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  • 94
    Millipore xestospongin c
    Diacylglycerol but not phosphatidylinositol-3-phosphate or arachidonic acid is involved in amino acid-signaling in the lateral MOE. A , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (cyan and blue trace). Incubation with <t>Xestospongin</t> C (500 nM; application for 10 min; green-shaded panel) did not affect the responses. B , mean Ca 2+ transients (±SEM) of all three L-arginine-responsive ORNs of an acute slice preparation (lateral MOE). The responses were not affected by Xestospongin C (500 nM; 10 min; green-shaded panel). C , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (red and purple trace). Application of SAG (200 µM; 10 s, middle panel; 50 s, right-hand-panel) triggered Ca 2+ increases in both ORNs. D , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (black and grey trace). Both ORNs did not respond upon application of AA (50 µM; 10 s, middle panel; 60 s, right-hand-panel) E , mean responses (±SEM), expressed as percentage of control response to L-arginine, of 14 ORNs (4 slices) in standard (dark grey columns) and bath solution with Xestospongin C 500 nM (green columns; respectively 5, 10 and 15 min after application of Xestospongin C; washout time was 5 min). No significant reduction of the Ca 2+ responses was observed (p > 0.05; paired Student's t-test). F , mean response amplitudes (±SEM) upon application of L-arginine (dark grey columns) and SAG (purple columns; 200 and 500 µM; 7 ORNs, 2 slices and 9 ORNs, 2 slices, respectively). The response amplitudes to SAG were lower but not significanty different from the L-arginine responses (p > 0.05; paired Student's t-test). [AA, arachidonic acid].
    Xestospongin C, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 286 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Abcam xestospongin c
    Ca 2+ handling. ( a ) Analysis of Ca 2+ release in FDB fibres (area under the curve, AUC) at different stimulation frequencies using Magfluo4. Inset: Representative Ca 2+ transients at different stimulation frequencies. n is the number of fibres from at least three different mice. ( b ) Resting cytosolic Ca 2+ concentration relative to that of WT fibres assessed with Fura-2 in FDB fibres. n is the number of fibres from at least three different mice. ( c ) Analysis of the amplitudes of the Ca 2+ transients in FDB fibres from WT and IT mice with repetitive 100 Hz (200 ms train/1.5 s) stimulations. ( d ) Representative fibres loaded with MitoSOX from WT and IT mice with and without RU360 treatment. Scale bars are 10 μm. ( e ) Analysis of images in panel D. MitoSOX fluorescence in FDB fibres (with and without RU360 to inhibit MCU) from WT and IT mice was plotted as % WT control (littermate, same day). n is the number of fibres from three to four mice. ( f ) Effect of <t>Xestospongin</t> C on MitoSox fluorescence. ( g ) Negatively stained EM pictures of SR-MaMs from IT and WT soleus. Bar is 100 nm. ( h ) Analysis of the average length of the tethers between the SR and the interfibrillar mitochondria. ( i ) Distribution of tether length in WT and IT soleus. Data are shown as mean±s.e.m. * P
    Xestospongin C, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 30 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Tocris xestospongin c
    Phospholipase C (PLC)‐phosphatidylinositol 4,5‐bisphosphate(PIP 2 )‐protein kinase C (PKC) signaling mediates the effects of mGluR1 on mGluR6‐evoked currents. Raw traces depicting the effect of PKC stimulation on the rod bipolar cell (RBC) light response under four different conditions. (A) Light response of an RBC at break‐in and after dialysis with the PKC activator 1‐Oleoyl‐2‐acetyl‐sn‐glycerol (OAG). (B) As in (A) except that (RS)‐1‐Aminoindan‐1,5‐dicarboxylic acid (AIDA) was added to the bath prior to the experiment to block mGluR1 function. (C) Trpm1 current evoked at break‐in and after OAG dialysis in an internal solution containing 10 mmol/L BAPTA rather than EGTA. A pharmacological approach was used to activate Trpm1 current (see Methods). (D) Light‐evoked Trpm1 currents at break‐in (black trace) and after 5 min of dialysis with OAG and the IP 3  receptor inhibitor xestospongin C. (E) Summary data of the four experiments depicted in A–D ( n  = 5 for all conditions. *** P  = 0.006, ** P  = 0.01, * P  = 0.03). (F) Sample traces of Trpm1 current evoked by light in a cell dialyzed with the PLC inhibitor U73122 (10  μ mol/L) before and after bath application of AIDA. (G) Comparison of the response amplitudes after dialysis with U73122 and subsequent bath application of AIDA. Open and closed squares represent individual cells and the mean response respectively. AIDA application caused no significant change in response amplitude ( n  = 4;  P >  0.1, paired  t  test comparing U73122 alone vs. U73122+AIDA).
    Xestospongin C, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 47 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Cayman Chemical xestospongin c
    The inositol 1,4,5-trisphosphate receptor inhibitor <t>Xestospongin</t> C and the nonspecific PKC inhibitor calphostin C inhibited the proliferative effect of BW723C86 on ICC. A , 333 n m and 1 μ m Xestospongin ( Xesto ) C inhibited the increase in proliferation
    Xestospongin C, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 93/100, based on 65 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    FUJIFILM xestospongin c
    Specific inhibition of 2-APB-sensitive Ca 2+  channels failed to prevent H 2 O 2 -induced cardiomyocyte death. (A) Neonatal rat cardiomyocytes (NRCMs) were pretreated or not with xestospongin C, a specific IP 3 R inhibitor, for 1 hour, which was followed by H 2 O 2  treatment. Cell viability levels were determined. Results are shown as mean values ± SEM from three independent experiments. (B) Representative fura-2 ratio obtained using NRCMs pretreated or not with xestospongin C, followed by H 2 O 2  treatment. (C) The expression levels of 2-APB-sensitive TRP channels in NRCMs were analyzed by RT-PCR. A representative image with a 40-cycle amplification is shown. (D-F) NRCMs were pretreated or not with SKF-96365 (D, a TRPC inhibitor), AA-861 (E, a TRPM7 inhibitor) and mefenamic acid (F, a TRPM3 inhibitor), followed by H 2 O 2  treatment. Cell viability rate is presented. Results are presented as mean values ± SEM obtained in four independent experiments.
    Xestospongin C, supplied by FUJIFILM, used in various techniques. Bioz Stars score: 92/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Enzo Biochem xestospongin c
    Long-lasting increase of fIPSPs after DHPG application is mediated by IP 3 receptors activation. DHPG failed to increase fIPSPs in all CA1 (a) and specifically in its different sub-regions (b–g) in presence of the cell-permeable IP 3 receptors blockers 2-APB or <t>Xestospongin</t> C (XestoC). In all figures, left panel shows the time course, while right panel is showing mean over time. Statistical analysis in right panel figures is one-way ANOVA followed by Dunnet post-hoc test. Vehicles of both IP 3 receptors antagonists have been pooled together since they are not different. n = (slices, mice): Vehicle group = (11, 9), 2-APB group = (5, 5), Xestospongin C group (5, 3). Data are mean ± s.e.m. *p
    Xestospongin C, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 92/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Biomol GmbH xestospongin c
    IL-6–induced enhancement of GSIS is abrogated by an IP 3 receptor antagonist but not by a PKA inhibitor. MIN-6 cells were pretreated with vehicle or a pharmacological inhibitor (1 μmol/L H-89 [ A ] or 10 μmol/L <t>Xestospongin</t> C [ B ]) with or without concomitant 1,200 pg/mL IL-6 for 24 h, followed by measurement of insulin secretion for 60 min in KRBB supplemented with either 1.67 or 16.7 mmol/L glucose ( n = 6 per group). ** P
    Xestospongin C, supplied by Biomol GmbH, used in various techniques. Bioz Stars score: 92/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Merck KGaA xestospongin c
    After cells were treated with 1.2% isoflurane for 8 h, cytosolic calcium concentration ([Ca 2+ ] c ) was determined by flow cytometry. Briefly, the cells were harvested, stained with Fluo-3/AM and were then analyzed. (A-C) Representative results from one of six independent experiments on mutated β-amyloid precursor protein (APP)-transfected SH-SY5Y cells treated with (A) the control condition (Con), (B) <t>xestospongin</t> C plus isoflurane (Xes) and (C) isoflurane (Iso). (D-F) Representative results from vector-transfected SH-SY5Y cells treated with (D) Con, (E) Xes and (F) Iso. The positive rate of [Ca 2+ ] c loading with Fluo-3/AM was > 99%. (A-F) X-axis refers to the average value of calcium fluorescence intensity, and Y-axis refers to cell count. (G) Data are presented as the mean ± standard deviation of at least three separate experiments. *P
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    Image Search Results


