rabbit anti kir4 1  (Alomone Labs)


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    Structured Review

    Alomone Labs rabbit anti kir4 1
    Experimental detachment of the porcine retina changes the immunoreactivities of various proteins involved in Müller cell swelling. The slices were derived from nonoperated control retinas and from detached retinal areas at 7 days after surgery. A: Immunoreactivity for <t>Kir4.1.</t> The arrows and the arrowhead mark the prominent expression of the Kir4.1 immunoreactivity around vessels and at the inner limiting membrane, respectively, in the control retina. B: Immunoreactivity for COX-2. Cell nuclei were stained with Hoechst 33258 (blue). The arrows point to Müller cell fibers that pass through the IPL. C: Immunoreactivities for COX-2 and glutamine synthetase (GS) in the INL. D: Immunoreactivities for COX-2 and vimentin. The arrowheads point to somata of two vimentin-expressing Müller cells with COX-2 expressing somata. Note the thick vimentin-positive Müller cell fibers in the detached retina, likely reflecting the hypertrophy of the cells. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer. Scale bars = 20 μm.
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    Images

    1) Product Images from "Changes in Membrane Conductance Play a Pathogenic Role in Osmotic Glial Cell Swelling in Detached Retinas"

    Article Title: Changes in Membrane Conductance Play a Pathogenic Role in Osmotic Glial Cell Swelling in Detached Retinas

    Journal: The American Journal of Pathology

    doi: 10.2353/ajpath.2006.060628

    Experimental detachment of the porcine retina changes the immunoreactivities of various proteins involved in Müller cell swelling. The slices were derived from nonoperated control retinas and from detached retinal areas at 7 days after surgery. A: Immunoreactivity for Kir4.1. The arrows and the arrowhead mark the prominent expression of the Kir4.1 immunoreactivity around vessels and at the inner limiting membrane, respectively, in the control retina. B: Immunoreactivity for COX-2. Cell nuclei were stained with Hoechst 33258 (blue). The arrows point to Müller cell fibers that pass through the IPL. C: Immunoreactivities for COX-2 and glutamine synthetase (GS) in the INL. D: Immunoreactivities for COX-2 and vimentin. The arrowheads point to somata of two vimentin-expressing Müller cells with COX-2 expressing somata. Note the thick vimentin-positive Müller cell fibers in the detached retina, likely reflecting the hypertrophy of the cells. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer. Scale bars = 20 μm.
    Figure Legend Snippet: Experimental detachment of the porcine retina changes the immunoreactivities of various proteins involved in Müller cell swelling. The slices were derived from nonoperated control retinas and from detached retinal areas at 7 days after surgery. A: Immunoreactivity for Kir4.1. The arrows and the arrowhead mark the prominent expression of the Kir4.1 immunoreactivity around vessels and at the inner limiting membrane, respectively, in the control retina. B: Immunoreactivity for COX-2. Cell nuclei were stained with Hoechst 33258 (blue). The arrows point to Müller cell fibers that pass through the IPL. C: Immunoreactivities for COX-2 and glutamine synthetase (GS) in the INL. D: Immunoreactivities for COX-2 and vimentin. The arrowheads point to somata of two vimentin-expressing Müller cells with COX-2 expressing somata. Note the thick vimentin-positive Müller cell fibers in the detached retina, likely reflecting the hypertrophy of the cells. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer. Scale bars = 20 μm.

    Techniques Used: Derivative Assay, Expressing, Staining

    2) Product Images from "Expression of Kir4.1 and Kir5.1 inwardly rectifying potassium channels in oligodendrocytes, the myelinating cells of the CNS"

    Article Title: Expression of Kir4.1 and Kir5.1 inwardly rectifying potassium channels in oligodendrocytes, the myelinating cells of the CNS

    Journal: Brain Structure & Function

    doi: 10.1007/s00429-016-1199-8

    Glial Kir5.1 expression is reduced in the absence of Kir4.1 subunit. Immunolabelling for Kir5.1 was determined in optic nerve explants cultures, comparing wild-type mice ( A , Kir4.1 +/+ ) with Kir4.1 knock-out mice ( B , Kir4.1 −/− ), and following transfection with scrambled shRNA ( C ) or Kir4.1 shRNA ( D ); transfected cells were identified by the expression of GFP (appears green ) and insets demonstrate Kir4.1 expression in controls ( Ai , Ci ) and complete ablation in Kir4.1 −/− mice ( Bi ) and Kir4.1 shRNA ( Di ). Scale bars 10 μm. Quantification of expression of Kir4.1 ( E ) and Kir5.1 ( F ) in Kir4.1 +/+ , Kir4.1 −/− , scrambled control and Kir4.1shRNA glia; analysis was performed on 10–12 cells in each group, and data are expressed as mean ± SEM number of voxels per µm 3 , *** p
    Figure Legend Snippet: Glial Kir5.1 expression is reduced in the absence of Kir4.1 subunit. Immunolabelling for Kir5.1 was determined in optic nerve explants cultures, comparing wild-type mice ( A , Kir4.1 +/+ ) with Kir4.1 knock-out mice ( B , Kir4.1 −/− ), and following transfection with scrambled shRNA ( C ) or Kir4.1 shRNA ( D ); transfected cells were identified by the expression of GFP (appears green ) and insets demonstrate Kir4.1 expression in controls ( Ai , Ci ) and complete ablation in Kir4.1 −/− mice ( Bi ) and Kir4.1 shRNA ( Di ). Scale bars 10 μm. Quantification of expression of Kir4.1 ( E ) and Kir5.1 ( F ) in Kir4.1 +/+ , Kir4.1 −/− , scrambled control and Kir4.1shRNA glia; analysis was performed on 10–12 cells in each group, and data are expressed as mean ± SEM number of voxels per µm 3 , *** p

    Techniques Used: Expressing, Mouse Assay, Knock-Out, Transfection, shRNA

    Functional implications of homomeric Kir4.1 and heteromeric Kir4.1/Kir5.1 channels in oligodendrocytes. Oligodendroglial expression of Kir4.1 channels indicates they may be important in uptake of excess K + released during axonal action potential propagation, a function largely attribiuted to astrocytes. Due to their wrapping of axons, oligodendrocytes are exposed to large ionic and pH shifts during axonal electrical activity, and it is likely weakly rectifying homomeric Kir4.1 and strongly rectifying Kir4.1/Kir5.1 heteromeric channels are important in maintaining the negative resting membrane potential, which is essential for oligodendroglial and myelin integrity. Weakly rectifying homomeric Kir4.1 channels may preferentially extrude K + and supply extracellular K + for the Na + –K + -pumps, as described in transporting epithelia. In contrast, the pH sensitivity of heteromeric Kir4.1/Kir5.1 channels is likely to have a role in the CO 2 /pH chemosensation in glia, involving carbonic anhydrase that is enriched in astrocytes and oligodendrocytes. Furthermore, intracellular acidification and inhibition of Kir4.1/Kir5.1 channels has been shown to trigger release of ATP from astrocytes, which would act on oligodendroglial P2X and P2Y receptors to provide a mechanism of astrocyte–oligodendrocyte signaling in response to metabolic challenges, which has important implications for white matter physiology and pathology
    Figure Legend Snippet: Functional implications of homomeric Kir4.1 and heteromeric Kir4.1/Kir5.1 channels in oligodendrocytes. Oligodendroglial expression of Kir4.1 channels indicates they may be important in uptake of excess K + released during axonal action potential propagation, a function largely attribiuted to astrocytes. Due to their wrapping of axons, oligodendrocytes are exposed to large ionic and pH shifts during axonal electrical activity, and it is likely weakly rectifying homomeric Kir4.1 and strongly rectifying Kir4.1/Kir5.1 heteromeric channels are important in maintaining the negative resting membrane potential, which is essential for oligodendroglial and myelin integrity. Weakly rectifying homomeric Kir4.1 channels may preferentially extrude K + and supply extracellular K + for the Na + –K + -pumps, as described in transporting epithelia. In contrast, the pH sensitivity of heteromeric Kir4.1/Kir5.1 channels is likely to have a role in the CO 2 /pH chemosensation in glia, involving carbonic anhydrase that is enriched in astrocytes and oligodendrocytes. Furthermore, intracellular acidification and inhibition of Kir4.1/Kir5.1 channels has been shown to trigger release of ATP from astrocytes, which would act on oligodendroglial P2X and P2Y receptors to provide a mechanism of astrocyte–oligodendrocyte signaling in response to metabolic challenges, which has important implications for white matter physiology and pathology

