rabbit polyclonal anti p2y1  (Alomone Labs)


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  • 94

    Structured Review

    Alomone Labs rabbit polyclonal anti p2y1
    P2Y receptors and nucleotide agonists.
    Rabbit Polyclonal Anti P2y1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal anti p2y1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal anti p2y1 - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Gi- and Gq-coupled ADP (P2Y) receptors act in opposition to modulate nociceptive signaling and inflammatory pain behavior"

    Article Title: Gi- and Gq-coupled ADP (P2Y) receptors act in opposition to modulate nociceptive signaling and inflammatory pain behavior

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-6-21

    P2Y receptors and nucleotide agonists.
    Figure Legend Snippet: P2Y receptors and nucleotide agonists.

    Techniques Used:

    P2Y Gi receptor mRNA levels are regulated in response to inflammatory injury . A ) Amplification of DRG cDNA by conventional RT-PCR using the P2Y Gi real-time PCR primers produced a single band for each receptor of the expected size (100-150 bp). B ) Real-time PCR was used to analyze mRNA levels for each of the Gi-coupled P2Y receptors and the Gq-coupled P2Y1 at 1, 4 and 15 days after induction of inflammatory hyperalgesia by injection of complete Freund's adjuvant into the hindpaw. The shaded box indicates the period of significant heat hyperalgesia determined using the Hargreaves test. Data are normalized against baseline values. *p < 0.01, ‡ p < 0.05, For PCR, n = 5 mice/time point. For behavior, n = 10 mice/time point.
    Figure Legend Snippet: P2Y Gi receptor mRNA levels are regulated in response to inflammatory injury . A ) Amplification of DRG cDNA by conventional RT-PCR using the P2Y Gi real-time PCR primers produced a single band for each receptor of the expected size (100-150 bp). B ) Real-time PCR was used to analyze mRNA levels for each of the Gi-coupled P2Y receptors and the Gq-coupled P2Y1 at 1, 4 and 15 days after induction of inflammatory hyperalgesia by injection of complete Freund's adjuvant into the hindpaw. The shaded box indicates the period of significant heat hyperalgesia determined using the Hargreaves test. Data are normalized against baseline values. *p < 0.01, ‡ p < 0.05, For PCR, n = 5 mice/time point. For behavior, n = 10 mice/time point.

    Techniques Used: Amplification, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction, Produced, Injection

    ADP evokes Ca ++ transients through  P2Y1.
    Figure Legend Snippet: ADP evokes Ca ++ transients through P2Y1.

    Techniques Used:

    P2Y Gi agonists inhibit depolarization-evoked increases in intracellular Ca ++ . Fura-2 Ca ++ imaging was used to measure the effect of P2Y receptor agonists on Ca ++ transients evoked by administration of 50 mM K + . Application of ADP (100 μM) for 3 minutes reduced subsequent depolarization-evoked transients in wildtype ( A ) and P2Y1-/- ( B ) mice. The P2Y13 agonist IDP ( C ) and the P2Y14 agonist UDPG ( D ) also inhibited depolarization-evoked transients.
    Figure Legend Snippet: P2Y Gi agonists inhibit depolarization-evoked increases in intracellular Ca ++ . Fura-2 Ca ++ imaging was used to measure the effect of P2Y receptor agonists on Ca ++ transients evoked by administration of 50 mM K + . Application of ADP (100 μM) for 3 minutes reduced subsequent depolarization-evoked transients in wildtype ( A ) and P2Y1-/- ( B ) mice. The P2Y13 agonist IDP ( C ) and the P2Y14 agonist UDPG ( D ) also inhibited depolarization-evoked transients.

    Techniques Used: Imaging

    Extent of inhibition by P2Y Gi receptor agonists.
    Figure Legend Snippet: Extent of inhibition by P2Y Gi receptor agonists.

    Techniques Used: Inhibition

    The inhibitory effect of ADP is enhanced in the absence of P2Y1 signaling . The magnitudes of depolarization-evoked Ca ++ transients in sensory neurons were measured before, and 5, 10 and 15 minutes after agonist application. Ca ++ transients were not affected by application of buffer alone (dashed lines), but were significantly reduced after application of ADP ( A-B ), IDP ( C ), or UDPG ( D ; solid lines). Inhibition was prolonged by application of the selective P2Y1 antagonist MRS2179 ( A ) and in neurons from P2Y1-/- mice ( B ). There was no effect of MRS2179 in P2Y1-/- neurons ( B ). Values are mean ± SEM; n = 10 mice/timepoint each treatment. *p < 0.02 versus control for each treatment.
    Figure Legend Snippet: The inhibitory effect of ADP is enhanced in the absence of P2Y1 signaling . The magnitudes of depolarization-evoked Ca ++ transients in sensory neurons were measured before, and 5, 10 and 15 minutes after agonist application. Ca ++ transients were not affected by application of buffer alone (dashed lines), but were significantly reduced after application of ADP ( A-B ), IDP ( C ), or UDPG ( D ; solid lines). Inhibition was prolonged by application of the selective P2Y1 antagonist MRS2179 ( A ) and in neurons from P2Y1-/- mice ( B ). There was no effect of MRS2179 in P2Y1-/- neurons ( B ). Values are mean ± SEM; n = 10 mice/timepoint each treatment. *p < 0.02 versus control for each treatment.

    Techniques Used: Inhibition

    ADP has opposing effects on behavioral nociceptive thresholds in the presence and absence of P2Y1 . ADP has opposite effects on withdrawal latencies to noxious heat stimuli (Hargreaves test) in the presence and absence of P2Y1. A) P2Y1-/- mice show a deficit in thermal hyperalgesia at day 3 following CFA injection, compared to wildtype mice. B) Injection of ADP into the hindpaw of naïve mice caused thermal hyperalgesia in wildtype mice, but hypoalgesia in P2Y1-/- mice. C) Mice were injected with ADP in the hindpaw three days after CFA injection and thermal response thresholds were measured. ADP injection had no effect on thermal thresholds in inflamed wildtype mice, but reversed thermal hyperalgesia in P2Y1-/- mice. D) Hindpaw injection of MRS2500, a P2Y1 antagonist, in inflamed wildtype mice acutely reversed thermal hyperalgesia compared to saline injection. Injection of either IDP ( E ) or UDPG ( F ) into the inflamed hindpaw reversed inflammation-evoked thermal hyperalgesia. n = 10 mice/cohort.
    Figure Legend Snippet: ADP has opposing effects on behavioral nociceptive thresholds in the presence and absence of P2Y1 . ADP has opposite effects on withdrawal latencies to noxious heat stimuli (Hargreaves test) in the presence and absence of P2Y1. A) P2Y1-/- mice show a deficit in thermal hyperalgesia at day 3 following CFA injection, compared to wildtype mice. B) Injection of ADP into the hindpaw of naïve mice caused thermal hyperalgesia in wildtype mice, but hypoalgesia in P2Y1-/- mice. C) Mice were injected with ADP in the hindpaw three days after CFA injection and thermal response thresholds were measured. ADP injection had no effect on thermal thresholds in inflamed wildtype mice, but reversed thermal hyperalgesia in P2Y1-/- mice. D) Hindpaw injection of MRS2500, a P2Y1 antagonist, in inflamed wildtype mice acutely reversed thermal hyperalgesia compared to saline injection. Injection of either IDP ( E ) or UDPG ( F ) into the inflamed hindpaw reversed inflammation-evoked thermal hyperalgesia. n = 10 mice/cohort.