    Diacylglycerol but not phosphatidylinositol-3-phosphate or arachidonic acid is involved in amino acid-signaling in the lateral MOE. A , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (cyan and blue trace). Incubation with Xestospongin C (500 nM; application for 10 min; green-shaded panel) did not affect the responses. B , mean Ca 2+ transients (±SEM) of all three L-arginine-responsive ORNs of an acute slice preparation (lateral MOE). The responses were not affected by Xestospongin C (500 nM; 10 min; green-shaded panel). C , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (red and purple trace). Application of SAG (200 µM; 10 s, middle panel; 50 s, right-hand-panel) triggered Ca 2+ increases in both ORNs. D , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (black and grey trace). Both ORNs did not respond upon application of AA (50 µM; 10 s, middle panel; 60 s, right-hand-panel) E , mean responses (±SEM), expressed as percentage of control response to L-arginine, of 14 ORNs (4 slices) in standard (dark grey columns) and bath solution with Xestospongin C 500 nM (green columns; respectively 5, 10 and 15 min after application of Xestospongin C; washout time was 5 min). No significant reduction of the Ca 2+ responses was observed (p > 0.05; paired Student's t-test). F , mean response amplitudes (±SEM) upon application of L-arginine (dark grey columns) and SAG (purple columns; 200 and 500 µM; 7 ORNs, 2 slices and 9 ORNs, 2 slices, respectively). The response amplitudes to SAG were lower but not significanty different from the L-arginine responses (p > 0.05; paired Student's t-test). [AA, arachidonic acid].

