rabbit polyclonal  (Alomone Labs)


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    Alomone Labs rabbit polyclonal

    Rabbit Polyclonal, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal - by Bioz Stars, 2023-09
    92/100 stars

    Images

    1) Product Images from "Megalencephalic leukoencephalopathy with subcortical cysts is a developmental disorder of the gliovascular unit"

    Article Title: Megalencephalic leukoencephalopathy with subcortical cysts is a developmental disorder of the gliovascular unit

    Journal: eLife

    doi: 10.7554/eLife.71379


    Figure Legend Snippet:

    Techniques Used: Sequencing, Western Blot, Immunofluorescence, Transduction

    rabbit polyclonal anti kir4 1 extracellular  (Alomone Labs)


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    Alomone Labs rabbit polyclonal anti kir4 1 extracellular
    RACK1 KO in astrocytes leads to higher levels of <t>Kir4.1</t> in astrocyte somata and PAPs (A) Generation of a mouse line with RACK1 KO in astrocytes (RACK1 cKO). Shown is a schematic of the RACK1 fl/fl and Aldh1l1-Cre/ERT2 alleles. Deletion of exon 2 in Gnb2l1 (the gene coding for RACK1) is induced in astrocytes by tamoxifen injection; this results in a frameshift and premature termination of Gnb2l1 translation. Primers are indicated by red arrows. (B) PCR assays for Gnb2l1 KO in brain DNA from RACK1 fl/fl or Aldh1l1-CreERT2: RACK1 fl/fl tamoxifen-injected mice (RACK1 cKO). The 898-bp band corresponds to the floxed allele ( <xref ref-type=Table S4 ). The 672-bp band corresponds to the exon 2-deleted allele. (C) Confocal images of RACK1 immunofluorescence (red) in the hippocampus in RACK1 fl/fl and RACK1 cKO mice. Astrocytes are co-immunolabeled for GFAP (green). Some astrocytes are indicated by white arrowheads. Nuclei are stained with DAPI. The bottom panel gives a higher-magnification view of the boxed areas in the RACK1 fl/fl and RACK1 cKO images, which shows that RACK1 is specifically depleted in astrocytes ( ∗ ) and is still expressed by neurons (°). Scale bars, 20 μm. (D), Western blot detection and analysis of Kir4.1 and GLT-1 in protein extracts from whole brain, hippocampus, whole-brain synaptogliosomes, hippocampal synaptogliosomes, or whole-brain microvessels purified from RACK1 fl/fl or RACK1 cKO mice. The position of molecular weight markers is indicated on the right. Signals were normalized against that of stain-free membranes except for the experiment on purified microvessels, where histone 3 was used. The data are quoted as the mean ± SD (N = 5 samples per genotype, 1 mouse per sample); two-tailed unpaired t test or Mann-Whitney test. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 and Figure S2 . " width="250" height="auto" />
    Rabbit Polyclonal Anti Kir4 1 Extracellular, 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 anti kir4 1 extracellular/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal anti kir4 1 extracellular - by Bioz Stars, 2023-09
    86/100 stars

    Images

    1) Product Images from "The ribosome-associated protein RACK1 represses Kir4.1 translation in astrocytes and influences neuronal activity"

    Article Title: The ribosome-associated protein RACK1 represses Kir4.1 translation in astrocytes and influences neuronal activity