    Techniques Used: Injection

    rabbit polyclonal anti p2y1  (Alomone Labs)


    Bioz Verified Symbol Alomone Labs is a verified supplier
    Bioz Manufacturer Symbol Alomone Labs manufactures this product  
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  • 94

    Structured Review

    Alomone Labs rabbit polyclonal anti p2y1
    P2Y receptors and nucleotide agonists.
    Rabbit Polyclonal Anti P2y1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal anti p2y1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal anti p2y1 - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Gi- and Gq-coupled ADP (P2Y) receptors act in opposition to modulate nociceptive signaling and inflammatory pain behavior"

    Article Title: Gi- and Gq-coupled ADP (P2Y) receptors act in opposition to modulate nociceptive signaling and inflammatory pain behavior

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-6-21

    P2Y receptors and nucleotide agonists.
    Figure Legend Snippet: P2Y receptors and nucleotide agonists.

    Techniques Used:

    P2Y Gi receptor mRNA levels are regulated in response to inflammatory injury . A ) Amplification of DRG cDNA by conventional RT-PCR using the P2Y Gi real-time PCR primers produced a single band for each receptor of the expected size (100-150 bp). B ) Real-time PCR was used to analyze mRNA levels for each of the Gi-coupled P2Y receptors and the Gq-coupled P2Y1 at 1, 4 and 15 days after induction of inflammatory hyperalgesia by injection of complete Freund's adjuvant into the hindpaw. The shaded box indicates the period of significant heat hyperalgesia determined using the Hargreaves test. Data are normalized against baseline values. *p < 0.01, ‡ p < 0.05, For PCR, n = 5 mice/time point. For behavior, n = 10 mice/time point.
    Figure Legend Snippet: P2Y Gi receptor mRNA levels are regulated in response to inflammatory injury . A ) Amplification of DRG cDNA by conventional RT-PCR using the P2Y Gi real-time PCR primers produced a single band for each receptor of the expected size (100-150 bp). B ) Real-time PCR was used to analyze mRNA levels for each of the Gi-coupled P2Y receptors and the Gq-coupled P2Y1 at 1, 4 and 15 days after induction of inflammatory hyperalgesia by injection of complete Freund's adjuvant into the hindpaw. The shaded box indicates the period of significant heat hyperalgesia determined using the Hargreaves test. Data are normalized against baseline values. *p < 0.01, ‡ p < 0.05, For PCR, n = 5 mice/time point. For behavior, n = 10 mice/time point.

    Techniques Used: Amplification, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction, Produced, Injection

    ADP evokes Ca ++ transients through  P2Y1.
    Figure Legend Snippet: ADP evokes Ca ++ transients through P2Y1.

    Techniques Used:

    P2Y Gi agonists inhibit depolarization-evoked increases in intracellular Ca ++ . Fura-2 Ca ++ imaging was used to measure the effect of P2Y receptor agonists on Ca ++ transients evoked by administration of 50 mM K + . Application of ADP (100 μM) for 3 minutes reduced subsequent depolarization-evoked transients in wildtype ( A ) and P2Y1-/- ( B ) mice. The P2Y13 agonist IDP ( C ) and the P2Y14 agonist UDPG ( D ) also inhibited depolarization-evoked transients.
    Figure Legend Snippet: P2Y Gi agonists inhibit depolarization-evoked increases in intracellular Ca ++ . Fura-2 Ca ++ imaging was used to measure the effect of P2Y receptor agonists on Ca ++ transients evoked by administration of 50 mM K + . Application of ADP (100 μM) for 3 minutes reduced subsequent depolarization-evoked transients in wildtype ( A ) and P2Y1-/- ( B ) mice. The P2Y13 agonist IDP ( C ) and the P2Y14 agonist UDPG ( D ) also inhibited depolarization-evoked transients.

    Techniques Used: Imaging

    Extent of inhibition by P2Y Gi receptor agonists.
    Figure Legend Snippet: Extent of inhibition by P2Y Gi receptor agonists.

    Techniques Used: Inhibition

    The inhibitory effect of ADP is enhanced in the absence of P2Y1 signaling . The magnitudes of depolarization-evoked Ca ++ transients in sensory neurons were measured before, and 5, 10 and 15 minutes after agonist application. Ca ++ transients were not affected by application of buffer alone (dashed lines), but were significantly reduced after application of ADP ( A-B ), IDP ( C ), or UDPG ( D ; solid lines). Inhibition was prolonged by application of the selective P2Y1 antagonist MRS2179 ( A ) and in neurons from P2Y1-/- mice ( B ). There was no effect of MRS2179 in P2Y1-/- neurons ( B ). Values are mean ± SEM; n = 10 mice/timepoint each treatment. *p < 0.02 versus control for each treatment.
    Figure Legend Snippet: The inhibitory effect of ADP is enhanced in the absence of P2Y1 signaling . The magnitudes of depolarization-evoked Ca ++ transients in sensory neurons were measured before, and 5, 10 and 15 minutes after agonist application. Ca ++ transients were not affected by application of buffer alone (dashed lines), but were significantly reduced after application of ADP ( A-B ), IDP ( C ), or UDPG ( D ; solid lines). Inhibition was prolonged by application of the selective P2Y1 antagonist MRS2179 ( A ) and in neurons from P2Y1-/- mice ( B ). There was no effect of MRS2179 in P2Y1-/- neurons ( B ). Values are mean ± SEM; n = 10 mice/timepoint each treatment. *p < 0.02 versus control for each treatment.

    Techniques Used: Inhibition

    ADP has opposing effects on behavioral nociceptive thresholds in the presence and absence of P2Y1 . ADP has opposite effects on withdrawal latencies to noxious heat stimuli (Hargreaves test) in the presence and absence of P2Y1. A) P2Y1-/- mice show a deficit in thermal hyperalgesia at day 3 following CFA injection, compared to wildtype mice. B) Injection of ADP into the hindpaw of naïve mice caused thermal hyperalgesia in wildtype mice, but hypoalgesia in P2Y1-/- mice. C) Mice were injected with ADP in the hindpaw three days after CFA injection and thermal response thresholds were measured. ADP injection had no effect on thermal thresholds in inflamed wildtype mice, but reversed thermal hyperalgesia in P2Y1-/- mice. D) Hindpaw injection of MRS2500, a P2Y1 antagonist, in inflamed wildtype mice acutely reversed thermal hyperalgesia compared to saline injection. Injection of either IDP ( E ) or UDPG ( F ) into the inflamed hindpaw reversed inflammation-evoked thermal hyperalgesia. n = 10 mice/cohort.
    Figure Legend Snippet: ADP has opposing effects on behavioral nociceptive thresholds in the presence and absence of P2Y1 . ADP has opposite effects on withdrawal latencies to noxious heat stimuli (Hargreaves test) in the presence and absence of P2Y1. A) P2Y1-/- mice show a deficit in thermal hyperalgesia at day 3 following CFA injection, compared to wildtype mice. B) Injection of ADP into the hindpaw of naïve mice caused thermal hyperalgesia in wildtype mice, but hypoalgesia in P2Y1-/- mice. C) Mice were injected with ADP in the hindpaw three days after CFA injection and thermal response thresholds were measured. ADP injection had no effect on thermal thresholds in inflamed wildtype mice, but reversed thermal hyperalgesia in P2Y1-/- mice. D) Hindpaw injection of MRS2500, a P2Y1 antagonist, in inflamed wildtype mice acutely reversed thermal hyperalgesia compared to saline injection. Injection of either IDP ( E ) or UDPG ( F ) into the inflamed hindpaw reversed inflammation-evoked thermal hyperalgesia. n = 10 mice/cohort.

