rabbit multiclonal anti kir4 2  (Alomone Labs)


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    Structured Review

    Alomone Labs rabbit multiclonal anti kir4 2
    Molecular models of <t>Kir4.2</t> channel with polymyxin B 1 . A The Kir4.2 channel model is shown in NewCartoon presentation (subunits are in yellow, blue, grey and purple). B Binding of polymyxin B 1 to the Kir4.2 channel. Polymyxin B 1 are shown in green, and the binding amino acids are in red. C Gate distance of the channel in the inactivate state (orange) and the state after polymyxin B 1 bound. Purple balls represent K + atoms. Independent simulations were conducted three times
    Rabbit Multiclonal Anti Kir4 2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit multiclonal anti kir4 2/product/Alomone Labs
    Average 94 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    rabbit multiclonal anti kir4 2 - by Bioz Stars, 2022-12
    94/100 stars

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    1) Product Images from "Inwardly rectifying potassium channels mediate polymyxin-induced nephrotoxicity"

    Article Title: Inwardly rectifying potassium channels mediate polymyxin-induced nephrotoxicity

    Journal: Cellular and Molecular Life Sciences

    doi: 10.1007/s00018-022-04316-z

    Molecular models of Kir4.2 channel with polymyxin B 1 . A The Kir4.2 channel model is shown in NewCartoon presentation (subunits are in yellow, blue, grey and purple). B Binding of polymyxin B 1 to the Kir4.2 channel. Polymyxin B 1 are shown in green, and the binding amino acids are in red. C Gate distance of the channel in the inactivate state (orange) and the state after polymyxin B 1 bound. Purple balls represent K + atoms. Independent simulations were conducted three times
    Figure Legend Snippet: Molecular models of Kir4.2 channel with polymyxin B 1 . A The Kir4.2 channel model is shown in NewCartoon presentation (subunits are in yellow, blue, grey and purple). B Binding of polymyxin B 1 to the Kir4.2 channel. Polymyxin B 1 are shown in green, and the binding amino acids are in red. C Gate distance of the channel in the inactivate state (orange) and the state after polymyxin B 1 bound. Purple balls represent K + atoms. Independent simulations were conducted three times

    Techniques Used: Binding Assay

    Intracellular accumulation of polymyxin B in wild-type, KCNJ15 KO and KCNJ16 KO HK-2 cells with the treatment of 25 µM polymyxin B and 50 µM BaCl 2 for 6 h. A Polymyxin B was immunostained with polymyxin antibody and visualized using Alexa Fluor-594 dye (red). The nucleus was counterstained with DAPI (blue). B The plots showing mean fluorescence intensities from each group. The value from control group has been deducted and the mean value from each replicate was plotted ( n = 4)
    Figure Legend Snippet: Intracellular accumulation of polymyxin B in wild-type, KCNJ15 KO and KCNJ16 KO HK-2 cells with the treatment of 25 µM polymyxin B and 50 µM BaCl 2 for 6 h. A Polymyxin B was immunostained with polymyxin antibody and visualized using Alexa Fluor-594 dye (red). The nucleus was counterstained with DAPI (blue). B The plots showing mean fluorescence intensities from each group. The value from control group has been deducted and the mean value from each replicate was plotted ( n = 4)