    Techniques Used: Functional Assay, Expressing, Activity Assay, Inhibition

    Specific reduction in plasmalemmal Kir5.1 in the absence of Kir4.1. Immunolocalization of Kir5.1 with the membrane bound Na–K-ATPase α1 subunit in optic nerve explant astrocytes identified by expression of GFAP, following transfection with scrambled shRNA ( A ) or Kir4.1 shRNA ( B ); transfected cells were identified by co-transfection with GFP (appears green ) and the co-localization channel indicates voxels in which Kir5.1 and Na–K-ATPase immunolabelling was at the same intensity ( Avi , Bvi ). Scale bars 20 μm. C Quantification of plasmalemmal Kir5.1 expressed as percentage of total Kir5.1 + voxels (data are mean ± SEM, n = 11–13 per group; * p
    Figure Legend Snippet: Specific reduction in plasmalemmal Kir5.1 in the absence of Kir4.1. Immunolocalization of Kir5.1 with the membrane bound Na–K-ATPase α1 subunit in optic nerve explant astrocytes identified by expression of GFAP, following transfection with scrambled shRNA ( A ) or Kir4.1 shRNA ( B ); transfected cells were identified by co-transfection with GFP (appears green ) and the co-localization channel indicates voxels in which Kir5.1 and Na–K-ATPase immunolabelling was at the same intensity ( Avi , Bvi ). Scale bars 20 μm. C Quantification of plasmalemmal Kir5.1 expressed as percentage of total Kir5.1 + voxels (data are mean ± SEM, n = 11–13 per group; * p

    Techniques Used: Expressing, Transfection, shRNA, Cotransfection

    Reduction of Kir5.1 in oligodendrocytes and myelin in the absence of Kir4.1. Immunolocalization of Kir5.1 with myelin basic protein, MBP ( A , B ) and the oligodenrocyte marker APC/CC1 ( C – F ), in brain tissue from wild-type Kir4.1 +/+ mice ( A , C , E ) compared to Kir4.1 −/− knock-out mice ( B , D , F ). Scale bars 20 μm. Western blot analysis of Kir5.1 from total lysates of optic nerve ( G ) and brain ( H ) from wild-type Kir4.1 +/+ and Kir4.1 −/− knock-out mice, and mean (±SEM) integrated density normalised against β-actin ( I , n = 3, ** p
    Figure Legend Snippet: Reduction of Kir5.1 in oligodendrocytes and myelin in the absence of Kir4.1. Immunolocalization of Kir5.1 with myelin basic protein, MBP ( A , B ) and the oligodenrocyte marker APC/CC1 ( C – F ), in brain tissue from wild-type Kir4.1 +/+ mice ( A , C , E ) compared to Kir4.1 −/− knock-out mice ( B , D , F ). Scale bars 20 μm. Western blot analysis of Kir5.1 from total lysates of optic nerve ( G ) and brain ( H ) from wild-type Kir4.1 +/+ and Kir4.1 −/− knock-out mice, and mean (±SEM) integrated density normalised against β-actin ( I , n = 3, ** p

    Techniques Used: Marker, Mouse Assay, Knock-Out, Western Blot

    Expression of Kir4.1 and Kir5.1 in oligodendrocytes and astrocytes in the cerebellum. Immunolabelling for Kir4.1 and Kir5.1, in combination with GFAP for astrocytes ( A , C ), and APC/CC1 for oligodendrocytes ( B , D ). Immunolabelling for Kir4.1 ( E ) and Kir5.1 ( F ) in mice in which EGFP is under the control of the oligodendrocyte-specific Sox10 promoter. G Double immunolabelling for Kir4.1 ( red ) and the oligodenrocyte-specific marker Olig2 ( green ). Insets in Aiv and Civ illustrate negative controls, in the Kir4.1 KO mouse ( Aiv ) and following preincubation with the Kir5.1 blocking peptide ( Civ ). Scale bars 20 μm. Western blot analysis of the brain and optic and nerve for Kir4.1 ( I ) and Kir5.1 ( J ); bands were absent in the negative controls, in the Kir4.1 knock-out mouse ( I ) following preincubation in the Kir5.1 blocking peptide ( J )
    Figure Legend Snippet: Expression of Kir4.1 and Kir5.1 in oligodendrocytes and astrocytes in the cerebellum. Immunolabelling for Kir4.1 and Kir5.1, in combination with GFAP for astrocytes ( A , C ), and APC/CC1 for oligodendrocytes ( B , D ). Immunolabelling for Kir4.1 ( E ) and Kir5.1 ( F ) in mice in which EGFP is under the control of the oligodendrocyte-specific Sox10 promoter. G Double immunolabelling for Kir4.1 ( red ) and the oligodenrocyte-specific marker Olig2 ( green ). Insets in Aiv and Civ illustrate negative controls, in the Kir4.1 KO mouse ( Aiv ) and following preincubation with the Kir5.1 blocking peptide ( Civ ). Scale bars 20 μm. Western blot analysis of the brain and optic and nerve for Kir4.1 ( I ) and Kir5.1 ( J ); bands were absent in the negative controls, in the Kir4.1 knock-out mouse ( I ) following preincubation in the Kir5.1 blocking peptide ( J )

    Techniques Used: Expressing, Mouse Assay, Marker, Blocking Assay, Western Blot, Knock-Out

    Expression of Kir4.1 and Kir5.1 in optic nerve oligodendrocytes and astrocytes. Immunolabelling for Kir4.1 ( A , C ) and Kir5.1 ( B , D ), in GFAP-GFP mice to identify astrocytes ( A , B ) and PLP-DsRED mice to identify oligodendrocytes ( C , D ). Cellular expression of Kir4.1 and Kir5.1 is demonstrated by the generation of colocalisation channels ( Av , Bv , Cv , Dv ) from confocal z -stacks ( Aiv , Biv , Civ , Div ), and green and red channels of equal intensity appear yellow . Scale bars 20 μm
    Figure Legend Snippet: Expression of Kir4.1 and Kir5.1 in optic nerve oligodendrocytes and astrocytes. Immunolabelling for Kir4.1 ( A , C ) and Kir5.1 ( B , D ), in GFAP-GFP mice to identify astrocytes ( A , B ) and PLP-DsRED mice to identify oligodendrocytes ( C , D ). Cellular expression of Kir4.1 and Kir5.1 is demonstrated by the generation of colocalisation channels ( Av , Bv , Cv , Dv ) from confocal z -stacks ( Aiv , Biv , Civ , Div ), and green and red channels of equal intensity appear yellow . Scale bars 20 μm

