1 mM), to cause relaxation of the rat internal anal sphincter. The values are expressed as percent of papaverine (100 mM)-induced relaxation. The results given are from at least three experiments. The vertical bars represent standard error of the mean. * Represents significant difference from CNP (100 nM) alone (p < 0.05).
Sp 8 Br Camps, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology rp 8 cptcamps
Fig. 3. The ability of C-type natriuretic peptide (CNP), in the presence or absence of the protein kinase A inhibitor <t>Rp-cAMPS</t> (1 mM), protein kinase G inhibitor Rp-8CPT- cGMPS (1 mM) and potassium channel blocker charybdotoxin (0.1 mM), to cause relaxation of the rat internal anal sphincter. The values are expressed as percent of papaverine (100 mM)-induced relaxation. The results given are from at least three experiments. The vertical bars represent standard error of the mean. * Represents significant difference from CNP (100 nM) alone (p < 0.05).
Rp 8 Cptcamps, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Effects of <t>CPT-cAMPS</t> and PKA inhibitors on EGF-induced cell migration. NR6WT cells were grown to confluence and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum before treatment or not with EGF (10 nM), CPT-cAMPS (1 μM), <t>Rp-8Br-cAMPS</t> and/or Rp-8Br-cGMPS (5 μM) (A), and H-89 (at indicated concentrations) (B). The datum for nontreated control cells is labeled as nTx. Basal and EGF-induced cell migrations were assessed as the ability of the cells to move into an acellular area after 24 h of EGF treatment. The data are shown as the ratios to the 10 nM EGF-induced cell migration activity. The data are the means ± SEM of at least three independent studies, each performed in triplicate. Statistical analysis was performed by Student's t test. n.s., not significant.
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Effects of <t>CPT-cAMPS</t> and PKA inhibitors on EGF-induced cell migration. NR6WT cells were grown to confluence and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum before treatment or not with EGF (10 nM), CPT-cAMPS (1 μM), <t>Rp-8Br-cAMPS</t> and/or Rp-8Br-cGMPS (5 μM) (A), and H-89 (at indicated concentrations) (B). The datum for nontreated control cells is labeled as nTx. Basal and EGF-induced cell migrations were assessed as the ability of the cells to move into an acellular area after 24 h of EGF treatment. The data are shown as the ratios to the 10 nM EGF-induced cell migration activity. The data are the means ± SEM of at least three independent studies, each performed in triplicate. Statistical analysis was performed by Student's t test. n.s., not significant.
Camps, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Effects of <t>CPT-cAMPS</t> and PKA inhibitors on EGF-induced cell migration. NR6WT cells were grown to confluence and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum before treatment or not with EGF (10 nM), CPT-cAMPS (1 μM), <t>Rp-8Br-cAMPS</t> and/or Rp-8Br-cGMPS (5 μM) (A), and H-89 (at indicated concentrations) (B). The datum for nontreated control cells is labeled as nTx. Basal and EGF-induced cell migrations were assessed as the ability of the cells to move into an acellular area after 24 h of EGF treatment. The data are shown as the ratios to the 10 nM EGF-induced cell migration activity. The data are the means ± SEM of at least three independent studies, each performed in triplicate. Statistical analysis was performed by Student's t test. n.s., not significant.
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Effects of <t>CPT-cAMPS</t> and PKA inhibitors on EGF-induced cell migration. NR6WT cells were grown to confluence and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum before treatment or not with EGF (10 nM), CPT-cAMPS (1 μM), <t>Rp-8Br-cAMPS</t> and/or Rp-8Br-cGMPS (5 μM) (A), and H-89 (at indicated concentrations) (B). The datum for nontreated control cells is labeled as nTx. Basal and EGF-induced cell migrations were assessed as the ability of the cells to move into an acellular area after 24 h of EGF treatment. The data are shown as the ratios to the 10 nM EGF-induced cell migration activity. The data are the means ± SEM of at least three independent studies, each performed in triplicate. Statistical analysis was performed by Student's t test. n.s., not significant.
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Effects of <t>CPT-cAMPS</t> and PKA inhibitors on EGF-induced cell migration. NR6WT cells were grown to confluence and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum before treatment or not with EGF (10 nM), CPT-cAMPS (1 μM), <t>Rp-8Br-cAMPS</t> and/or Rp-8Br-cGMPS (5 μM) (A), and H-89 (at indicated concentrations) (B). The datum for nontreated control cells is labeled as nTx. Basal and EGF-induced cell migrations were assessed as the ability of the cells to move into an acellular area after 24 h of EGF treatment. The data are shown as the ratios to the 10 nM EGF-induced cell migration activity. The data are the means ± SEM of at least three independent studies, each performed in triplicate. Statistical analysis was performed by Student's t test. n.s., not significant.
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Effects of <t>CPT-cAMPS</t> and PKA inhibitors on EGF-induced cell migration. NR6WT cells were grown to confluence and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum before treatment or not with EGF (10 nM), CPT-cAMPS (1 μM), <t>Rp-8Br-cAMPS</t> and/or Rp-8Br-cGMPS (5 μM) (A), and H-89 (at indicated concentrations) (B). The datum for nontreated control cells is labeled as nTx. Basal and EGF-induced cell migrations were assessed as the ability of the cells to move into an acellular area after 24 h of EGF treatment. The data are shown as the ratios to the 10 nM EGF-induced cell migration activity. The data are the means ± SEM of at least three independent studies, each performed in triplicate. Statistical analysis was performed by Student's t test. n.s., not significant.
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Image Search Results


Fig. 3. The ability of C-type natriuretic peptide (CNP), in the presence or absence of the protein kinase A inhibitor Rp-cAMPS (1 mM), protein kinase G inhibitor Rp-8CPT- cGMPS (1 mM) and potassium channel blocker charybdotoxin (0.1 mM), to cause relaxation of the rat internal anal sphincter. The values are expressed as percent of papaverine (100 mM)-induced relaxation. The results given are from at least three experiments. The vertical bars represent standard error of the mean. * Represents significant difference from CNP (100 nM) alone (p < 0.05).