    Techniques Used: Injection

    cav3 1  (Alomone Labs)


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  • 94

    Structured Review

    Alomone Labs cav3 1
    NmbR mediates the Nmb-induced I T increase. A, western blot analysis of NmbR in mouse TGs. A prominent band was also observed in the spinal cord of mice. Blots depicted are representative of three independent experiments. B, double immunostaining of NmbR with calcitonin gene-related peptide (CGRP), isolectin B4 (IB 4 ), or neurofilament 200 (NF200) in mouse TG sections. Arrows in white indicate the co-localization. Scale bar, 30 µm. C, time course ( left panel ) and summary data ( right panel ) show the effects of 100 nM Nmb on I T in TG neurons pretreated with BIM23042 (0.5 µM) ( n = 7). Bath application of 0.5 µM BIM23042 alone did not affect I T ( n = 6). Inset s indicate the exemplary current traces. The Arabic numbers represent points used for representative traces. *** p < 0.001 versus Nmb, two-tailed t test. D, double immunostaining of NmbR with <t>Cav3.2</t> in TG neurons of naïve mice. Arrows in white show the colocalization. Scale bars, 30 µm. Insets indicate the percentage of double-labeled neurons in NmbR + or Cav3.2 + neurons. E, total contact number of orofacial operant test with mechanical stimulation was comparable between normal saline (NS)- and CFA-treated mice. BL, baseline. F, total contact time was significantly decreased from 1 to 7 d after CFA injection, compared to NS group. * P < 0.05, ** P < 0.01 versus NS, two-way ANOVA followed by Bonferroni post hoc test. G, mechanical hypersensitivity induced by CFA injection. Decreased escape threshold was observed at the 12th h after CFA injection and lasted to ~7 d ( n = 9 mice per group). * p < 0.05 and ** p < 0.01 versus normal saline (NS) at the corresponding time point, two-way ANOVA followed by Bonferroni post hoc test. H, representative immunoblots show that Nmb expression was increased in the local inflamed tissue of mice at 2 d after CFA. Blots depicted are representative of three independent experiments. # p < 0.05 versus NS, two-tailed t test. I, abundance of NmbR protein in mouse TGs at 2 d after NS- or CFA- treatment. Blots depicted are representative of three independent experiments. ## p < 0.01 versus NS, two-tailed t test.
    Cav3 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cav3 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cav3 1 - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Neuromedin B receptor stimulation of Cav3.2 T-type Ca 2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity"

    Article Title: Neuromedin B receptor stimulation of Cav3.2 T-type Ca 2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity

    Journal: Theranostics

    doi: 10.7150/thno.62255

    NmbR mediates the Nmb-induced I T increase. A, western blot analysis of NmbR in mouse TGs. A prominent band was also observed in the spinal cord of mice. Blots depicted are representative of three independent experiments. B, double immunostaining of NmbR with calcitonin gene-related peptide (CGRP), isolectin B4 (IB 4 ), or neurofilament 200 (NF200) in mouse TG sections. Arrows in white indicate the co-localization. Scale bar, 30 µm. C, time course ( left panel ) and summary data ( right panel ) show the effects of 100 nM Nmb on I T in TG neurons pretreated with BIM23042 (0.5 µM) ( n = 7). Bath application of 0.5 µM BIM23042 alone did not affect I T ( n = 6). Inset s indicate the exemplary current traces. The Arabic numbers represent points used for representative traces. *** p < 0.001 versus Nmb, two-tailed t test. D, double immunostaining of NmbR with Cav3.2 in TG neurons of naïve mice. Arrows in white show the colocalization. Scale bars, 30 µm. Insets indicate the percentage of double-labeled neurons in NmbR + or Cav3.2 + neurons. E, total contact number of orofacial operant test with mechanical stimulation was comparable between normal saline (NS)- and CFA-treated mice. BL, baseline. F, total contact time was significantly decreased from 1 to 7 d after CFA injection, compared to NS group. * P < 0.05, ** P < 0.01 versus NS, two-way ANOVA followed by Bonferroni post hoc test. G, mechanical hypersensitivity induced by CFA injection. Decreased escape threshold was observed at the 12th h after CFA injection and lasted to ~7 d ( n = 9 mice per group). * p < 0.05 and ** p < 0.01 versus normal saline (NS) at the corresponding time point, two-way ANOVA followed by Bonferroni post hoc test. H, representative immunoblots show that Nmb expression was increased in the local inflamed tissue of mice at 2 d after CFA. Blots depicted are representative of three independent experiments. # p < 0.05 versus NS, two-tailed t test. I, abundance of NmbR protein in mouse TGs at 2 d after NS- or CFA- treatment. Blots depicted are representative of three independent experiments. ## p < 0.01 versus NS, two-tailed t test.
    Figure Legend Snippet: NmbR mediates the Nmb-induced I T increase. A, western blot analysis of NmbR in mouse TGs. A prominent band was also observed in the spinal cord of mice. Blots depicted are representative of three independent experiments. B, double immunostaining of NmbR with calcitonin gene-related peptide (CGRP), isolectin B4 (IB 4 ), or neurofilament 200 (NF200) in mouse TG sections. Arrows in white indicate the co-localization. Scale bar, 30 µm. C, time course ( left panel ) and summary data ( right panel ) show the effects of 100 nM Nmb on I T in TG neurons pretreated with BIM23042 (0.5 µM) ( n = 7). Bath application of 0.5 µM BIM23042 alone did not affect I T ( n = 6). Inset s indicate the exemplary current traces. The Arabic numbers represent points used for representative traces. *** p < 0.001 versus Nmb, two-tailed t test. D, double immunostaining of NmbR with Cav3.2 in TG neurons of naïve mice. Arrows in white show the colocalization. Scale bars, 30 µm. Insets indicate the percentage of double-labeled neurons in NmbR + or Cav3.2 + neurons. E, total contact number of orofacial operant test with mechanical stimulation was comparable between normal saline (NS)- and CFA-treated mice. BL, baseline. F, total contact time was significantly decreased from 1 to 7 d after CFA injection, compared to NS group. * P < 0.05, ** P < 0.01 versus NS, two-way ANOVA followed by Bonferroni post hoc test. G, mechanical hypersensitivity induced by CFA injection. Decreased escape threshold was observed at the 12th h after CFA injection and lasted to ~7 d ( n = 9 mice per group). * p < 0.05 and ** p < 0.01 versus normal saline (NS) at the corresponding time point, two-way ANOVA followed by Bonferroni post hoc test. H, representative immunoblots show that Nmb expression was increased in the local inflamed tissue of mice at 2 d after CFA. Blots depicted are representative of three independent experiments. # p < 0.05 versus NS, two-tailed t test. I, abundance of NmbR protein in mouse TGs at 2 d after NS- or CFA- treatment. Blots depicted are representative of three independent experiments. ## p < 0.01 versus NS, two-tailed t test.

