pctx 1  (Alomone Labs)


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    Alomone Labs pctx 1
    Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with <t>Pctx-1</t> compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.
    Pctx 1, supplied by Alomone Labs, 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/pctx 1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pctx 1 - by Bioz Stars, 2023-03
    93/100 stars

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    1) Product Images from "Signaling Pathways in Proton and Non-proton ASIC1a Activation"

    Article Title: Signaling Pathways in Proton and Non-proton ASIC1a Activation

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2021.735414

    Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with Pctx-1 compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.
    Figure Legend Snippet: Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with Pctx-1 compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.

    Techniques Used: Activation Assay

    Proton and non-proton activation of overexpressed ASIC1a channels. (A) Representative membranes of lysates of cells control (ctr) or transfected with eGFP-ASIC1a (eASIC) at two levels (1x or x3) to obtained different levels of expression of the protein (“eASICx1 or eASICx3”), and treated with pH6 or MitTx with or without pre-incubation of Pctx-1 or untreated. (B) Plots showing the increase in pERK and pCaMKII levels calculated from membranes as that shown in (A) , consistent with the increase in eASIC expressed. Notice the level of increase achievable via MitTx incubation at the highest overexpressed level of eASIC, higher than that obtained via pH6. (C) Representative membrane showing the different levels of eASIC in cells overexpressing the channel (1x or 3x), detected with an ASIC1 antibody. (D) Comparison between the different ASIC1 proteins expressed (the endogenous human ASIC1a; of approx. 67 kDa) and the overexpressed eASIC (approx. 110 kDa, and expressed at different levels; x1 or x3). (A) Notice that plots are the result of the signal intensity of the band detected,—tERK and tubulin are used as loading controls between loaded samples—and expressed relative to eASICx1 levels. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments and conditions were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; ns: no significant differences. Mean values expressed relative to eASICx1 levels ± SEM are as follows: eASICx3 3.16 ± 0.06; eASIC MitTx 3.42 ± 0.15; eASICx3 MitTx 9.96 ± 0.12; eASIC MitTx Pctx 1.10 ± 0.05; eASIC pH6 2’ 1.85 ± 0.08; eASIC pH6 2’ Pctx 1.08 ± 0.05; eASICx3 pH6 2’ 4.00 ± 0.12.
    Figure Legend Snippet: Proton and non-proton activation of overexpressed ASIC1a channels. (A) Representative membranes of lysates of cells control (ctr) or transfected with eGFP-ASIC1a (eASIC) at two levels (1x or x3) to obtained different levels of expression of the protein (“eASICx1 or eASICx3”), and treated with pH6 or MitTx with or without pre-incubation of Pctx-1 or untreated. (B) Plots showing the increase in pERK and pCaMKII levels calculated from membranes as that shown in (A) , consistent with the increase in eASIC expressed. Notice the level of increase achievable via MitTx incubation at the highest overexpressed level of eASIC, higher than that obtained via pH6. (C) Representative membrane showing the different levels of eASIC in cells overexpressing the channel (1x or 3x), detected with an ASIC1 antibody. (D) Comparison between the different ASIC1 proteins expressed (the endogenous human ASIC1a; of approx. 67 kDa) and the overexpressed eASIC (approx. 110 kDa, and expressed at different levels; x1 or x3). (A) Notice that plots are the result of the signal intensity of the band detected,—tERK and tubulin are used as loading controls between loaded samples—and expressed relative to eASICx1 levels. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments and conditions were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; ns: no significant differences. Mean values expressed relative to eASICx1 levels ± SEM are as follows: eASICx3 3.16 ± 0.06; eASIC MitTx 3.42 ± 0.15; eASICx3 MitTx 9.96 ± 0.12; eASIC MitTx Pctx 1.10 ± 0.05; eASIC pH6 2’ 1.85 ± 0.08; eASIC pH6 2’ Pctx 1.08 ± 0.05; eASICx3 pH6 2’ 4.00 ± 0.12.

    Techniques Used: Activation Assay, Transfection, Expressing, Incubation

    pctx 1  (Alomone Labs)


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    Alomone Labs pctx 1
    Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with <t>Pctx-1</t> compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.
    Pctx 1, supplied by Alomone Labs, 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/pctx 1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pctx 1 - by Bioz Stars, 2023-03
    93/100 stars

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    1) Product Images from "Signaling Pathways in Proton and Non-proton ASIC1a Activation"

    Article Title: Signaling Pathways in Proton and Non-proton ASIC1a Activation

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2021.735414

    Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with Pctx-1 compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.
    Figure Legend Snippet: Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with Pctx-1 compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.

