p2x7  (Alomone Labs)


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    Structured Review

    Alomone Labs p2x7
    <t>P2X7</t> receptor activity occurs exclusively in HUVEC under atheroprone flow. Representative single cell ATP-induced calcium responses in atheroprotected ( A ) or atheroprone ( B, C ) flow conditioned HUVEC after thapsigargin pre-treatment ± the P2X7 inhibitor 10 µM A438079 (P2X7i) or siRNA control and P2X7 knockdown ( C ) and analysed by measuring the average area under the curve ( n = 4, 175 cells per donor, * indicates P ≤ 0.05 using a paired t -test). Values are mean ± S.E.M.
    P2x7, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 10 article reviews
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    Images

    1) Product Images from "Atheroprone flow activates inflammation via endothelial ATP-dependent P2X7-p38 signalling"

    Article Title: Atheroprone flow activates inflammation via endothelial ATP-dependent P2X7-p38 signalling

    Journal: Cardiovascular Research

    doi: 10.1093/cvr/cvx213

    P2X7 receptor activity occurs exclusively in HUVEC under atheroprone flow. Representative single cell ATP-induced calcium responses in atheroprotected ( A ) or atheroprone ( B, C ) flow conditioned HUVEC after thapsigargin pre-treatment ± the P2X7 inhibitor 10 µM A438079 (P2X7i) or siRNA control and P2X7 knockdown ( C ) and analysed by measuring the average area under the curve ( n = 4, 175 cells per donor, * indicates P ≤ 0.05 using a paired t -test). Values are mean ± S.E.M.
    Figure Legend Snippet: P2X7 receptor activity occurs exclusively in HUVEC under atheroprone flow. Representative single cell ATP-induced calcium responses in atheroprotected ( A ) or atheroprone ( B, C ) flow conditioned HUVEC after thapsigargin pre-treatment ± the P2X7 inhibitor 10 µM A438079 (P2X7i) or siRNA control and P2X7 knockdown ( C ) and analysed by measuring the average area under the curve ( n = 4, 175 cells per donor, * indicates P ≤ 0.05 using a paired t -test). Values are mean ± S.E.M.

    Techniques Used: Activity Assay

    Expression of ATP-gated P2X7 receptors is enhanced under atheroprone flow. ( A ) Western blot and densitometry of P2X7 in flow conditioned HUVEC using the ibidi flow system ( n = 6, ** indicates P ≤ 0.01 using a paired t -test). P2X7 is shown by an arrow, validated by P2X7 knockdown, shown in Supplementary material online , Figure 4 B. ( B ) Western blot and densitometry of P2X7 in flow conditioned HUVEC using the orbital shaker system ( n = 4, ** indicates P ≤ 0.01 using a paired t -test). ( C ) Representative en face immunostaining for P2X7 (red) on wildtype C57BL/6 mice at atheroprotective (outer curvature) and atheroprone (inner curvature) regions of the aorta (scale = 25 µm). Endothelial cells were identified by staining with CD31 (green) and cell nuclei were stained using TO-PRO (blue). P2X7 expression was analysed by measuring the relative fluorescent intensity at sites protected or prone to atherosclerosis. Surface expression was measured by measuring P2X7 fluorescence at sites co-localized with the endothelial cell surface marker CD31. Relative fluorescent intensities for P2X7 were corrected against the relative fluorescent intensity of IgG performed on the descending aorta ( n = 5, * indicates P ≤ 0.05 and *** indicates P ≤ 0.001 using a paired t -test). Values are mean ± S.E.M.
    Figure Legend Snippet: Expression of ATP-gated P2X7 receptors is enhanced under atheroprone flow. ( A ) Western blot and densitometry of P2X7 in flow conditioned HUVEC using the ibidi flow system ( n = 6, ** indicates P ≤ 0.01 using a paired t -test). P2X7 is shown by an arrow, validated by P2X7 knockdown, shown in Supplementary material online , Figure 4 B. ( B ) Western blot and densitometry of P2X7 in flow conditioned HUVEC using the orbital shaker system ( n = 4, ** indicates P ≤ 0.01 using a paired t -test). ( C ) Representative en face immunostaining for P2X7 (red) on wildtype C57BL/6 mice at atheroprotective (outer curvature) and atheroprone (inner curvature) regions of the aorta (scale = 25 µm). Endothelial cells were identified by staining with CD31 (green) and cell nuclei were stained using TO-PRO (blue). P2X7 expression was analysed by measuring the relative fluorescent intensity at sites protected or prone to atherosclerosis. Surface expression was measured by measuring P2X7 fluorescence at sites co-localized with the endothelial cell surface marker CD31. Relative fluorescent intensities for P2X7 were corrected against the relative fluorescent intensity of IgG performed on the descending aorta ( n = 5, * indicates P ≤ 0.05 and *** indicates P ≤ 0.001 using a paired t -test). Values are mean ± S.E.M.