    Techniques Used: Western Blot, Double Immunostaining, Two Tailed Test, Labeling, Injection, Expressing

    The G βγ -dependent AMPK/PKA pathway mediates the NmbR response. A, time course of I T changes induced by 100 nM Nmb in TG neurons dialyzed with QEHA (10 μM). Inset s indicate the exemplary current traces. The Arabic numbers represent points used for representative traces. B, summary data indicate the effect of 100 nM Nmb on I T in TG neurons dialyzed with QEHA (10 μM, n = 6) or SKEE (10 μM, n = 7). ** p < 0.01 versus control, two-tailed t test. C, protein expression of G β in cells transduced with G β shRNA (G β -shRNA) or negative control shRNA (NC-shRNA). Blots depicted are representative of three independent experiments. # p < 0.05 versus NC-shRNA, two-tailed t test. D, summary data show the effect of Nmb (100 nM) on I T in TG neurons transduced with NC-shRNA ( n = 9) or G β -shRNA ( n = 8). * p < 0.05 versus NC-shRNA + control, one-way ANOVA followed by Bonferroni post hoc test. E, time course ( left panel ) and summary data ( right panel ) show the effect of Nmb (100 nM) on I T in cells pre-incubated with KT-5720 (1 μM, n = 7). Inset s indicate the exemplary current traces. The Arabic numbers represent points used for representative traces. ** p < 0.01 versus control, two-tailed t test. F, exemplary current traces and summary of results show the effect of forskolin (10 µM) on I T in TG neurons in the absence ( n = 7) or presence of KT-5720 (1 μM, n = 6). ** p < 0.01 versus control, two-tailed t test. G, representative immunoblot and summary data show that treatment of TG cells with 100 nM Nmb did not affect the protein expression level of Cav3.2. GAPDH was used as the loading control. H, pretreatment of TG cells with 0.5 µM BIM23042, but not 1 μM KT-5720, attenuates the increased expression level of phosphorylated AMPK ( p -AMPK) induced by 100 nM Nmb. GAPDH was used as the loading control. Blots depicted are representative of three independent experiments. * p < 0.05 versus control, two-tailed t test. I, summary data show the effect of 100 nM Nmb on PKA activity in TG cells pretreated with 0.5 µM BIM23042 or 10 µM compound C. All experiments were performed in triplicate with similar results. # p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. J, time course ( left panel ) and summary of results ( right panel ) indicate the effect of 100 nM Nmb on I T in TG neurons pretreated with compound C (10 µM, n = 7). Inset s show the exemplary current traces. The Arabic numbers represent points used for representative traces. *** p < 0.001 versus control, two-tailed t test.
    Figure Legend Snippet: The G βγ -dependent AMPK/PKA pathway mediates the NmbR response. A, time course of I T changes induced by 100 nM Nmb in TG neurons dialyzed with QEHA (10 μM). Inset s indicate the exemplary current traces. The Arabic numbers represent points used for representative traces. B, summary data indicate the effect of 100 nM Nmb on I T in TG neurons dialyzed with QEHA (10 μM, n = 6) or SKEE (10 μM, n = 7). ** p < 0.01 versus control, two-tailed t test. C, protein expression of G β in cells transduced with G β shRNA (G β -shRNA) or negative control shRNA (NC-shRNA). Blots depicted are representative of three independent experiments. # p < 0.05 versus NC-shRNA, two-tailed t test. D, summary data show the effect of Nmb (100 nM) on I T in TG neurons transduced with NC-shRNA ( n = 9) or G β -shRNA ( n = 8). * p < 0.05 versus NC-shRNA + control, one-way ANOVA followed by Bonferroni post hoc test. E, time course ( left panel ) and summary data ( right panel ) show the effect of Nmb (100 nM) on I T in cells pre-incubated with KT-5720 (1 μM, n = 7). Inset s indicate the exemplary current traces. The Arabic numbers represent points used for representative traces. ** p < 0.01 versus control, two-tailed t test. F, exemplary current traces and summary of results show the effect of forskolin (10 µM) on I T in TG neurons in the absence ( n = 7) or presence of KT-5720 (1 μM, n = 6). ** p < 0.01 versus control, two-tailed t test. G, representative immunoblot and summary data show that treatment of TG cells with 100 nM Nmb did not affect the protein expression level of Cav3.2. GAPDH was used as the loading control. H, pretreatment of TG cells with 0.5 µM BIM23042, but not 1 μM KT-5720, attenuates the increased expression level of phosphorylated AMPK ( p -AMPK) induced by 100 nM Nmb. GAPDH was used as the loading control. Blots depicted are representative of three independent experiments. * p < 0.05 versus control, two-tailed t test. I, summary data show the effect of 100 nM Nmb on PKA activity in TG cells pretreated with 0.5 µM BIM23042 or 10 µM compound C. All experiments were performed in triplicate with similar results. # p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. J, time course ( left panel ) and summary of results ( right panel ) indicate the effect of 100 nM Nmb on I T in TG neurons pretreated with compound C (10 µM, n = 7). Inset s show the exemplary current traces. The Arabic numbers represent points used for representative traces. *** p < 0.001 versus control, two-tailed t test.

    Techniques Used: Two Tailed Test, Expressing, Transduction, shRNA, Negative Control, Incubation, Western Blot, Activity Assay

    Activation of NmbR stimulates recombinant Cav3.2 channels heterologously expressed in HEK293 cells. A, western blot analysis of NmbR in HEK293 cells transiently transfected with NmbR cDNA. Blots depicted are representative of three independent experiments. B, membrane localization of NmbR in transfected HEK293 cells. Alphabets a through c in the diagram indicate the differential interference contrast (DIC, a ), the EGFP fluorescent signals of NmbR ( b ), and the merged image ( c ), respectively. C, exemplary current traces show the effect of Nmb (100 nM) on Cav3.1 (α1G), Cav3.2 (α1H) and Cav3.3 (α1I) channel currents. Currents were elicited by a 100 ms depolarizing step pulse from the holding potential of -110 mV to -30 mV. D, summary data show the effect of 100 nM Nmb on Cav3.1 ( n = 10), Cav3.2 ( n = 9) and Cav3.3 ( n = 7) channel currents. ** p < 0.01 versus control, two-tailed t test. E, dose-dependent effects of Nmb on Cav3.2 channel currents. Solid line represents the sigmoidal dose-response fits. Numbers in parentheses denote n cells tested at each concentration. F, summary data show the effect of Nmb (100 nM) on Cav3.2 channel currents in cells pre-incubated with 10 µM compound C ( n = 8), in cells pretreated with 1 µM KT-5720 ( n = 9), and in cells dialyzed with 10 μM PKC 19-36 ( n = 9), respectively. ** p < 0.01 and *** p < 0.001 versus control, two-tailed t test.
    Figure Legend Snippet: Activation of NmbR stimulates recombinant Cav3.2 channels heterologously expressed in HEK293 cells. A, western blot analysis of NmbR in HEK293 cells transiently transfected with NmbR cDNA. Blots depicted are representative of three independent experiments. B, membrane localization of NmbR in transfected HEK293 cells. Alphabets a through c in the diagram indicate the differential interference contrast (DIC, a ), the EGFP fluorescent signals of NmbR ( b ), and the merged image ( c ), respectively. C, exemplary current traces show the effect of Nmb (100 nM) on Cav3.1 (α1G), Cav3.2 (α1H) and Cav3.3 (α1I) channel currents. Currents were elicited by a 100 ms depolarizing step pulse from the holding potential of -110 mV to -30 mV. D, summary data show the effect of 100 nM Nmb on Cav3.1 ( n = 10), Cav3.2 ( n = 9) and Cav3.3 ( n = 7) channel currents. ** p < 0.01 versus control, two-tailed t test. E, dose-dependent effects of Nmb on Cav3.2 channel currents. Solid line represents the sigmoidal dose-response fits. Numbers in parentheses denote n cells tested at each concentration. F, summary data show the effect of Nmb (100 nM) on Cav3.2 channel currents in cells pre-incubated with 10 µM compound C ( n = 8), in cells pretreated with 1 µM KT-5720 ( n = 9), and in cells dialyzed with 10 μM PKC 19-36 ( n = 9), respectively. ** p < 0.01 and *** p < 0.001 versus control, two-tailed t test.

