trk inhibitor k252a Search Results


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    Millipore k252a
    The proliferative effect of NT3 on human AVICs is mediated by the <t>Trk</t> receptors. Normal AVICs were treated with NT3 for 3 days in the presence or absence of Trk inhibitor <t>K252a</t> (0.20 µM) or isoform-selective inhibitors (Fc chimeras specific for TrkA, TrkB, and TrkC; 2.0 µg/ml each) for 3 days. Inhibition of Trk markedly reduces NT3-induced BrdU incorporation and formazan dye formation. Each isoform-selective inhibitor attenuates the BrdU incorporation and formazan dye formation induced by NT3. Data are presented as means ± SE of 5 experiments using different cell isolates from distinct donor valves. Statistical analyses were performed using ANOVA with the post hoc Bonferroni/Dunn test and confirmed using nonparametric Kruskal-Wallis test. * P
    K252a, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    The proliferative effect of NT3 on human AVICs is mediated by the Trk receptors. Normal AVICs were treated with NT3 for 3 days in the presence or absence of Trk inhibitor K252a (0.20 µM) or isoform-selective inhibitors (Fc chimeras specific for TrkA, TrkB, and TrkC; 2.0 µg/ml each) for 3 days. Inhibition of Trk markedly reduces NT3-induced BrdU incorporation and formazan dye formation. Each isoform-selective inhibitor attenuates the BrdU incorporation and formazan dye formation induced by NT3. Data are presented as means ± SE of 5 experiments using different cell isolates from distinct donor valves. Statistical analyses were performed using ANOVA with the post hoc Bonferroni/Dunn test and confirmed using nonparametric Kruskal-Wallis test. * P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Neurotrophin 3 upregulates proliferation and collagen production in human aortic valve interstitial cells: a potential role in aortic valve sclerosis

    doi: 10.1152/ajpcell.00292.2016

    Figure Lengend Snippet: The proliferative effect of NT3 on human AVICs is mediated by the Trk receptors. Normal AVICs were treated with NT3 for 3 days in the presence or absence of Trk inhibitor K252a (0.20 µM) or isoform-selective inhibitors (Fc chimeras specific for TrkA, TrkB, and TrkC; 2.0 µg/ml each) for 3 days. Inhibition of Trk markedly reduces NT3-induced BrdU incorporation and formazan dye formation. Each isoform-selective inhibitor attenuates the BrdU incorporation and formazan dye formation induced by NT3. Data are presented as means ± SE of 5 experiments using different cell isolates from distinct donor valves. Statistical analyses were performed using ANOVA with the post hoc Bonferroni/Dunn test and confirmed using nonparametric Kruskal-Wallis test. * P

    Article Snippet: The Trk inhibitor K252a was obtained from Calbiochem (La Jolla, CA).

    Techniques: Inhibition, BrdU Incorporation Assay

    NT3 upregulates collagen deposition through Trk receptors. A : normal AVICs were treated with NT3 in the presence or absence of the Trk inhibitor K252a (0.20 µM) for 3 days. Representative immunoblots and densitometric data show that inhibition of Trk suppresses NT3-induced expression of collagen III and MMP-9. Data are presented as means ± SE of 5 experiments using different cell isolates from distinct donor valves. Statistical analyses were performed using ANOVA with the post hoc Bonferroni/Dunn test and confirmed using nonparametric Kruskal-Wallis test. * P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Neurotrophin 3 upregulates proliferation and collagen production in human aortic valve interstitial cells: a potential role in aortic valve sclerosis

    doi: 10.1152/ajpcell.00292.2016

    Figure Lengend Snippet: NT3 upregulates collagen deposition through Trk receptors. A : normal AVICs were treated with NT3 in the presence or absence of the Trk inhibitor K252a (0.20 µM) for 3 days. Representative immunoblots and densitometric data show that inhibition of Trk suppresses NT3-induced expression of collagen III and MMP-9. Data are presented as means ± SE of 5 experiments using different cell isolates from distinct donor valves. Statistical analyses were performed using ANOVA with the post hoc Bonferroni/Dunn test and confirmed using nonparametric Kruskal-Wallis test. * P

    Article Snippet: The Trk inhibitor K252a was obtained from Calbiochem (La Jolla, CA).

    Techniques: Western Blot, Inhibition, Expressing

    Involvement of PKA and Trk receptor in BDNF-induced Ser916/898 phosphorylation of RasGRF1. (A, B) Cortical neurons at 3 DIV were pretreated with 10 μM H-89 (A) or 100 nM K252a (B) for 45 min, and then treated with 50 ng/mL of BDNF for 30 min. Phosphorylated RasGRF1 (Ser916/898) was analyzed by immunoblotting with the anti-pSer916/898 antibody. (C, D) Densitometry analysis was performed, and p-RasGRF1/total RasGRF1 ratio was determined. Relative levels of p-RasGRF1/total RasGRF1 compared to vehicle-treated cells are shown. Data are presented as the means ± SEM of four independent preparations, *p

    Journal: Biochemistry and Biophysics Reports

    Article Title: RasGRF1 mediates brain-derived neurotrophic factor-induced axonal growth in primary cultured cortical neurons

    doi: 10.1016/j.bbrep.2018.11.011

    Figure Lengend Snippet: Involvement of PKA and Trk receptor in BDNF-induced Ser916/898 phosphorylation of RasGRF1. (A, B) Cortical neurons at 3 DIV were pretreated with 10 μM H-89 (A) or 100 nM K252a (B) for 45 min, and then treated with 50 ng/mL of BDNF for 30 min. Phosphorylated RasGRF1 (Ser916/898) was analyzed by immunoblotting with the anti-pSer916/898 antibody. (C, D) Densitometry analysis was performed, and p-RasGRF1/total RasGRF1 ratio was determined. Relative levels of p-RasGRF1/total RasGRF1 compared to vehicle-treated cells are shown. Data are presented as the means ± SEM of four independent preparations, *p

    Article Snippet: 2.2 Reagents and antibodies The following reagents were purchased commercially: Poly-L -lysine, dbcAMP, forskolin, and the pharmacological Trk receptor inhibitor K252a (Sigma-Aldrich); recombinant human BDNF (PeproTech); and the pharmacological PKA inhibitor H-89 (Cell Signaling Technology).

    Techniques: