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ip3r antagonist  (MedChemExpress)


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    MedChemExpress ip3r antagonist
    Ip3r Antagonist, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 110 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ip3r+antagonist/10__7554_slash_elife__97373__3-408-13-19?v=MedChemExpress
    Average 95 stars, based on 110 article reviews
    ip3r antagonist - by Bioz Stars, 2026-07
    95/100 stars

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    Expression of markers involved in Ca 2+ signaling in RYR2 –/– -iPSC-CMs compared to Ctrl-iPSC-CMs. (A) Reverse transcription-PCR analyses showing mRNA expression of transcripts for Ca 2+ handling-related genes ( RYR2, IP3R1, IP3R2 , and CACNA1C ), genes encoding sarcomeric proteins ( TNNT2 and ACTN2 ), and the housekeeping gene GAPDH in Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 6 and RYR2 –/– -A3: n = 6 different differentiation experiments). M: DNA molecular-weight size marker. (B) Western blot showing expression of Ca 2+ handling-associated proteins <t>(IP3R,</t> SERCA2A, and NCX1) in both Ctrl- and A3 RYR2 –/– -iPSC-CMs. (C–E) Scatter dot plot showing protein levels of IP3R (C) , SERCA2A (D) , and NCX1 (E) normalized to GAPDH between Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 4 and A3 RYR2 –/– : n = 5 different differentiation experiments). (F) Representative immunostaining of Ctrl- and RYR2 –/– -iPSC-CMs for IP3R (green) and α-actinin (red). Cells were counterstained with DAPI (blue). Scale bar, 100 μm.
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    Expression of markers involved in Ca 2+ signaling in RYR2 –/– -iPSC-CMs compared to Ctrl-iPSC-CMs. (A) Reverse transcription-PCR analyses showing mRNA expression of transcripts for Ca 2+ handling-related genes ( RYR2, IP3R1, IP3R2 , and CACNA1C ), genes encoding sarcomeric proteins ( TNNT2 and ACTN2 ), and the housekeeping gene GAPDH in Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 6 and RYR2 –/– -A3: n = 6 different differentiation experiments). M: DNA molecular-weight size marker. (B) Western blot showing expression of Ca 2+ handling-associated proteins <t>(IP3R,</t> SERCA2A, and NCX1) in both Ctrl- and A3 RYR2 –/– -iPSC-CMs. (C–E) Scatter dot plot showing protein levels of IP3R (C) , SERCA2A (D) , and NCX1 (E) normalized to GAPDH between Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 4 and A3 RYR2 –/– : n = 5 different differentiation experiments). (F) Representative immunostaining of Ctrl- and RYR2 –/– -iPSC-CMs for IP3R (green) and α-actinin (red). Cells were counterstained with DAPI (blue). Scale bar, 100 μm.
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    ip3r antagonist xestospongin c  (Cayman Chemical)
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    Expression of markers involved in Ca 2+ signaling in RYR2 –/– -iPSC-CMs compared to Ctrl-iPSC-CMs. (A) Reverse transcription-PCR analyses showing mRNA expression of transcripts for Ca 2+ handling-related genes ( RYR2, IP3R1, IP3R2 , and CACNA1C ), genes encoding sarcomeric proteins ( TNNT2 and ACTN2 ), and the housekeeping gene GAPDH in Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 6 and RYR2 –/– -A3: n = 6 different differentiation experiments). M: DNA molecular-weight size marker. (B) Western blot showing expression of Ca 2+ handling-associated proteins <t>(IP3R,</t> SERCA2A, and NCX1) in both Ctrl- and A3 RYR2 –/– -iPSC-CMs. (C–E) Scatter dot plot showing protein levels of IP3R (C) , SERCA2A (D) , and NCX1 (E) normalized to GAPDH between Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 4 and A3 RYR2 –/– : n = 5 different differentiation experiments). (F) Representative immunostaining of Ctrl- and RYR2 –/– -iPSC-CMs for IP3R (green) and α-actinin (red). Cells were counterstained with DAPI (blue). Scale bar, 100 μm.
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    Expression of markers involved in Ca 2+ signaling in RYR2 –/– -iPSC-CMs compared to Ctrl-iPSC-CMs. (A) Reverse transcription-PCR analyses showing mRNA expression of transcripts for Ca 2+ handling-related genes ( RYR2, IP3R1, IP3R2 , and CACNA1C ), genes encoding sarcomeric proteins ( TNNT2 and ACTN2 ), and the housekeeping gene GAPDH in Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 6 and RYR2 –/– -A3: n = 6 different differentiation experiments). M: DNA molecular-weight size marker. (B) Western blot showing expression of Ca 2+ handling-associated proteins (IP3R, SERCA2A, and NCX1) in both Ctrl- and A3 RYR2 –/– -iPSC-CMs. (C–E) Scatter dot plot showing protein levels of IP3R (C) , SERCA2A (D) , and NCX1 (E) normalized to GAPDH between Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 4 and A3 RYR2 –/– : n = 5 different differentiation experiments). (F) Representative immunostaining of Ctrl- and RYR2 –/– -iPSC-CMs for IP3R (green) and α-actinin (red). Cells were counterstained with DAPI (blue). Scale bar, 100 μm.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: IP3R-Mediated Compensatory Mechanism for Calcium Handling in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes With Cardiac Ryanodine Receptor Deficiency