    Journal: PLoS ONE

    Article Title: Phospholipase C and Diacylglycerol Mediate Olfactory Responses to Amino Acids in the Main Olfactory Epithelium of an Amphibian

    doi: 10.1371/journal.pone.0087721

    Figure Lengend Snippet: Diacylglycerol but not phosphatidylinositol-3-phosphate or arachidonic acid is involved in amino acid-signaling in the lateral MOE. A , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (cyan and blue trace). Incubation with Xestospongin C (500 nM; application for 10 min; green-shaded panel) did not affect the responses. B , mean Ca 2+ transients (±SEM) of all three L-arginine-responsive ORNs of an acute slice preparation (lateral MOE). The responses were not affected by Xestospongin C (500 nM; 10 min; green-shaded panel). C , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (red and purple trace). Application of SAG (200 µM; 10 s, middle panel; 50 s, right-hand-panel) triggered Ca 2+ increases in both ORNs. D , L-arginine-induced Ca 2+ responses of two ORNs of an individual slice of the lateral MOE (black and grey trace). Both ORNs did not respond upon application of AA (50 µM; 10 s, middle panel; 60 s, right-hand-panel) E , mean responses (±SEM), expressed as percentage of control response to L-arginine, of 14 ORNs (4 slices) in standard (dark grey columns) and bath solution with Xestospongin C 500 nM (green columns; respectively 5, 10 and 15 min after application of Xestospongin C; washout time was 5 min). No significant reduction of the Ca 2+ responses was observed (p > 0.05; paired Student's t-test). F , mean response amplitudes (±SEM) upon application of L-arginine (dark grey columns) and SAG (purple columns; 200 and 500 µM; 7 ORNs, 2 slices and 9 ORNs, 2 slices, respectively). The response amplitudes to SAG were lower but not significanty different from the L-arginine responses (p > 0.05; paired Student's t-test). [AA, arachidonic acid].

    Article Snippet: U-73122, U-73343, Xestospongin C and 1-Stearoyl-2-arachidonoyl-sn-glycerol (SAG) were from Calbiochem (Darmstadt, Germany), and SKF-96365 from Abcam (Cambridge, United Kingdom).

    Techniques: Incubation, Slice Preparation

    Inhibition of IP3R by xestospongin C (XeC) or MCU by ruthenium red (RuR) reverses the opening of mPTP in Cdk5 −/− MEFs. a Wt and Cdk5 −/− MEFs pretreated with or without XeC (3 µM) or RuR (3 µM) were loaded with calcein-AM, then treated with or without CoCl 2 . Cell were then analysed by flow cytometry. Cells treated with the potent mPTP desensitizers, cyclosporin A (CsA, 1 µM) or sanglifehrin A (SFA, 2 µM), were used as positive controls. b Quantitative analysis of the relative calcein fluorescence in wt and Cdk5 −/− MEFs in the presence or absence of the treatments indicated above. Untreated cells and cells treated with ionomycin served as controls. Values are means ± SEM from three ( n = 3) independent experiments. * p

    Journal: Oncogene

    Article Title: mPTP opening caused by Cdk5 loss is due to increased mitochondrial Ca2+ uptake

    doi: 10.1038/s41388-020-1188-5

    Figure Lengend Snippet: Inhibition of IP3R by xestospongin C (XeC) or MCU by ruthenium red (RuR) reverses the opening of mPTP in Cdk5 −/− MEFs. a Wt and Cdk5 −/− MEFs pretreated with or without XeC (3 µM) or RuR (3 µM) were loaded with calcein-AM, then treated with or without CoCl 2 . Cell were then analysed by flow cytometry. Cells treated with the potent mPTP desensitizers, cyclosporin A (CsA, 1 µM) or sanglifehrin A (SFA, 2 µM), were used as positive controls. b Quantitative analysis of the relative calcein fluorescence in wt and Cdk5 −/− MEFs in the presence or absence of the treatments indicated above. Untreated cells and cells treated with ionomycin served as controls. Values are means ± SEM from three ( n = 3) independent experiments. * p

    Article Snippet: The protease inhibitor cocktail, Cyclosporine A (CsA), Ruthenium Red (RuR), ATP, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) and Xestospongin C (XeC) were from Sigma.

    Techniques: Inhibition, Flow Cytometry, Fluorescence

    Ca 2+ handling. ( a ) Analysis of Ca 2+ release in FDB fibres (area under the curve, AUC) at different stimulation frequencies using Magfluo4. Inset: Representative Ca 2+ transients at different stimulation frequencies. n is the number of fibres from at least three different mice. ( b ) Resting cytosolic Ca 2+ concentration relative to that of WT fibres assessed with Fura-2 in FDB fibres. n is the number of fibres from at least three different mice. ( c ) Analysis of the amplitudes of the Ca 2+ transients in FDB fibres from WT and IT mice with repetitive 100 Hz (200 ms train/1.5 s) stimulations. ( d ) Representative fibres loaded with MitoSOX from WT and IT mice with and without RU360 treatment. Scale bars are 10 μm. ( e ) Analysis of images in panel D. MitoSOX fluorescence in FDB fibres (with and without RU360 to inhibit MCU) from WT and IT mice was plotted as % WT control (littermate, same day). n is the number of fibres from three to four mice. ( f ) Effect of Xestospongin C on MitoSox fluorescence. ( g ) Negatively stained EM pictures of SR-MaMs from IT and WT soleus. Bar is 100 nm. ( h ) Analysis of the average length of the tethers between the SR and the interfibrillar mitochondria. ( i ) Distribution of tether length in WT and IT soleus. Data are shown as mean±s.e.m. * P