    Journal: Cell Reports

    doi: 10.1016/j.celrep.2023.112456

    RACK1 KO in astrocytes leads to higher levels of Kir4.1 in astrocyte somata and PAPs (A) Generation of a mouse line with RACK1 KO in astrocytes (RACK1 cKO). Shown is a schematic of the RACK1 fl/fl and Aldh1l1-Cre/ERT2 alleles. Deletion of exon 2 in Gnb2l1 (the gene coding for RACK1) is induced in astrocytes by tamoxifen injection; this results in a frameshift and premature termination of Gnb2l1 translation. Primers are indicated by red arrows. (B) PCR assays for Gnb2l1 KO in brain DNA from RACK1 fl/fl or Aldh1l1-CreERT2: RACK1 fl/fl tamoxifen-injected mice (RACK1 cKO). The 898-bp band corresponds to the floxed allele ( <xref ref-type=Table S4 ). The 672-bp band corresponds to the exon 2-deleted allele. (C) Confocal images of RACK1 immunofluorescence (red) in the hippocampus in RACK1 fl/fl and RACK1 cKO mice. Astrocytes are co-immunolabeled for GFAP (green). Some astrocytes are indicated by white arrowheads. Nuclei are stained with DAPI. The bottom panel gives a higher-magnification view of the boxed areas in the RACK1 fl/fl and RACK1 cKO images, which shows that RACK1 is specifically depleted in astrocytes ( ∗ ) and is still expressed by neurons (°). Scale bars, 20 μm. (D), Western blot detection and analysis of Kir4.1 and GLT-1 in protein extracts from whole brain, hippocampus, whole-brain synaptogliosomes, hippocampal synaptogliosomes, or whole-brain microvessels purified from RACK1 fl/fl or RACK1 cKO mice. The position of molecular weight markers is indicated on the right. Signals were normalized against that of stain-free membranes except for the experiment on purified microvessels, where histone 3 was used. The data are quoted as the mean ± SD (N = 5 samples per genotype, 1 mouse per sample); two-tailed unpaired t test or Mann-Whitney test. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 and Figure S2 . " title="... KO in astrocytes leads to higher levels of Kir4.1 in astrocyte somata and PAPs (A) Generation of ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: RACK1 KO in astrocytes leads to higher levels of Kir4.1 in astrocyte somata and PAPs (A) Generation of a mouse line with RACK1 KO in astrocytes (RACK1 cKO). Shown is a schematic of the RACK1 fl/fl and Aldh1l1-Cre/ERT2 alleles. Deletion of exon 2 in Gnb2l1 (the gene coding for RACK1) is induced in astrocytes by tamoxifen injection; this results in a frameshift and premature termination of Gnb2l1 translation. Primers are indicated by red arrows. (B) PCR assays for Gnb2l1 KO in brain DNA from RACK1 fl/fl or Aldh1l1-CreERT2: RACK1 fl/fl tamoxifen-injected mice (RACK1 cKO). The 898-bp band corresponds to the floxed allele ( Table S4 ). The 672-bp band corresponds to the exon 2-deleted allele. (C) Confocal images of RACK1 immunofluorescence (red) in the hippocampus in RACK1 fl/fl and RACK1 cKO mice. Astrocytes are co-immunolabeled for GFAP (green). Some astrocytes are indicated by white arrowheads. Nuclei are stained with DAPI. The bottom panel gives a higher-magnification view of the boxed areas in the RACK1 fl/fl and RACK1 cKO images, which shows that RACK1 is specifically depleted in astrocytes ( ∗ ) and is still expressed by neurons (°). Scale bars, 20 μm. (D), Western blot detection and analysis of Kir4.1 and GLT-1 in protein extracts from whole brain, hippocampus, whole-brain synaptogliosomes, hippocampal synaptogliosomes, or whole-brain microvessels purified from RACK1 fl/fl or RACK1 cKO mice. The position of molecular weight markers is indicated on the right. Signals were normalized against that of stain-free membranes except for the experiment on purified microvessels, where histone 3 was used. The data are quoted as the mean ± SD (N = 5 samples per genotype, 1 mouse per sample); two-tailed unpaired t test or Mann-Whitney test. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 and Figure S2 .

    Techniques Used: Injection, Immunofluorescence, Immunolabeling, Staining, Western Blot, Purification, Molecular Weight, Two Tailed Test, MANN-WHITNEY

    Absence of RACK1 in astrocytes leads to higher Kir4.1-mediated astrocytic inward K + currents and cell volumes (A) Schematic of electrode positions used to record astrocyte whole-cell currents evoked by Schaffer collateral (SC) stimulation in the CA1 region of hippocampal slices. (B) Left: representative traces of astrocytic whole-cell currents induced by 150-ms voltage steps (from −200 mV to +100 mV, 10-mV steps; black traces at the bottom) in RACK1 fl/fl and RACK1 cKO mice before (black and pink) and after (blue) application of a KIR 4.1 antagonist (VU). Scale bars, 50 ms, 5 nA. Right: current-voltage (I-V) plot in RACK1 fl/fl (white filled dots) and in RACK1 cKO (pink-filled dots) mice before (black) and after (blue) application of VU (N = 7 and 10 astrocytes for RACK1 fl/fl and RACK1 cKO mice, respectively; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons) The data are quoted as the mean ± SD. (C) Left: representative astrocytic Kir4.1 (VU-sensitive) currents induced by SC stimulation (10 Hz, 1 s) in RACK1 fl/fl (black) and RACK1 cKO (pink) mice. Scale bars, 200 ms, 50 pA. Right: quantification of astrocytic Kir4.1 current peak amplitude after each stimulus during SC stimulation (10 Hz, 1 s) in RACK1 fl/fl (white filled dots) and RACK1 cKO (pink filled dots) mice (N = 6 and 5 astrocytes for RACK1 fl/fl and RACK1 cKO mice, respectively; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons). The data are quoted as the mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Illustration of the imaging method with a representative raw confocal image of an isolated RACK1 fl/fl CA1 astrocyte expressing tdTomato. (E–G) Imaris analysis: filament tracing (E), convex hull volume (F), and a 3D Sholl analysis (G). (H) Mean territory volume and filament length of RACK1 fl/fl and RACK1 cKO astrocytes. Shown is a histogram of the data, presented as the mean ± SD (N = 4 mice per genotype, 45 astrocytes); two-tailed t test. The data are quoted as the mean ± SD. (I) A Sholl analysis of the ramification complexity of RACK1 fl/fl and RACK1 cKO astrocytes. Two-way analysis of variance. ∗ p < 0.05, ∗∗ p < 0.01. The data are quoted as the mean ± SD. The raw data are presented in <xref ref-type=Table S3 . " title="Absence of RACK1 in astrocytes leads to higher Kir4.1-mediated astrocytic inward K + currents and cell volumes ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Absence of RACK1 in astrocytes leads to higher Kir4.1-mediated astrocytic inward K + currents and cell volumes (A) Schematic of electrode positions used to record astrocyte whole-cell currents evoked by Schaffer collateral (SC) stimulation in the CA1 region of hippocampal slices. (B) Left: representative traces of astrocytic whole-cell currents induced by 150-ms voltage steps (from −200 mV to +100 mV, 10-mV steps; black traces at the bottom) in RACK1 fl/fl and RACK1 cKO mice before (black and pink) and after (blue) application of a KIR 4.1 antagonist (VU). Scale bars, 50 ms, 5 nA. Right: current-voltage (I-V) plot in RACK1 fl/fl (white filled dots) and in RACK1 cKO (pink-filled dots) mice before (black) and after (blue) application of VU (N = 7 and 10 astrocytes for RACK1 fl/fl and RACK1 cKO mice, respectively; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons) The data are quoted as the mean ± SD. (C) Left: representative astrocytic Kir4.1 (VU-sensitive) currents induced by SC stimulation (10 Hz, 1 s) in RACK1 fl/fl (black) and RACK1 cKO (pink) mice. Scale bars, 200 ms, 50 pA. Right: quantification of astrocytic Kir4.1 current peak amplitude after each stimulus during SC stimulation (10 Hz, 1 s) in RACK1 fl/fl (white filled dots) and RACK1 cKO (pink filled dots) mice (N = 6 and 5 astrocytes for RACK1 fl/fl and RACK1 cKO mice, respectively; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons). The data are quoted as the mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Illustration of the imaging method with a representative raw confocal image of an isolated RACK1 fl/fl CA1 astrocyte expressing tdTomato. (E–G) Imaris analysis: filament tracing (E), convex hull volume (F), and a 3D Sholl analysis (G). (H) Mean territory volume and filament length of RACK1 fl/fl and RACK1 cKO astrocytes. Shown is a histogram of the data, presented as the mean ± SD (N = 4 mice per genotype, 45 astrocytes); two-tailed t test. The data are quoted as the mean ± SD. (I) A Sholl analysis of the ramification complexity of RACK1 fl/fl and RACK1 cKO astrocytes. Two-way analysis of variance. ∗ p < 0.05, ∗∗ p < 0.01. The data are quoted as the mean ± SD. The raw data are presented in Table S3 .

    Techniques Used: Imaging, Isolation, Expressing, Two Tailed Test

    Absence of RACK1 in astrocytes alters network population activity and neuronal responses to intense stimulation (A) Schematic of electrode positions used to record field excitatory postsynaptic potentials (fEPSPs) evoked by SC stimulation in the CA1 region of hippocampal slices. (B) Input-output curves for basal synaptic transmission. Left: representative recordings in RACK1 fl/fl mice (black) and RACK1 cKO mice before (pink) and after (blue) application of a Kir 4.1 antagonist (VU). Scale bars, 10 ms, 0.5 mV. Right: quantification of the fEPSP slope for different fiber volley amplitudes after SC stimulation. The data are quoted as the mean ± SD. RACK1 fl/fl: n = 5 slices from 4 mice; p = 0.0087; RACK1 cKO: n = 5 slices from 5 mice; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons. (C) Top: a representative recording of fEPSPs evoked by repetitive stimulation (10 Hz, 30 s) of CA1 SCs in RACK1 fl/fl mice under control conditions. Scale bars, 5 s, 0.2 mV. Bottom: enlarged view of fEPSPs evoked by the first 10 stimuli. Scale bars, 200 ms, 0.2 mV. (D) Changes in the fEPSP slope induced by 10-Hz stimulation relative to responses measured before the onset of stimulation (baseline responses) in RACK1 fl/fl mice (white filled dots) and in RACK1 cKO mice (pink-filled dots) before (black) and after (blue) application of VU. The data are quoted as the mean ± SD. RACK1 fl/fl: n = 5 from 5 mice; RACK1 cKO: n = 6 slices from 4 mice; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons. (E) Schematic (left) and picture (right) of a hippocampal slice placed on a multielectrode array (MEA). Scale bar, 200 μm. (F) Representative MEA recordings of burst activity induced in hippocampal slices of RACK1 fl/fl (black) and RACK1 cKO (pink) mice by incubation in Mg 2+ -free ACSF containing 6 mM KCl. The expanded recordings of the bursts (surrounded by gray rectangles) are shown on the right. Scale bars, 10 s (left)/200 ms (right), 50 μV. (G) Quantification of burst frequency (top) and burst duration (bottom) in RACK1 fl/fl (white) and RACK1 cKO (pink) hippocampal slices. The data are quoted as the mean ± SD. n = 15 slices from 5 mice for RACK1 fl/fl and n = 18 slices from 6 mice for RACK1 cKO; unpaired t test. (H) Representative MEA recordings of hippocampal bursting activity in RACK1 fl/fl (top) and RACK1 cKO (bottom) slices in control (Ct) and during 25-min treatment with the Kir4.1 blocker VU0134992 (VU). The corresponding time-frequency plots are shown under the traces. Scale bar, 20 s/2 min, 50 μV. (I) Quantification of VU’s effect on burst frequency (top) and duration (bottom) in RACK1 fl/fl (white) and RACK1 cKO (pink) hippocampal slices (RACK1 fl/fl: n = 15 slices from 5 mice for burst frequency and duration, respectively; RACK1 cKO: n = 18 slices from 6 mice for burst frequency and duration; paired t test. The data are quoted as the mean ± SD. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in <xref ref-type=Table S3 . " title="... control (Ct) and during 25-min treatment with the Kir4.1 blocker VU0134992 (VU). The corresponding time-frequency plots are ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Absence of RACK1 in astrocytes alters network population activity and neuronal responses to intense stimulation (A) Schematic of electrode positions used to record field excitatory postsynaptic potentials (fEPSPs) evoked by SC stimulation in the CA1 region of hippocampal slices. (B) Input-output curves for basal synaptic transmission. Left: representative recordings in RACK1 fl/fl mice (black) and RACK1 cKO mice before (pink) and after (blue) application of a Kir 4.1 antagonist (VU). Scale bars, 10 ms, 0.5 mV. Right: quantification of the fEPSP slope for different fiber volley amplitudes after SC stimulation. The data are quoted as the mean ± SD. RACK1 fl/fl: n = 5 slices from 4 mice; p = 0.0087; RACK1 cKO: n = 5 slices from 5 mice; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons. (C) Top: a representative recording of fEPSPs evoked by repetitive stimulation (10 Hz, 30 s) of CA1 SCs in RACK1 fl/fl mice under control conditions. Scale bars, 5 s, 0.2 mV. Bottom: enlarged view of fEPSPs evoked by the first 10 stimuli. Scale bars, 200 ms, 0.2 mV. (D) Changes in the fEPSP slope induced by 10-Hz stimulation relative to responses measured before the onset of stimulation (baseline responses) in RACK1 fl/fl mice (white filled dots) and in RACK1 cKO mice (pink-filled dots) before (black) and after (blue) application of VU. The data are quoted as the mean ± SD. RACK1 fl/fl: n = 5 from 5 mice; RACK1 cKO: n = 6 slices from 4 mice; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons. (E) Schematic (left) and picture (right) of a hippocampal slice placed on a multielectrode array (MEA). Scale bar, 200 μm. (F) Representative MEA recordings of burst activity induced in hippocampal slices of RACK1 fl/fl (black) and RACK1 cKO (pink) mice by incubation in Mg 2+ -free ACSF containing 6 mM KCl. The expanded recordings of the bursts (surrounded by gray rectangles) are shown on the right. Scale bars, 10 s (left)/200 ms (right), 50 μV. (G) Quantification of burst frequency (top) and burst duration (bottom) in RACK1 fl/fl (white) and RACK1 cKO (pink) hippocampal slices. The data are quoted as the mean ± SD. n = 15 slices from 5 mice for RACK1 fl/fl and n = 18 slices from 6 mice for RACK1 cKO; unpaired t test. (H) Representative MEA recordings of hippocampal bursting activity in RACK1 fl/fl (top) and RACK1 cKO (bottom) slices in control (Ct) and during 25-min treatment with the Kir4.1 blocker VU0134992 (VU). The corresponding time-frequency plots are shown under the traces. Scale bar, 20 s/2 min, 50 μV. (I) Quantification of VU’s effect on burst frequency (top) and duration (bottom) in RACK1 fl/fl (white) and RACK1 cKO (pink) hippocampal slices (RACK1 fl/fl: n = 15 slices from 5 mice for burst frequency and duration, respectively; RACK1 cKO: n = 18 slices from 6 mice for burst frequency and duration; paired t test. The data are quoted as the mean ± SD. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 .