    Techniques Used: Expressing, Mouse Assay, Plasmid Purification

    Co-expression of Kir4.1 and Kir5.1 in optic nerve oligodendrocytes and astrocytes. Co-immunolocalization of Kir4.1 and Kir5.1 in optic nerve explant cultures, in astrocytes identified by GFAP immunolabelling ( A ) and oligodendrocytes identified by PLP-DsRED ( B ). The overlay and individual channels are illustrated, together with the co-localisation channel for Kir4.1/Kir5.1 ( Aii, Bii ). Boxed areas on overlay images ( Ai , Bi ) are enlarged in Avi – Aviii and Bvi – Bviii , to illustrate punctate colocalization of Kir4.1 and Kir5.1 along processes (some indicated by arrows ). Scale bars 20 μm. Quantification of the number of voxels that were positive for Kir4.1 and Kir5.1 alone and of Kir4.1/Kir5.1 together, in astrocytes ( C , n = 15) and oligodendrocytes ( D , n = 13); data are mean ± SEM. Co-immunoprecipitation of Kir4.1 with Kir5.1 ( E ) and of Kir5.1 with Kir4.1 ( F ) from total brain and optic nerve (ON) lysates; negative controls were Kir4.1 knock-out mice (−/−) for Kir4.1, and using the blocking peptide for Kir5.1
    Figure Legend Snippet: Co-expression of Kir4.1 and Kir5.1 in optic nerve oligodendrocytes and astrocytes. Co-immunolocalization of Kir4.1 and Kir5.1 in optic nerve explant cultures, in astrocytes identified by GFAP immunolabelling ( A ) and oligodendrocytes identified by PLP-DsRED ( B ). The overlay and individual channels are illustrated, together with the co-localisation channel for Kir4.1/Kir5.1 ( Aii, Bii ). Boxed areas on overlay images ( Ai , Bi ) are enlarged in Avi – Aviii and Bvi – Bviii , to illustrate punctate colocalization of Kir4.1 and Kir5.1 along processes (some indicated by arrows ). Scale bars 20 μm. Quantification of the number of voxels that were positive for Kir4.1 and Kir5.1 alone and of Kir4.1/Kir5.1 together, in astrocytes ( C , n = 15) and oligodendrocytes ( D , n = 13); data are mean ± SEM. Co-immunoprecipitation of Kir4.1 with Kir5.1 ( E ) and of Kir5.1 with Kir4.1 ( F ) from total brain and optic nerve (ON) lysates; negative controls were Kir4.1 knock-out mice (−/−) for Kir4.1, and using the blocking peptide for Kir5.1

    Techniques Used: Expressing, Plasmid Purification, Immunoprecipitation, Knock-Out, Mouse Assay, Blocking Assay

    Plasmalemmal expression of Kir4.1 and Kir5.1 subunit in optic nerve glia. Immunolocalization of Kir4.1 and Kir5.1 with the membrane bound Na–K-ATPase α1 subunit in optic nerve explants of astrocytes identified by GFAP ( A , B ) and oligodendrocytes identified by PLP-DsRed ( C , D ). Scale bars 20 μm. Quantification in astrocytes and oligodendrocytes of total number of voxels immunopositive for Kir4.1 and Kir5.1, compared to voxels that were identified as colocalized for Kir4.1/Na–K-ATPase ( E ) and Kir5.1/Na–K-ATPase ( F ); data are mean ± SEM, n = 13 cells for each analysis. Western blot analysis of Kir5.1 ( G ) and Kir4.1 ( H ) in total optic nerve lysate and plasma membrane fraction. Co-immunoprecipitation of Kir4.1 ( I ) and Kir5.1 ( J ) with PSD95, in total brain and optic nerve (ON) lysate; negative controls were Kir4.1 knock-out mice (−/−) for Kir4.1 and preincubation with the blocking peptide for Kir5.1
    Figure Legend Snippet: Plasmalemmal expression of Kir4.1 and Kir5.1 subunit in optic nerve glia. Immunolocalization of Kir4.1 and Kir5.1 with the membrane bound Na–K-ATPase α1 subunit in optic nerve explants of astrocytes identified by GFAP ( A , B ) and oligodendrocytes identified by PLP-DsRed ( C , D ). Scale bars 20 μm. Quantification in astrocytes and oligodendrocytes of total number of voxels immunopositive for Kir4.1 and Kir5.1, compared to voxels that were identified as colocalized for Kir4.1/Na–K-ATPase ( E ) and Kir5.1/Na–K-ATPase ( F ); data are mean ± SEM, n = 13 cells for each analysis. Western blot analysis of Kir5.1 ( G ) and Kir4.1 ( H ) in total optic nerve lysate and plasma membrane fraction. Co-immunoprecipitation of Kir4.1 ( I ) and Kir5.1 ( J ) with PSD95, in total brain and optic nerve (ON) lysate; negative controls were Kir4.1 knock-out mice (−/−) for Kir4.1 and preincubation with the blocking peptide for Kir5.1

    Techniques Used: Expressing, Plasmid Purification, Western Blot, Immunoprecipitation, Knock-Out, Mouse Assay, Blocking Assay

    3) Product Images from "Age-dependent alterations of Kir4.1 expression in neural crest-derived cells of the mouse and human cochlea"

    Article Title: Age-dependent alterations of Kir4.1 expression in neural crest-derived cells of the mouse and human cochlea

    Journal: Neurobiology of aging

    doi: 10.1016/j.neurobiolaging.2019.04.009

    Age-related alterations in the Kir4.1 immunostaining pattern in satellite cells. The honeycomb-like Kir4.1 expression pattern reflects satellite cells ensheathing SGNs in the basal turn of young (A) and aged (B) CBA/CaJ mice. Notable alterations in the immunostaining pattern for Kir4.1 were seen in satellite cells of aged mice including discontinuities and thinning of Kir4.1 + components (arrows). The far right panels shows regions randomly selected from images in the left panels. Nuclei were counterstained with PI (red). Scale bar: 8 mm in A (applies to B, except for the right panels).
    Figure Legend Snippet: Age-related alterations in the Kir4.1 immunostaining pattern in satellite cells. The honeycomb-like Kir4.1 expression pattern reflects satellite cells ensheathing SGNs in the basal turn of young (A) and aged (B) CBA/CaJ mice. Notable alterations in the immunostaining pattern for Kir4.1 were seen in satellite cells of aged mice including discontinuities and thinning of Kir4.1 + components (arrows). The far right panels shows regions randomly selected from images in the left panels. Nuclei were counterstained with PI (red). Scale bar: 8 mm in A (applies to B, except for the right panels).

    Techniques Used: Immunostaining, Expressing, Crocin Bleaching Assay, Mouse Assay

    Age-related reduction of Kir4.1 expression in the mouse cochlear lateral wall. (A,C) Semiquantation of Kir4.1 expression levels as judged by measurements of fluorescence intensity in the middle and basal turns of the young versus aged group, revealed a significant decline of in the basal but not the middle turns of aged mice. (D-F) Immunostaining for Kir4.1 also declined in OSC root processes of the spiral ligament. A significant reduction of Kir4.1 fluorescence intensity was found in both the middle and basal turns of the aged mice. Data are presented as mean ± SEM (* p
    Figure Legend Snippet: Age-related reduction of Kir4.1 expression in the mouse cochlear lateral wall. (A,C) Semiquantation of Kir4.1 expression levels as judged by measurements of fluorescence intensity in the middle and basal turns of the young versus aged group, revealed a significant decline of in the basal but not the middle turns of aged mice. (D-F) Immunostaining for Kir4.1 also declined in OSC root processes of the spiral ligament. A significant reduction of Kir4.1 fluorescence intensity was found in both the middle and basal turns of the aged mice. Data are presented as mean ± SEM (* p

    Techniques Used: Expressing, Fluorescence, Mouse Assay, Immunostaining

    Immunostaining patterns for Kir4.1 in the STV from six temporal bones of different ages. (A-F) Kir4.1 immunoreactivity for intermediate cells in the STV generally appeared stronger and more uniform in the ears from the 31, 42 and 55 year-old donors (A-C). (D-E) There was a partial loss or reduction of Kir4.1 immunoreactivity in the STV (arrowheads) of the three human temporal bones from the 75, 86 and 91-year-old donors. All images were taken from the middle turn of the cochlea. Nuclei were counterstained with PI (red). Scale bar: 12 μm in A (applies to B-F).
    Figure Legend Snippet: Immunostaining patterns for Kir4.1 in the STV from six temporal bones of different ages. (A-F) Kir4.1 immunoreactivity for intermediate cells in the STV generally appeared stronger and more uniform in the ears from the 31, 42 and 55 year-old donors (A-C). (D-E) There was a partial loss or reduction of Kir4.1 immunoreactivity in the STV (arrowheads) of the three human temporal bones from the 75, 86 and 91-year-old donors. All images were taken from the middle turn of the cochlea. Nuclei were counterstained with PI (red). Scale bar: 12 μm in A (applies to B-F).