    Journal: Nature Communications

    Article Title: A chemical chaperone improves muscle function in mice with a RyR1 mutation

    doi: 10.1038/ncomms14659

    Figure Lengend Snippet: Ca 2+ handling. ( a ) Analysis of Ca 2+ release in FDB fibres (area under the curve, AUC) at different stimulation frequencies using Magfluo4. Inset: Representative Ca 2+ transients at different stimulation frequencies. n is the number of fibres from at least three different mice. ( b ) Resting cytosolic Ca 2+ concentration relative to that of WT fibres assessed with Fura-2 in FDB fibres. n is the number of fibres from at least three different mice. ( c ) Analysis of the amplitudes of the Ca 2+ transients in FDB fibres from WT and IT mice with repetitive 100 Hz (200 ms train/1.5 s) stimulations. ( d ) Representative fibres loaded with MitoSOX from WT and IT mice with and without RU360 treatment. Scale bars are 10 μm. ( e ) Analysis of images in panel D. MitoSOX fluorescence in FDB fibres (with and without RU360 to inhibit MCU) from WT and IT mice was plotted as % WT control (littermate, same day). n is the number of fibres from three to four mice. ( f ) Effect of Xestospongin C on MitoSox fluorescence. ( g ) Negatively stained EM pictures of SR-MaMs from IT and WT soleus. Bar is 100 nm. ( h ) Analysis of the average length of the tethers between the SR and the interfibrillar mitochondria. ( i ) Distribution of tether length in WT and IT soleus. Data are shown as mean±s.e.m. * P

    Article Snippet: Xestospongin C was obtained from Abcam.

    Techniques: Mouse Assay, Concentration Assay, Mass Spectrometry, Fluorescence, Staining, Micro-arrays for Mass Spectrometry

    UgU induces an increase in intracellular calcium (Ca 2+ ). (A, B) Representative traces (black) of the effects of UgU on intracellular Ca 2+ mobilization in human monocytes are shown. LPS-primed human monocytes (5×10 5 cells/ml) were labeled with Fura-2/AM and then stimulated with UgU (10 μM) in Ca 2+ -free HBSS. Fluorescence was monitored at 37 °C. A phospholipase C (PLC) inhibitor (U73122, 10 μM, 15 min) (A, red) or inositol triphosphate receptor (IP 3 R) inhibitor (Xestospongin C, XeC, 5 μM, 30 min) (B, red) was added before human monocytes were stimulated with UgU. Representative images from one of five independent experiments are shown.

    Journal: Redox Biology

    Article Title: Ugonin U stimulates NLRP3 inflammasome activation and enhances inflammasome-mediated pathogen clearance

    doi: 10.1016/j.redox.2016.12.018

    Figure Lengend Snippet: UgU induces an increase in intracellular calcium (Ca 2+ ). (A, B) Representative traces (black) of the effects of UgU on intracellular Ca 2+ mobilization in human monocytes are shown. LPS-primed human monocytes (5×10 5 cells/ml) were labeled with Fura-2/AM and then stimulated with UgU (10 μM) in Ca 2+ -free HBSS. Fluorescence was monitored at 37 °C. A phospholipase C (PLC) inhibitor (U73122, 10 μM, 15 min) (A, red) or inositol triphosphate receptor (IP 3 R) inhibitor (Xestospongin C, XeC, 5 μM, 30 min) (B, red) was added before human monocytes were stimulated with UgU. Representative images from one of five independent experiments are shown.

    Article Snippet: Xestospongin C (XeC) and Z-YVAD-FMK were purchased from Abcam (Cambridge, MA, USA).

    Techniques: Labeling, Fluorescence, Planar Chromatography

    Phospholipase C (PLC)‐phosphatidylinositol 4,5‐bisphosphate(PIP 2 )‐protein kinase C (PKC) signaling mediates the effects of mGluR1 on mGluR6‐evoked currents. Raw traces depicting the effect of PKC stimulation on the rod bipolar cell (RBC) light response under four different conditions. (A) Light response of an RBC at break‐in and after dialysis with the PKC activator 1‐Oleoyl‐2‐acetyl‐sn‐glycerol (OAG). (B) As in (A) except that (RS)‐1‐Aminoindan‐1,5‐dicarboxylic acid (AIDA) was added to the bath prior to the experiment to block mGluR1 function. (C) Trpm1 current evoked at break‐in and after OAG dialysis in an internal solution containing 10 mmol/L BAPTA rather than EGTA. A pharmacological approach was used to activate Trpm1 current (see Methods). (D) Light‐evoked Trpm1 currents at break‐in (black trace) and after 5 min of dialysis with OAG and the IP 3  receptor inhibitor xestospongin C. (E) Summary data of the four experiments depicted in A–D ( n  = 5 for all conditions. *** P  = 0.006, ** P  = 0.01, * P  = 0.03). (F) Sample traces of Trpm1 current evoked by light in a cell dialyzed with the PLC inhibitor U73122 (10  μ mol/L) before and after bath application of AIDA. (G) Comparison of the response amplitudes after dialysis with U73122 and subsequent bath application of AIDA. Open and closed squares represent individual cells and the mean response respectively. AIDA application caused no significant change in response amplitude ( n  = 4;  P >  0.1, paired  t  test comparing U73122 alone vs. U73122+AIDA).