    Techniques Used: Activation Assay, Recombinant, Western Blot, Transfection, Two Tailed Test, Concentration Assay, Incubation

    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or TTA-P2 (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.
    Figure Legend Snippet: Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or TTA-P2 (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.

    Techniques Used: Injection, Produced, Expressing, Two Tailed Test

    Proposed mechanisms of NmbR signalling on Cav3.2 channels in TG neurons. The binding of Nmb triggers NmbR to activate G q protein and releases the G βγ subunits. The released G βγ dimer then stimulates AMPK activity, induces the activation of PKA and subsequently phosphorylates Cav3.2 channels to increase I T . Neither PLC/PKC nor direct binding of G βγ to Cav3.2 channels is required for T-type channel response mediated by NmbR.
    Figure Legend Snippet: Proposed mechanisms of NmbR signalling on Cav3.2 channels in TG neurons. The binding of Nmb triggers NmbR to activate G q protein and releases the G βγ subunits. The released G βγ dimer then stimulates AMPK activity, induces the activation of PKA and subsequently phosphorylates Cav3.2 channels to increase I T . Neither PLC/PKC nor direct binding of G βγ to Cav3.2 channels is required for T-type channel response mediated by NmbR.

    Techniques Used: Binding Assay, Activity Assay, Activation Assay

    rabbit anti a 2b ar  (Alomone Labs)


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    Alomone Labs rabbit anti a 2b ar
    Rabbit Anti A 2b Ar, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rb anti k v 3 3 kcn3 pab  (Alomone Labs)


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    Alomone Labs rb anti k v 3 3 kcn3 pab
    Primary and Secondary Antibody Sources and Working Dilutions.
    Rb Anti K V 3 3 Kcn3 Pab, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Immunohistochemical Characterization of the Chemosensory Pulmonary Neuroepithelial Bodies in the Naked Mole-Rat Reveals a Unique Adaptive Phenotype"

    Article Title: Immunohistochemical Characterization of the Chemosensory Pulmonary Neuroepithelial Bodies in the Naked Mole-Rat Reveals a Unique Adaptive Phenotype

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0112623

    Primary and Secondary Antibody Sources and Working Dilutions.
    Figure Legend Snippet: Primary and Secondary Antibody Sources and Working Dilutions.

    Techniques Used:

    rb anti k v 4 3 kcn4 pab  (Alomone Labs)


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    Alomone Labs rb anti k v 4 3 kcn4 pab
    Primary and Secondary Antibody Sources and Working Dilutions.
    Rb Anti K V 4 3 Kcn4 Pab, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Immunohistochemical Characterization of the Chemosensory Pulmonary Neuroepithelial Bodies in the Naked Mole-Rat Reveals a Unique Adaptive Phenotype"

    Article Title: Immunohistochemical Characterization of the Chemosensory Pulmonary Neuroepithelial Bodies in the Naked Mole-Rat Reveals a Unique Adaptive Phenotype

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0112623

    Primary and Secondary Antibody Sources and Working Dilutions.
    Figure Legend Snippet: Primary and Secondary Antibody Sources and Working Dilutions.

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    anti p2y1  (Alomone Labs)


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    Alomone Labs anti p2y1
    Western blotting showed components for calcium wave propagation (CWP) were expressed abundantly at ST36. Components tested were the ATP-releasing hemichannels pannexin 1 (PanX 1) and connexin 43 (Cx 43) and the purinergic receptors <t>P2Y1</t> and P2Y2. Tissues from nerve (Ner), muscle (Mus), epimysium (Epi), and subcutaneous loose connective tissue (ScLCT) of ST36 or sham were collected in a manner similar to that described for mechanosensitive channel western blotting. (A, B, C, and D) Pannexin 1, connexin 43, P2Y1, and P2Y2 were expressed in nerve and muscle. (A) Pannexin 1 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.05). (B) Connexin 43 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.01). (C) P2Y1 was more abundantly expressed in ST36 muscle compared with the sham ( P < 0.05) and in ST36 ScLCT compared with ST36 epimysium ( P < 0.01) and sham ScLCT ( P < 0.01.) (D) P2Y2 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.01). All four components were expressed in muscle and the epimysium of ST36. These two layers also abundantly expressed TRPV1. The relative levels of target proteins were calculated in a manner similar to that used for western blotting of mechanosensitive channels (* P < 0.05, ** P < 0.01; Mann–Whitney rank sum test; pannexin 1, n = 8–12; connexin 43, n = 6; P2Y1, n = 5–9; P2Y2, n = 7). Data are means ± S.E.M.
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    1) Product Images from "Abundant expression and functional participation of TRPV1 at Zusanli acupoint (ST36) in mice: mechanosensitive TRPV1 as an “acupuncture-responding channel”"

    Article Title: Abundant expression and functional participation of TRPV1 at Zusanli acupoint (ST36) in mice: mechanosensitive TRPV1 as an “acupuncture-responding channel”