    Techniques Used: Immunostaining

    Immunolocalization of Kir4.1 in the human cochlea. (A-D) Similar to the mouse, the Kir4.1 immunoactivity was present in cells of the STV (A), OSCs (B), support cells in the Organ of Corti (C) and satellite cells surrounding SGNs within RC (D, arrows). The cochlear sections were taken from an 86 year-old donor (AC) Nuclei were counterstained with PI (red). Scale bar: 12 mm in A (applies to B-D).
    Figure Legend Snippet: Immunolocalization of Kir4.1 in the human cochlea. (A-D) Similar to the mouse, the Kir4.1 immunoactivity was present in cells of the STV (A), OSCs (B), support cells in the Organ of Corti (C) and satellite cells surrounding SGNs within RC (D, arrows). The cochlear sections were taken from an 86 year-old donor (AC) Nuclei were counterstained with PI (red). Scale bar: 12 mm in A (applies to B-D).

    Techniques Used:

    Expression of Kir4.1 in neural crest-derived cells of the young adult mouse cochlea. Immunostaining patterns for Kir4.1 (red) and Sox10 (a neural crest-derived cell marker; green) are illustrated in the middle turn of a 2 month-old mouse. (A) Kir4.1 and Sox10 proteins were co-localized in the intermediate cells in the stria vascularis (STV). (B) Outer sulcus cells (OSCs) and their root processes were also co-expressed Sox10, and Kir4.1. (C) Immunoreactive Kir4.1 and Sox10 were also found in supporting cells in the organ of Corti (OCT). (D) A honeycomb-like staining pattern for Kir4.1 reflected in the Sox10 + satellite cells ensheathing spiral ganglion neurons in Rosenthal’s canal (RC). Nuclei were counterstained with Dapi (blue). Scale bars, 25 μm in A; 12 μm in B (applies to C,D).
    Figure Legend Snippet: Expression of Kir4.1 in neural crest-derived cells of the young adult mouse cochlea. Immunostaining patterns for Kir4.1 (red) and Sox10 (a neural crest-derived cell marker; green) are illustrated in the middle turn of a 2 month-old mouse. (A) Kir4.1 and Sox10 proteins were co-localized in the intermediate cells in the stria vascularis (STV). (B) Outer sulcus cells (OSCs) and their root processes were also co-expressed Sox10, and Kir4.1. (C) Immunoreactive Kir4.1 and Sox10 were also found in supporting cells in the organ of Corti (OCT). (D) A honeycomb-like staining pattern for Kir4.1 reflected in the Sox10 + satellite cells ensheathing spiral ganglion neurons in Rosenthal’s canal (RC). Nuclei were counterstained with Dapi (blue). Scale bars, 25 μm in A; 12 μm in B (applies to C,D).

    Techniques Used: Expressing, Derivative Assay, Immunostaining, Marker, Staining

    4) Product Images from "Dystrophin Dp71 Is Critical for the Clustered Localization of Potassium Channels in Retinal Glial Cells"

    Article Title: Dystrophin Dp71 Is Critical for the Clustered Localization of Potassium Channels in Retinal Glial Cells

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.22-11-04321.2002

    Kir4.1 localization in wild-type ( wt ) and mdx 3Cv whole-mount retinal tissue. In both mice, optical sections were taken from the OPL ( A , B ), the IPL ( C , D ), the GCL ( E , F ), and the inner limiting membrane ( ILM ; D , H ). In the wild-type mouse ( A , C , E , G ), Kir4.1 was prominently detected in processes surrounding blood vessels ( green ) in the OPL, IPL, and GCL, respectively, whereas glutamine synthetase staining ( red ) revealed the location of Müller cells. Colocalization is indicated by yellow areas. Kir4.1 staining is prominently displayed at the inner limiting membrane of the wild type ( G ). Arrowheads ( B , D , F ) delineate blood vessels present in the OPL, IPL, and GCL, respectively, of the mdx 3Cv mouse that were not noticeably stained for Kir4.1. Uneven staining intensity in G and H resulted from the retina not being completely flat. Scale bar, 25 μm.
    Figure Legend Snippet: Kir4.1 localization in wild-type ( wt ) and mdx 3Cv whole-mount retinal tissue. In both mice, optical sections were taken from the OPL ( A , B ), the IPL ( C , D ), the GCL ( E , F ), and the inner limiting membrane ( ILM ; D , H ). In the wild-type mouse ( A , C , E , G ), Kir4.1 was prominently detected in processes surrounding blood vessels ( green ) in the OPL, IPL, and GCL, respectively, whereas glutamine synthetase staining ( red ) revealed the location of Müller cells. Colocalization is indicated by yellow areas. Kir4.1 staining is prominently displayed at the inner limiting membrane of the wild type ( G ). Arrowheads ( B , D , F ) delineate blood vessels present in the OPL, IPL, and GCL, respectively, of the mdx 3Cv mouse that were not noticeably stained for Kir4.1. Uneven staining intensity in G and H resulted from the retina not being completely flat. Scale bar, 25 μm.

    Techniques Used: Mouse Assay, Staining

    A , A Western blot was performed using brain lysates from wild-type ( wt ) and mdx 3Cv mice and was exposed to an antibody specific for the hydrophobic C terminus of dystrophin. The lack of immunodetection in the mdx 3Cv lane confirms a lack of Dp71 in the mutant mouse. B , A Western blot showing expression levels of Kir4.1 in wild-type versus mdx 3Cv brain and retina. A band at ∼200 kDa represents Kir4.1 in its tetrameric form. Brain tissue from the Kir4.1 knock-out ( KO ) mouse was used as a negative control ( far right lane ). There was no distinguishable difference in Kir4.1 expression between wild-type and mdx 3Cv mouse.
    Figure Legend Snippet: A , A Western blot was performed using brain lysates from wild-type ( wt ) and mdx 3Cv mice and was exposed to an antibody specific for the hydrophobic C terminus of dystrophin. The lack of immunodetection in the mdx 3Cv lane confirms a lack of Dp71 in the mutant mouse. B , A Western blot showing expression levels of Kir4.1 in wild-type versus mdx 3Cv brain and retina. A band at ∼200 kDa represents Kir4.1 in its tetrameric form. Brain tissue from the Kir4.1 knock-out ( KO ) mouse was used as a negative control ( far right lane ). There was no distinguishable difference in Kir4.1 expression between wild-type and mdx 3Cv mouse.

    Techniques Used: Western Blot, Mouse Assay, Immunodetection, Mutagenesis, Expressing, Knock-Out, Negative Control

    Kir4.1 localization in wild-type ( wt ) and mdx 3Cv retinal sections. A , Kir4.1 is concentrated at the inner limiting membrane ( arrow ) and to processes around blood vessels in wild-type retina ( arrowheads ). B , In the mdx 3Cv mouse, Kir4.1 appeared to be evenly distributed throughout the retina, and there appeared to be a reduction in staining at the inner limiting membrane ( arrow ) and no apparent enrichment of Kir4.1 around blood vessels ( arrowheads ). The Müller-specific marker glutamine synthetase ( GS ; C , D ) and merged images ( merged ; E , F ) suggest the localization of Kir4.1 to Müller cells. POS , Photoreceptor outer segments; ONL , outer nuclear layer; INL , inner nuclear layer. G , H , Retinal sections from wild type and mdx 3Cv were stained for GLAST. The structural integrity of Müller cells and their fine processes in the mutant mouse appeared to be intact and indistinguishable from that of the wild type. Scale bar, 25 μm.
    Figure Legend Snippet: Kir4.1 localization in wild-type ( wt ) and mdx 3Cv retinal sections. A , Kir4.1 is concentrated at the inner limiting membrane ( arrow ) and to processes around blood vessels in wild-type retina ( arrowheads ). B , In the mdx 3Cv mouse, Kir4.1 appeared to be evenly distributed throughout the retina, and there appeared to be a reduction in staining at the inner limiting membrane ( arrow ) and no apparent enrichment of Kir4.1 around blood vessels ( arrowheads ). The Müller-specific marker glutamine synthetase ( GS ; C , D ) and merged images ( merged ; E , F ) suggest the localization of Kir4.1 to Müller cells. POS , Photoreceptor outer segments; ONL , outer nuclear layer; INL , inner nuclear layer. G , H , Retinal sections from wild type and mdx 3Cv were stained for GLAST. The structural integrity of Müller cells and their fine processes in the mutant mouse appeared to be intact and indistinguishable from that of the wild type. Scale bar, 25 μm.