    Techniques Used: Activation Assay

    Proton and non-proton activation of overexpressed ASIC1a channels. (A) Representative membranes of lysates of cells control (ctr) or transfected with eGFP-ASIC1a (eASIC) at two levels (1x or x3) to obtained different levels of expression of the protein (“eASICx1 or eASICx3”), and treated with pH6 or MitTx with or without pre-incubation of Pctx-1 or untreated. (B) Plots showing the increase in pERK and pCaMKII levels calculated from membranes as that shown in (A) , consistent with the increase in eASIC expressed. Notice the level of increase achievable via MitTx incubation at the highest overexpressed level of eASIC, higher than that obtained via pH6. (C) Representative membrane showing the different levels of eASIC in cells overexpressing the channel (1x or 3x), detected with an ASIC1 antibody. (D) Comparison between the different ASIC1 proteins expressed (the endogenous human ASIC1a; of approx. 67 kDa) and the overexpressed eASIC (approx. 110 kDa, and expressed at different levels; x1 or x3). (A) Notice that plots are the result of the signal intensity of the band detected,—tERK and tubulin are used as loading controls between loaded samples—and expressed relative to eASICx1 levels. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments and conditions were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; ns: no significant differences. Mean values expressed relative to eASICx1 levels ± SEM are as follows: eASICx3 3.16 ± 0.06; eASIC MitTx 3.42 ± 0.15; eASICx3 MitTx 9.96 ± 0.12; eASIC MitTx Pctx 1.10 ± 0.05; eASIC pH6 2’ 1.85 ± 0.08; eASIC pH6 2’ Pctx 1.08 ± 0.05; eASICx3 pH6 2’ 4.00 ± 0.12.
    Figure Legend Snippet: Proton and non-proton activation of overexpressed ASIC1a channels. (A) Representative membranes of lysates of cells control (ctr) or transfected with eGFP-ASIC1a (eASIC) at two levels (1x or x3) to obtained different levels of expression of the protein (“eASICx1 or eASICx3”), and treated with pH6 or MitTx with or without pre-incubation of Pctx-1 or untreated. (B) Plots showing the increase in pERK and pCaMKII levels calculated from membranes as that shown in (A) , consistent with the increase in eASIC expressed. Notice the level of increase achievable via MitTx incubation at the highest overexpressed level of eASIC, higher than that obtained via pH6. (C) Representative membrane showing the different levels of eASIC in cells overexpressing the channel (1x or 3x), detected with an ASIC1 antibody. (D) Comparison between the different ASIC1 proteins expressed (the endogenous human ASIC1a; of approx. 67 kDa) and the overexpressed eASIC (approx. 110 kDa, and expressed at different levels; x1 or x3). (A) Notice that plots are the result of the signal intensity of the band detected,—tERK and tubulin are used as loading controls between loaded samples—and expressed relative to eASICx1 levels. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments and conditions were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; ns: no significant differences. Mean values expressed relative to eASICx1 levels ± SEM are as follows: eASICx3 3.16 ± 0.06; eASIC MitTx 3.42 ± 0.15; eASICx3 MitTx 9.96 ± 0.12; eASIC MitTx Pctx 1.10 ± 0.05; eASIC pH6 2’ 1.85 ± 0.08; eASIC pH6 2’ Pctx 1.08 ± 0.05; eASICx3 pH6 2’ 4.00 ± 0.12.

    Techniques Used: Activation Assay, Transfection, Expressing, Incubation

    pctx 1  (Alomone Labs)


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    Alomone Labs pctx 1
    Pctx 1, supplied by Alomone Labs, 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/pctx 1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
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    pctx 1 - by Bioz Stars, 2023-03
    93/100 stars

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    pctx 1  (Alomone Labs)


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    Alomone Labs pctx 1
    The effect of psalmotoxin-1 <t>(PcTx-1)</t> on the pressor response-evoked byto static contraction of the triceps surae muscles with freely perfused (n = 8; left) or ligated femoral arteries (n = 10; right). Data are presented as individual (●) and group mean (gray bars) for the peak increase in mean arterial pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) to static contraction. The pressor responses evoked from the freely perfused and ligated legs were obtained from the same rats. ○, Data points that could be obtained in only 1 leg. Baseline values for blood pressure and tension (in g) are presented below the x-axes of their respective graphs. Contractions were evoked before and at 10 and 20 min following PcTx-1 (200 ng/kg, 100 μL) injection in the superficial epigastric artery. *P < 0.05, significant difference compared with before ASIC1a blockade.
    Pctx 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pctx 1/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pctx 1 - by Bioz Stars, 2023-03
    86/100 stars

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    1) Product Images from "ASIC1a does not play a role in evoking the metabolic component of the exercise pressor reflex in a rat model of peripheral artery disease"

    Article Title: ASIC1a does not play a role in evoking the metabolic component of the exercise pressor reflex in a rat model of peripheral artery disease

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    doi: 10.1152/ajpheart.00257.2020

    The effect of psalmotoxin-1 (PcTx-1) on the pressor response-evoked byto static contraction of the triceps surae muscles with freely perfused (n = 8; left) or ligated femoral arteries (n = 10; right). Data are presented as individual (●) and group mean (gray bars) for the peak increase in mean arterial pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) to static contraction. The pressor responses evoked from the freely perfused and ligated legs were obtained from the same rats. ○, Data points that could be obtained in only 1 leg. Baseline values for blood pressure and tension (in g) are presented below the x-axes of their respective graphs. Contractions were evoked before and at 10 and 20 min following PcTx-1 (200 ng/kg, 100 μL) injection in the superficial epigastric artery. *P < 0.05, significant difference compared with before ASIC1a blockade.
    Figure Legend Snippet: The effect of psalmotoxin-1 (PcTx-1) on the pressor response-evoked byto static contraction of the triceps surae muscles with freely perfused (n = 8; left) or ligated femoral arteries (n = 10; right). Data are presented as individual (●) and group mean (gray bars) for the peak increase in mean arterial pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) to static contraction. The pressor responses evoked from the freely perfused and ligated legs were obtained from the same rats. ○, Data points that could be obtained in only 1 leg. Baseline values for blood pressure and tension (in g) are presented below the x-axes of their respective graphs. Contractions were evoked before and at 10 and 20 min following PcTx-1 (200 ng/kg, 100 μL) injection in the superficial epigastric artery. *P < 0.05, significant difference compared with before ASIC1a blockade.

