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  • 97
    Millipore k252a
    BDNF-induced suppression of eIPSCs is dependent on both postsynaptic trkB receptors and postsynaptic calcium elevation. A : individual example of the lack of effect of BDNF (20 ng/ml) on eIPSC amplitude, with 200 nM <t>K252a</t> intracellularly loaded through
    K252a, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 1175 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/k252a/product/Millipore
    Average 97 stars, based on 1175 article reviews
    Price from $9.99 to $1999.99
    k252a - by Bioz Stars, 2020-05
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    93
    Tocris k252 a
    Bar histograms showing the group data of the effects of <t>K252a</t> and TrkB antibody on the latency of epileptiform activity induced by CTZ in anaesthetised rats. Comparing to the injection of CTZ (5 μmol, i.c.v.) alone, rats pre-injected with K252a
    K252 A, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/k252 a/product/Tocris
    Average 93 stars, based on 8 article reviews
    Price from $9.99 to $1999.99
    k252 a - by Bioz Stars, 2020-05
    93/100 stars
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    88
    Abcam k 252b
    Bar histograms showing the group data of the effects of <t>K252a</t> and TrkB antibody on the latency of epileptiform activity induced by CTZ in anaesthetised rats. Comparing to the injection of CTZ (5 μmol, i.c.v.) alone, rats pre-injected with K252a
    K 252b, supplied by Abcam, used in various techniques. Bioz Stars score: 88/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/k 252b/product/Abcam
    Average 88 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    k 252b - by Bioz Stars, 2020-05
    88/100 stars
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    93
    Tocris 200 n m k252a
    Bar histograms showing the group data of the effects of <t>K252a</t> and TrkB antibody on the latency of epileptiform activity induced by CTZ in anaesthetised rats. Comparing to the injection of CTZ (5 μmol, i.c.v.) alone, rats pre-injected with K252a
    200 N M K252a, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/200 n m k252a/product/Tocris
    Average 93 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
    200 n m k252a - by Bioz Stars, 2020-05
    93/100 stars
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    Image Search Results


    BDNF-induced suppression of eIPSCs is dependent on both postsynaptic trkB receptors and postsynaptic calcium elevation. A : individual example of the lack of effect of BDNF (20 ng/ml) on eIPSC amplitude, with 200 nM K252a intracellularly loaded through

    Journal: Journal of Neurophysiology

    Article Title: BDNF Evokes Release of Endogenous Cannabinoids at Layer 2/3 Inhibitory Synapses in the Neocortex

    doi: 10.1152/jn.00472.2010

    Figure Lengend Snippet: BDNF-induced suppression of eIPSCs is dependent on both postsynaptic trkB receptors and postsynaptic calcium elevation. A : individual example of the lack of effect of BDNF (20 ng/ml) on eIPSC amplitude, with 200 nM K252a intracellularly loaded through

    Article Snippet: We addressed the question of which subset of trkB receptors are involved in the BDNF-induced suppression of eIPSCs by including K252a (200 nM) in the internal patch pipette solution.

    Techniques:

    K252a induces apoptosis of primary AML cells . Cell viability was analyzed using the annexin-V assay. Results are presented as the percentage of living cells in the presence of K252a (100% value derived from untreated control). (A) Cells were from patient

    Journal: Blood

    Article Title: High-affinity neurotrophin receptors and ligands promote leukemogenesis

    doi: 10.1182/blood-2008-05-155200

    Figure Lengend Snippet: K252a induces apoptosis of primary AML cells . Cell viability was analyzed using the annexin-V assay. Results are presented as the percentage of living cells in the presence of K252a (100% value derived from untreated control). (A) Cells were from patient

    Article Snippet: Inhibitors K252a, AG879 (Calbiochem) and anti–human BDNF antibody (Promega, Mannheim, Germany) were used.

    Techniques: Annexin V Assay, Derivative Assay

    Effect of chronic physical exercise on the number of β-cells in Langerhans islet in a healthy state. The high intensity training reduces the number of β-cells per islet. On the other hand, the K252a treatment did not modify the high intensity training effect on the β-cell number per islet. ** p = 0.007 vs C-K252a, *** p

    Journal: Islets

    Article Title: Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

    doi: 10.1080/19382014.2016.1260796

    Figure Lengend Snippet: Effect of chronic physical exercise on the number of β-cells in Langerhans islet in a healthy state. The high intensity training reduces the number of β-cells per islet. On the other hand, the K252a treatment did not modify the high intensity training effect on the β-cell number per islet. ** p = 0.007 vs C-K252a, *** p

    Article Snippet: The groups +K252a received K252a intraperitoneal (ip) injections during the seventh and eighth week at 50 µg/kg body weight (Sigma Aldrich Mexico) diluted in a final concentration of 25% DMSO, 1.5 mL total volume ip injections.

    Techniques:

    Effect of chronic physical exercise on islet/mm 2 pancreas in healthy rats. The intensities of chronic exercise did not change the Langerhans islet number per mm 2 . Besides, the K252a administration had any effect on the Langerhans islet number area.

    Journal: Islets

    Article Title: Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

    doi: 10.1080/19382014.2016.1260796

    Figure Lengend Snippet: Effect of chronic physical exercise on islet/mm 2 pancreas in healthy rats. The intensities of chronic exercise did not change the Langerhans islet number per mm 2 . Besides, the K252a administration had any effect on the Langerhans islet number area.

    Article Snippet: The groups +K252a received K252a intraperitoneal (ip) injections during the seventh and eighth week at 50 µg/kg body weight (Sigma Aldrich Mexico) diluted in a final concentration of 25% DMSO, 1.5 mL total volume ip injections.

    Techniques:

    Effects of chronic exercise intensity on β-cell size, under unblocked BDNF receptors conditions (−K252a) and under blocked BDNF receptor conditions (+K252a) in healthy state. The chronic training exercise induced β-cell hypertrophy with respect to C group. The K252a administration has not impact on exercise effects to increase the β-cell size. * p

    Journal: Islets

    Article Title: Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

    doi: 10.1080/19382014.2016.1260796

    Figure Lengend Snippet: Effects of chronic exercise intensity on β-cell size, under unblocked BDNF receptors conditions (−K252a) and under blocked BDNF receptor conditions (+K252a) in healthy state. The chronic training exercise induced β-cell hypertrophy with respect to C group. The K252a administration has not impact on exercise effects to increase the β-cell size. * p

    Article Snippet: The groups +K252a received K252a intraperitoneal (ip) injections during the seventh and eighth week at 50 µg/kg body weight (Sigma Aldrich Mexico) diluted in a final concentration of 25% DMSO, 1.5 mL total volume ip injections.

    Techniques:

    Effect of chronic physical exercise on β-cell density in Langerhans islets in healthy state. The high intensity training reduces the percentage of β-cell per islet. (*** p = 0.008 when compared with C- K252a treatment. The K252a administration affects the β-cell density in pancreatic islets. In sedentary conditions, the blocking of BDNF receptor reduced the β-cell density ( and p

    Journal: Islets

    Article Title: Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

    doi: 10.1080/19382014.2016.1260796

    Figure Lengend Snippet: Effect of chronic physical exercise on β-cell density in Langerhans islets in healthy state. The high intensity training reduces the percentage of β-cell per islet. (*** p = 0.008 when compared with C- K252a treatment. The K252a administration affects the β-cell density in pancreatic islets. In sedentary conditions, the blocking of BDNF receptor reduced the β-cell density ( and p

    Article Snippet: The groups +K252a received K252a intraperitoneal (ip) injections during the seventh and eighth week at 50 µg/kg body weight (Sigma Aldrich Mexico) diluted in a final concentration of 25% DMSO, 1.5 mL total volume ip injections.

    Techniques: Blocking Assay

    Effects of chronic exercise intensity on the total insulin area in healthy rats. (A) Representative images (objective 5X) for the 6 experimental groups (duodenal pancreas in rats). Islets were stained with insulin antibody (brown color); high intensity training reduced the presence of insulin in the islet. (B) The K252a treatment shows a strong tendency to affect the total insulin area.