    Techniques Used: Staining, Marker, Mutagenesis

    5) Product Images from "Dystrophin Dp71 Is Critical for the Clustered Localization of Potassium Channels in Retinal Glial Cells"

    Article Title: Dystrophin Dp71 Is Critical for the Clustered Localization of Potassium Channels in Retinal Glial Cells

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.22-11-04321.2002

    Kir4.1 localization in wild-type ( wt ) and mdx 3Cv whole-mount retinal tissue. In both mice, optical sections were taken from the OPL ( A , B ), the IPL ( C , D ), the GCL ( E , F ), and the inner limiting membrane ( ILM ; D , H ). In the wild-type mouse ( A , C , E , G ), Kir4.1 was prominently detected in processes surrounding blood vessels ( green ) in the OPL, IPL, and GCL, respectively, whereas glutamine synthetase staining ( red ) revealed the location of Müller cells. Colocalization is indicated by yellow areas. Kir4.1 staining is prominently displayed at the inner limiting membrane of the wild type ( G ). Arrowheads ( B , D , F ) delineate blood vessels present in the OPL, IPL, and GCL, respectively, of the mdx 3Cv mouse that were not noticeably stained for Kir4.1. Uneven staining intensity in G and H resulted from the retina not being completely flat. Scale bar, 25 μm.
    Figure Legend Snippet: Kir4.1 localization in wild-type ( wt ) and mdx 3Cv whole-mount retinal tissue. In both mice, optical sections were taken from the OPL ( A , B ), the IPL ( C , D ), the GCL ( E , F ), and the inner limiting membrane ( ILM ; D , H ). In the wild-type mouse ( A , C , E , G ), Kir4.1 was prominently detected in processes surrounding blood vessels ( green ) in the OPL, IPL, and GCL, respectively, whereas glutamine synthetase staining ( red ) revealed the location of Müller cells. Colocalization is indicated by yellow areas. Kir4.1 staining is prominently displayed at the inner limiting membrane of the wild type ( G ). Arrowheads ( B , D , F ) delineate blood vessels present in the OPL, IPL, and GCL, respectively, of the mdx 3Cv mouse that were not noticeably stained for Kir4.1. Uneven staining intensity in G and H resulted from the retina not being completely flat. Scale bar, 25 μm.

    Techniques Used: Mouse Assay, Staining

    A , A Western blot was performed using brain lysates from wild-type ( wt ) and mdx 3Cv mice and was exposed to an antibody specific for the hydrophobic C terminus of dystrophin. The lack of immunodetection in the mdx 3Cv lane confirms a lack of Dp71 in the mutant mouse. B , A Western blot showing expression levels of Kir4.1 in wild-type versus mdx 3Cv brain and retina. A band at ∼200 kDa represents Kir4.1 in its tetrameric form. Brain tissue from the Kir4.1 knock-out ( KO ) mouse was used as a negative control ( far right lane ). There was no distinguishable difference in Kir4.1 expression between wild-type and mdx 3Cv mouse.
    Figure Legend Snippet: A , A Western blot was performed using brain lysates from wild-type ( wt ) and mdx 3Cv mice and was exposed to an antibody specific for the hydrophobic C terminus of dystrophin. The lack of immunodetection in the mdx 3Cv lane confirms a lack of Dp71 in the mutant mouse. B , A Western blot showing expression levels of Kir4.1 in wild-type versus mdx 3Cv brain and retina. A band at ∼200 kDa represents Kir4.1 in its tetrameric form. Brain tissue from the Kir4.1 knock-out ( KO ) mouse was used as a negative control ( far right lane ). There was no distinguishable difference in Kir4.1 expression between wild-type and mdx 3Cv mouse.

    Techniques Used: Western Blot, Mouse Assay, Immunodetection, Mutagenesis, Expressing, Knock-Out, Negative Control

    Kir4.1 localization in wild-type ( wt ) and mdx 3Cv retinal sections. A , Kir4.1 is concentrated at the inner limiting membrane ( arrow ) and to processes around blood vessels in wild-type retina ( arrowheads ). B , In the mdx 3Cv mouse, Kir4.1 appeared to be evenly distributed throughout the retina, and there appeared to be a reduction in staining at the inner limiting membrane ( arrow ) and no apparent enrichment of Kir4.1 around blood vessels ( arrowheads ). The Müller-specific marker glutamine synthetase ( GS ; C , D ) and merged images ( merged ; E , F ) suggest the localization of Kir4.1 to Müller cells. POS , Photoreceptor outer segments; ONL , outer nuclear layer; INL , inner nuclear layer. G , H , Retinal sections from wild type and mdx 3Cv were stained for GLAST. The structural integrity of Müller cells and their fine processes in the mutant mouse appeared to be intact and indistinguishable from that of the wild type. Scale bar, 25 μm.
    Figure Legend Snippet: Kir4.1 localization in wild-type ( wt ) and mdx 3Cv retinal sections. A , Kir4.1 is concentrated at the inner limiting membrane ( arrow ) and to processes around blood vessels in wild-type retina ( arrowheads ). B , In the mdx 3Cv mouse, Kir4.1 appeared to be evenly distributed throughout the retina, and there appeared to be a reduction in staining at the inner limiting membrane ( arrow ) and no apparent enrichment of Kir4.1 around blood vessels ( arrowheads ). The Müller-specific marker glutamine synthetase ( GS ; C , D ) and merged images ( merged ; E , F ) suggest the localization of Kir4.1 to Müller cells. POS , Photoreceptor outer segments; ONL , outer nuclear layer; INL , inner nuclear layer. G , H , Retinal sections from wild type and mdx 3Cv were stained for GLAST. The structural integrity of Müller cells and their fine processes in the mutant mouse appeared to be intact and indistinguishable from that of the wild type. Scale bar, 25 μm.

    Techniques Used: Staining, Marker, Mutagenesis

    6) Product Images from "Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat"

    Article Title: Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat

    Journal: Molecular Vision

    doi:

    Immunohistochemical detection of Kir4.1, aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.
    Figure Legend Snippet: Immunohistochemical detection of Kir4.1, aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.

    Techniques Used: Immunohistochemistry, Staining, Immunostaining, Injection

    Time course of Kir4.1 and aquaporin-4 mRNA expression in lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Total RNA (1 μg) was used for reverse transcriptase polymerase chain reaction (RT-PCR). A 330-bp product for aquaporin-4 (AQP4), a 225-bp product for Kir4.1, and a 240-bp product for β-actin were separated on a 2.0% agarose gel. B , C : The relative levels of Kir4.1 and AQP4 mRNA expression were quantified. Compared with the control, there was a significant decline in Kir4.1 in lipopolysaccharide (LPS)-treated animals, whereas there was no change in AQP4 after LPS injection (means±SEM, n=4; asterisk (*) indicates p
    Figure Legend Snippet: Time course of Kir4.1 and aquaporin-4 mRNA expression in lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Total RNA (1 μg) was used for reverse transcriptase polymerase chain reaction (RT-PCR). A 330-bp product for aquaporin-4 (AQP4), a 225-bp product for Kir4.1, and a 240-bp product for β-actin were separated on a 2.0% agarose gel. B , C : The relative levels of Kir4.1 and AQP4 mRNA expression were quantified. Compared with the control, there was a significant decline in Kir4.1 in lipopolysaccharide (LPS)-treated animals, whereas there was no change in AQP4 after LPS injection (means±SEM, n=4; asterisk (*) indicates p

    Techniques Used: Expressing, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Agarose Gel Electrophoresis, Injection