    Journal: BMC Complementary and Alternative Medicine

    doi: 10.1186/1472-6882-14-96

    Western blotting showed components for calcium wave propagation (CWP) were expressed abundantly at ST36. Components tested were the ATP-releasing hemichannels pannexin 1 (PanX 1) and connexin 43 (Cx 43) and the purinergic receptors P2Y1 and P2Y2. Tissues from nerve (Ner), muscle (Mus), epimysium (Epi), and subcutaneous loose connective tissue (ScLCT) of ST36 or sham were collected in a manner similar to that described for mechanosensitive channel western blotting. (A, B, C, and D) Pannexin 1, connexin 43, P2Y1, and P2Y2 were expressed in nerve and muscle. (A) Pannexin 1 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.05). (B) Connexin 43 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.01). (C) P2Y1 was more abundantly expressed in ST36 muscle compared with the sham ( P < 0.05) and in ST36 ScLCT compared with ST36 epimysium ( P < 0.01) and sham ScLCT ( P < 0.01.) (D) P2Y2 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.01). All four components were expressed in muscle and the epimysium of ST36. These two layers also abundantly expressed TRPV1. The relative levels of target proteins were calculated in a manner similar to that used for western blotting of mechanosensitive channels (* P < 0.05, ** P < 0.01; Mann–Whitney rank sum test; pannexin 1, n = 8–12; connexin 43, n = 6; P2Y1, n = 5–9; P2Y2, n = 7). Data are means ± S.E.M.
    Figure Legend Snippet: Western blotting showed components for calcium wave propagation (CWP) were expressed abundantly at ST36. Components tested were the ATP-releasing hemichannels pannexin 1 (PanX 1) and connexin 43 (Cx 43) and the purinergic receptors P2Y1 and P2Y2. Tissues from nerve (Ner), muscle (Mus), epimysium (Epi), and subcutaneous loose connective tissue (ScLCT) of ST36 or sham were collected in a manner similar to that described for mechanosensitive channel western blotting. (A, B, C, and D) Pannexin 1, connexin 43, P2Y1, and P2Y2 were expressed in nerve and muscle. (A) Pannexin 1 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.05). (B) Connexin 43 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.01). (C) P2Y1 was more abundantly expressed in ST36 muscle compared with the sham ( P < 0.05) and in ST36 ScLCT compared with ST36 epimysium ( P < 0.01) and sham ScLCT ( P < 0.01.) (D) P2Y2 was more abundantly expressed at ST36 epimysium compared with ST36 ScLCT ( P < 0.05) and sham ScLCT ( P < 0.01). All four components were expressed in muscle and the epimysium of ST36. These two layers also abundantly expressed TRPV1. The relative levels of target proteins were calculated in a manner similar to that used for western blotting of mechanosensitive channels (* P < 0.05, ** P < 0.01; Mann–Whitney rank sum test; pannexin 1, n = 8–12; connexin 43, n = 6; P2Y1, n = 5–9; P2Y2, n = 7). Data are means ± S.E.M.

    Techniques Used: Western Blot, MANN-WHITNEY

    glp 1r  (Alomone Labs)


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    Alomone Labs glp 1r
    Activation of cortical neuron expressed <t>GLP-1</t> receptor <t>(GLP-1R)</t> protected cortical neurons from oxidative insults. (A) mRNA and (B) protein expressions of GLP-1R were detected in the 8-day in vitro primary cortical neurons. (C) Immunofluorescence staining of GLP-1R (green), TUJ-1 (red), and DAPI (blue) in the 8-day in vitro primary cortical neurons. Merged bright field (100X) and immunostained (100X) images indicated that GLP-1R is mostly distributed in neuronal bodies but also exist in both axons and dendrites. (D) GLP-1or (E) EX-4 pretreated cortical neurons were continually treated with 100 nM GLP-1 or EX-4 after an oxidative insult and neuronal viability was measured at 0, 6, 12, 24 hr time points. Neuronal viability of ligand administrated neurons (GLP-1:~82%, EX-4:~67%) was approximately 20% higher than the menadione-treated group (GLP-1~65%, EX-4:~48%) 24-hour after menadione-induced oxidative insults. (M±SE; * p<0.05, ** p< 0.01, *** p< 0.001; compared to the 24-hr value of the menadione alone group, n=6).
    Glp 1r, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Activation of GLP-1 Receptor Enhances Neuronal Base Excision Repair via PI3K-AKT-Induced Expression of Apurinic/Apyrimidinic Endonuclease 1"

    Article Title: Activation of GLP-1 Receptor Enhances Neuronal Base Excision Repair via PI3K-AKT-Induced Expression of Apurinic/Apyrimidinic Endonuclease 1

    Journal: Theranostics

    doi: 10.7150/thno.15993

    Activation of cortical neuron expressed GLP-1 receptor (GLP-1R) protected cortical neurons from oxidative insults. (A) mRNA and (B) protein expressions of GLP-1R were detected in the 8-day in vitro primary cortical neurons. (C) Immunofluorescence staining of GLP-1R (green), TUJ-1 (red), and DAPI (blue) in the 8-day in vitro primary cortical neurons. Merged bright field (100X) and immunostained (100X) images indicated that GLP-1R is mostly distributed in neuronal bodies but also exist in both axons and dendrites. (D) GLP-1or (E) EX-4 pretreated cortical neurons were continually treated with 100 nM GLP-1 or EX-4 after an oxidative insult and neuronal viability was measured at 0, 6, 12, 24 hr time points. Neuronal viability of ligand administrated neurons (GLP-1:~82%, EX-4:~67%) was approximately 20% higher than the menadione-treated group (GLP-1~65%, EX-4:~48%) 24-hour after menadione-induced oxidative insults. (M±SE; * p<0.05, ** p< 0.01, *** p< 0.001; compared to the 24-hr value of the menadione alone group, n=6).
    Figure Legend Snippet: Activation of cortical neuron expressed GLP-1 receptor (GLP-1R) protected cortical neurons from oxidative insults. (A) mRNA and (B) protein expressions of GLP-1R were detected in the 8-day in vitro primary cortical neurons. (C) Immunofluorescence staining of GLP-1R (green), TUJ-1 (red), and DAPI (blue) in the 8-day in vitro primary cortical neurons. Merged bright field (100X) and immunostained (100X) images indicated that GLP-1R is mostly distributed in neuronal bodies but also exist in both axons and dendrites. (D) GLP-1or (E) EX-4 pretreated cortical neurons were continually treated with 100 nM GLP-1 or EX-4 after an oxidative insult and neuronal viability was measured at 0, 6, 12, 24 hr time points. Neuronal viability of ligand administrated neurons (GLP-1:~82%, EX-4:~67%) was approximately 20% higher than the menadione-treated group (GLP-1~65%, EX-4:~48%) 24-hour after menadione-induced oxidative insults. (M±SE; * p<0.05, ** p< 0.01, *** p< 0.001; compared to the 24-hr value of the menadione alone group, n=6).

    Techniques Used: Activation Assay, In Vitro, Immunofluorescence, Staining

    The downstream PI3K-AKT signaling axis of GLP-1R is the major pathway that regulates expression of APE1. (A) Western blot analyses of pAKT, pERK1/2, pCREB, APE1, and actin levels in neuronal cultures treated with 100 nM of GLP-1(100nM), GLP-1 plus MEK inhibitors U0126, or GLP-1 plus PI3K inhibitor LY294002. (B) LY294002 specifically inhibited GLP-1-induced AKT phosphorylation. (C) U0126 specifically inhibited GLP-1-induced pERK1/2 phosphorylation. (D) pCREB levels and (E) APE1 were specifically inhibited by LY294002 but not U0126. The results suggested that PI3K-AKT-CREB is the predominant downstream signaling pathway of GLP-1R elevating APE1 expression. (M±SE; *p< 0.05; ** p< 0.01; ***p<0.001; compared to the value of control group, n=4).
    Figure Legend Snippet: The downstream PI3K-AKT signaling axis of GLP-1R is the major pathway that regulates expression of APE1. (A) Western blot analyses of pAKT, pERK1/2, pCREB, APE1, and actin levels in neuronal cultures treated with 100 nM of GLP-1(100nM), GLP-1 plus MEK inhibitors U0126, or GLP-1 plus PI3K inhibitor LY294002. (B) LY294002 specifically inhibited GLP-1-induced AKT phosphorylation. (C) U0126 specifically inhibited GLP-1-induced pERK1/2 phosphorylation. (D) pCREB levels and (E) APE1 were specifically inhibited by LY294002 but not U0126. The results suggested that PI3K-AKT-CREB is the predominant downstream signaling pathway of GLP-1R elevating APE1 expression. (M±SE; *p< 0.05; ** p< 0.01; ***p<0.001; compared to the value of control group, n=4).