    Journal: Islets

    Article Title: Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

    doi: 10.1080/19382014.2016.1260796

    Figure Lengend Snippet: Effects of chronic exercise intensity on the total insulin area in healthy rats. (A) Representative images (objective 5X) for the 6 experimental groups (duodenal pancreas in rats). Islets were stained with insulin antibody (brown color); high intensity training reduced the presence of insulin in the islet. (B) The K252a treatment shows a strong tendency to affect the total insulin area.

    Article Snippet: The groups +K252a received K252a intraperitoneal (ip) injections during the seventh and eighth week at 50 µg/kg body weight (Sigma Aldrich Mexico) diluted in a final concentration of 25% DMSO, 1.5 mL total volume ip injections.

    Techniques: Staining

    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

    Kinase inhibitors decrease sensitivity to ABA-mediated postgermination arrest. Wild-type and hyl1 seeds were plated on filter paper saturated with MS solution alone or MS containing either PD98059 (100 μM) or K252a (1 μM). ABA was present at the indicated concentrations. After 2 days at 4°C, seeds were transferred to constant light at 22°C. Pictures were taken 10 days after stratification.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Mitogen-activated protein kinase signaling in postgermination arrest of development by abscisic acid

    doi: 10.1073/pnas.242607499

    Figure Lengend Snippet: Kinase inhibitors decrease sensitivity to ABA-mediated postgermination arrest. Wild-type and hyl1 seeds were plated on filter paper saturated with MS solution alone or MS containing either PD98059 (100 μM) or K252a (1 μM). ABA was present at the indicated concentrations. After 2 days at 4°C, seeds were transferred to constant light at 22°C. Pictures were taken 10 days after stratification.

    Article Snippet: ABA (Sigma), the MAPK kinase (MAPKK)-specific inhibitor PD98059 (Sigma), and the general kinase inhibitor K252a (Calbiochem) were added to the medium where indicated.

    Techniques: Mass Spectrometry

    Relationship between VHL status and MT1-MMP transcription and synthesis—effects of EGFR and MET inhibition. Panel I: VHL+/+ Caki-1 and VHL−/− 786-O clear cell carcinoma cells were transiently transfected with the MT1-MMP luciferase reporter construct in the presence or absence of the EGFR inhibitor 4557w (2.5 μM) or the MET inhibitor K252a (10 nM). After 48 h, the cells were lysed and luciferase activity determined. Data expressed as mean ± SD of triplicate to quadruplicate measurements where the control pGL3 vector was assigned a relative activity of 100%. (* P

    Journal: Carcinogenesis

    Article Title: Graded activation of the MEK1/MT1-MMP axis determines renal epithelial cell tumor phenotype

    doi: 10.1093/carcin/bgr216

    Figure Lengend Snippet: Relationship between VHL status and MT1-MMP transcription and synthesis—effects of EGFR and MET inhibition. Panel I: VHL+/+ Caki-1 and VHL−/− 786-O clear cell carcinoma cells were transiently transfected with the MT1-MMP luciferase reporter construct in the presence or absence of the EGFR inhibitor 4557w (2.5 μM) or the MET inhibitor K252a (10 nM). After 48 h, the cells were lysed and luciferase activity determined. Data expressed as mean ± SD of triplicate to quadruplicate measurements where the control pGL3 vector was assigned a relative activity of 100%. (* P

    Article Snippet: To assess the transcriptional activity of MT1-MMP within the context of VHL+/+ and VHL−/− status, Caki-1 and 786-O renal cell carcinoma cell lines were transiently transfected as detailed above in the presence or absence of the EGFR/ErbB-2 inhibitor 4557W (2.5 μM; Calbiochem, San Diego, CA) or MET inhibitor K252a (10 nM; Sigma-Aldrich, St. Louis, MO) for 48 h, followed by lysis and analysis as detailed above.