    Time courses of Kir4.1 and aquaporin-4 protein expression in retinas from lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Equal amounts of protein (30 μg) were subjected to immunoblotting analysis. A band at about 200 kDa represents Kir4.1 in its tetrameric form; aquaporin-4 (AQP4) consists of two bands, representing its M1 and M23 forms. B , C : The relative levels of Kir4.1 and AQP4 protein expression were quantified. Compared with that of the control, the expression of Kir4.1 was significantly reduced after LPS injection. In contrast, there was only a slight, statistically insignificant decline in AQP4 expression from 1 day to 7 day after LPS injection. (means±SEM, n=5; double asterisks (**) p
    Figure Legend Snippet: Time courses of Kir4.1 and aquaporin-4 protein expression in retinas from lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Equal amounts of protein (30 μg) were subjected to immunoblotting analysis. A band at about 200 kDa represents Kir4.1 in its tetrameric form; aquaporin-4 (AQP4) consists of two bands, representing its M1 and M23 forms. B , C : The relative levels of Kir4.1 and AQP4 protein expression were quantified. Compared with that of the control, the expression of Kir4.1 was significantly reduced after LPS injection. In contrast, there was only a slight, statistically insignificant decline in AQP4 expression from 1 day to 7 day after LPS injection. (means±SEM, n=5; double asterisks (**) p

    Techniques Used: Expressing, Injection

    7) Product Images from "Progressive irreversible hearing loss is caused by stria vascularis degeneration in an Slc26a4-insufficient mouse model of large vestibular aqueduct syndrome"

    Article Title: Progressive irreversible hearing loss is caused by stria vascularis degeneration in an Slc26a4-insufficient mouse model of large vestibular aqueduct syndrome

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2015.09.016

    Stria vascularis protein expression. Representative immunostaining of KCNQ1 (green) and KCNJ10 (red) in cryosections (A, C) or KCNQ1 (green) and F-actin (red) in whole-mounted specimens (B, D) of control (A, B) or experimental stria vascularis (C, D) in the middle turn. n = 6 ears for control mice, and n = 12 ears for experimental mice. MC, marginal cells. KCNQ1 fluorescence was reduced and KCNJ10 staining was absent in experimental ears at 12 months of age. Some marginal cells were expanded and lacked detectable KCNQ1, while others were abnormally small with KCNQ1 concentrated or aggregated within small cell surfaces (D). Apical surface areas of marginal cells for 3 control ears (E; n = 30 cells) and 3 experimental ears (F; n = 96 cells). Bin area = 50 μm 2 . If the surface area was > 1050 μm 2 , it was included in the 1000–1050 μm 2 bin.
    Figure Legend Snippet: Stria vascularis protein expression. Representative immunostaining of KCNQ1 (green) and KCNJ10 (red) in cryosections (A, C) or KCNQ1 (green) and F-actin (red) in whole-mounted specimens (B, D) of control (A, B) or experimental stria vascularis (C, D) in the middle turn. n = 6 ears for control mice, and n = 12 ears for experimental mice. MC, marginal cells. KCNQ1 fluorescence was reduced and KCNJ10 staining was absent in experimental ears at 12 months of age. Some marginal cells were expanded and lacked detectable KCNQ1, while others were abnormally small with KCNQ1 concentrated or aggregated within small cell surfaces (D). Apical surface areas of marginal cells for 3 control ears (E; n = 30 cells) and 3 experimental ears (F; n = 96 cells). Bin area = 50 μm 2 . If the surface area was > 1050 μm 2 , it was included in the 1000–1050 μm 2 bin.

    Techniques Used: Expressing, Immunostaining, Mouse Assay, Fluorescence, Staining

    8) Product Images from "AQUAPORIN-4 INDEPENDENT Kir4.1 K+ CHANNEL FUNCTION IN BRAIN GLIAL CELLS"

    Article Title: AQUAPORIN-4 INDEPENDENT Kir4.1 K+ CHANNEL FUNCTION IN BRAIN GLIAL CELLS

    Journal: Molecular and cellular neurosciences

    doi: 10.1016/j.mcn.2007.08.007

    Single-channel patch-clamp of Kir4.1 K + channels in freshly isolated astroglial cells
    Figure Legend Snippet: Single-channel patch-clamp of Kir4.1 K + channels in freshly isolated astroglial cells

    Techniques Used: Patch Clamp, Isolation

    Kir4.1 inhibition or knock-down does not affect AQP4 water permeability
    Figure Legend Snippet: Kir4.1 inhibition or knock-down does not affect AQP4 water permeability

    Techniques Used: Inhibition, Permeability

    Kir4.1 and AQP4 expression in mouse brain and isolated astroglial cells
    Figure Legend Snippet: Kir4.1 and AQP4 expression in mouse brain and isolated astroglial cells

    Techniques Used: Expressing, Isolation

    9) Product Images from "Modeling human‐specific interlaminar astrocytes in the mouse cerebral cortex. Modeling human‐specific interlaminar astrocytes in the mouse cerebral cortex"

    Article Title: Modeling human‐specific interlaminar astrocytes in the mouse cerebral cortex. Modeling human‐specific interlaminar astrocytes in the mouse cerebral cortex

    Journal: The Journal of Comparative Neurology

    doi: 10.1002/cne.24979

    Interlaminar astrocytes in the mouse cortex express canonical astrocytic markers. Sections from 9‐month‐old mouse engrafted with RFP expressing hiPSC‐astrocytes and immunostained with the antibodies against hGFAP, hCD44, S100B, Kir4.1, and AQP4. Scale = 10 μm [Color figure can be viewed at wileyonlinelibrary.com ]
    Figure Legend Snippet: Interlaminar astrocytes in the mouse cortex express canonical astrocytic markers. Sections from 9‐month‐old mouse engrafted with RFP expressing hiPSC‐astrocytes and immunostained with the antibodies against hGFAP, hCD44, S100B, Kir4.1, and AQP4. Scale = 10 μm [Color figure can be viewed at wileyonlinelibrary.com ]

    Techniques Used: Expressing

    10) Product Images from "A Nanoscale Interface Promoting Molecular and Functional Differentiation of Neural Cells"

    Article Title: A Nanoscale Interface Promoting Molecular and Functional Differentiation of Neural Cells

    Journal: Scientific Reports

    doi: 10.1038/srep31226

    Western blot analyses and quantification of protein expression of AQP4 ( a ) Kir4.1 ( b ) and Cx43 ( c ) on astrocytes plated on PDL and HTlc. β-actin ( a,b , lower panels) and α-tubulin were re-blotted and used as controls for signal normalization. Histogram plots evidencing change in protein expression with respect to the control are reported in the right panels of the figures. Values are the mean ± SE. (n = 3; *p
    Figure Legend Snippet: Western blot analyses and quantification of protein expression of AQP4 ( a ) Kir4.1 ( b ) and Cx43 ( c ) on astrocytes plated on PDL and HTlc. β-actin ( a,b , lower panels) and α-tubulin were re-blotted and used as controls for signal normalization. Histogram plots evidencing change in protein expression with respect to the control are reported in the right panels of the figures. Values are the mean ± SE. (n = 3; *p

    Techniques Used: Western Blot, Expressing

    Functional properties of HTlc-plated astrocytes. ( a,b ) Typical current traces evoked by a holding potential (Vh) of −60 mV stimulating astrocytes with a voltage ramp or voltage step family (insets). Astrocytes (left panels) plated on PDL displayed only voltage-dependent outward rectifying K + conductance. Astrocytes plated on HTlc coated coverslips (Right panels), display an inward conductance in response to a hyperpolarizing stimulus that is inhibited after extracellular superfusion with Ba 2+ ( a , inset, red trace 2). Note inhibition by Ba 2+ of outward currents in HTLc-treated astrocytes, suggesting a weak rectification profile of the inward current typical of Kir4.1. ( c ) Micrograph of calcein-loaded astrocytes showing the different shape of astrocytes grown on PDL vs those grown on HTlc. Histogram summarizing the swelling rates (τ) for the astrocytes grown on PDL or on HTlc. Value is the mean ± SE. (n = 30; P
    Figure Legend Snippet: Functional properties of HTlc-plated astrocytes. ( a,b ) Typical current traces evoked by a holding potential (Vh) of −60 mV stimulating astrocytes with a voltage ramp or voltage step family (insets). Astrocytes (left panels) plated on PDL displayed only voltage-dependent outward rectifying K + conductance. Astrocytes plated on HTlc coated coverslips (Right panels), display an inward conductance in response to a hyperpolarizing stimulus that is inhibited after extracellular superfusion with Ba 2+ ( a , inset, red trace 2). Note inhibition by Ba 2+ of outward currents in HTLc-treated astrocytes, suggesting a weak rectification profile of the inward current typical of Kir4.1. ( c ) Micrograph of calcein-loaded astrocytes showing the different shape of astrocytes grown on PDL vs those grown on HTlc. Histogram summarizing the swelling rates (τ) for the astrocytes grown on PDL or on HTlc. Value is the mean ± SE. (n = 30; P

