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  • 99
    Millipore aprotinin a
    Active TK, but not inactive form, induces HaCaT cell migration independent of kinin, kinin B2 receptor and NO formation, and stimulates EGFR and ERK phosphorylation. (A) Treatment with kinin (1 μM) or inactive TK (1 μM) for 48 hours had no effect on cell migration by scratch method. Cells were pretreated with kinin B2 receptor antagonist (icatibant, 200 μM) or NOS inhibitor (L-NAME, 200 μM) for 45 minutes, and then stimulated with TK (1 μM) for 48 hours. (B) TK (1 μM), but not kinin (1 μM), stimulated cell migration after 18 hour incubation in modified Boyden chambers. <t>Aprotinin</t> (5 μM), but not icatibant (200 μM) or L-NAME (200 μM) blocked TK-induced cell migration. (C) Stimulation with active TK (1 μM), but not inactive TK (1 μM), for 15 minutes induced EGFR phosphorylation as determined by immunoprecipitation and Western blot. (D) Stimulation with active TK (1 μM), but not inactive TK (1 μM) for 15 minutes, induced ERK phosphorylation. Three independent measurements were performed in triplicate. Values are represented as mean ± SEM. * P
    Aprotinin A, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 164 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aprotinin a/product/Millipore
    Average 99 stars, based on 164 article reviews
    Price from $9.99 to $1999.99
    aprotinin a - by Bioz Stars, 2020-05
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    93
    Tocris aprotinin
    Active TK, but not inactive form, induces HaCaT cell migration independent of kinin, kinin B2 receptor and NO formation, and stimulates EGFR and ERK phosphorylation. (A) Treatment with kinin (1 μM) or inactive TK (1 μM) for 48 hours had no effect on cell migration by scratch method. Cells were pretreated with kinin B2 receptor antagonist (icatibant, 200 μM) or NOS inhibitor (L-NAME, 200 μM) for 45 minutes, and then stimulated with TK (1 μM) for 48 hours. (B) TK (1 μM), but not kinin (1 μM), stimulated cell migration after 18 hour incubation in modified Boyden chambers. <t>Aprotinin</t> (5 μM), but not icatibant (200 μM) or L-NAME (200 μM) blocked TK-induced cell migration. (C) Stimulation with active TK (1 μM), but not inactive TK (1 μM), for 15 minutes induced EGFR phosphorylation as determined by immunoprecipitation and Western blot. (D) Stimulation with active TK (1 μM), but not inactive TK (1 μM) for 15 minutes, induced ERK phosphorylation. Three independent measurements were performed in triplicate. Values are represented as mean ± SEM. * P
    Aprotinin, 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
    https://www.bioz.com/result/aprotinin/product/Tocris
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    aprotinin - by Bioz Stars, 2020-05
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    91
    Selleck Chemicals aprotinin
    Active TK, but not inactive form, induces HaCaT cell migration independent of kinin, kinin B2 receptor and NO formation, and stimulates EGFR and ERK phosphorylation. (A) Treatment with kinin (1 μM) or inactive TK (1 μM) for 48 hours had no effect on cell migration by scratch method. Cells were pretreated with kinin B2 receptor antagonist (icatibant, 200 μM) or NOS inhibitor (L-NAME, 200 μM) for 45 minutes, and then stimulated with TK (1 μM) for 48 hours. (B) TK (1 μM), but not kinin (1 μM), stimulated cell migration after 18 hour incubation in modified Boyden chambers. <t>Aprotinin</t> (5 μM), but not icatibant (200 μM) or L-NAME (200 μM) blocked TK-induced cell migration. (C) Stimulation with active TK (1 μM), but not inactive TK (1 μM), for 15 minutes induced EGFR phosphorylation as determined by immunoprecipitation and Western blot. (D) Stimulation with active TK (1 μM), but not inactive TK (1 μM) for 15 minutes, induced ERK phosphorylation. Three independent measurements were performed in triplicate. Values are represented as mean ± SEM. * P
    Aprotinin, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 91/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aprotinin/product/Selleck Chemicals
    Average 91 stars, based on 7 article reviews
    Price from $9.99 to $1999.99
    aprotinin - by Bioz Stars, 2020-05
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    Image Search Results


    Active TK, but not inactive form, induces HaCaT cell migration independent of kinin, kinin B2 receptor and NO formation, and stimulates EGFR and ERK phosphorylation. (A) Treatment with kinin (1 μM) or inactive TK (1 μM) for 48 hours had no effect on cell migration by scratch method. Cells were pretreated with kinin B2 receptor antagonist (icatibant, 200 μM) or NOS inhibitor (L-NAME, 200 μM) for 45 minutes, and then stimulated with TK (1 μM) for 48 hours. (B) TK (1 μM), but not kinin (1 μM), stimulated cell migration after 18 hour incubation in modified Boyden chambers. Aprotinin (5 μM), but not icatibant (200 μM) or L-NAME (200 μM) blocked TK-induced cell migration. (C) Stimulation with active TK (1 μM), but not inactive TK (1 μM), for 15 minutes induced EGFR phosphorylation as determined by immunoprecipitation and Western blot. (D) Stimulation with active TK (1 μM), but not inactive TK (1 μM) for 15 minutes, induced ERK phosphorylation. Three independent measurements were performed in triplicate. Values are represented as mean ± SEM. * P