    Techniques Used: Fluorescence

    Polymyxin B induced significant electrophysiological changes and membrane depolarization in HK-2 cells. A The resting membrane potential in wild-type, KCNJ15 KO and KCNJ16 KO cells ( n = 34, 18 and 10, respectively). B Input resistances in wild-type, KCNJ15 KO and KCNJ16 KO cells ( n = 20, 18 and 10, respectively). C In current clamp mode, polymyxin B induced approximately 30 mV depolarization in WT cells and this was reversible. Depolarization was not induced in KCNJ15 KO cells. Polymyxin B induced membrane potential changes are shown aside ( n = 9, 10 and 7, respectively). D In voltage clamp mode, polymyxin B induced a statistically significant inward current (green) in wild-type HK-2 cells ( n = 8), but not in KCNJ15 KO cells ( n = 8). The current and reversal potential values are shown aside. E Fluorescent signal detection in HK-2 cells with DiBAC, 25 μM polymyxin B, and DiBAC plus 25 μM polymyxin B. F Proportions of DiBAC-positive in wild-type, KCNJ15 KO, and KCNJ16 KO HK-2 cells measured by flow cytometry. G Proportions of DiBAC-positive HK-2 cells in the control and BaCl 2 (10 μM) groups with or without 25 μM polymyxin B treatment measured by flow cytometry ( n = 5 for WT and n = 4 for KOs). Data are shown as box and whisker plots. One-way (for WT) or two-way (for KOs) ANOVA was employed for multi-group comparisons. ** p
    Figure Legend Snippet: Polymyxin B induced significant electrophysiological changes and membrane depolarization in HK-2 cells. A The resting membrane potential in wild-type, KCNJ15 KO and KCNJ16 KO cells ( n = 34, 18 and 10, respectively). B Input resistances in wild-type, KCNJ15 KO and KCNJ16 KO cells ( n = 20, 18 and 10, respectively). C In current clamp mode, polymyxin B induced approximately 30 mV depolarization in WT cells and this was reversible. Depolarization was not induced in KCNJ15 KO cells. Polymyxin B induced membrane potential changes are shown aside ( n = 9, 10 and 7, respectively). D In voltage clamp mode, polymyxin B induced a statistically significant inward current (green) in wild-type HK-2 cells ( n = 8), but not in KCNJ15 KO cells ( n = 8). The current and reversal potential values are shown aside. E Fluorescent signal detection in HK-2 cells with DiBAC, 25 μM polymyxin B, and DiBAC plus 25 μM polymyxin B. F Proportions of DiBAC-positive in wild-type, KCNJ15 KO, and KCNJ16 KO HK-2 cells measured by flow cytometry. G Proportions of DiBAC-positive HK-2 cells in the control and BaCl 2 (10 μM) groups with or without 25 μM polymyxin B treatment measured by flow cytometry ( n = 5 for WT and n = 4 for KOs). Data are shown as box and whisker plots. One-way (for WT) or two-way (for KOs) ANOVA was employed for multi-group comparisons. ** p

    Techniques Used: Flow Cytometry, Whisker Assay

    Knockout or inhibition of Kir4.2 and Kir5.1 prevented polymyxin-induced toxicity in HK-2 cells. A Western blot showing the expression levels of KCNJ15 and KCNJ16 after knockout; actin was used as an internal control. B Viability of wild-type HK-2, KCNJ15 KO and KCNJ16 KO cells following 24-h exposure to 10 and 25 µM polymyxin B ( n = 6). C Viability of HK-2 cells following 24-h exposure to 0–100 µM BaCl 2 with or without 25 µM polymyxin B ( n = 5). D Viability of HK-2 cells following the treatment of 0–25 µM VU0134992 alone or in combination with 25 µM polymyxin B for 24 h ( n = 3 for controls, and n = 4 for treatment groups). E Morphologies of wild-type, KNCJ15 KO, and KCNJ16 KO HK-2 cells with the treatment of 25 µM polymyxin B or polymyxin B with the combination of 50 µM BaCl 2 , or 5 µM VU0134992 to wild-type cells . Two-way ANOVA was employed for multi-group comparisons and Tukey's multiple comparison test was employed for post-test. * p
    Figure Legend Snippet: Knockout or inhibition of Kir4.2 and Kir5.1 prevented polymyxin-induced toxicity in HK-2 cells. A Western blot showing the expression levels of KCNJ15 and KCNJ16 after knockout; actin was used as an internal control. B Viability of wild-type HK-2, KCNJ15 KO and KCNJ16 KO cells following 24-h exposure to 10 and 25 µM polymyxin B ( n = 6). C Viability of HK-2 cells following 24-h exposure to 0–100 µM BaCl 2 with or without 25 µM polymyxin B ( n = 5). D Viability of HK-2 cells following the treatment of 0–25 µM VU0134992 alone or in combination with 25 µM polymyxin B for 24 h ( n = 3 for controls, and n = 4 for treatment groups). E Morphologies of wild-type, KNCJ15 KO, and KCNJ16 KO HK-2 cells with the treatment of 25 µM polymyxin B or polymyxin B with the combination of 50 µM BaCl 2 , or 5 µM VU0134992 to wild-type cells . Two-way ANOVA was employed for multi-group comparisons and Tukey's multiple comparison test was employed for post-test. * p