    Techniques Used: Injection

    Average time course of the pressor response to static contraction following acid-sensing ion channel 1a (ASIC1a) blockade. ASIC1as were antagonized by injecting psalmotoxin-1 (PcTx-1; n = 8 and 10, 200 ng/kg, 100 μL; A) or mambalgin-1 (Mamb-1; n = 5 and 6, 6.5 μg/kg, 100 μL; B) into the superficial epigastric artery. The pressor responses to contraction were evoked at 10 and at 20 min after injection of the ASIC1a antagonist. The averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. The pressor responses evoked from the freely perfused and ligated legs were obtained from the same rats. Sample sizes are different because in 2 and 1 of the experiments with PcTx-1 and Mamb-1, respectively, we could not obtain a pressor response from the freely perfused leg. For clarity, error bars were omitted. MAP, mean arterial pressure. *P < 0.05, significant difference between before and 10 min after ASIC1a blockade; ***P < 0.001.
    Figure Legend Snippet: Average time course of the pressor response to static contraction following acid-sensing ion channel 1a (ASIC1a) blockade. ASIC1as were antagonized by injecting psalmotoxin-1 (PcTx-1; n = 8 and 10, 200 ng/kg, 100 μL; A) or mambalgin-1 (Mamb-1; n = 5 and 6, 6.5 μg/kg, 100 μL; B) into the superficial epigastric artery. The pressor responses to contraction were evoked at 10 and at 20 min after injection of the ASIC1a antagonist. The averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. The pressor responses evoked from the freely perfused and ligated legs were obtained from the same rats. Sample sizes are different because in 2 and 1 of the experiments with PcTx-1 and Mamb-1, respectively, we could not obtain a pressor response from the freely perfused leg. For clarity, error bars were omitted. MAP, mean arterial pressure. *P < 0.05, significant difference between before and 10 min after ASIC1a blockade; ***P < 0.001.

    Techniques Used: Injection

    The effect of psalmotoxin-1 (PcTx-1) on the pressor response to tendon stretch of the triceps surae muscles with freely perfused (n = 5; left) or ligated femoral arteries (n = 5; right). Data are presented as individual (●) and group mean (gray bars) for the peak increase in mean arterial pressure (MAP) and blood pressure index (BPI) evoked by tendon stretch. The pressor responses evoked from the freely perfused and ligated legs were obtained from the same rats. Baseline values for blood pressure are presented below the x-axes of the graphs. Tendon stretches were evoked before and 10 min following PcTx-1 (200 ng/kg, 100 μL) injection in the superficial epigastric artery.
    Figure Legend Snippet: The effect of psalmotoxin-1 (PcTx-1) on the pressor response to tendon stretch of the triceps surae muscles with freely perfused (n = 5; left) or ligated femoral arteries (n = 5; right). Data are presented as individual (●) and group mean (gray bars) for the peak increase in mean arterial pressure (MAP) and blood pressure index (BPI) evoked by tendon stretch. The pressor responses evoked from the freely perfused and ligated legs were obtained from the same rats. Baseline values for blood pressure are presented below the x-axes of the graphs. Tendon stretches were evoked before and 10 min following PcTx-1 (200 ng/kg, 100 μL) injection in the superficial epigastric artery.

    Techniques Used: Injection

    The effect of psalmotoxin-1 (PcTx-1) on the pressor response to injection of diprotonated phosphate into the arterial circulation of the triceps surae muscles with freely perfused (n = 6; left) or ligated femoral arteries (n = 6; middle). Data are presented as individual (●) and group mean (gray bars) for the peak increase in mean arterial pressure (MAP) evoked by injection of diprotonated phosphate (86 mM, pH 6.0). Data are also presented as the %change in the peak MAP response evoked by injection of diprotonated phosphate from baseline compared with 10 min after injecting PcTx-1 (right). The pressor responses evoked from the freely perfused and ligated legs were obtained within the same animals. Baseline values for blood pressure are presented below the x-axes of the graphs. The pressor responses were evoked before and 10 and 20 min following PcTx-1 (200 ng/kg, 100 μL) injection in the superficial epigastric artery. *P < 0.05, significant difference compared with before acid-sensing ion channel 1a (ASIC1a) blockade; **P < 0.01. i.a., intra-arterial.
    Figure Legend Snippet: The effect of psalmotoxin-1 (PcTx-1) on the pressor response to injection of diprotonated phosphate into the arterial circulation of the triceps surae muscles with freely perfused (n = 6; left) or ligated femoral arteries (n = 6; middle). Data are presented as individual (●) and group mean (gray bars) for the peak increase in mean arterial pressure (MAP) evoked by injection of diprotonated phosphate (86 mM, pH 6.0). Data are also presented as the %change in the peak MAP response evoked by injection of diprotonated phosphate from baseline compared with 10 min after injecting PcTx-1 (right). The pressor responses evoked from the freely perfused and ligated legs were obtained within the same animals. Baseline values for blood pressure are presented below the x-axes of the graphs. The pressor responses were evoked before and 10 and 20 min following PcTx-1 (200 ng/kg, 100 μL) injection in the superficial epigastric artery. *P < 0.05, significant difference compared with before acid-sensing ion channel 1a (ASIC1a) blockade; **P < 0.01. i.a., intra-arterial.