    Techniques Used: Expressing, Western Blot, Immunostaining, Mouse Assay, Staining, Fluorescence, Marker

    P2X7 regulates E-selectin expression at sites susceptible to atherosclerosis in vivo . Representative en face immunostaining for E-selectin (red) on wildtype or P2X7 −/− BALB/c mice at atheroprotective (outer curvature) and atheroprone (inner curvature) sites of the aorta ( n = 4–5) (scale = 25 µm). Endothelial cells were identified by staining with CD31 (green) and cell nuclei were stained using TO-PRO (blue). E-selectin expression was analysed by measuring the relative fluorescent intensity at sites of protected or prone to atherosclerosis ( n = 4–5, * indicates P ≤ 0.05, ** indicates P ≤ 0.01 and *** indicates P ≤ 0.001 using a two-way ANOVA). Relative fluorescent intensities for P2X7 were corrected against the relative fluorescent intensity of IgG. Values are mean ± S.E.M.
    Figure Legend Snippet: P2X7 regulates E-selectin expression at sites susceptible to atherosclerosis in vivo . Representative en face immunostaining for E-selectin (red) on wildtype or P2X7 −/− BALB/c mice at atheroprotective (outer curvature) and atheroprone (inner curvature) sites of the aorta ( n = 4–5) (scale = 25 µm). Endothelial cells were identified by staining with CD31 (green) and cell nuclei were stained using TO-PRO (blue). E-selectin expression was analysed by measuring the relative fluorescent intensity at sites of protected or prone to atherosclerosis ( n = 4–5, * indicates P ≤ 0.05, ** indicates P ≤ 0.01 and *** indicates P ≤ 0.001 using a two-way ANOVA). Relative fluorescent intensities for P2X7 were corrected against the relative fluorescent intensity of IgG. Values are mean ± S.E.M.

    Techniques Used: Expressing, In Vivo, Immunostaining, Mouse Assay, Staining

    Atheroprone flow mediated inflammatory signalling is regulated by P2X7 responses. qPCR analysis of E-selectin ( A ) and IL-8 ( B ) in HUVEC conditioned with atheroprotective or atheroprone flow using the ibidi system ± the P2X7 inhibitor 10 µM A438079 (P2X7i) ( n = 5, * indicates P ≤ 0.05 using a two-way ANOVA). ( C ) IL-8 release measured by ELISA in the supernatant of HUVEC conditioned under atheroprotective or atheroprone flow using the ibidi system ± the P2X7 inhibitor 10 µM A438079 (P2X7i) ( n = 9, * indicates P ≤ 0.05, *** indicates p =
    Figure Legend Snippet: Atheroprone flow mediated inflammatory signalling is regulated by P2X7 responses. qPCR analysis of E-selectin ( A ) and IL-8 ( B ) in HUVEC conditioned with atheroprotective or atheroprone flow using the ibidi system ± the P2X7 inhibitor 10 µM A438079 (P2X7i) ( n = 5, * indicates P ≤ 0.05 using a two-way ANOVA). ( C ) IL-8 release measured by ELISA in the supernatant of HUVEC conditioned under atheroprotective or atheroprone flow using the ibidi system ± the P2X7 inhibitor 10 µM A438079 (P2X7i) ( n = 9, * indicates P ≤ 0.05, *** indicates p =

    Techniques Used: Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    2) Product Images from "Transient P2X7 Receptor Antagonism Produces Lasting Reductions in Spontaneous Seizures and Gliosis in Experimental Temporal Lobe Epilepsy"

    Article Title: Transient P2X7 Receptor Antagonism Produces Lasting Reductions in Spontaneous Seizures and Gliosis in Experimental Temporal Lobe Epilepsy

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4009-15.2016

    Increased expression of P2X7R in experimental and human epilepsy. A , Photomicrograph showing EGFP immunofluorescence in the hippocampus of a control P2rx7-EGFP mouse. Scale bar, 125 μm. Panels below show higher-power images of CA1 (i) and DG (ii) hippocampal subfields from the P2rx7-EGFP control animal. Scale bar, 50 μm. Note that the constitutive EGFP appears mainly in cells of the DG. B , Photomicrograph showing EGFP immunofluorescence in the hippocampus of an epileptic P2rx7-EGFP mouse 14 d after status epilepticus. Scale bar, 125 μm. Panels below show higher-power images of CA1 (i) and DG (ii) hippocampal subfields from the P2rx7-EGFP epileptic animal. Scale bar, 50 μm. C , Double-stained confocal immunofluorescence images showing EGFP (green, GFP) and neuronal marker NeuN (red), in the CA1 and DG subfields from epileptic P2rx7-EGFP mice. Scale bar, 50 μm. D , Immunofluorescence staining showing EGFP (green, GFP) and microglia marker Iba1 (red) in the CA3 subfield of a P2rx7-EGFP epileptic mouse. Scale bar, 20 μm. Images are representative of data from n = 5 animals per group. E , Graph showing P2rx7 mRNA levels in the CA1, CA3, and DG subfields of control (Con) and epileptic (Epi) mice ( n = 9/group; ANOVA with Bonferroni test, * p
    Figure Legend Snippet: Increased expression of P2X7R in experimental and human epilepsy. A , Photomicrograph showing EGFP immunofluorescence in the hippocampus of a control P2rx7-EGFP mouse. Scale bar, 125 μm. Panels below show higher-power images of CA1 (i) and DG (ii) hippocampal subfields from the P2rx7-EGFP control animal. Scale bar, 50 μm. Note that the constitutive EGFP appears mainly in cells of the DG. B , Photomicrograph showing EGFP immunofluorescence in the hippocampus of an epileptic P2rx7-EGFP mouse 14 d after status epilepticus. Scale bar, 125 μm. Panels below show higher-power images of CA1 (i) and DG (ii) hippocampal subfields from the P2rx7-EGFP epileptic animal. Scale bar, 50 μm. C , Double-stained confocal immunofluorescence images showing EGFP (green, GFP) and neuronal marker NeuN (red), in the CA1 and DG subfields from epileptic P2rx7-EGFP mice. Scale bar, 50 μm. D , Immunofluorescence staining showing EGFP (green, GFP) and microglia marker Iba1 (red) in the CA3 subfield of a P2rx7-EGFP epileptic mouse. Scale bar, 20 μm. Images are representative of data from n = 5 animals per group. E , Graph showing P2rx7 mRNA levels in the CA1, CA3, and DG subfields of control (Con) and epileptic (Epi) mice ( n = 9/group; ANOVA with Bonferroni test, * p

    Techniques Used: Expressing, Immunofluorescence, Staining, Marker, Mouse Assay

    Decreased astrogliosis and microgliosis in JNJ-47965567-treated epileptic mice. A–D , Photomicrographs of representative Iba1 staining of the hippocampus from vehicle- (Veh) and JNJ-47965567 (JNJ)-treated epileptic mice showing field views ( A ) and 20× lens magnifications ( B–D ) of individual subfields from the same animal. Note, the decrease in the number of Iba1 + cells and the immunoreactivity in mice treated with the specific P2X7R inhibitor JNJ-47965567. E , Graph showing the quantification of Iba1 + microglia found in each hippocampal subfield of vehicle- and JNJ-47965567-treated mice killed 6 d after drug washout at the end of recordings ( n = 9/group; ANOVA with Bonferroni test, ** p
    Figure Legend Snippet: Decreased astrogliosis and microgliosis in JNJ-47965567-treated epileptic mice. A–D , Photomicrographs of representative Iba1 staining of the hippocampus from vehicle- (Veh) and JNJ-47965567 (JNJ)-treated epileptic mice showing field views ( A ) and 20× lens magnifications ( B–D ) of individual subfields from the same animal. Note, the decrease in the number of Iba1 + cells and the immunoreactivity in mice treated with the specific P2X7R inhibitor JNJ-47965567. E , Graph showing the quantification of Iba1 + microglia found in each hippocampal subfield of vehicle- and JNJ-47965567-treated mice killed 6 d after drug washout at the end of recordings ( n = 9/group; ANOVA with Bonferroni test, ** p

    Techniques Used: Mouse Assay, Staining

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    Alomone Labs rabbit polyclonal p2x7 c terminus antibody
    The N terminus is important for the sensitivity of P2X7 receptor activity to cholesterol depletion. A , amino acid sequence alignment of the N-terminal region of human P2X1, P2X2, and P2X7 receptors, with conserved amino acids highlighted in  gray , P2X1 aa20–23 and equivalent residues in P2X2  underlined , and the P2X7 residues Lys 17  and Val 18  in  red. B , time course of dye uptake mediated by the K17R/V18M mutant and wild type P2X7, alone, pretreated with MCD and loaded with cholesterol ( chol ), normalized to the untreated WT P2X7.  C , bar graph of the relative rate of dye uptake normalized to the untreated WT P2X7. Dye uptake mediated by the K17R/V18M mutant is not potentiated by MCD, but is inhibited by cholesterol loading (WT:  n  = 14 alone,  n  = 11 MCD,  n  = 3 cholesterol; mutants:  n  = 12 alone,  n  = 11 MCD,  n  = 3 cholesterol; *,  p
    Rabbit Polyclonal P2x7 C Terminus Antibody, 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/rabbit polyclonal p2x7 c terminus antibody/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
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    Alomone Labs nav1 5
    Human UhiPS cells differentiated into functional cardiomyocytes. A, Transcriptional profile of control hiPS cells derived from skin fibroblasts (control FhiPS-CMs) and from urine cells (control UhiPS-CMs and A561P-UhiPS CMs) at days 5, 18, and 28 of cardiac differentiation. Quantitative reverse transcription polymerase chain reaction analysis was performed on pluripotent stem cell markers ( OCT3/4 , NANOG , SOX2 ), on cardiomyocyte markers ( NKX2-5 , GJA1 , GJA5 , RYR2 ), and on key genes encoding cardiac ion channels ( <t>SCN5A</t> , CACNA1C , CACNA1G , KCND3 , KCNQ1 , KCNH2 and KCNJ2 ) to show enrichment for the cardiomyocyte population. The expression for each gene and sample (n=5 per condition) was normalized to the ß-actin gene ACTB and was calculated relative to the median expression level. Raw minimum and maximum values were taken as a reference for heat map representation. B, (top) In control UhiPS-CMs, representative immunofluorescence images of the cardiac sarcomeric protein α-actinin (green, left) and costaining of myosin light chain 2a (MLC2a; green, middle) and myosin light chain 2v (MLC2v; red, middle) and troponin I and connexin 43 (green and red, respectively, right); (bottom) in A561P-UhiPS CMs, representative immunofluorescence images of α-actinin (red, left), costaining of MLC2a (red; middle) and MLC2v (green, middle) and troponin I and connexin 43 (green and red, respectively, right). Scale=5 μm. CM indicates cardiomyocytes; FhiPS, foreskin fibroblast–derived human induced pluripotent stem cells; max, maximum; min, minimum; UhiPS, urine-derived human induced pluripotent stem cells.
    Nav1 5, 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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    94
    Alomone Labs rabbit anti extracellular p2x7r igg
    The effects of L-NAME and/or PDI knockdown on the amounts of SNO-thiol and total thiol-PDI or <t>-P2X7R,</t> and PDI-P2X7R bindings following SE. As compared to vehicle (V), L-NAME (L) reduces the amount of SNO-thiol-PDI and PDI-P2X7R bindings without affecting PDI expression and the amount of total thiol-PDI under physiological condition. Thus, S -nitrosylation ratio of PDI is decreased. L-NAME abrogates SE-induced alterations in PDI-P2X7R bindings and S -nitrosylation ratio of PDI, except PDI expression. As compared to control siRNA (C), PDI siRNA (P) abolishes the changes in PDI-P2X7R bindings and S -nitrosylation ratio of P2X7R following SE, except its expression. a Representative Western blot for S -nitrosylation and thiolization on PDI and its expression. b Quantification of analyses of S -nitrosylation and thiolization on PDI and its expression. Open circles indicate each individual value. Horizontal bars indicate the mean value. Error bars indicate SEM ( * # p
    Rabbit Anti Extracellular P2x7r Igg, 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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    Alomone Labs rabbit anti nav1 7
    ALA downregulated <t>NaV1.7</t> and NaV1.8 expression. Notes: (A) Western blots for NaV1.7 of T13-L2 DRGs from NS- and ALA-treatment rats. Bar graph showed mean density relative to GAPHD for NaV1.7. ALA treatment greatly reduced expressions of NaV1.7 (n=4 for each group, ** p
    Rabbit Anti Nav1 7, 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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    The N terminus is important for the sensitivity of P2X7 receptor activity to cholesterol depletion. A , amino acid sequence alignment of the N-terminal region of human P2X1, P2X2, and P2X7 receptors, with conserved amino acids highlighted in  gray , P2X1 aa20–23 and equivalent residues in P2X2  underlined , and the P2X7 residues Lys 17  and Val 18  in  red. B , time course of dye uptake mediated by the K17R/V18M mutant and wild type P2X7, alone, pretreated with MCD and loaded with cholesterol ( chol ), normalized to the untreated WT P2X7.  C , bar graph of the relative rate of dye uptake normalized to the untreated WT P2X7. Dye uptake mediated by the K17R/V18M mutant is not potentiated by MCD, but is inhibited by cholesterol loading (WT:  n  = 14 alone,  n  = 11 MCD,  n  = 3 cholesterol; mutants:  n  = 12 alone,  n  = 11 MCD,  n  = 3 cholesterol; *,  p

    Journal: The Journal of Biological Chemistry

    Article Title: Plasma Membrane Cholesterol as a Regulator of Human and Rodent P2X7 Receptor Activation and Sensitization *

    doi: 10.1074/jbc.M114.574699

    Figure Lengend Snippet: The N terminus is important for the sensitivity of P2X7 receptor activity to cholesterol depletion. A , amino acid sequence alignment of the N-terminal region of human P2X1, P2X2, and P2X7 receptors, with conserved amino acids highlighted in gray , P2X1 aa20–23 and equivalent residues in P2X2 underlined , and the P2X7 residues Lys 17 and Val 18 in red. B , time course of dye uptake mediated by the K17R/V18M mutant and wild type P2X7, alone, pretreated with MCD and loaded with cholesterol ( chol ), normalized to the untreated WT P2X7. C , bar graph of the relative rate of dye uptake normalized to the untreated WT P2X7. Dye uptake mediated by the K17R/V18M mutant is not potentiated by MCD, but is inhibited by cholesterol loading (WT: n = 14 alone, n = 11 MCD, n = 3 cholesterol; mutants: n = 12 alone, n = 11 MCD, n = 3 cholesterol; *, p

    Article Snippet: Rabbit polyclonal P2X7 C terminus antibody was obtained from Alomone Labs (Jerusalem, Israel), and anti-mouse and anti-rabbit HRP-conjugated secondary antibodies were from Thermo Fisher Scientific and Bio-Rad, respectively.

    Techniques: Activity Assay, Sequencing, Mutagenesis, Relative Rate

    Human UhiPS cells differentiated into functional cardiomyocytes. A, Transcriptional profile of control hiPS cells derived from skin fibroblasts (control FhiPS-CMs) and from urine cells (control UhiPS-CMs and A561P-UhiPS CMs) at days 5, 18, and 28 of cardiac differentiation. Quantitative reverse transcription polymerase chain reaction analysis was performed on pluripotent stem cell markers ( OCT3/4 , NANOG , SOX2 ), on cardiomyocyte markers ( NKX2-5 , GJA1 , GJA5 , RYR2 ), and on key genes encoding cardiac ion channels ( SCN5A , CACNA1C , CACNA1G , KCND3 , KCNQ1 , KCNH2 and KCNJ2 ) to show enrichment for the cardiomyocyte population. The expression for each gene and sample (n=5 per condition) was normalized to the ß-actin gene ACTB and was calculated relative to the median expression level. Raw minimum and maximum values were taken as a reference for heat map representation. B, (top) In control UhiPS-CMs, representative immunofluorescence images of the cardiac sarcomeric protein α-actinin (green, left) and costaining of myosin light chain 2a (MLC2a; green, middle) and myosin light chain 2v (MLC2v; red, middle) and troponin I and connexin 43 (green and red, respectively, right); (bottom) in A561P-UhiPS CMs, representative immunofluorescence images of α-actinin (red, left), costaining of MLC2a (red; middle) and MLC2v (green, middle) and troponin I and connexin 43 (green and red, respectively, right). Scale=5 μm. CM indicates cardiomyocytes; FhiPS, foreskin fibroblast–derived human induced pluripotent stem cells; max, maximum; min, minimum; UhiPS, urine-derived human induced pluripotent stem cells.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Toward Personalized Medicine: Using Cardiomyocytes Differentiated From Urine-Derived Pluripotent Stem Cells to Recapitulate Electrophysiological Characteristics of Type 2 Long QT Syndrome

    doi: 10.1161/JAHA.115.002159

    Figure Lengend Snippet: Human UhiPS cells differentiated into functional cardiomyocytes. A, Transcriptional profile of control hiPS cells derived from skin fibroblasts (control FhiPS-CMs) and from urine cells (control UhiPS-CMs and A561P-UhiPS CMs) at days 5, 18, and 28 of cardiac differentiation. Quantitative reverse transcription polymerase chain reaction analysis was performed on pluripotent stem cell markers ( OCT3/4 , NANOG , SOX2 ), on cardiomyocyte markers ( NKX2-5 , GJA1 , GJA5 , RYR2 ), and on key genes encoding cardiac ion channels ( SCN5A , CACNA1C , CACNA1G , KCND3 , KCNQ1 , KCNH2 and KCNJ2 ) to show enrichment for the cardiomyocyte population. The expression for each gene and sample (n=5 per condition) was normalized to the ß-actin gene ACTB and was calculated relative to the median expression level. Raw minimum and maximum values were taken as a reference for heat map representation. B, (top) In control UhiPS-CMs, representative immunofluorescence images of the cardiac sarcomeric protein α-actinin (green, left) and costaining of myosin light chain 2a (MLC2a; green, middle) and myosin light chain 2v (MLC2v; red, middle) and troponin I and connexin 43 (green and red, respectively, right); (bottom) in A561P-UhiPS CMs, representative immunofluorescence images of α-actinin (red, left), costaining of MLC2a (red; middle) and MLC2v (green, middle) and troponin I and connexin 43 (green and red, respectively, right). Scale=5 μm. CM indicates cardiomyocytes; FhiPS, foreskin fibroblast–derived human induced pluripotent stem cells; max, maximum; min, minimum; UhiPS, urine-derived human induced pluripotent stem cells.

    Article Snippet: For type 2 cells, after methanol fixation, cells were permeabilized with 0.1% Triton X-100, blocked with 5% PBS-BSA and stained with primary antibodies against α-actinin (Abcam), troponin I (Santa Cruz Biotechnology), MLC2a (Abcam), MLC2v (Proteintech Europe), connexin 43 (Chemicon), HERG (Santa Cruz Biotechnology), or Nav1.5 (Alomone Labs).