    Techniques: Inhibition, Transfection, Luciferase, Construct, Activity Assay, Plasmid Preparation

    K252a reduced nicotine withdrawal-induced downregulation of KCC2 expression in the spinal cord. A. Western blot of KCC2 protein expression in the spinal cord of the control, NW, NW+DMSO, and NW+K252a groups. Blockade of TrkB with K252a increased the KCC2 protein level in NW rats on day 4. B. The relative expression of KCC2 was normalized to the expression of β-actin (n = 3,*P

    Journal: Translational Neuroscience

    Article Title: BDNF/TRK/KCC2 pathway in nicotine withdrawal-induced hyperalgesia

    doi: 10.1515/tnsci-2015-0022

    Figure Lengend Snippet: K252a reduced nicotine withdrawal-induced downregulation of KCC2 expression in the spinal cord. A. Western blot of KCC2 protein expression in the spinal cord of the control, NW, NW+DMSO, and NW+K252a groups. Blockade of TrkB with K252a increased the KCC2 protein level in NW rats on day 4. B. The relative expression of KCC2 was normalized to the expression of β-actin (n = 3,*P

    Article Snippet: The animals were randomly assigned to five groups: control group (n = 12) receiving no treatment, normal saline group (NS group, n = 12) receiving subcutaneous injection of saline for 7 days, nicotine withdrawal group (NW group, n = 30) receiving subcutaneous injection of nicotine for 7 days, NW + DMSO group (n = 12) receiving intrathecal injection of dimethyl sulfoxide (DMSO, 10 μl) for 3 days after nicotine withdrawal, and NW+K252a group (n = 12) receiving intrathecal injection of K252a (Sigma, St. Louis, MO, USA, 10 μg in 10 μl of saline) for three days after nicotine withdrawal.

    Techniques: Expressing, Western Blot

    K252a reduced nicotine withdrawal-induced hyperalgesia in rats. The thermal withdrawal latency (TWL) was measured from 1 to 7 days after the last injection in rats in the control, NS, NW, NW+DMSO, and NW+K252a groups (*P

    Journal: Translational Neuroscience

    Article Title: BDNF/TRK/KCC2 pathway in nicotine withdrawal-induced hyperalgesia

    doi: 10.1515/tnsci-2015-0022

    Figure Lengend Snippet: K252a reduced nicotine withdrawal-induced hyperalgesia in rats. The thermal withdrawal latency (TWL) was measured from 1 to 7 days after the last injection in rats in the control, NS, NW, NW+DMSO, and NW+K252a groups (*P

    Article Snippet: The animals were randomly assigned to five groups: control group (n = 12) receiving no treatment, normal saline group (NS group, n = 12) receiving subcutaneous injection of saline for 7 days, nicotine withdrawal group (NW group, n = 30) receiving subcutaneous injection of nicotine for 7 days, NW + DMSO group (n = 12) receiving intrathecal injection of dimethyl sulfoxide (DMSO, 10 μl) for 3 days after nicotine withdrawal, and NW+K252a group (n = 12) receiving intrathecal injection of K252a (Sigma, St. Louis, MO, USA, 10 μg in 10 μl of saline) for three days after nicotine withdrawal.

    Techniques: Injection

    In vitro migration of bone marrow (BM)- and peripheral blood (PB)-derived mononuclear cells (MNCs) towards NGF . ( a–c ) Identification by flow cytometry of c-kit pos /TrkA pos cells in human BM-derived MNCs. ( a ) Forward and side scatter shows the total population analyzed (P1). ( b ) c-kit pos cells (P2) were gated from the total cells population and double-positive cells for c-kit and TrkA ( c ) are shown in P3. ( d–f ) Quantitative analysis of human BM-derived MNCs (obtained from noncardiovascular patients) after in vitro Transwell migration towards NGF shows migration of human MNCs ( d ) and enrichment for CD34 pos /c-kit pos ( e ) and CD34 pos /c-kit pos /TrkA pos ( f ). The TrkA inhibitor K252a was used to repress NGF. ( g ) Bar graphs show the percentage of CD34 pos /c-kit pos /TrkA pos cells in the PB of either healthy subjects or patients with an acute MI (within 5 days following MI). BSA and SDF-1 have been used as negative and positive controls, respectively. Data are expressed as mean ± SEM. ** P