    Techniques Used: Injection

    pctx 1  (Alomone Labs)


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    Alomone Labs pctx 1
    Representative traces and time course of the pressor response to static contraction before and after psalmotoxin-1 <t>(PcTx-1)</t> injection. Acid-sensing ion channels 1a were antagonized by injecting PcTx-1 (n = 8; 200 ng/kg, 100 μL) into the superficial epigastric artery. A: representative traces of the pressor responses to contraction before and 10 min after PcTx-1 in the same rat. B: averaged time course of the pressor response to contraction, which was evoked before, at 10 min after, and at 20 min after PcTx-1. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. For clarity, error bars were omitted. *P < 0.05, significant difference between before and 10 min after PcTx-1. BP, blood pressure; bpm, beats/min; HR, heart rate; MAP, mean arterial pressure.
    Pctx 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pctx 1/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pctx 1 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "ASIC1a plays a key role in evoking the metabolic component of the exercise pressor reflex in rats"

    Article Title: ASIC1a plays a key role in evoking the metabolic component of the exercise pressor reflex in rats

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    doi: 10.1152/ajpheart.00565.2019

    Representative traces and time course of the pressor response to static contraction before and after psalmotoxin-1 (PcTx-1) injection. Acid-sensing ion channels 1a were antagonized by injecting PcTx-1 (n = 8; 200 ng/kg, 100 μL) into the superficial epigastric artery. A: representative traces of the pressor responses to contraction before and 10 min after PcTx-1 in the same rat. B: averaged time course of the pressor response to contraction, which was evoked before, at 10 min after, and at 20 min after PcTx-1. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. For clarity, error bars were omitted. *P < 0.05, significant difference between before and 10 min after PcTx-1. BP, blood pressure; bpm, beats/min; HR, heart rate; MAP, mean arterial pressure.
    Figure Legend Snippet: Representative traces and time course of the pressor response to static contraction before and after psalmotoxin-1 (PcTx-1) injection. Acid-sensing ion channels 1a were antagonized by injecting PcTx-1 (n = 8; 200 ng/kg, 100 μL) into the superficial epigastric artery. A: representative traces of the pressor responses to contraction before and 10 min after PcTx-1 in the same rat. B: averaged time course of the pressor response to contraction, which was evoked before, at 10 min after, and at 20 min after PcTx-1. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. For clarity, error bars were omitted. *P < 0.05, significant difference between before and 10 min after PcTx-1. BP, blood pressure; bpm, beats/min; HR, heart rate; MAP, mean arterial pressure.

    Techniques Used: Injection

    Effect of acid-sensing ion channel 1a (ASIC1a) blockade on the pressor response to static contraction. Data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP; A), blood pressure index (BPI; B), peak increase in tension (C), and time-tension index (TTI; D) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. Contractions were evoked before, at 10 min after, and at 20 min after psalmotoxin-1 (PcTx-1; n = 8; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5; 6.5 μg/kg, 100 μL) injection into the superficial epigastric artery. *P < 0.05, significant difference compared with before ASIC1a blockade. ia, intra-arterial.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a (ASIC1a) blockade on the pressor response to static contraction. Data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP; A), blood pressure index (BPI; B), peak increase in tension (C), and time-tension index (TTI; D) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. Contractions were evoked before, at 10 min after, and at 20 min after psalmotoxin-1 (PcTx-1; n = 8; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5; 6.5 μg/kg, 100 μL) injection into the superficial epigastric artery. *P < 0.05, significant difference compared with before ASIC1a blockade. ia, intra-arterial.

    Techniques Used: Injection

    Effect of injecting psalmotoxin-1 (PcTx-1) intravenously on the pressor response to static contraction. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. E: the averaged increase in blood pressure over time. For clarity, error bars were omitted. The averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. Contractions were evoked before and at 10 min following intravenous (iv) injection of PcTx-1 (n = 5; 200 ng/kg, 100 μL) into the right jugular vein.
    Figure Legend Snippet: Effect of injecting psalmotoxin-1 (PcTx-1) intravenously on the pressor response to static contraction. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. E: the averaged increase in blood pressure over time. For clarity, error bars were omitted. The averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. Contractions were evoked before and at 10 min following intravenous (iv) injection of PcTx-1 (n = 5; 200 ng/kg, 100 μL) into the right jugular vein.

    Techniques Used: IV Injection

    Effect of acid-sensing ion channel 1a blockade and μ- and δ-opioid receptor blockade on the pressor response to static contraction. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. E: averaged increase in blood pressure over time. For clarity, error bars were omitted. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. Contractions were evoked before and at 10 min after naloxone infusion (100 μg/kg, 100 μL, 10 min) and at 10 min and 20 min after psalmotoxin-1 (PcTx-1; n = 4; 200 ng/kg, 100 μL) injection. Both drugs were injected into the superficial epigastric artery. **P < 0.01, significant difference compared with before injections, after naloxone (5 min), and after PcTx-1 (20 min). ia, intra-articular.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a blockade and μ- and δ-opioid receptor blockade on the pressor response to static contraction. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. E: averaged increase in blood pressure over time. For clarity, error bars were omitted. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. Contractions were evoked before and at 10 min after naloxone infusion (100 μg/kg, 100 μL, 10 min) and at 10 min and 20 min after psalmotoxin-1 (PcTx-1; n = 4; 200 ng/kg, 100 μL) injection. Both drugs were injected into the superficial epigastric artery. **P < 0.01, significant difference compared with before injections, after naloxone (5 min), and after PcTx-1 (20 min). ia, intra-articular.