    Journal: Physiological Reports

    Article Title: A group I metabotropic glutamate receptor controls synaptic gain between rods and rod bipolar cells in the mouse retina. A group I metabotropic glutamate receptor controls synaptic gain between rods and rod bipolar cells in the mouse retina

    doi: 10.14814/phy2.13885

    Figure Lengend Snippet: Phospholipase C (PLC)‐phosphatidylinositol 4,5‐bisphosphate(PIP 2 )‐protein kinase C (PKC) signaling mediates the effects of mGluR1 on mGluR6‐evoked currents. Raw traces depicting the effect of PKC stimulation on the rod bipolar cell (RBC) light response under four different conditions. (A) Light response of an RBC at break‐in and after dialysis with the PKC activator 1‐Oleoyl‐2‐acetyl‐sn‐glycerol (OAG). (B) As in (A) except that (RS)‐1‐Aminoindan‐1,5‐dicarboxylic acid (AIDA) was added to the bath prior to the experiment to block mGluR1 function. (C) Trpm1 current evoked at break‐in and after OAG dialysis in an internal solution containing 10 mmol/L BAPTA rather than EGTA. A pharmacological approach was used to activate Trpm1 current (see Methods). (D) Light‐evoked Trpm1 currents at break‐in (black trace) and after 5 min of dialysis with OAG and the IP 3 receptor inhibitor xestospongin C. (E) Summary data of the four experiments depicted in A–D ( n  = 5 for all conditions. *** P  = 0.006, ** P  = 0.01, * P  = 0.03). (F) Sample traces of Trpm1 current evoked by light in a cell dialyzed with the PLC inhibitor U73122 (10  μ mol/L) before and after bath application of AIDA. (G) Comparison of the response amplitudes after dialysis with U73122 and subsequent bath application of AIDA. Open and closed squares represent individual cells and the mean response respectively. AIDA application caused no significant change in response amplitude ( n  = 4; P >  0.1, paired t test comparing U73122 alone vs. U73122+AIDA).

    Article Snippet: LY341495 (500 μ mol/L, cat. # 1209), U73122 (10 μ mol/L, cat. # 1268), xestospongin C (1 μ mol/L, cat. # 1280) were purchased from Tocris Bioscience, while 1‐Oleoyl‐2‐acetyl‐sn‐glycerol (OAG) (100 μ mol/L, cat. # O6754) was purchased from Sigma‐Aldrich.

    Techniques: Planar Chromatography, Blocking Assay

    ER-released Ca 2+ is essential for the fast polyspermy block. Representative fertilization recordings made in the presence of 500 nM Xestospongin C (XC; A), vehicle (2% DMSO; C), or 100 µM 2-APB (F). Dashed line denotes 0 mV, and arrows indicate sperm additions. Tukey box plot distributions of the resting (B) and fertilization (D) potentials, as well as the depolarization rates (E), from recordings made in the indicated treatments ( n = 5–8, 2–4 experiment days per treatment). In B and D, the gray lines behind the box plots represent the Tukey box plot distributions for the control (MR/5) data, where the solid line represents the median value, the dashed lines denote the data spread from 25 and 75%, and the whiskers reflect 10–90%. (G) Proportion of polyspermic embryos out of total developed embryos in vehicle (2% DMSO in MR/5), Xestospongin C, control (MR/5), and 2-APB ( n = 3, recorded over 3 experiment days per treatment, the mean values ± SEM are reported). *, P

    Journal: The Journal of General Physiology

    Article Title: PLC and IP3-evoked Ca2+ release initiate the fast block to polyspermy in Xenopus laevis eggs

    doi: 10.1085/jgp.201812069

    Figure Lengend Snippet: ER-released Ca 2+ is essential for the fast polyspermy block. Representative fertilization recordings made in the presence of 500 nM Xestospongin C (XC; A), vehicle (2% DMSO; C), or 100 µM 2-APB (F). Dashed line denotes 0 mV, and arrows indicate sperm additions. Tukey box plot distributions of the resting (B) and fertilization (D) potentials, as well as the depolarization rates (E), from recordings made in the indicated treatments ( n = 5–8, 2–4 experiment days per treatment). In B and D, the gray lines behind the box plots represent the Tukey box plot distributions for the control (MR/5) data, where the solid line represents the median value, the dashed lines denote the data spread from 25 and 75%, and the whiskers reflect 10–90%. (G) Proportion of polyspermic embryos out of total developed embryos in vehicle (2% DMSO in MR/5), Xestospongin C, control (MR/5), and 2-APB ( n = 3, recorded over 3 experiment days per treatment, the mean values ± SEM are reported). *, P

    Article Snippet: Reagents Xestospongin C, GdCl3 , U-73343, and 2-aminoethoxydiphenyl borate (2-APB) were purchased from Tocris, and human chorionic gonadotropin was purchased from Henry Schien.