    Journal: Molecular Therapy

    Article Title: Cardiac Nerve Growth Factor Overexpression Induces Bone Marrow–derived Progenitor Cells Mobilization and Homing to the Infarcted Heart

    doi: 10.1038/mt.2015.167

    Figure Lengend Snippet: In vitro migration of bone marrow (BM)- and peripheral blood (PB)-derived mononuclear cells (MNCs) towards NGF . ( a–c ) Identification by flow cytometry of c-kit pos /TrkA pos cells in human BM-derived MNCs. ( a ) Forward and side scatter shows the total population analyzed (P1). ( b ) c-kit pos cells (P2) were gated from the total cells population and double-positive cells for c-kit and TrkA ( c ) are shown in P3. ( d–f ) Quantitative analysis of human BM-derived MNCs (obtained from noncardiovascular patients) after in vitro Transwell migration towards NGF shows migration of human MNCs ( d ) and enrichment for CD34 pos /c-kit pos ( e ) and CD34 pos /c-kit pos /TrkA pos ( f ). The TrkA inhibitor K252a was used to repress NGF. ( g ) Bar graphs show the percentage of CD34 pos /c-kit pos /TrkA pos cells in the PB of either healthy subjects or patients with an acute MI (within 5 days following MI). BSA and SDF-1 have been used as negative and positive controls, respectively. Data are expressed as mean ± SEM. ** P

    Article Snippet: Endothelial Basal Medium-2 supplemented with NGF (100 ng/ml; Millipore) alone or in combination with the TrkA inhibitor K252a (100 nmol/l; Sigma Aldrich) was placed in the lower wells.

    Techniques: In Vitro, Migration, Derivative Assay, Flow Cytometry, Cytometry

    Loss of TrkC leads to loss of cell viability. (A) Cleavage of procaspase-3 and PARP of U937 control-shRNA or U937 TrkC-shRNA cells was analyzed by Western blotting. (B) Cell viability of U937 cells after treatment with K252a (100 nM) or vehicle control

    Journal: Molecules and Cells

    Article Title: TrkC Promotes Survival and Growth of Leukemia Cells Through Akt-mTOR-Dependent Up-Regulation of PLK-1 and Twist-1

    doi: 10.1007/s10059-013-0061-6

    Figure Lengend Snippet: Loss of TrkC leads to loss of cell viability. (A) Cleavage of procaspase-3 and PARP of U937 control-shRNA or U937 TrkC-shRNA cells was analyzed by Western blotting. (B) Cell viability of U937 cells after treatment with K252a (100 nM) or vehicle control

    Article Snippet: The protein kinase inhibitor K252a was purchased from Calbiochem (USA).

    Techniques: shRNA, Western Blot

    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:

    Bar histograms showing the group data of the effects of K252a and TrkB antibody on the latency of epileptiform activity induced by CTZ in anaesthetised rats. Comparing to the injection of CTZ (5 μmol, i.c.v.) alone, rats pre-injected with K252a

    Journal:

    Article Title: BDNF-TrkB signaling pathway mediates the induction of epileptiform activity induced by a convulsant drug cyclothiazide

    doi: 10.1016/j.neuropharm.2009.04.007

    Figure Lengend Snippet: Bar histograms showing the group data of the effects of K252a and TrkB antibody on the latency of epileptiform activity induced by CTZ in anaesthetised rats. Comparing to the injection of CTZ (5 μmol, i.c.v.) alone, rats pre-injected with K252a

    Article Snippet: The following drugs were freshly made before each experiment: Cyclothiazide (1 M or 0.2 M in DMSO for in vivo injection) and K252a (0.25 M in DMSO for in vivo injection) were purchased from Tocris (Northpoint, Bristol); anti-TrkB mouse antibody (TrkB antibody) was from BD Biosciences (San Jose, California); Pontamine sky blue dye (20 mg ml-1 ; BDH, Poole) was dissolved in 0.5 M sodium acetate; Urethane (25%; Sigma Aldrich Chemical Co., Poole, Dorset) was dissolved in distilled water.