Journal: Tzu Chi Medical Journal

Article Title: C-type atriuretic peptide causes relaxation of the internal anal sphincter through natriuretic peptide receptor B

doi: 10.1016/j.tcmj.2015.05.002

Figure Lengend Snippet: Fig. 3. The ability of C-type natriuretic peptide (CNP), in the presence or absence of the protein kinase A inhibitor Rp-cAMPS (1 mM), protein kinase G inhibitor Rp-8CPT- cGMPS (1 mM) and potassium channel blocker charybdotoxin (0.1 mM), to cause relaxation of the rat internal anal sphincter. The values are expressed as percent of papaverine (100 mM)-induced relaxation. The results given are from at least three experiments. The vertical bars represent standard error of the mean. * Represents significant difference from CNP (100 nM) alone (p < 0.05).

Article Snippet: Rp-8-(4chlorophenylthio)-guanosine 30,50-cyclic monophosphorothioate (Rp-8CPT-cGMPS), Rp-adenosine 30,50-cyclic monophosphorothioate (Rp-cAMPS), and rabbit polyclonal anti-NPR-B antibody (sc-25486) were obtained from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques:

Effects of CPT-cAMPS and PKA inhibitors on EGF-induced cell migration. NR6WT cells were grown to confluence and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum before treatment or not with EGF (10 nM), CPT-cAMPS (1 μM), Rp-8Br-cAMPS and/or Rp-8Br-cGMPS (5 μM) (A), and H-89 (at indicated concentrations) (B). The datum for nontreated control cells is labeled as nTx. Basal and EGF-induced cell migrations were assessed as the ability of the cells to move into an acellular area after 24 h of EGF treatment. The data are shown as the ratios to the 10 nM EGF-induced cell migration activity. The data are the means ± SEM of at least three independent studies, each performed in triplicate. Statistical analysis was performed by Student's t test. n.s., not significant.

Journal:

Article Title: Activation of m-Calpain (Calpain II) by Epidermal Growth Factor Is Limited by Protein Kinase A Phosphorylation of m-Calpain

doi: 10.1128/MCB.22.8.2716-2727.2002

Figure Lengend Snippet: Effects of CPT-cAMPS and PKA inhibitors on EGF-induced cell migration. NR6WT cells were grown to confluence and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum before treatment or not with EGF (10 nM), CPT-cAMPS (1 μM), Rp-8Br-cAMPS and/or Rp-8Br-cGMPS (5 μM) (A), and H-89 (at indicated concentrations) (B). The datum for nontreated control cells is labeled as nTx. Basal and EGF-induced cell migrations were assessed as the ability of the cells to move into an acellular area after 24 h of EGF treatment. The data are shown as the ratios to the 10 nM EGF-induced cell migration activity. The data are the means ± SEM of at least three independent studies, each performed in triplicate. Statistical analysis was performed by Student's t test. n.s., not significant.

Article Snippet: Cells were treated or not with CPT-cAMPS (1 μM) and/or Rp-8Br-cAMPS (5 μM) and incubated for 30 min in the presence of 30 μM BOC-LM-CMAC (Molecular Probes, Eugene, Oreg.).

Techniques: Migration, Labeling, Activity Assay

EGF-induced calpain activation. NR6WT cells were plated on tissue culture chamber slides (Nunc) and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum. Cells were treated or not with CPT-cAMPS (1 μM), Rp-8Br-cAMPS (5 μM), and/or Rp-8Br-cGMPS (5 μM) 30 min prior to EGF (10 nM) treatment in the presence of BOC-LM-CMAC (Molecular Probes). Then cells were treated or not with EGF (10 nM) for 5 min. Calpain activation was assessed by fluorescence microscopy. The fluorescence indicates calpain activity. The panel for nontreated control cells is labeled as nTx. The pictures shown are representative of n = 9.

Journal:

Article Title: Activation of m-Calpain (Calpain II) by Epidermal Growth Factor Is Limited by Protein Kinase A Phosphorylation of m-Calpain

doi: 10.1128/MCB.22.8.2716-2727.2002

Figure Lengend Snippet: EGF-induced calpain activation. NR6WT cells were plated on tissue culture chamber slides (Nunc) and made quiescent for 24 h in MEMα with 0.5% dialyzed fetal calf serum. Cells were treated or not with CPT-cAMPS (1 μM), Rp-8Br-cAMPS (5 μM), and/or Rp-8Br-cGMPS (5 μM) 30 min prior to EGF (10 nM) treatment in the presence of BOC-LM-CMAC (Molecular Probes). Then cells were treated or not with EGF (10 nM) for 5 min. Calpain activation was assessed by fluorescence microscopy. The fluorescence indicates calpain activity. The panel for nontreated control cells is labeled as nTx. The pictures shown are representative of n = 9.

Article Snippet: Cells were treated or not with CPT-cAMPS (1 μM) and/or Rp-8Br-cAMPS (5 μM) and incubated for 30 min in the presence of 30 μM BOC-LM-CMAC (Molecular Probes, Eugene, Oreg.).

Techniques: Activation Assay, Fluorescence, Microscopy, Activity Assay, Labeling