    Techniques: Blocking Assay

    The inositol 1,4,5-trisphosphate receptor inhibitor Xestospongin C and the nonspecific PKC inhibitor calphostin C inhibited the proliferative effect of BW723C86 on ICC. A , 333 n m and 1 μ m Xestospongin ( Xesto ) C inhibited the increase in proliferation

    Journal:

    Article Title: Protein Kinase C? Mediates Regulation of Proliferation by the Serotonin 5-Hydroxytryptamine Receptor 2B *

    doi: 10.1074/jbc.M109.015859

    Figure Lengend Snippet: The inositol 1,4,5-trisphosphate receptor inhibitor Xestospongin C and the nonspecific PKC inhibitor calphostin C inhibited the proliferative effect of BW723C86 on ICC. A , 333 n m and 1 μ m Xestospongin ( Xesto ) C inhibited the increase in proliferation

    Article Snippet: BW723C86 was purchased from Tocris Cookson Inc. (Ellisville, MO); was from Invitrogen; was from Calbiochem (Gibbstown, NJ); LY294002 was from Cell Signaling Technology (Beverly, MA); calphostin C, Gö6976, and Gö6983 were from Calbiochem, 3-(2-aminoethyl)-5-((4-ethoxyphenyl)methylene)-2,4-thiazolidinedione hydrochloride (ERK inhibitor) was from Sigma-Aldrich; SB204741 was from Tocris Cookson Inc.; and Xestospongin C was from Cayman Chemicals (Ann Arbor, MI).

    Techniques: Immunocytochemistry

    Specific inhibition of 2-APB-sensitive Ca 2+  channels failed to prevent H 2 O 2 -induced cardiomyocyte death. (A) Neonatal rat cardiomyocytes (NRCMs) were pretreated or not with xestospongin C, a specific IP 3 R inhibitor, for 1 hour, which was followed by H 2 O 2  treatment. Cell viability levels were determined. Results are shown as mean values ± SEM from three independent experiments. (B) Representative fura-2 ratio obtained using NRCMs pretreated or not with xestospongin C, followed by H 2 O 2  treatment. (C) The expression levels of 2-APB-sensitive TRP channels in NRCMs were analyzed by RT-PCR. A representative image with a 40-cycle amplification is shown. (D-F) NRCMs were pretreated or not with SKF-96365 (D, a TRPC inhibitor), AA-861 (E, a TRPM7 inhibitor) and mefenamic acid (F, a TRPM3 inhibitor), followed by H 2 O 2  treatment. Cell viability rate is presented. Results are presented as mean values ± SEM obtained in four independent experiments.

    Journal: PLoS ONE

    Article Title: 2-aminoethoxydiphenyl borate provides an anti-oxidative effect and mediates cardioprotection during ischemia reperfusion in mice

    doi: 10.1371/journal.pone.0189948

    Figure Lengend Snippet: Specific inhibition of 2-APB-sensitive Ca 2+ channels failed to prevent H 2 O 2 -induced cardiomyocyte death. (A) Neonatal rat cardiomyocytes (NRCMs) were pretreated or not with xestospongin C, a specific IP 3 R inhibitor, for 1 hour, which was followed by H 2 O 2 treatment. Cell viability levels were determined. Results are shown as mean values ± SEM from three independent experiments. (B) Representative fura-2 ratio obtained using NRCMs pretreated or not with xestospongin C, followed by H 2 O 2 treatment. (C) The expression levels of 2-APB-sensitive TRP channels in NRCMs were analyzed by RT-PCR. A representative image with a 40-cycle amplification is shown. (D-F) NRCMs were pretreated or not with SKF-96365 (D, a TRPC inhibitor), AA-861 (E, a TRPM7 inhibitor) and mefenamic acid (F, a TRPM3 inhibitor), followed by H 2 O 2 treatment. Cell viability rate is presented. Results are presented as mean values ± SEM obtained in four independent experiments.

    Article Snippet: Reagents Reagents used in this study included H2 O2 (31 wt%; Santoku Chemical Industries Co, Japan), BAPTA-AM (Merck Millipore, Billerica, MA), xestospongin C (Wako Pure Chemical Industries, Japan), SKF-96365 (Focus Biomolecules, Plymouth Meeting, PA), mefenamic acid (Tokyo Chemical Industry Co, Japan), 2-APB, AA-861 and phenylephrine (Sigma-Aldrich, St. Louis, MO).