    Techniques Used: Injection

    Effect of acid-sensing ion channel 1a blockade on popliteal blood flow during contraction. A: the averaged time course of popliteal artery blood flow and tension development during static contraction and the following 30 s of recovery (n = 3). The gray shaded area represents the contraction period. B: individual (black dots) and group means (gray bars) represent the mean percent changes in blood flow measured from the popliteal artery. Blood flow was calculated as the percent difference from baseline measurement. Baseline means and standard deviations for blood flow are presented below the x-axis of B. For clarity, error bars were omitted in A. The averaged time course of blood flow includes 2 s of baseline, 30 s of contraction, and 32 s after the end of contraction. Contractions were evoked before and at 10 min after psalmotoxin-1 (PcTx-1; 200 ng/kg, 100 μL) injection into the superficial epigastric artery. ia, intra-articular.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a blockade on popliteal blood flow during contraction. A: the averaged time course of popliteal artery blood flow and tension development during static contraction and the following 30 s of recovery (n = 3). The gray shaded area represents the contraction period. B: individual (black dots) and group means (gray bars) represent the mean percent changes in blood flow measured from the popliteal artery. Blood flow was calculated as the percent difference from baseline measurement. Baseline means and standard deviations for blood flow are presented below the x-axis of B. For clarity, error bars were omitted in A. The averaged time course of blood flow includes 2 s of baseline, 30 s of contraction, and 32 s after the end of contraction. Contractions were evoked before and at 10 min after psalmotoxin-1 (PcTx-1; 200 ng/kg, 100 μL) injection into the superficial epigastric artery. ia, intra-articular.

    Techniques Used: Injection

    Effect of acid-sensing ion channel 1a blockade on the pressor response to stretch. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) to stretch. Baseline means and standard deviations for blood pressure and tension are presented below the x-axis of their respective figures. E: averaged increase in blood pressure over time. For clarity, error bars were omitted. The averaged time course of blood pressure includes 2 s of baseline, 30 s of stretch, and 2 s after the end of stretch. Stretches were evoked before and 10 min after psalmotoxin-1 (PcTx-1; n = 6; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5; 6.5 μg/kg, 100 μL) injection into the superficial epigastric artery.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a blockade on the pressor response to stretch. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) to stretch. Baseline means and standard deviations for blood pressure and tension are presented below the x-axis of their respective figures. E: averaged increase in blood pressure over time. For clarity, error bars were omitted. The averaged time course of blood pressure includes 2 s of baseline, 30 s of stretch, and 2 s after the end of stretch. Stretches were evoked before and 10 min after psalmotoxin-1 (PcTx-1; n = 6; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5; 6.5 μg/kg, 100 μL) injection into the superficial epigastric artery.

    Techniques Used: Injection

    Effect of acid-sensing ion channel 1a (ASIC1a) blockade on the pressor response to injection of lactic acid and diprotonated phosphate. Data are presented as individual (black dots) and group means (gray bars) for the peak pressor response to lactic acid (24 mM, 100 μL, pH 2.66) (A) and diprotonated phosphate (86 mM, 100 μL, pH 6.0) (B) injections. Baseline means and standard deviations for blood pressure are presented below the x-axis. Lactic acid and diprotonated phosphate were injected into the superficial epigastric artery before and at 10, 20, and 30 min after psalmotoxin-1 (PcTx-1; n = 6; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5 and 6; 6.5 μg/kg, 100 μL) injection. *P < 0.05, significant difference compared with before ASIC1a blockade. MAP, mean arterial pressure.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a (ASIC1a) blockade on the pressor response to injection of lactic acid and diprotonated phosphate. Data are presented as individual (black dots) and group means (gray bars) for the peak pressor response to lactic acid (24 mM, 100 μL, pH 2.66) (A) and diprotonated phosphate (86 mM, 100 μL, pH 6.0) (B) injections. Baseline means and standard deviations for blood pressure are presented below the x-axis. Lactic acid and diprotonated phosphate were injected into the superficial epigastric artery before and at 10, 20, and 30 min after psalmotoxin-1 (PcTx-1; n = 6; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5 and 6; 6.5 μg/kg, 100 μL) injection. *P < 0.05, significant difference compared with before ASIC1a blockade. MAP, mean arterial pressure.

    Techniques Used: Injection

    pctx 1  (Alomone Labs)


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    Structured Review

    Alomone Labs pctx 1
    Representative traces and time course of the pressor response to static contraction before and after psalmotoxin-1 <t>(PcTx-1)</t> injection. Acid-sensing ion channels 1a were antagonized by injecting PcTx-1 (n = 8; 200 ng/kg, 100 μL) into the superficial epigastric artery. A: representative traces of the pressor responses to contraction before and 10 min after PcTx-1 in the same rat. B: averaged time course of the pressor response to contraction, which was evoked before, at 10 min after, and at 20 min after PcTx-1. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. For clarity, error bars were omitted. *P < 0.05, significant difference between before and 10 min after PcTx-1. BP, blood pressure; bpm, beats/min; HR, heart rate; MAP, mean arterial pressure.
    Pctx 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pctx 1/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pctx 1 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "ASIC1a plays a key role in evoking the metabolic component of the exercise pressor reflex in rats"

    Article Title: ASIC1a plays a key role in evoking the metabolic component of the exercise pressor reflex in rats

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    doi: 10.1152/ajpheart.00565.2019