    Techniques Used: Functional Assay, Inhibition

    AQP4 and Kir 4.1 protein expression in astrocytes plated on PDL and HTlc. ( a) Confocal imaging of astrocytes grown on HTLc NPs (upper panels) and PDL (lower panels) and stained for AQP4 (red), and Actin (green). ( b) Confocal imaging of astrocytes grown on HTLc NPs (upper panels) and PDL (lower panels) and stained for Kir4.1 (red), and GFAP(green). A merged image of the channels is reported on the right side of the panel, revealing that AQP4 and Kir 4.1 are highly up-regulated in the endfeet of astrocytes grown on HTlc NPs.
    Figure Legend Snippet: AQP4 and Kir 4.1 protein expression in astrocytes plated on PDL and HTlc. ( a) Confocal imaging of astrocytes grown on HTLc NPs (upper panels) and PDL (lower panels) and stained for AQP4 (red), and Actin (green). ( b) Confocal imaging of astrocytes grown on HTLc NPs (upper panels) and PDL (lower panels) and stained for Kir4.1 (red), and GFAP(green). A merged image of the channels is reported on the right side of the panel, revealing that AQP4 and Kir 4.1 are highly up-regulated in the endfeet of astrocytes grown on HTlc NPs.

    Techniques Used: Expressing, Imaging, Staining

    11) Product Images from "Caveolin-1 regulates corneal wound healing by modulating Kir4.1 activity"

    Article Title: Caveolin-1 regulates corneal wound healing by modulating Kir4.1 activity

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00023.2016

    Knockout of Cav1 suppresses Kir4.1 and enhances the phosphorylation of EGFR Y845 in corneas. A : Western blot shows that Cav1 knockout decreased Kir4.1 expression. B : normalized expression of Kir4.1 in corneas from both Cav1 −/− and WT mice is shown ( P
    Figure Legend Snippet: Knockout of Cav1 suppresses Kir4.1 and enhances the phosphorylation of EGFR Y845 in corneas. A : Western blot shows that Cav1 knockout decreased Kir4.1 expression. B : normalized expression of Kir4.1 in corneas from both Cav1 −/− and WT mice is shown ( P

    Techniques Used: Knock-Out, Western Blot, Expressing, Mouse Assay

    Inhibition of Cav1 by siRNA or inhibition of Kir4.1 by Ba 2+ incubation enhances the phosphorylation of EGFR Y845 in human corneal epithelial cells (HCE). A , top : expression of phosphorylation of EGFR Y845 from both control and siRNA-Cav1 groups. A , bottom : total EGFR expression in the groups. B : normalized expression of EGFR Y845 was quantitated by densitometry ( P
    Figure Legend Snippet: Inhibition of Cav1 by siRNA or inhibition of Kir4.1 by Ba 2+ incubation enhances the phosphorylation of EGFR Y845 in human corneal epithelial cells (HCE). A , top : expression of phosphorylation of EGFR Y845 from both control and siRNA-Cav1 groups. A , bottom : total EGFR expression in the groups. B : normalized expression of EGFR Y845 was quantitated by densitometry ( P

    Techniques Used: Inhibition, Incubation, Expressing

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    Alomone Labs kir4 1
    Posthypoxic effects in retinal water/ion channels, gliosis and cell death. (a) AQP-4 immunostaining of retina in control (a), 1h (b) and 18h (c) animals. (d-f) <t>Kir4.1</t> immunostaining. (g-i) GFAP immunostaining (green) and DAPI nuclei labeling (blue). (j-l) TUNEL (red, arrows) and DAPI (blue). (m, n) Bar graph of quantification of AQP-4 (m) and Kir4.1 (n) expression levels in the retina and correlation with retinal thickness. (o) Bar graph of quantification of GFAP + processes across the IPL and correlation with retinal thickness. (p) Bar graph of quantification of the number of TUNEL + cells in each retina layer per retinal section. GCL: ganglion cell layer; INL: inner nuclear layer; IPL: inner plexiform layer; OPL: outer plexiform layer, ONL: outer nuclear layer.
    Kir4 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/kir4 1/product/Alomone Labs
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    Alomone Labs kir4 1 ab
    In vivo intravitreal application of <t>Kir4.1-Ab:carrier</t> reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.
    Kir4 1 Ab, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Posthypoxic effects in retinal water/ion channels, gliosis and cell death. (a) AQP-4 immunostaining of retina in control (a), 1h (b) and 18h (c) animals. (d-f) Kir4.1 immunostaining. (g-i) GFAP immunostaining (green) and DAPI nuclei labeling (blue). (j-l) TUNEL (red, arrows) and DAPI (blue). (m, n) Bar graph of quantification of AQP-4 (m) and Kir4.1 (n) expression levels in the retina and correlation with retinal thickness. (o) Bar graph of quantification of GFAP + processes across the IPL and correlation with retinal thickness. (p) Bar graph of quantification of the number of TUNEL + cells in each retina layer per retinal section. GCL: ganglion cell layer; INL: inner nuclear layer; IPL: inner plexiform layer; OPL: outer plexiform layer, ONL: outer nuclear layer.

    Journal: PLoS ONE

    Article Title: Hypoxia-induced inflammation: Profiling the first 24-hour posthypoxic plasma and central nervous system changes

    doi: 10.1371/journal.pone.0246681

    Figure Lengend Snippet: Posthypoxic effects in retinal water/ion channels, gliosis and cell death. (a) AQP-4 immunostaining of retina in control (a), 1h (b) and 18h (c) animals. (d-f) Kir4.1 immunostaining. (g-i) GFAP immunostaining (green) and DAPI nuclei labeling (blue). (j-l) TUNEL (red, arrows) and DAPI (blue). (m, n) Bar graph of quantification of AQP-4 (m) and Kir4.1 (n) expression levels in the retina and correlation with retinal thickness. (o) Bar graph of quantification of GFAP + processes across the IPL and correlation with retinal thickness. (p) Bar graph of quantification of the number of TUNEL + cells in each retina layer per retinal section. GCL: ganglion cell layer; INL: inner nuclear layer; IPL: inner plexiform layer; OPL: outer plexiform layer, ONL: outer nuclear layer.

    Article Snippet: Retina immunostainingRetinae were immunostained with primary antibodies to detect and AQP-4 (1:50, mouse; catalog number sc-32739, Santa Cruz Biotechnology, Inc. Dallas, Texas, USA), Kir4.1 (1:200, rabbit, catalog number APC-035, Alomone Labs, Jerusalem, Israel) and glial fibrillary acidic protein (GFAP) (1:1000, rabbit; catalog number ab7260; Abcam, Cambridge, MA, USA).