    Techniques: Functional Assay, Derivative Assay, Reverse Transcription Polymerase Chain Reaction, Expressing, Immunofluorescence

    The effects of L-NAME and/or PDI knockdown on the amounts of SNO-thiol and total thiol-PDI or -P2X7R, and PDI-P2X7R bindings following SE. As compared to vehicle (V), L-NAME (L) reduces the amount of SNO-thiol-PDI and PDI-P2X7R bindings without affecting PDI expression and the amount of total thiol-PDI under physiological condition. Thus, S -nitrosylation ratio of PDI is decreased. L-NAME abrogates SE-induced alterations in PDI-P2X7R bindings and S -nitrosylation ratio of PDI, except PDI expression. As compared to control siRNA (C), PDI siRNA (P) abolishes the changes in PDI-P2X7R bindings and S -nitrosylation ratio of P2X7R following SE, except its expression. a Representative Western blot for S -nitrosylation and thiolization on PDI and its expression. b Quantification of analyses of S -nitrosylation and thiolization on PDI and its expression. Open circles indicate each individual value. Horizontal bars indicate the mean value. Error bars indicate SEM ( * # p

    Journal: Journal of Neuroinflammation

    Article Title: Protein disulfide isomerase-mediated S-nitrosylation facilitates surface expression of P2X7 receptor following status epilepticus

    doi: 10.1186/s12974-020-02058-y

    Figure Lengend Snippet: The effects of L-NAME and/or PDI knockdown on the amounts of SNO-thiol and total thiol-PDI or -P2X7R, and PDI-P2X7R bindings following SE. As compared to vehicle (V), L-NAME (L) reduces the amount of SNO-thiol-PDI and PDI-P2X7R bindings without affecting PDI expression and the amount of total thiol-PDI under physiological condition. Thus, S -nitrosylation ratio of PDI is decreased. L-NAME abrogates SE-induced alterations in PDI-P2X7R bindings and S -nitrosylation ratio of PDI, except PDI expression. As compared to control siRNA (C), PDI siRNA (P) abolishes the changes in PDI-P2X7R bindings and S -nitrosylation ratio of P2X7R following SE, except its expression. a Representative Western blot for S -nitrosylation and thiolization on PDI and its expression. b Quantification of analyses of S -nitrosylation and thiolization on PDI and its expression. Open circles indicate each individual value. Horizontal bars indicate the mean value. Error bars indicate SEM ( * # p

    Article Snippet: The primary antibodies were mouse anti-PDI (1:1,000, Abcam, ab2792) and rabbit anti-extracellular P2X7R IgG (1:200, Alomone labs, APR-008).

    Techniques: Expressing, Western Blot

    Scheme of the role of PDI-mediated S -nitrosylation of P2X7R in its trafficking to the cell membrane. SE elevates NO synthesis, which S -nitrosylates PDI. SNO-PDI transfers NO to the reduced (immature) P2X7R. In turn, SNO-P2X7R is oxidized by denitrosylases (presumably Trx-1 [ 8 ]), which facilitates its trafficking to the cell surface

    Journal: Journal of Neuroinflammation

    Article Title: Protein disulfide isomerase-mediated S-nitrosylation facilitates surface expression of P2X7 receptor following status epilepticus

    doi: 10.1186/s12974-020-02058-y

    Figure Lengend Snippet: Scheme of the role of PDI-mediated S -nitrosylation of P2X7R in its trafficking to the cell membrane. SE elevates NO synthesis, which S -nitrosylates PDI. SNO-PDI transfers NO to the reduced (immature) P2X7R. In turn, SNO-P2X7R is oxidized by denitrosylases (presumably Trx-1 [ 8 ]), which facilitates its trafficking to the cell surface

    Article Snippet: The primary antibodies were mouse anti-PDI (1:1,000, Abcam, ab2792) and rabbit anti-extracellular P2X7R IgG (1:200, Alomone labs, APR-008).

    Techniques:

    The effects of L-NAME and PDI knockdown on the surface expression of P2X7R. As compared to control animals, SE increases the membrane P2X7R expressions, which are abrogated by both L-NAME and PDI siRNA. a Representative Western blot for surface expression of P2X7R following SE. b Quantification of analyses of P2X7R expression in membrane fractions. Open circles indicate each individual value. Horizontal bars indicate the mean value. Error bars indicate SEM ( * # p

    Journal: Journal of Neuroinflammation

    Article Title: Protein disulfide isomerase-mediated S-nitrosylation facilitates surface expression of P2X7 receptor following status epilepticus

    doi: 10.1186/s12974-020-02058-y

    Figure Lengend Snippet: The effects of L-NAME and PDI knockdown on the surface expression of P2X7R. As compared to control animals, SE increases the membrane P2X7R expressions, which are abrogated by both L-NAME and PDI siRNA. a Representative Western blot for surface expression of P2X7R following SE. b Quantification of analyses of P2X7R expression in membrane fractions. Open circles indicate each individual value. Horizontal bars indicate the mean value. Error bars indicate SEM ( * # p

    Article Snippet: The primary antibodies were mouse anti-PDI (1:1,000, Abcam, ab2792) and rabbit anti-extracellular P2X7R IgG (1:200, Alomone labs, APR-008).