    Journal: Experimental cell research

    Article Title: A Novel Signaling Pathway of Tissue Kallikrein in Promoting Keratinocyte Migration: Activation of Proteinase-Activated Receptor 1 and Epidermal Growth Factor Receptor

    doi: 10.1016/j.yexcr.2009.10.022

    Figure Lengend Snippet: Active TK, but not inactive form, induces HaCaT cell migration independent of kinin, kinin B2 receptor and NO formation, and stimulates EGFR and ERK phosphorylation. (A) Treatment with kinin (1 μM) or inactive TK (1 μM) for 48 hours had no effect on cell migration by scratch method. Cells were pretreated with kinin B2 receptor antagonist (icatibant, 200 μM) or NOS inhibitor (L-NAME, 200 μM) for 45 minutes, and then stimulated with TK (1 μM) for 48 hours. (B) TK (1 μM), but not kinin (1 μM), stimulated cell migration after 18 hour incubation in modified Boyden chambers. Aprotinin (5 μM), but not icatibant (200 μM) or L-NAME (200 μM) blocked TK-induced cell migration. (C) Stimulation with active TK (1 μM), but not inactive TK (1 μM), for 15 minutes induced EGFR phosphorylation as determined by immunoprecipitation and Western blot. (D) Stimulation with active TK (1 μM), but not inactive TK (1 μM) for 15 minutes, induced ERK phosphorylation. Three independent measurements were performed in triplicate. Values are represented as mean ± SEM. * P

    Article Snippet: Active TK (3 μg) with or without AG1478 (2 μg) (Calbiochem) and icatibant (12 μg) (Sigma), as well as aprotinin (3 μg) (Sigma), neutralizing antibody to rat TK, control IgG (50 μg), or saline in 100 μl final volume was injected intradermally at 6 different sites around the wound edge once a day for 8 days.

    Techniques: Migration, Incubation, Modification, Immunoprecipitation, Western Blot

    EGFR, Src or ERK activition are required for EGF-induced HaCaT cell migration. (A) EGFR antagonist (AG), Src antagonist (PP2) and ERK antagonist (PD), but not PAR 1 antagonist (SCH), PKC antagonist (CHE) or aprotinin blocked TK-induced cell migration by scratch method. Cells were pretreated with AG (300nM), SCH (1 μM), CHE (5 μM), PP2 (5 μM) or PD (5 μM) for 45 minutes, then stimulated with EGF (5 ng/mL) for 48 hours. (B) AG, PP2 and PD, but not SCH, CHE or aprotinin blocked EGF-induced cell migration in modified Boyden chambers. Cells were treated with EGF (5 ng/mL) in the presence or absence of AG (300nM), SCH (1 μM), CHE (5 μM), PP2 (5 μM) or PD (5 μM) for 18 hours. Three independent measurements were performed in triplicate. Values are represented as mean ± SEM. * P

    Journal: Experimental cell research

    Article Title: A Novel Signaling Pathway of Tissue Kallikrein in Promoting Keratinocyte Migration: Activation of Proteinase-Activated Receptor 1 and Epidermal Growth Factor Receptor

    doi: 10.1016/j.yexcr.2009.10.022

    Figure Lengend Snippet: EGFR, Src or ERK activition are required for EGF-induced HaCaT cell migration. (A) EGFR antagonist (AG), Src antagonist (PP2) and ERK antagonist (PD), but not PAR 1 antagonist (SCH), PKC antagonist (CHE) or aprotinin blocked TK-induced cell migration by scratch method. Cells were pretreated with AG (300nM), SCH (1 μM), CHE (5 μM), PP2 (5 μM) or PD (5 μM) for 45 minutes, then stimulated with EGF (5 ng/mL) for 48 hours. (B) AG, PP2 and PD, but not SCH, CHE or aprotinin blocked EGF-induced cell migration in modified Boyden chambers. Cells were treated with EGF (5 ng/mL) in the presence or absence of AG (300nM), SCH (1 μM), CHE (5 μM), PP2 (5 μM) or PD (5 μM) for 18 hours. Three independent measurements were performed in triplicate. Values are represented as mean ± SEM. * P

    Article Snippet: Active TK (3 μg) with or without AG1478 (2 μg) (Calbiochem) and icatibant (12 μg) (Sigma), as well as aprotinin (3 μg) (Sigma), neutralizing antibody to rat TK, control IgG (50 μg), or saline in 100 μl final volume was injected intradermally at 6 different sites around the wound edge once a day for 8 days.

    Techniques: Migration, Modification