    Techniques: Immunostaining, Labeling, TUNEL Assay, Expressing

    Expression of astrocyte-enriched proteins . Western blot analyses of astrocyte-enriched proteins in striatal protein homogenate from 13- to 14-month-old mice. ( A ) Western blots using Glt-1 and βactin as loading control (top panel), Kir4.1 and α-tubulin as loading control (middle panel) and αB-crystallin with βactin as loading control (bottom panel). Charts demonstrating no significant differences in the expression level of ( B ) Glt-1 [ F ) = 0.69, P = 0.54] or ( C ) Kir4.1, [ F ) = 3.4, P = 0.101] in the striatum of BACHD mice at this age. ( D ) Expression of αB-crystallin is changed in the group of samples [ F ) = 24.45, P = 0.0013]. It is decreased in BACHD mice ( P = 0029) and normalized in BACHD/GFAP-CreER T2 mice ( P = 0.7994) as compared to wild-type levels. BACHD/GFAP-CreER T2 levels are significantly increased as compared to BACHD levels. n = 3 BACHD, n = 3 BACHD/GFAP-CreER T2 , n = 3 wild type. Data are mean ± SEM. ** P

    Journal: Human Molecular Genetics

    Article Title: Mutant huntingtin reduction in astrocytes slows disease progression in the BACHD conditional Huntington’s disease mouse model

    doi: 10.1093/hmg/ddy363

    Figure Lengend Snippet: Expression of astrocyte-enriched proteins . Western blot analyses of astrocyte-enriched proteins in striatal protein homogenate from 13- to 14-month-old mice. ( A ) Western blots using Glt-1 and βactin as loading control (top panel), Kir4.1 and α-tubulin as loading control (middle panel) and αB-crystallin with βactin as loading control (bottom panel). Charts demonstrating no significant differences in the expression level of ( B ) Glt-1 [ F ) = 0.69, P = 0.54] or ( C ) Kir4.1, [ F ) = 3.4, P = 0.101] in the striatum of BACHD mice at this age. ( D ) Expression of αB-crystallin is changed in the group of samples [ F ) = 24.45, P = 0.0013]. It is decreased in BACHD mice ( P = 0029) and normalized in BACHD/GFAP-CreER T2 mice ( P = 0.7994) as compared to wild-type levels. BACHD/GFAP-CreER T2 levels are significantly increased as compared to BACHD levels. n = 3 BACHD, n = 3 BACHD/GFAP-CreER T2 , n = 3 wild type. Data are mean ± SEM. ** P

    Article Snippet: Gels were loaded with 25–30 μg of protein and immunoblots were probed with antibodies against HTT, (1:3000, MAB2166, mouse, EMD Millipore Burlington, MA) and either α-tubulin (1:3000, T9026, mouse, Sigma-Aldrich, St. Louis, MO) or βactin (1:5000, A7811, mouse, Sigma-Aldrich, St. Louis, MO) in 5% non-fat dry milk shaking overnight at 4°C; 5–10 □g of protein was used for Kir4.1 (1:1000, APC-035, rabbit, Alomone Labs Ltd., Jerusalem, Israel), GLT-1 (1:10,000, AB1783, guinea pig, EMD Millipore Burlington, MA) and αB-crystallin (1:2000, ADI-SPA-223, Enzo Biochem, New York, NY) in 5% non-fat dry milk.

    Techniques: Expressing, Western Blot, Mouse Assay

    The diabetes-induced decrease in Kir4.1-positive potassium channels level was restored after repeated THR-149 administration. ( A ) Representative graph and ( B ) images demonstrating a significant increase in the Kir4.1-positive retinal area after repeated administration of THR-149 at 4 weeks after diabetes onset. A single IVT injection of the PKal inhibitor did not significantly change the Kir4.1-positive retinal area compared with its vehicle ( n = 7 eyes for non-diabetic and n = 4 eyes for all diabetic groups). Individual data points and mean ± SEM are shown. * P

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Targeting Plasma Kallikrein With a Novel Bicyclic Peptide Inhibitor (THR-149) Reduces Retinal Thickening in a Diabetic Rat Model

    doi: 10.1167/iovs.62.13.18

    Figure Lengend Snippet: The diabetes-induced decrease in Kir4.1-positive potassium channels level was restored after repeated THR-149 administration. ( A ) Representative graph and ( B ) images demonstrating a significant increase in the Kir4.1-positive retinal area after repeated administration of THR-149 at 4 weeks after diabetes onset. A single IVT injection of the PKal inhibitor did not significantly change the Kir4.1-positive retinal area compared with its vehicle ( n = 7 eyes for non-diabetic and n = 4 eyes for all diabetic groups). Individual data points and mean ± SEM are shown. * P

    Article Snippet: Sections were incubated overnight with primary antibody for Iba1 (1/800; 019-19741; Sopachem, Ede, Netherlands), vimentin (1/400; V5255; Sigma-Aldrich), IL-6 (1/250; ab9324; Abcam, Cambridge, UK), IL-1β (1/1000; ab9722; Abcam), Kir 4.1 (1/200; APC-035; Alomone Labs, Jerusalem, Israel), or AQP4 (1/200; AQP-004; Alomone Labs).

    Techniques: Injection

    In vivo intravitreal application of Kir4.1-Ab:carrier reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Probing potassium channel function in vivo by intracellular delivery of antibodies in a rat model of retinal neurodegeneration

    doi: 10.1073/pnas.0913472107

    Figure Lengend Snippet: In vivo intravitreal application of Kir4.1-Ab:carrier reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.

    Article Snippet: Primary antibodies were polyclonal rabbit anti-human Kir2.1-Ab and Kir4.1-Ab (1:50 dilution; Alomone Labs), monoclonal mouse anti-human protein kinase C alpha (PKCα-Ab 1:200; Santa Cruz Biotechnology) to label rod BCs , monoclonal mouse anti-human protein kinase C beta (PKCβ-Ab, 1:200; Santa Cruz Biotechnology) to label cone BCs , polyclonal guinea-pig anti-rat vesicular glutamate transporter 1 (VGLUT1-Ab, 1:5,000; Chemicon) to label rod and cone BCs , polyclonal goat anti-human synapsin Ia/b-Ab (1:50; Santa Cruz Biotechnology) and IIa-Ab (1:100; Santa Cruz Biotechnology) as amacrine cell markers that label phosphoproteins of conventional synapses but not ribbon-containing terminals , and polyclonal GFAP-Ab (Sigma, 1:200) as Müller cell marker.

    Techniques: In Vivo, Injection

    IHC of rat retina shows Kir4.1 colocalization with Müller cell GFAP marker. ( A ) Conventional postmortem double labeling with Kir4.1-Ab (red) and GFAP-Ab (green) shows colocalization with Müller cells in a dystrophic 14 wk-old RCS retina. ( B ) In vivo intravitreal application of Kir4.1-Ab:carrier complex gives prominent labeling of Müller cell endfeet with extensions along Müller cell processes in the IPL (red) in a 15-wk-old dystrophic RCS rat and colocalizes with GFAP (green). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Probing potassium channel function in vivo by intracellular delivery of antibodies in a rat model of retinal neurodegeneration

    doi: 10.1073/pnas.0913472107

    Figure Lengend Snippet: IHC of rat retina shows Kir4.1 colocalization with Müller cell GFAP marker. ( A ) Conventional postmortem double labeling with Kir4.1-Ab (red) and GFAP-Ab (green) shows colocalization with Müller cells in a dystrophic 14 wk-old RCS retina. ( B ) In vivo intravitreal application of Kir4.1-Ab:carrier complex gives prominent labeling of Müller cell endfeet with extensions along Müller cell processes in the IPL (red) in a 15-wk-old dystrophic RCS rat and colocalizes with GFAP (green). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer.

    Article Snippet: Primary antibodies were polyclonal rabbit anti-human Kir2.1-Ab and Kir4.1-Ab (1:50 dilution; Alomone Labs), monoclonal mouse anti-human protein kinase C alpha (PKCα-Ab 1:200; Santa Cruz Biotechnology) to label rod BCs , monoclonal mouse anti-human protein kinase C beta (PKCβ-Ab, 1:200; Santa Cruz Biotechnology) to label cone BCs , polyclonal guinea-pig anti-rat vesicular glutamate transporter 1 (VGLUT1-Ab, 1:5,000; Chemicon) to label rod and cone BCs , polyclonal goat anti-human synapsin Ia/b-Ab (1:50; Santa Cruz Biotechnology) and IIa-Ab (1:100; Santa Cruz Biotechnology) as amacrine cell markers that label phosphoproteins of conventional synapses but not ribbon-containing terminals , and polyclonal GFAP-Ab (Sigma, 1:200) as Müller cell marker.

    Techniques: Immunohistochemistry, Marker, Labeling, In Vivo