    Techniques: Activity Assay, Injection

    Acute application of K252a blocked action potential firing in cultured hippocampal neurons. (A) One example showing that acute application of K252a (250 nM) significantly reduced the action potential firing rate when bath applied to cultured hippocampal

    Journal:

    Article Title: BDNF-TrkB signaling pathway mediates the induction of epileptiform activity induced by a convulsant drug cyclothiazide

    doi: 10.1016/j.neuropharm.2009.04.007

    Figure Lengend Snippet: Acute application of K252a blocked action potential firing in cultured hippocampal neurons. (A) One example showing that acute application of K252a (250 nM) significantly reduced the action potential firing rate when bath applied to cultured hippocampal

    Article Snippet: The following drugs were freshly made before each experiment: Cyclothiazide (1 M or 0.2 M in DMSO for in vivo injection) and K252a (0.25 M in DMSO for in vivo injection) were purchased from Tocris (Northpoint, Bristol); anti-TrkB mouse antibody (TrkB antibody) was from BD Biosciences (San Jose, California); Pontamine sky blue dye (20 mg ml-1 ; BDH, Poole) was dissolved in 0.5 M sodium acetate; Urethane (25%; Sigma Aldrich Chemical Co., Poole, Dorset) was dissolved in distilled water.

    Techniques: Cell Culture

    Effects of K252a and TrkB antibody on CTZ-induced spontaneous epileptiform bursts in hippocampal CA1 pyramidal cell layer in anaesthetised rats sampled before, 45, 90 and 180 min after CTZ injection (5 μmol, i.c.v.). (A) Original traces from a

    Journal:

    Article Title: BDNF-TrkB signaling pathway mediates the induction of epileptiform activity induced by a convulsant drug cyclothiazide

    doi: 10.1016/j.neuropharm.2009.04.007

    Figure Lengend Snippet: Effects of K252a and TrkB antibody on CTZ-induced spontaneous epileptiform bursts in hippocampal CA1 pyramidal cell layer in anaesthetised rats sampled before, 45, 90 and 180 min after CTZ injection (5 μmol, i.c.v.). (A) Original traces from a

    Article Snippet: The following drugs were freshly made before each experiment: Cyclothiazide (1 M or 0.2 M in DMSO for in vivo injection) and K252a (0.25 M in DMSO for in vivo injection) were purchased from Tocris (Northpoint, Bristol); anti-TrkB mouse antibody (TrkB antibody) was from BD Biosciences (San Jose, California); Pontamine sky blue dye (20 mg ml-1 ; BDH, Poole) was dissolved in 0.5 M sodium acetate; Urethane (25%; Sigma Aldrich Chemical Co., Poole, Dorset) was dissolved in distilled water.

    Techniques: Injection

    Chronic blocking TrkB receptors suppressed CTZ-induced epileptiform activity in cultured hippocampal neurons. (A-C) Typical neuronal activity after chronic treatment with CTZ alone (5 μM, 48 hrs) (A), CTZ+K252a (500 nM) (B), or CTZ+TrkB antibody

    Journal:

    Article Title: BDNF-TrkB signaling pathway mediates the induction of epileptiform activity induced by a convulsant drug cyclothiazide

    doi: 10.1016/j.neuropharm.2009.04.007

    Figure Lengend Snippet: Chronic blocking TrkB receptors suppressed CTZ-induced epileptiform activity in cultured hippocampal neurons. (A-C) Typical neuronal activity after chronic treatment with CTZ alone (5 μM, 48 hrs) (A), CTZ+K252a (500 nM) (B), or CTZ+TrkB antibody

    Article Snippet: The following drugs were freshly made before each experiment: Cyclothiazide (1 M or 0.2 M in DMSO for in vivo injection) and K252a (0.25 M in DMSO for in vivo injection) were purchased from Tocris (Northpoint, Bristol); anti-TrkB mouse antibody (TrkB antibody) was from BD Biosciences (San Jose, California); Pontamine sky blue dye (20 mg ml-1 ; BDH, Poole) was dissolved in 0.5 M sodium acetate; Urethane (25%; Sigma Aldrich Chemical Co., Poole, Dorset) was dissolved in distilled water.