    Techniques Used: Knock-Out, Inhibition, Western Blot, Expressing

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    Alomone Labs rabbit multiclonal anti kir4 2
    Molecular models of <t>Kir4.2</t> channel with polymyxin B 1 . A The Kir4.2 channel model is shown in NewCartoon presentation (subunits are in yellow, blue, grey and purple). B Binding of polymyxin B 1 to the Kir4.2 channel. Polymyxin B 1 are shown in green, and the binding amino acids are in red. C Gate distance of the channel in the inactivate state (orange) and the state after polymyxin B 1 bound. Purple balls represent K + atoms. Independent simulations were conducted three times
    Rabbit Multiclonal Anti Kir4 2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit multiclonal anti kir4 2/product/Alomone Labs
    Average 94 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    rabbit multiclonal anti kir4 2 - by Bioz Stars, 2022-12
    94/100 stars
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    Molecular models of Kir4.2 channel with polymyxin B 1 . A The Kir4.2 channel model is shown in NewCartoon presentation (subunits are in yellow, blue, grey and purple). B Binding of polymyxin B 1 to the Kir4.2 channel. Polymyxin B 1 are shown in green, and the binding amino acids are in red. C Gate distance of the channel in the inactivate state (orange) and the state after polymyxin B 1 bound. Purple balls represent K + atoms. Independent simulations were conducted three times

    Journal: Cellular and Molecular Life Sciences

    Article Title: Inwardly rectifying potassium channels mediate polymyxin-induced nephrotoxicity

    doi: 10.1007/s00018-022-04316-z

    Figure Lengend Snippet: Molecular models of Kir4.2 channel with polymyxin B 1 . A The Kir4.2 channel model is shown in NewCartoon presentation (subunits are in yellow, blue, grey and purple). B Binding of polymyxin B 1 to the Kir4.2 channel. Polymyxin B 1 are shown in green, and the binding amino acids are in red. C Gate distance of the channel in the inactivate state (orange) and the state after polymyxin B 1 bound. Purple balls represent K + atoms. Independent simulations were conducted three times

    Article Snippet: Rabbit multiclonal anti-Kir4.2 (KCNJ15) and anti-Kir5.1 (KCNJ16) antibodies were purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Binding Assay

    Intracellular accumulation of polymyxin B in wild-type, KCNJ15 KO and KCNJ16 KO HK-2 cells with the treatment of 25 µM polymyxin B and 50 µM BaCl 2 for 6 h. A Polymyxin B was immunostained with polymyxin antibody and visualized using Alexa Fluor-594 dye (red). The nucleus was counterstained with DAPI (blue). B The plots showing mean fluorescence intensities from each group. The value from control group has been deducted and the mean value from each replicate was plotted ( n = 4)

    Journal: Cellular and Molecular Life Sciences

    Article Title: Inwardly rectifying potassium channels mediate polymyxin-induced nephrotoxicity

    doi: 10.1007/s00018-022-04316-z

    Figure Lengend Snippet: Intracellular accumulation of polymyxin B in wild-type, KCNJ15 KO and KCNJ16 KO HK-2 cells with the treatment of 25 µM polymyxin B and 50 µM BaCl 2 for 6 h. A Polymyxin B was immunostained with polymyxin antibody and visualized using Alexa Fluor-594 dye (red). The nucleus was counterstained with DAPI (blue). B The plots showing mean fluorescence intensities from each group. The value from control group has been deducted and the mean value from each replicate was plotted ( n = 4)

    Article Snippet: Rabbit multiclonal anti-Kir4.2 (KCNJ15) and anti-Kir5.1 (KCNJ16) antibodies were purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Fluorescence

    Polymyxin B induced significant electrophysiological changes and membrane depolarization in HK-2 cells. A The resting membrane potential in wild-type, KCNJ15 KO and KCNJ16 KO cells ( n = 34, 18 and 10, respectively). B Input resistances in wild-type, KCNJ15 KO and KCNJ16 KO cells ( n = 20, 18 and 10, respectively). C In current clamp mode, polymyxin B induced approximately 30 mV depolarization in WT cells and this was reversible. Depolarization was not induced in KCNJ15 KO cells. Polymyxin B induced membrane potential changes are shown aside ( n = 9, 10 and 7, respectively). D In voltage clamp mode, polymyxin B induced a statistically significant inward current (green) in wild-type HK-2 cells ( n = 8), but not in KCNJ15 KO cells ( n = 8). The current and reversal potential values are shown aside. E Fluorescent signal detection in HK-2 cells with DiBAC, 25 μM polymyxin B, and DiBAC plus 25 μM polymyxin B. F Proportions of DiBAC-positive in wild-type, KCNJ15 KO, and KCNJ16 KO HK-2 cells measured by flow cytometry. G Proportions of DiBAC-positive HK-2 cells in the control and BaCl 2 (10 μM) groups with or without 25 μM polymyxin B treatment measured by flow cytometry ( n = 5 for WT and n = 4 for KOs). Data are shown as box and whisker plots. One-way (for WT) or two-way (for KOs) ANOVA was employed for multi-group comparisons. ** p