    Techniques: Inhibition, Expressing, Reverse Transcription Polymerase Chain Reaction, Amplification

    Long-lasting increase of fIPSPs after DHPG application is mediated by IP 3 receptors activation. DHPG failed to increase fIPSPs in all CA1 (a) and specifically in its different sub-regions (b–g) in presence of the cell-permeable IP 3 receptors blockers 2-APB or Xestospongin C (XestoC). In all figures, left panel shows the time course, while right panel is showing mean over time. Statistical analysis in right panel figures is one-way ANOVA followed by Dunnet post-hoc test. Vehicles of both IP 3 receptors antagonists have been pooled together since they are not different. n = (slices, mice): Vehicle group = (11, 9), 2-APB group = (5, 5), Xestospongin C group (5, 3). Data are mean ± s.e.m. *p

    Journal: Scientific Reports

    Article Title: Layer-specific potentiation of network GABAergic inhibition in the CA1 area of the hippocampus

    doi: 10.1038/srep28454

    Figure Lengend Snippet: Long-lasting increase of fIPSPs after DHPG application is mediated by IP 3 receptors activation. DHPG failed to increase fIPSPs in all CA1 (a) and specifically in its different sub-regions (b–g) in presence of the cell-permeable IP 3 receptors blockers 2-APB or Xestospongin C (XestoC). In all figures, left panel shows the time course, while right panel is showing mean over time. Statistical analysis in right panel figures is one-way ANOVA followed by Dunnet post-hoc test. Vehicles of both IP 3 receptors antagonists have been pooled together since they are not different. n = (slices, mice): Vehicle group = (11, 9), 2-APB group = (5, 5), Xestospongin C group (5, 3). Data are mean ± s.e.m. *p

    Article Snippet: Xestospongin C was from Enzo Life Sciences (France) and dissolved in DMSO (DMSO < 0.1%).

    Techniques: Activation Assay, Mouse Assay

    IL-6–induced enhancement of GSIS is abrogated by an IP 3 receptor antagonist but not by a PKA inhibitor. MIN-6 cells were pretreated with vehicle or a pharmacological inhibitor (1 μmol/L H-89 [ A ] or 10 μmol/L Xestospongin C [ B ]) with or without concomitant 1,200 pg/mL IL-6 for 24 h, followed by measurement of insulin secretion for 60 min in KRBB supplemented with either 1.67 or 16.7 mmol/L glucose ( n = 6 per group). ** P

    Journal: Diabetes

    Article Title: Interleukin-6 Enhances Glucose-Stimulated Insulin Secretion From Pancreatic ?-Cells

    doi: 10.2337/db10-0796

    Figure Lengend Snippet: IL-6–induced enhancement of GSIS is abrogated by an IP 3 receptor antagonist but not by a PKA inhibitor. MIN-6 cells were pretreated with vehicle or a pharmacological inhibitor (1 μmol/L H-89 [ A ] or 10 μmol/L Xestospongin C [ B ]) with or without concomitant 1,200 pg/mL IL-6 for 24 h, followed by measurement of insulin secretion for 60 min in KRBB supplemented with either 1.67 or 16.7 mmol/L glucose ( n = 6 per group). ** P

    Article Snippet: Recombinant murine IL-6 (PeproTech, London, U.K.), U-73343, U-73122, neomycin (Sigma), Xestospongin C (Biomol, Plymouth Meeting, PA), and H-89 (Millipore, Billerica, MA) were commercially obtained.

    Techniques:

    After cells were treated with 1.2% isoflurane for 8 h, cytosolic calcium concentration ([Ca 2+ ] c ) was determined by flow cytometry. Briefly, the cells were harvested, stained with Fluo-3/AM and were then analyzed. (A-C) Representative results from one of six independent experiments on mutated β-amyloid precursor protein (APP)-transfected SH-SY5Y cells treated with (A) the control condition (Con), (B) xestospongin C plus isoflurane (Xes) and (C) isoflurane (Iso). (D-F) Representative results from vector-transfected SH-SY5Y cells treated with (D) Con, (E) Xes and (F) Iso. The positive rate of [Ca 2+ ] c loading with Fluo-3/AM was > 99%. (A-F) X-axis refers to the average value of calcium fluorescence intensity, and Y-axis refers to cell count. (G) Data are presented as the mean ± standard deviation of at least three separate experiments. *P

    Journal: Molecular Medicine Reports

    Article Title: A mutation in β-amyloid precursor protein renders SH-SY5Y cells vulnerable to isoflurane toxicity: The role of inositol 1,4,5-trisphosphate receptors

    doi: 10.3892/mmr.2016.5930

    Figure Lengend Snippet: After cells were treated with 1.2% isoflurane for 8 h, cytosolic calcium concentration ([Ca 2+ ] c ) was determined by flow cytometry. Briefly, the cells were harvested, stained with Fluo-3/AM and were then analyzed. (A-C) Representative results from one of six independent experiments on mutated β-amyloid precursor protein (APP)-transfected SH-SY5Y cells treated with (A) the control condition (Con), (B) xestospongin C plus isoflurane (Xes) and (C) isoflurane (Iso). (D-F) Representative results from vector-transfected SH-SY5Y cells treated with (D) Con, (E) Xes and (F) Iso. The positive rate of [Ca 2+ ] c loading with Fluo-3/AM was > 99%. (A-F) X-axis refers to the average value of calcium fluorescence intensity, and Y-axis refers to cell count. (G) Data are presented as the mean ± standard deviation of at least three separate experiments. *P

    Article Snippet: However, due to the findings of xestospongin C experiments in PC12 cells and rat cerebral cortical neurons it is likely that isoflurane acts directly on IP3R to enhance calcium release.