    Techniques: Blocking Assay, Activity Assay, Cell Culture

    Bar histograms showing the group data of the effects of K252a and TrkB antibody on the CTZ-induction of epileptiform activity in anaesthetised rats. All CTZ injection was at the dose of 5 μmol. Injection of K252a 30 min prior to the injection

    Journal:

    Article Title: BDNF-TrkB signaling pathway mediates the induction of epileptiform activity induced by a convulsant drug cyclothiazide

    doi: 10.1016/j.neuropharm.2009.04.007

    Figure Lengend Snippet: Bar histograms showing the group data of the effects of K252a and TrkB antibody on the CTZ-induction of epileptiform activity in anaesthetised rats. All CTZ injection was at the dose of 5 μmol. Injection of K252a 30 min prior to the injection

    Article Snippet: The following drugs were freshly made before each experiment: Cyclothiazide (1 M or 0.2 M in DMSO for in vivo injection) and K252a (0.25 M in DMSO for in vivo injection) were purchased from Tocris (Northpoint, Bristol); anti-TrkB mouse antibody (TrkB antibody) was from BD Biosciences (San Jose, California); Pontamine sky blue dye (20 mg ml-1 ; BDH, Poole) was dissolved in 0.5 M sodium acetate; Urethane (25%; Sigma Aldrich Chemical Co., Poole, Dorset) was dissolved in distilled water.

    Techniques: Activity Assay, Injection

    Representative traces illustrating that acute application of K252a suppressed the epileptiform activity induced by chronic or acute treatment of CTZ in cultured hippocampal neurons. (A) Epileptiform bursts persisted after long-term CTZ treatment (7 days).

    Journal:

    Article Title: BDNF-TrkB signaling pathway mediates the induction of epileptiform activity induced by a convulsant drug cyclothiazide

    doi: 10.1016/j.neuropharm.2009.04.007

    Figure Lengend Snippet: Representative traces illustrating that acute application of K252a suppressed the epileptiform activity induced by chronic or acute treatment of CTZ in cultured hippocampal neurons. (A) Epileptiform bursts persisted after long-term CTZ treatment (7 days).

    Article Snippet: The following drugs were freshly made before each experiment: Cyclothiazide (1 M or 0.2 M in DMSO for in vivo injection) and K252a (0.25 M in DMSO for in vivo injection) were purchased from Tocris (Northpoint, Bristol); anti-TrkB mouse antibody (TrkB antibody) was from BD Biosciences (San Jose, California); Pontamine sky blue dye (20 mg ml-1 ; BDH, Poole) was dissolved in 0.5 M sodium acetate; Urethane (25%; Sigma Aldrich Chemical Co., Poole, Dorset) was dissolved in distilled water.

    Techniques: Activity Assay, Cell Culture

    Bar histograms showing the effect of K252a and TrkB antibody on CTZ-induced synchronized bursts. (A) Pre-injection of K252a 60 min prior to CTZ (5 μmol) injection significantly reduced the frequency of synchronized bursts. (B) Pre-injection of

    Journal:

    Article Title: BDNF-TrkB signaling pathway mediates the induction of epileptiform activity induced by a convulsant drug cyclothiazide

    doi: 10.1016/j.neuropharm.2009.04.007

    Figure Lengend Snippet: Bar histograms showing the effect of K252a and TrkB antibody on CTZ-induced synchronized bursts. (A) Pre-injection of K252a 60 min prior to CTZ (5 μmol) injection significantly reduced the frequency of synchronized bursts. (B) Pre-injection of

    Article Snippet: The following drugs were freshly made before each experiment: Cyclothiazide (1 M or 0.2 M in DMSO for in vivo injection) and K252a (0.25 M in DMSO for in vivo injection) were purchased from Tocris (Northpoint, Bristol); anti-TrkB mouse antibody (TrkB antibody) was from BD Biosciences (San Jose, California); Pontamine sky blue dye (20 mg ml-1 ; BDH, Poole) was dissolved in 0.5 M sodium acetate; Urethane (25%; Sigma Aldrich Chemical Co., Poole, Dorset) was dissolved in distilled water.