    Representative traces and time course of the pressor response to static contraction before and after psalmotoxin-1 (PcTx-1) injection. Acid-sensing ion channels 1a were antagonized by injecting PcTx-1 (n = 8; 200 ng/kg, 100 μL) into the superficial epigastric artery. A: representative traces of the pressor responses to contraction before and 10 min after PcTx-1 in the same rat. B: averaged time course of the pressor response to contraction, which was evoked before, at 10 min after, and at 20 min after PcTx-1. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. For clarity, error bars were omitted. *P < 0.05, significant difference between before and 10 min after PcTx-1. BP, blood pressure; bpm, beats/min; HR, heart rate; MAP, mean arterial pressure.
    Figure Legend Snippet: Representative traces and time course of the pressor response to static contraction before and after psalmotoxin-1 (PcTx-1) injection. Acid-sensing ion channels 1a were antagonized by injecting PcTx-1 (n = 8; 200 ng/kg, 100 μL) into the superficial epigastric artery. A: representative traces of the pressor responses to contraction before and 10 min after PcTx-1 in the same rat. B: averaged time course of the pressor response to contraction, which was evoked before, at 10 min after, and at 20 min after PcTx-1. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. For clarity, error bars were omitted. *P < 0.05, significant difference between before and 10 min after PcTx-1. BP, blood pressure; bpm, beats/min; HR, heart rate; MAP, mean arterial pressure.

    Techniques Used: Injection

    Effect of acid-sensing ion channel 1a (ASIC1a) blockade on the pressor response to static contraction. Data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP; A), blood pressure index (BPI; B), peak increase in tension (C), and time-tension index (TTI; D) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. Contractions were evoked before, at 10 min after, and at 20 min after psalmotoxin-1 (PcTx-1; n = 8; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5; 6.5 μg/kg, 100 μL) injection into the superficial epigastric artery. *P < 0.05, significant difference compared with before ASIC1a blockade. ia, intra-arterial.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a (ASIC1a) blockade on the pressor response to static contraction. Data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP; A), blood pressure index (BPI; B), peak increase in tension (C), and time-tension index (TTI; D) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. Contractions were evoked before, at 10 min after, and at 20 min after psalmotoxin-1 (PcTx-1; n = 8; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5; 6.5 μg/kg, 100 μL) injection into the superficial epigastric artery. *P < 0.05, significant difference compared with before ASIC1a blockade. ia, intra-arterial.

    Techniques Used: Injection

    Effect of injecting psalmotoxin-1 (PcTx-1) intravenously on the pressor response to static contraction. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. E: the averaged increase in blood pressure over time. For clarity, error bars were omitted. The averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. Contractions were evoked before and at 10 min following intravenous (iv) injection of PcTx-1 (n = 5; 200 ng/kg, 100 μL) into the right jugular vein.
    Figure Legend Snippet: Effect of injecting psalmotoxin-1 (PcTx-1) intravenously on the pressor response to static contraction. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. E: the averaged increase in blood pressure over time. For clarity, error bars were omitted. The averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. Contractions were evoked before and at 10 min following intravenous (iv) injection of PcTx-1 (n = 5; 200 ng/kg, 100 μL) into the right jugular vein.

    Techniques Used: IV Injection

    Effect of acid-sensing ion channel 1a blockade and μ- and δ-opioid receptor blockade on the pressor response to static contraction. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. E: averaged increase in blood pressure over time. For clarity, error bars were omitted. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. Contractions were evoked before and at 10 min after naloxone infusion (100 μg/kg, 100 μL, 10 min) and at 10 min and 20 min after psalmotoxin-1 (PcTx-1; n = 4; 200 ng/kg, 100 μL) injection. Both drugs were injected into the superficial epigastric artery. **P < 0.01, significant difference compared with before injections, after naloxone (5 min), and after PcTx-1 (20 min). ia, intra-articular.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a blockade and μ- and δ-opioid receptor blockade on the pressor response to static contraction. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) evoked by static contraction. Baseline means and standard deviations for blood pressure and tension (in g) are presented below the x-axis of their respective figures. E: averaged increase in blood pressure over time. For clarity, error bars were omitted. Averaged time course of blood pressure includes 2 s of baseline, 30 s of contraction, and 2 s after the end of contraction. Contractions were evoked before and at 10 min after naloxone infusion (100 μg/kg, 100 μL, 10 min) and at 10 min and 20 min after psalmotoxin-1 (PcTx-1; n = 4; 200 ng/kg, 100 μL) injection. Both drugs were injected into the superficial epigastric artery. **P < 0.01, significant difference compared with before injections, after naloxone (5 min), and after PcTx-1 (20 min). ia, intra-articular.

    Techniques Used: Injection

    Effect of acid-sensing ion channel 1a blockade on popliteal blood flow during contraction. A: the averaged time course of popliteal artery blood flow and tension development during static contraction and the following 30 s of recovery (n = 3). The gray shaded area represents the contraction period. B: individual (black dots) and group means (gray bars) represent the mean percent changes in blood flow measured from the popliteal artery. Blood flow was calculated as the percent difference from baseline measurement. Baseline means and standard deviations for blood flow are presented below the x-axis of B. For clarity, error bars were omitted in A. The averaged time course of blood flow includes 2 s of baseline, 30 s of contraction, and 32 s after the end of contraction. Contractions were evoked before and at 10 min after psalmotoxin-1 (PcTx-1; 200 ng/kg, 100 μL) injection into the superficial epigastric artery. ia, intra-articular.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a blockade on popliteal blood flow during contraction. A: the averaged time course of popliteal artery blood flow and tension development during static contraction and the following 30 s of recovery (n = 3). The gray shaded area represents the contraction period. B: individual (black dots) and group means (gray bars) represent the mean percent changes in blood flow measured from the popliteal artery. Blood flow was calculated as the percent difference from baseline measurement. Baseline means and standard deviations for blood flow are presented below the x-axis of B. For clarity, error bars were omitted in A. The averaged time course of blood flow includes 2 s of baseline, 30 s of contraction, and 32 s after the end of contraction. Contractions were evoked before and at 10 min after psalmotoxin-1 (PcTx-1; 200 ng/kg, 100 μL) injection into the superficial epigastric artery. ia, intra-articular.