    Journal: Cellular and Molecular Life Sciences

    Article Title: Inwardly rectifying potassium channels mediate polymyxin-induced nephrotoxicity

    doi: 10.1007/s00018-022-04316-z

    Figure Lengend Snippet: Polymyxin B induced significant electrophysiological changes and membrane depolarization in HK-2 cells. A The resting membrane potential in wild-type, KCNJ15 KO and KCNJ16 KO cells ( n = 34, 18 and 10, respectively). B Input resistances in wild-type, KCNJ15 KO and KCNJ16 KO cells ( n = 20, 18 and 10, respectively). C In current clamp mode, polymyxin B induced approximately 30 mV depolarization in WT cells and this was reversible. Depolarization was not induced in KCNJ15 KO cells. Polymyxin B induced membrane potential changes are shown aside ( n = 9, 10 and 7, respectively). D In voltage clamp mode, polymyxin B induced a statistically significant inward current (green) in wild-type HK-2 cells ( n = 8), but not in KCNJ15 KO cells ( n = 8). The current and reversal potential values are shown aside. E Fluorescent signal detection in HK-2 cells with DiBAC, 25 μM polymyxin B, and DiBAC plus 25 μM polymyxin B. F Proportions of DiBAC-positive in wild-type, KCNJ15 KO, and KCNJ16 KO HK-2 cells measured by flow cytometry. G Proportions of DiBAC-positive HK-2 cells in the control and BaCl 2 (10 μM) groups with or without 25 μM polymyxin B treatment measured by flow cytometry ( n = 5 for WT and n = 4 for KOs). Data are shown as box and whisker plots. One-way (for WT) or two-way (for KOs) ANOVA was employed for multi-group comparisons. ** p

    Article Snippet: Rabbit multiclonal anti-Kir4.2 (KCNJ15) and anti-Kir5.1 (KCNJ16) antibodies were purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Flow Cytometry, Whisker Assay

    Knockout or inhibition of Kir4.2 and Kir5.1 prevented polymyxin-induced toxicity in HK-2 cells. A Western blot showing the expression levels of KCNJ15 and KCNJ16 after knockout; actin was used as an internal control. B Viability of wild-type HK-2, KCNJ15 KO and KCNJ16 KO cells following 24-h exposure to 10 and 25 µM polymyxin B ( n = 6). C Viability of HK-2 cells following 24-h exposure to 0–100 µM BaCl 2 with or without 25 µM polymyxin B ( n = 5). D Viability of HK-2 cells following the treatment of 0–25 µM VU0134992 alone or in combination with 25 µM polymyxin B for 24 h ( n = 3 for controls, and n = 4 for treatment groups). E Morphologies of wild-type, KNCJ15 KO, and KCNJ16 KO HK-2 cells with the treatment of 25 µM polymyxin B or polymyxin B with the combination of 50 µM BaCl 2 , or 5 µM VU0134992 to wild-type cells . Two-way ANOVA was employed for multi-group comparisons and Tukey's multiple comparison test was employed for post-test. * p

    Journal: Cellular and Molecular Life Sciences

    Article Title: Inwardly rectifying potassium channels mediate polymyxin-induced nephrotoxicity

    doi: 10.1007/s00018-022-04316-z

    Figure Lengend Snippet: Knockout or inhibition of Kir4.2 and Kir5.1 prevented polymyxin-induced toxicity in HK-2 cells. A Western blot showing the expression levels of KCNJ15 and KCNJ16 after knockout; actin was used as an internal control. B Viability of wild-type HK-2, KCNJ15 KO and KCNJ16 KO cells following 24-h exposure to 10 and 25 µM polymyxin B ( n = 6). C Viability of HK-2 cells following 24-h exposure to 0–100 µM BaCl 2 with or without 25 µM polymyxin B ( n = 5). D Viability of HK-2 cells following the treatment of 0–25 µM VU0134992 alone or in combination with 25 µM polymyxin B for 24 h ( n = 3 for controls, and n = 4 for treatment groups). E Morphologies of wild-type, KNCJ15 KO, and KCNJ16 KO HK-2 cells with the treatment of 25 µM polymyxin B or polymyxin B with the combination of 50 µM BaCl 2 , or 5 µM VU0134992 to wild-type cells . Two-way ANOVA was employed for multi-group comparisons and Tukey's multiple comparison test was employed for post-test. * p

    Article Snippet: Rabbit multiclonal anti-Kir4.2 (KCNJ15) and anti-Kir5.1 (KCNJ16) antibodies were purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Knock-Out, Inhibition, Western Blot, Expressing