    Techniques: Expressing, Western Blot

    The effects of L-NAME on the amounts of SNO-thiol- and total thiol-P2X7R following SE. As compared to vehicle (V), L-NAME (L) reduces the amount of SNO-thiol-P2X7R and increased that of total thiol-P2X7R without altering P2X7R expression under physiological condition. Thus, S -nitrosylation ratio of P2X7R is decreased. SE upregulates P2X7R expression and S -nitrosylation ratio of P2X7R due to the reduced the amount of total thiol without the altered that of SNO-thiol-P2X7R. L-NAME inhibits these alterations induced by SE, except P2X7R expression. a Representative Western blot for S -nitrosylation and thiolization on P2X7R and its expression. b-e Quantification of analyses of S -nitrosylation and thiolization on P2X7R and its expression. Open circles indicate each individual value. Horizontal bars indicate the mean value. Error bars indicate SEM ( * # p

    Journal: Journal of Neuroinflammation

    Article Title: Protein disulfide isomerase-mediated S-nitrosylation facilitates surface expression of P2X7 receptor following status epilepticus

    doi: 10.1186/s12974-020-02058-y

    Figure Lengend Snippet: The effects of L-NAME on the amounts of SNO-thiol- and total thiol-P2X7R following SE. As compared to vehicle (V), L-NAME (L) reduces the amount of SNO-thiol-P2X7R and increased that of total thiol-P2X7R without altering P2X7R expression under physiological condition. Thus, S -nitrosylation ratio of P2X7R is decreased. SE upregulates P2X7R expression and S -nitrosylation ratio of P2X7R due to the reduced the amount of total thiol without the altered that of SNO-thiol-P2X7R. L-NAME inhibits these alterations induced by SE, except P2X7R expression. a Representative Western blot for S -nitrosylation and thiolization on P2X7R and its expression. b-e Quantification of analyses of S -nitrosylation and thiolization on P2X7R and its expression. Open circles indicate each individual value. Horizontal bars indicate the mean value. Error bars indicate SEM ( * # p

    Article Snippet: The primary antibodies were mouse anti-PDI (1:1,000, Abcam, ab2792) and rabbit anti-extracellular P2X7R IgG (1:200, Alomone labs, APR-008).

    Techniques: Expressing, Western Blot

    ALA downregulated NaV1.7 and NaV1.8 expression. Notes: (A) Western blots for NaV1.7 of T13-L2 DRGs from NS- and ALA-treatment rats. Bar graph showed mean density relative to GAPHD for NaV1.7. ALA treatment greatly reduced expressions of NaV1.7 (n=4 for each group, ** p

    Journal: Journal of Pain Research

    Article Title: α-lipoic acid suppresses neuronal excitability and attenuates colonic hypersensitivity to colorectal distention in diabetic rats

    doi: 10.2147/JPR.S135017

    Figure Lengend Snippet: ALA downregulated NaV1.7 and NaV1.8 expression. Notes: (A) Western blots for NaV1.7 of T13-L2 DRGs from NS- and ALA-treatment rats. Bar graph showed mean density relative to GAPHD for NaV1.7. ALA treatment greatly reduced expressions of NaV1.7 (n=4 for each group, ** p

    Article Snippet: The primary antibodies used to probe the target proteins included rabbit anti-NaV1.7 or anti-NaV1.8 (1:200, Alomone Labs, Jerusalem, Israel), rabbit anti-GAPDH (1:1000, Biotechnology Co., CHN), and mouse anti-actin (1:1000; Chemicon, Temecula, CA, USA).

    Techniques: Expressing, Western Blot