    Techniques: Concentration Assay, Flow Cytometry, Cytometry, Staining, Transfection, Plasmid Preparation, Fluorescence, Cell Counting, Standard Deviation

    After cells were treated with 1.2% isoflurane for 8 h, apoptosis was determined by flow cytometry. Briefly, the cells were harvested, stained with annexin V-fluorescein isothiocyanate (FITC) and propidium iodide (PI), and were then analyzed. (A-C) Representative results from one of six independent experiments on mutated β-amyloid precursor protein (APP)-transfected SH-SY5Y cells treated with (A) the control condition (Con), (B) xestospongin C plus isoflurane (Xes) and (C) isoflurane (Iso). (D-F) Representative results from vector-transfected SH-SY5Y cells treated with (D) Con, (E) Xes and (F) Iso. The quadrants of each plot exhibit the following: Viable cells (Annexin − /PI − ; lower left), early apoptotic cells (Annexin + /PI − , lower right), necrotic cells (Annexin + /PI + , upper right), and late apoptotic cells (Annexin − /PI + , upper left). (G) Data are presented as a sum of the percentage of apoptotic cells in early apoptosis (annexin + /PI − ) and late apoptosis (annexin + /PI + ). Data are presented as the mean ± standard deviation of at least three separate experiments. ***P

    Journal: Molecular Medicine Reports

    Article Title: A mutation in β-amyloid precursor protein renders SH-SY5Y cells vulnerable to isoflurane toxicity: The role of inositol 1,4,5-trisphosphate receptors

    doi: 10.3892/mmr.2016.5930

    Figure Lengend Snippet: After cells were treated with 1.2% isoflurane for 8 h, apoptosis was determined by flow cytometry. Briefly, the cells were harvested, stained with annexin V-fluorescein isothiocyanate (FITC) and propidium iodide (PI), and were then analyzed. (A-C) Representative results from one of six independent experiments on mutated β-amyloid precursor protein (APP)-transfected SH-SY5Y cells treated with (A) the control condition (Con), (B) xestospongin C plus isoflurane (Xes) and (C) isoflurane (Iso). (D-F) Representative results from vector-transfected SH-SY5Y cells treated with (D) Con, (E) Xes and (F) Iso. The quadrants of each plot exhibit the following: Viable cells (Annexin − /PI − ; lower left), early apoptotic cells (Annexin + /PI − , lower right), necrotic cells (Annexin + /PI + , upper right), and late apoptotic cells (Annexin − /PI + , upper left). (G) Data are presented as a sum of the percentage of apoptotic cells in early apoptosis (annexin + /PI − ) and late apoptosis (annexin + /PI + ). Data are presented as the mean ± standard deviation of at least three separate experiments. ***P

    Article Snippet: However, due to the findings of xestospongin C experiments in PC12 cells and rat cerebral cortical neurons it is likely that isoflurane acts directly on IP3R to enhance calcium release.

    Techniques: Flow Cytometry, Cytometry, Staining, Transfection, Plasmid Preparation, Standard Deviation

    Isoflurane induces inositol 1,4,5-trisphosphate receptor (IP3R) activation in mutated β-amyloid precursor protein (APP)-transfected SH-SY5Y cells. (A and B) Treatment with 1.2% isoflurane (Iso) inducesd IP3R cleavage compared with in the control (Con) and xestospongin C (Xes) groups in both cell types. There was no significant difference in β-actin expression between the groups. (C) Treatment with 1.2% isoflurane induced a higher increase in IP3R protein expression in the mutated APP-transfected SH-SY5Y cells compared with vector-transfected SH-SY5Y cells. Data are presented as the mean ± standard deviation of at least three separate experiments. *P

    Journal: Molecular Medicine Reports

    Article Title: A mutation in β-amyloid precursor protein renders SH-SY5Y cells vulnerable to isoflurane toxicity: The role of inositol 1,4,5-trisphosphate receptors

    doi: 10.3892/mmr.2016.5930

    Figure Lengend Snippet: Isoflurane induces inositol 1,4,5-trisphosphate receptor (IP3R) activation in mutated β-amyloid precursor protein (APP)-transfected SH-SY5Y cells. (A and B) Treatment with 1.2% isoflurane (Iso) inducesd IP3R cleavage compared with in the control (Con) and xestospongin C (Xes) groups in both cell types. There was no significant difference in β-actin expression between the groups. (C) Treatment with 1.2% isoflurane induced a higher increase in IP3R protein expression in the mutated APP-transfected SH-SY5Y cells compared with vector-transfected SH-SY5Y cells. Data are presented as the mean ± standard deviation of at least three separate experiments. *P

    Article Snippet: However, due to the findings of xestospongin C experiments in PC12 cells and rat cerebral cortical neurons it is likely that isoflurane acts directly on IP3R to enhance calcium release.

    Techniques: Activation Assay, Transfection, Expressing, Plasmid Preparation, Standard Deviation