    Techniques Used: Injection

    Effect of acid-sensing ion channel 1a blockade on the pressor response to stretch. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) to stretch. Baseline means and standard deviations for blood pressure and tension are presented below the x-axis of their respective figures. E: averaged increase in blood pressure over time. For clarity, error bars were omitted. The averaged time course of blood pressure includes 2 s of baseline, 30 s of stretch, and 2 s after the end of stretch. Stretches were evoked before and 10 min after psalmotoxin-1 (PcTx-1; n = 6; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5; 6.5 μg/kg, 100 μL) injection into the superficial epigastric artery.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a blockade on the pressor response to stretch. A–D: data are presented as individual (black dots) and group means (gray bars) for the peak increase in mean arterial blood pressure (MAP), blood pressure index (BPI), peak increase in tension, and time-tension index (TTI) to stretch. Baseline means and standard deviations for blood pressure and tension are presented below the x-axis of their respective figures. E: averaged increase in blood pressure over time. For clarity, error bars were omitted. The averaged time course of blood pressure includes 2 s of baseline, 30 s of stretch, and 2 s after the end of stretch. Stretches were evoked before and 10 min after psalmotoxin-1 (PcTx-1; n = 6; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5; 6.5 μg/kg, 100 μL) injection into the superficial epigastric artery.

    Techniques Used: Injection

    Effect of acid-sensing ion channel 1a (ASIC1a) blockade on the pressor response to injection of lactic acid and diprotonated phosphate. Data are presented as individual (black dots) and group means (gray bars) for the peak pressor response to lactic acid (24 mM, 100 μL, pH 2.66) (A) and diprotonated phosphate (86 mM, 100 μL, pH 6.0) (B) injections. Baseline means and standard deviations for blood pressure are presented below the x-axis. Lactic acid and diprotonated phosphate were injected into the superficial epigastric artery before and at 10, 20, and 30 min after psalmotoxin-1 (PcTx-1; n = 6; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5 and 6; 6.5 μg/kg, 100 μL) injection. *P < 0.05, significant difference compared with before ASIC1a blockade. MAP, mean arterial pressure.
    Figure Legend Snippet: Effect of acid-sensing ion channel 1a (ASIC1a) blockade on the pressor response to injection of lactic acid and diprotonated phosphate. Data are presented as individual (black dots) and group means (gray bars) for the peak pressor response to lactic acid (24 mM, 100 μL, pH 2.66) (A) and diprotonated phosphate (86 mM, 100 μL, pH 6.0) (B) injections. Baseline means and standard deviations for blood pressure are presented below the x-axis. Lactic acid and diprotonated phosphate were injected into the superficial epigastric artery before and at 10, 20, and 30 min after psalmotoxin-1 (PcTx-1; n = 6; 200 ng/kg, 100 μL) or mambalgin-1 (Mamb-1; n = 5 and 6; 6.5 μg/kg, 100 μL) injection. *P < 0.05, significant difference compared with before ASIC1a blockade. MAP, mean arterial pressure.

    Techniques Used: Injection

    psalmotoxin 1 pctx  (Alomone Labs)


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    Alomone Labs psalmotoxin 1 pctx
    Psalmotoxin 1 Pctx, supplied by Alomone Labs, 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/psalmotoxin 1 pctx/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    psalmotoxin 1 pctx - by Bioz Stars, 2023-03
    93/100 stars

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    • pctx 1  (Alomone Labs)
    93
    Alomone Labs pctx 1
    Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with <t>Pctx-1</t> compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.
    Pctx 1, supplied by Alomone Labs, 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/pctx 1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pctx 1 - by Bioz Stars, 2023-03
    93/100 stars
    		  Buy from Supplier
    psalmotoxin 1 pctx  (Alomone Labs)
    93
    Alomone Labs psalmotoxin 1 pctx
    Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with <t>Pctx-1</t> compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.
    Psalmotoxin 1 Pctx, supplied by Alomone Labs, 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/psalmotoxin 1 pctx/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    psalmotoxin 1 pctx - by Bioz Stars, 2023-03
    93/100 stars
    		  Buy from Supplier