    doi: 10.3389/fcell.2020.00772

    Figure Lengend Snippet: Expression of markers involved in Ca 2+ signaling in RYR2 –/– -iPSC-CMs compared to Ctrl-iPSC-CMs. (A) Reverse transcription-PCR analyses showing mRNA expression of transcripts for Ca 2+ handling-related genes ( RYR2, IP3R1, IP3R2 , and CACNA1C ), genes encoding sarcomeric proteins ( TNNT2 and ACTN2 ), and the housekeeping gene GAPDH in Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 6 and RYR2 –/– -A3: n = 6 different differentiation experiments). M: DNA molecular-weight size marker. (B) Western blot showing expression of Ca 2+ handling-associated proteins (IP3R, SERCA2A, and NCX1) in both Ctrl- and A3 RYR2 –/– -iPSC-CMs. (C–E) Scatter dot plot showing protein levels of IP3R (C) , SERCA2A (D) , and NCX1 (E) normalized to GAPDH between Ctrl- and A3 RYR2 –/– -iPSC-CMs (Ctrl: n = 4 and A3 RYR2 –/– : n = 5 different differentiation experiments). (F) Representative immunostaining of Ctrl- and RYR2 –/– -iPSC-CMs for IP3R (green) and α-actinin (red). Cells were counterstained with DAPI (blue). Scale bar, 100 μm.

    Article Snippet: To investigate the role of IP3R-mediated Ca 2+ release in Ca 2+ handling of iPSC-CMs, spontaneous Ca 2+ transients were recorded before and after the application of the IP3R antagonists 2-aminoethoxydiphenyl borate (2-APB, 20 μM; Tocris) and Xestospongin C (XeC, 1 μM; abcam).

    Techniques: Expressing, Reverse Transcription, Molecular Weight, Marker, Western Blot, Immunostaining

    Contributions of IP3R-mediated Ca 2+ release to spontaneous Ca 2+ transients in Ctrl- and RYR2 –/– -iPSC-CMs. (A,B) Representative cytosolic Ca 2+ dynamics in Ctrl- (A) and RYR2 –/– -iPSC-CMs (B) before and after the addition of IP3R antagonist 2-APB (20 μM), and after the washout of the drug. (C) Pie charts depict the percentage of cells maintaining Ca 2+ transients after the treatment with 2-APB for 500 s. (D,E) Changes of Ca 2+ transient amplitude (D) and frequency (E) after the treatment and the following removal of 2-APB, which were normalized to those from the same cell under the basal condition (Ctrl: n = 13 cells from three differentiation experiments; A3 RYR2 –/– : n = 14 cells from three differentiation experiments). (F,G) Representative cytosolic Ca 2+ dynamics in Ctrl- (F) and RYR2 –/– -iPSC-CMs (G) before and after the addition of IP3R inhibitor Xestospongin C (XeC;1 μM), and after the washout of the drug. (H) Pie charts depict the percentage of cells maintaining Ca 2+ transients after the treatment with XeC for 200 s. (I,J) Changes of Ca 2+ transient amplitude (I) and frequency (J) after the treatment and following the washout of XeC, which were normalized to those from the same cell under the basal condition (Ctrl: n = 14 cells from three differentiation experiments; A3 RYR2 –/– : n = 13 cells from three differentiation experiments; A5 RYR2 –/– : n = 10 cells from two differentiation experiments). * P < 0.05; ** P < 0.01; *** P < 0.001;**** P < 0.0001 by using the one-way ANOVA with the Dunnett’s multiple comparison test.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: IP3R-Mediated Compensatory Mechanism for Calcium Handling in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes With Cardiac Ryanodine Receptor Deficiency

    doi: 10.3389/fcell.2020.00772

    Figure Lengend Snippet: Contributions of IP3R-mediated Ca 2+ release to spontaneous Ca 2+ transients in Ctrl- and RYR2 –/– -iPSC-CMs. (A,B) Representative cytosolic Ca 2+ dynamics in Ctrl- (A) and RYR2 –/– -iPSC-CMs (B) before and after the addition of IP3R antagonist 2-APB (20 μM), and after the washout of the drug. (C) Pie charts depict the percentage of cells maintaining Ca 2+ transients after the treatment with 2-APB for 500 s. (D,E) Changes of Ca 2+ transient amplitude (D) and frequency (E) after the treatment and the following removal of 2-APB, which were normalized to those from the same cell under the basal condition (Ctrl: n = 13 cells from three differentiation experiments; A3 RYR2 –/– : n = 14 cells from three differentiation experiments). (F,G) Representative cytosolic Ca 2+ dynamics in Ctrl- (F) and RYR2 –/– -iPSC-CMs (G) before and after the addition of IP3R inhibitor Xestospongin C (XeC;1 μM), and after the washout of the drug. (H) Pie charts depict the percentage of cells maintaining Ca 2+ transients after the treatment with XeC for 200 s. (I,J) Changes of Ca 2+ transient amplitude (I) and frequency (J) after the treatment and following the washout of XeC, which were normalized to those from the same cell under the basal condition (Ctrl: n = 14 cells from three differentiation experiments; A3 RYR2 –/– : n = 13 cells from three differentiation experiments; A5 RYR2 –/– : n = 10 cells from two differentiation experiments). * P < 0.05; ** P < 0.01; *** P < 0.001;**** P < 0.0001 by using the one-way ANOVA with the Dunnett’s multiple comparison test.

    Article Snippet: To investigate the role of IP3R-mediated Ca 2+ release in Ca 2+ handling of iPSC-CMs, spontaneous Ca 2+ transients were recorded before and after the application of the IP3R antagonists 2-aminoethoxydiphenyl borate (2-APB, 20 μM; Tocris) and Xestospongin C (XeC, 1 μM; abcam).

    Techniques: Comparison