    Techniques Used: Expressing, Western Blot

    This schematic diagram illustrates the mechanisms by which activated GLP-1R elevate repair of oxidative DNA damage and increase neuronal survival. The expression GLP-1 and its receptors occurs in the central nervous system and is involved in neuronal protection. Two major signaling pathways are triggered, including PKA-Erk (dotted-line arrow) and PI3K-AKT (filled-line arrow), when GLP-1R is activated. Results of our study suggested that PI3K-AKT is the key downstream signaling pathway regulating APE1 expression, elevation DNA repair efficiency, and increasing neuronal survival after oxidative insults. (AC: adenylyl cyclase; cAMP: cyclic adenosine monophosphate; PKA: protein kinase A; MEK: mitogen-activated protein kinase kinase; ERK: mitogen-activated protein kinase; PI3K: phosphatidylinositide 3-kinase; AKT: protein kinase B; CREB: cAMP response element binding protein).
    Figure Legend Snippet: This schematic diagram illustrates the mechanisms by which activated GLP-1R elevate repair of oxidative DNA damage and increase neuronal survival. The expression GLP-1 and its receptors occurs in the central nervous system and is involved in neuronal protection. Two major signaling pathways are triggered, including PKA-Erk (dotted-line arrow) and PI3K-AKT (filled-line arrow), when GLP-1R is activated. Results of our study suggested that PI3K-AKT is the key downstream signaling pathway regulating APE1 expression, elevation DNA repair efficiency, and increasing neuronal survival after oxidative insults. (AC: adenylyl cyclase; cAMP: cyclic adenosine monophosphate; PKA: protein kinase A; MEK: mitogen-activated protein kinase kinase; ERK: mitogen-activated protein kinase; PI3K: phosphatidylinositide 3-kinase; AKT: protein kinase B; CREB: cAMP response element binding protein).

    Techniques Used: Expressing, Binding Assay

    calcium modulated potassium channel bk  (Alomone Labs)


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    Alomone Labs calcium modulated potassium channel bk
    Calcium Modulated Potassium Channel Bk, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit polyclonal  (Alomone Labs)


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    Alomone Labs rabbit polyclonal
    (A) Whole-cell currents recorded from an apical outer hair cell in response to voltage steps (100 ms in duration) from −131 mV to 49 mV in 10 mV increments (with an interpulse holding potential of −81 mV) before (black line) and in the presence (grey line) of bath application of 100 nM IBTX, a specific blocker of BK channels, show little IBTX-sensitive currents. (For clarity only some of the traces are shown.) (B) No differences in voltage-gated currents were observed in response to IBTX application across all test potentials examined in apical outer hair cells. (C) Bar plot comparing the fractional contribution of IBTX- and linopirdine-sensitive currents to apical outer hair cells at 49 mV show that apical outer hair cells express predominantly linopirdine-sensitive KCNQ4 currents and little or no BK currents. Confocal micrograph (1 optical section) of an apical cochlear turn immunostained with a monoclonal antibody against the BK channel (red, D and F) shows immunoreactivity in the region corresponding to the neck of the inner hair cells (indicated with an open arrowhead) but no immunoreactivity in the region associated with the outer hair cells (indicated by the solid arrowheads), immunostained with a <t>polyclonal</t> antibody against prestin (green, E and F). Scale bar equals 10 µm.
    Rabbit Polyclonal, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "BK Channels Mediate Cholinergic Inhibition of High Frequency Cochlear Hair Cells"

    Article Title: BK Channels Mediate Cholinergic Inhibition of High Frequency Cochlear Hair Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0013836

    (A) Whole-cell currents recorded from an apical outer hair cell in response to voltage steps (100 ms in duration) from −131 mV to 49 mV in 10 mV increments (with an interpulse holding potential of −81 mV) before (black line) and in the presence (grey line) of bath application of 100 nM IBTX, a specific blocker of BK channels, show little IBTX-sensitive currents. (For clarity only some of the traces are shown.) (B) No differences in voltage-gated currents were observed in response to IBTX application across all test potentials examined in apical outer hair cells. (C) Bar plot comparing the fractional contribution of IBTX- and linopirdine-sensitive currents to apical outer hair cells at 49 mV show that apical outer hair cells express predominantly linopirdine-sensitive KCNQ4 currents and little or no BK currents. Confocal micrograph (1 optical section) of an apical cochlear turn immunostained with a monoclonal antibody against the BK channel (red, D and F) shows immunoreactivity in the region corresponding to the neck of the inner hair cells (indicated with an open arrowhead) but no immunoreactivity in the region associated with the outer hair cells (indicated by the solid arrowheads), immunostained with a polyclonal antibody against prestin (green, E and F). Scale bar equals 10 µm.
    Figure Legend Snippet: (A) Whole-cell currents recorded from an apical outer hair cell in response to voltage steps (100 ms in duration) from −131 mV to 49 mV in 10 mV increments (with an interpulse holding potential of −81 mV) before (black line) and in the presence (grey line) of bath application of 100 nM IBTX, a specific blocker of BK channels, show little IBTX-sensitive currents. (For clarity only some of the traces are shown.) (B) No differences in voltage-gated currents were observed in response to IBTX application across all test potentials examined in apical outer hair cells. (C) Bar plot comparing the fractional contribution of IBTX- and linopirdine-sensitive currents to apical outer hair cells at 49 mV show that apical outer hair cells express predominantly linopirdine-sensitive KCNQ4 currents and little or no BK currents. Confocal micrograph (1 optical section) of an apical cochlear turn immunostained with a monoclonal antibody against the BK channel (red, D and F) shows immunoreactivity in the region corresponding to the neck of the inner hair cells (indicated with an open arrowhead) but no immunoreactivity in the region associated with the outer hair cells (indicated by the solid arrowheads), immunostained with a polyclonal antibody against prestin (green, E and F). Scale bar equals 10 µm.