    Techniques: Injection

    Tnf mRNA and TNF protein abundance are increased in 17NF ovaries as compared to WT controls, and this increase in TNF production is abolished by blocking high affinity NTRK receptors. A , Tnf mRNA content in 30-day-old WT and 17NF ovaries measured by semi-quantitative PCR. Ppia = Peptidylprolyl isomerase A (cyclophilin A). B , TNF protein measured by ELISA in protein extracts from 28–30 day-old ovaries incubated for 3 h in KRB buffer at 37 C. Some ovaries were treated during this time with 100 ng/ml of K252a, a blocker of NTRK tyrosine kinase activity. MM = molecular marker; * = p

    Journal: Reproduction (Cambridge, England)

    Article Title: Excessive Ovarian Production of Nerve Growth Factor Elicits Granulosa Cell Apoptosis by Setting in Motion a Tumor Necrosis Factor alpha/Stathmin$Mediated Death Signaling Pathway

    doi: 10.1530/REP-11-0134

    Figure Lengend Snippet: Tnf mRNA and TNF protein abundance are increased in 17NF ovaries as compared to WT controls, and this increase in TNF production is abolished by blocking high affinity NTRK receptors. A , Tnf mRNA content in 30-day-old WT and 17NF ovaries measured by semi-quantitative PCR. Ppia = Peptidylprolyl isomerase A (cyclophilin A). B , TNF protein measured by ELISA in protein extracts from 28–30 day-old ovaries incubated for 3 h in KRB buffer at 37 C. Some ovaries were treated during this time with 100 ng/ml of K252a, a blocker of NTRK tyrosine kinase activity. MM = molecular marker; * = p

    Article Snippet: One ovary from each 17NF and WT mice was treated with 100 nM of the NTRK receptor inhibitor's K252a (Tocris Bioscience, Ellisville, MO).

    Techniques: Blocking Assay, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Incubation, Activity Assay, Marker

    Concentration-response and time-course analyses of 7,8-DHF effects on STEP 61 levels. (a) Primary rat cortical neurons (DIV12-14) were treated with various doses (100, 250 or 500 nM) of a TrkB agonist (7,8-dihydroxyflavone, DHF) in the absence or presence of the tyrosine kinase inhibitor, K252a (100 nM) for 30 min. (b) Cultures were treated with DHF (500 nM) for 5-30 min in the absence or presence of K252a (100 nM). Equal amounts of lysates were used for western blotting with phospho-specific and pan-antibodies as indicated in the figure. Quantification of phospho-protein levels was normalized to total protein levels and then to β-actin as a loading control. Data were expressed as mean ± SEM (* p

    Journal: Journal of neurochemistry

    Article Title: Down-regulation of BDNF in cell and animal models increases striatal-enriched protein tyrosine phosphatase 61 (STEP61) levels

    doi: 10.1111/jnc.13295

    Figure Lengend Snippet: Concentration-response and time-course analyses of 7,8-DHF effects on STEP 61 levels. (a) Primary rat cortical neurons (DIV12-14) were treated with various doses (100, 250 or 500 nM) of a TrkB agonist (7,8-dihydroxyflavone, DHF) in the absence or presence of the tyrosine kinase inhibitor, K252a (100 nM) for 30 min. (b) Cultures were treated with DHF (500 nM) for 5-30 min in the absence or presence of K252a (100 nM). Equal amounts of lysates were used for western blotting with phospho-specific and pan-antibodies as indicated in the figure. Quantification of phospho-protein levels was normalized to total protein levels and then to β-actin as a loading control. Data were expressed as mean ± SEM (* p

    Article Snippet: The tyrosine kinase inhibitor K252a, the TrkB agonists 7,8-dihydroxyflavone (7,8-DHF) and LM 22A4 were purchased from Tocris Biosciences (Ellisville, MO).

    Techniques: Concentration Assay, Western Blot