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    Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with Pctx-1 compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Signaling Pathways in Proton and Non-proton ASIC1a Activation

    doi: 10.3389/fncel.2021.735414

    Figure Lengend Snippet: Proton and non-proton activation of ASIC1a in HEK cells. (A) Representative membranes of lysates of HEK cells treated with pH6 or MitTx for 2 or 10 min or preincubated with Pctx-1 compared to untreated cells (control, Ctr) and detected with phosphoERK (pERK), total ERK (tERK), and ASIC1 antibodies. (B) Representative membrane of the same lysates to detect pCaMKII levels. (C) Plots showing detected levels of pERK (top panel) or pCaMKII (lower panel). Notice that the increase in kinase levels goes further at a later time point (2 vs. 10 min) in MitTx treated cultures compared to pH6 treated ones that show an increase at 2 min followed by a reversal to control levels consistent with the proton-activated desensitizing mechanism. (A) Notice that plots are the result of the signal intensity of the bands—with tERK and tubulin used as loading controls between loaded samples—and expressed relative to control samples. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments against the control were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; *** p 0.0001–0.001; ns: no significant differences. Mean values expressed relative to control ( Ctr ) levels ± SEM are as follows: for pERK/tERK: pH6 2’ 6.10 ± 0.13; pH6 10’ 1.23 ± 0.11; pH6 2’ Pctx 1.39 ± 0.08; MitTx 2’ 7.98 ± 0.10; Mittx10 ’ 10.90 ± 0.17; MitTx 2’ Pctx 1.18 ± 0.05 ; MitTx 10’ Pctx 1.42 ± 0.05. For pCaMKII/Tub: pH6 2’ 7.31 ± 0.21; pH6 10’ 1.16 ± 0.06; pH6 2’ Pctx 1.14±0.07; Mittx 2’ 8.88 ± 0.15; Mittx 10’ 10.76 ± 0.32; Mittx 2’ Pctx 1.17 ± 0.07.

    Article Snippet: Incubation of cells: ASIC inhibitors were used at the following concentrations before incubation with other reagents: Pctx-1 (Alomone, STP-200), 20 nM, 30 min before; as previously used in Salinas et al. ( ).

    Techniques: Activation Assay

    Proton and non-proton activation of overexpressed ASIC1a channels. (A) Representative membranes of lysates of cells control (ctr) or transfected with eGFP-ASIC1a (eASIC) at two levels (1x or x3) to obtained different levels of expression of the protein (“eASICx1 or eASICx3”), and treated with pH6 or MitTx with or without pre-incubation of Pctx-1 or untreated. (B) Plots showing the increase in pERK and pCaMKII levels calculated from membranes as that shown in (A) , consistent with the increase in eASIC expressed. Notice the level of increase achievable via MitTx incubation at the highest overexpressed level of eASIC, higher than that obtained via pH6. (C) Representative membrane showing the different levels of eASIC in cells overexpressing the channel (1x or 3x), detected with an ASIC1 antibody. (D) Comparison between the different ASIC1 proteins expressed (the endogenous human ASIC1a; of approx. 67 kDa) and the overexpressed eASIC (approx. 110 kDa, and expressed at different levels; x1 or x3). (A) Notice that plots are the result of the signal intensity of the band detected,—tERK and tubulin are used as loading controls between loaded samples—and expressed relative to eASICx1 levels. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments and conditions were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; ns: no significant differences. Mean values expressed relative to eASICx1 levels ± SEM are as follows: eASICx3 3.16 ± 0.06; eASIC MitTx 3.42 ± 0.15; eASICx3 MitTx 9.96 ± 0.12; eASIC MitTx Pctx 1.10 ± 0.05; eASIC pH6 2’ 1.85 ± 0.08; eASIC pH6 2’ Pctx 1.08 ± 0.05; eASICx3 pH6 2’ 4.00 ± 0.12.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Signaling Pathways in Proton and Non-proton ASIC1a Activation

    doi: 10.3389/fncel.2021.735414

    Figure Lengend Snippet: Proton and non-proton activation of overexpressed ASIC1a channels. (A) Representative membranes of lysates of cells control (ctr) or transfected with eGFP-ASIC1a (eASIC) at two levels (1x or x3) to obtained different levels of expression of the protein (“eASICx1 or eASICx3”), and treated with pH6 or MitTx with or without pre-incubation of Pctx-1 or untreated. (B) Plots showing the increase in pERK and pCaMKII levels calculated from membranes as that shown in (A) , consistent with the increase in eASIC expressed. Notice the level of increase achievable via MitTx incubation at the highest overexpressed level of eASIC, higher than that obtained via pH6. (C) Representative membrane showing the different levels of eASIC in cells overexpressing the channel (1x or 3x), detected with an ASIC1 antibody. (D) Comparison between the different ASIC1 proteins expressed (the endogenous human ASIC1a; of approx. 67 kDa) and the overexpressed eASIC (approx. 110 kDa, and expressed at different levels; x1 or x3). (A) Notice that plots are the result of the signal intensity of the band detected,—tERK and tubulin are used as loading controls between loaded samples—and expressed relative to eASICx1 levels. Data are presented as the mean ± SEM ANOVA and Dunnet post hoc test for treatments and conditions were performed, mean values above bars; n = 3 membranes, **** p < 0.0001; ns: no significant differences. Mean values expressed relative to eASICx1 levels ± SEM are as follows: eASICx3 3.16 ± 0.06; eASIC MitTx 3.42 ± 0.15; eASICx3 MitTx 9.96 ± 0.12; eASIC MitTx Pctx 1.10 ± 0.05; eASIC pH6 2’ 1.85 ± 0.08; eASIC pH6 2’ Pctx 1.08 ± 0.05; eASICx3 pH6 2’ 4.00 ± 0.12.

    Article Snippet: Incubation of cells: ASIC inhibitors were used at the following concentrations before incubation with other reagents: Pctx-1 (Alomone, STP-200), 20 nM, 30 min before; as previously used in Salinas et al. ( ).

    Techniques: Activation Assay, Transfection, Expressing, Incubation