    Techniques Used:

    (A) Whole-cell currents recorded from a basal outer hair cell in response to voltage steps (100 ms in duration) from −131 mV to 49 mV in 10 mV increments (with an interpulse holding potential of −81 mV) before (black line) and in the presence of either 100 µM linopirdine (red trace) or both 100 µM linopirdine and 100 nM IBTX (blue trace). (For clarity only 2 potentials, −131 mV and 49 mV are shown.) (B) At depolarizing membrane potentials, both linopirdine-sensitive KCNQ4 and IBTX-sensitive currents contribute to the voltage gated currents in basal outer hair cells. (C) Bar plot comparing the percent block of I Max at 49 mV in apical and basal OHCs in the presence of 100 µM linopirdine (black bars) or both 100 µM linopirdine and 100 nM IBTX (grey bars). (D) Confocal micrograph (1 optical section) of a basal cochlear turn immunostained with a monoclonal antibody against the BK channel (red, D and F) shows immunoreactivity in the region corresponding to the neck of the inner hair cells (indicated with an open arrowhead) as well as immunoreactivity in the outer hair cells (indicated by the solid arrowheads), immunostained with a polyclonal antibody against prestin (green, E and F). Scale bar equals 10 µm.
    Figure Legend Snippet: (A) Whole-cell currents recorded from a basal outer hair cell in response to voltage steps (100 ms in duration) from −131 mV to 49 mV in 10 mV increments (with an interpulse holding potential of −81 mV) before (black line) and in the presence of either 100 µM linopirdine (red trace) or both 100 µM linopirdine and 100 nM IBTX (blue trace). (For clarity only 2 potentials, −131 mV and 49 mV are shown.) (B) At depolarizing membrane potentials, both linopirdine-sensitive KCNQ4 and IBTX-sensitive currents contribute to the voltage gated currents in basal outer hair cells. (C) Bar plot comparing the percent block of I Max at 49 mV in apical and basal OHCs in the presence of 100 µM linopirdine (black bars) or both 100 µM linopirdine and 100 nM IBTX (grey bars). (D) Confocal micrograph (1 optical section) of a basal cochlear turn immunostained with a monoclonal antibody against the BK channel (red, D and F) shows immunoreactivity in the region corresponding to the neck of the inner hair cells (indicated with an open arrowhead) as well as immunoreactivity in the outer hair cells (indicated by the solid arrowheads), immunostained with a polyclonal antibody against prestin (green, E and F). Scale bar equals 10 µm.

    Techniques Used: Blocking Assay

    3D renderings of confocal z-stacks of apical (A), middle (B), and basal (C) cochlear turns immunostained with a monoclonal antibody against the BK channel (red) and a polyclonal antibody against synapsin (green) to label the efferent presynaptic terminals show that BK channel immunoreactivity in the three rows of outer hair cells (when present) is associated with efferent terminals. (D) Moreover, the size of BK channel immunopuncta increases from apical to middle and basal turns, paralleling an increase in size and likely number of efferent terminals. Data are presented as box plots representing the median (box interior), the 25th and 75th percentile (box boundaries), the 10th and 90th percentile (whiskers), and the 5th and 95th percentile (dots). (E) 3D renderings of confocal z-stacks of a middle cochlear turn immunostained with a polyclonal antibody against the BK channel (red) and a monoclonal antibody against the NaK-ATPase α3 (green) to label the efferent presynaptic terminal membrane shows adjacent but not co localized expression of the BK channel with the presynaptic efferent terminal membrane. The location of the three rows of outer hair cells are indicated (solid arrowheads). Grid dimensions equal 10 µm.
    Figure Legend Snippet: 3D renderings of confocal z-stacks of apical (A), middle (B), and basal (C) cochlear turns immunostained with a monoclonal antibody against the BK channel (red) and a polyclonal antibody against synapsin (green) to label the efferent presynaptic terminals show that BK channel immunoreactivity in the three rows of outer hair cells (when present) is associated with efferent terminals. (D) Moreover, the size of BK channel immunopuncta increases from apical to middle and basal turns, paralleling an increase in size and likely number of efferent terminals. Data are presented as box plots representing the median (box interior), the 25th and 75th percentile (box boundaries), the 10th and 90th percentile (whiskers), and the 5th and 95th percentile (dots). (E) 3D renderings of confocal z-stacks of a middle cochlear turn immunostained with a polyclonal antibody against the BK channel (red) and a monoclonal antibody against the NaK-ATPase α3 (green) to label the efferent presynaptic terminal membrane shows adjacent but not co localized expression of the BK channel with the presynaptic efferent terminal membrane. The location of the three rows of outer hair cells are indicated (solid arrowheads). Grid dimensions equal 10 µm.

    Techniques Used: Expressing

    3D renderings of confocal z-stacks of apical (A), middle (B), and basal (C) cochlear turns immunostained with a polyclonal antibody against the SK2 channel (green) show expression of the SK2 channel in the three rows of outer hair cells in all regions. Confocal z-stacks (23 optical sections) of basal cochlear turns immunostained with a polyclonal antibody against the SK2 channel (green, D) and monoclonal antibody against the BK channel (red, E) show colocalized expression (F) in the three rows of outer hair cells, further suggesting the localization of BK channels to the postsynaptic outer hair cell membrane. (Examination of single optical sections also shows colocalization of the SK2 and BK channel.) The size of the SK2 channel immunopuncta increases from apical to middle turns and then decreases in basal turns. Data are presented as box plots representing the median (box interior), the 25 th and 75 th percentile (box boundaries), the 10 th and 90 th percentile (whiskers), and the 5 th and 95 th percentile (dots). (G) 3D renderings of confocal z-stacks of basal cochlear turns immunostained with a polyclonal antibody against the SK2 channel (green), a monoclonal antibody against the BK channel (red), and a goat polyclonal antibody against synapsin (blue) confirm the colocalized expression of SK2 and BK channels in association with efferent terminals (H) in the three rows of outer hair cells. In basal turns, BK and SK2 channel immunoreactivity are colocalized. Grid dimensions equal 10 µm for top and bottom panels. Scale bar equals 10 µm for middle panels.
    Figure Legend Snippet: 3D renderings of confocal z-stacks of apical (A), middle (B), and basal (C) cochlear turns immunostained with a polyclonal antibody against the SK2 channel (green) show expression of the SK2 channel in the three rows of outer hair cells in all regions. Confocal z-stacks (23 optical sections) of basal cochlear turns immunostained with a polyclonal antibody against the SK2 channel (green, D) and monoclonal antibody against the BK channel (red, E) show colocalized expression (F) in the three rows of outer hair cells, further suggesting the localization of BK channels to the postsynaptic outer hair cell membrane. (Examination of single optical sections also shows colocalization of the SK2 and BK channel.) The size of the SK2 channel immunopuncta increases from apical to middle turns and then decreases in basal turns. Data are presented as box plots representing the median (box interior), the 25 th and 75 th percentile (box boundaries), the 10 th and 90 th percentile (whiskers), and the 5 th and 95 th percentile (dots). (G) 3D renderings of confocal z-stacks of basal cochlear turns immunostained with a polyclonal antibody against the SK2 channel (green), a monoclonal antibody against the BK channel (red), and a goat polyclonal antibody against synapsin (blue) confirm the colocalized expression of SK2 and BK channels in association with efferent terminals (H) in the three rows of outer hair cells. In basal turns, BK and SK2 channel immunoreactivity are colocalized. Grid dimensions equal 10 µm for top and bottom panels. Scale bar equals 10 µm for middle panels.

    Techniques Used: Expressing

    bk ca  (Alomone Labs)


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    Structured Review

    Alomone Labs bk ca
    Bk Ca, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bk ca/product/Alomone Labs
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bk ca - by Bioz Stars, 2023-02
    95/100 stars

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