    Techniques Used: Activity Assay, Transmission Assay, Incubation


    Figure Legend Snippet:

    Techniques Used: Transduction, Recombinant, Multiplex Assay, Mass Spectrometry, Software

    rabbit polyclonal  (Alomone Labs)


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    Alomone Labs rabbit polyclonal

    Rabbit Polyclonal, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal - by Bioz Stars, 2023-09
    92/100 stars

    Images

    1) Product Images from "Megalencephalic leukoencephalopathy with subcortical cysts is a developmental disorder of the gliovascular unit"

    Article Title: Megalencephalic leukoencephalopathy with subcortical cysts is a developmental disorder of the gliovascular unit

    Journal: eLife

    doi: 10.7554/eLife.71379


    Figure Legend Snippet:

    Techniques Used: Sequencing, Western Blot, Immunofluorescence, Transduction

    rabbit polyclonal anti kir4 1 extracellular  (Alomone Labs)


    Bioz Verified Symbol Alomone Labs is a verified supplier
    Bioz Manufacturer Symbol Alomone Labs manufactures this product  
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    Structured Review

    Alomone Labs rabbit polyclonal anti kir4 1 extracellular
    <t>Kir4.1</t> Upregulation in Ventral Horn AS around Large FαMN MNs (A and B) Kir4.1 mRNA is enriched in spinal cord compared to other CNS regions in humans (A) and mice ( <xref ref-type=Kasukawa et al., 2011 ) (B). Data are represented as mean ± SEM. (C and D) Perineuronal enrichment of Kir4.1 expression in human and mouse ventral spinal cord. (C) KIR4.1 is expressed around SMI32 + neurons in adult human ventral spinal cord (scale bars, 1 mm, left; 50 μm, right). Representative image of n = 3 control human spinal cord. Patient data are provided in . (D) Kir4.1 is expressed around ChAT + MNs in mouse ventral lumbar spinal cord at P16 (scale bars, 200 μm, left; 50 μm, right). Dotted line denotes gray/white matter boundary. WM, white matter. Arrowheads denote Kir4.1 enrichment around ventral horn neurons. High-resolution images are single-plane confocal images. (E) Increased ventral (V) compared to dorsal (D) Kir4.1 protein by western blot from mouse lumbar spinal cord at P30 (n = 4 mice, mean ± SEM, Welch’s t test). (F) Left: fold change of Kir4.1 mRNA levels between ventral and dorsal samples from cultured (n = 6 mice, mean ± SEM, one-sample t test) neonatal mouse spinal cord AS. Right: FACS-purified AS from P5 Aldh1l1-GFP + (n = 3 mice, mean ± SEM, one-sample t test) mouse spinal cord. (G) Kir4.1 mRNA levels in P5 Aldh1l1-GFP + FACS-purified AS compared to Aldh1l1-GFP − non-AS cells from mouse ventral spinal cord (n = 3 mice, mean ± SEM, one-sample t test). (H) Kir4.1 protein is preferentially found around larger MMP-9 + FαMNs (white arrowheads) compared to smaller MMP-9 − SαMNs (yellow arrowheads) at P30 (scale bar, 50 μm). (I) Quantification of Kir4.1 signal intensity around individual MMP-9 + or MMP-9 − MN (n = 4 mice, >100 MN counts/animal, boxplot, Mann-Whitney test). (J) Kir4.1 loss in AS from VGLUT1 KO animals at P26. VGLUT1 KO mice were crossed with EAAT2-td-Tomato reporter for AS visualization. (K) Quantification of Kir4.1 immunofluorescence intensity per AS (EAAT2-td-tomato + ) (n = 2 mice, >50 AS counts/animal, boxplot, Mann-Whitney test; scale bar, 40 μm, insert: 20 μm). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and the black line denoting the median value. " width="250" height="auto" />
    Rabbit Polyclonal Anti Kir4 1 Extracellular, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal anti kir4 1 extracellular/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal anti kir4 1 extracellular - by Bioz Stars, 2023-09
    92/100 stars

    Images

    1) Product Images from "Kir4.1-Dependent Astrocyte-Fast Motor Neuron Interactions Are Required for Peak Strength"

    Article Title: Kir4.1-Dependent Astrocyte-Fast Motor Neuron Interactions Are Required for Peak Strength

    Journal: Neuron

    doi: 10.1016/j.neuron.2018.03.010

    Kir4.1 Upregulation in Ventral Horn AS around Large FαMN MNs (A and B) Kir4.1 mRNA is enriched in spinal cord compared to other CNS regions in humans (A) and mice ( <xref ref-type=Kasukawa et al., 2011 ) (B). Data are represented as mean ± SEM. (C and D) Perineuronal enrichment of Kir4.1 expression in human and mouse ventral spinal cord. (C) KIR4.1 is expressed around SMI32 + neurons in adult human ventral spinal cord (scale bars, 1 mm, left; 50 μm, right). Representative image of n = 3 control human spinal cord. Patient data are provided in . (D) Kir4.1 is expressed around ChAT + MNs in mouse ventral lumbar spinal cord at P16 (scale bars, 200 μm, left; 50 μm, right). Dotted line denotes gray/white matter boundary. WM, white matter. Arrowheads denote Kir4.1 enrichment around ventral horn neurons. High-resolution images are single-plane confocal images. (E) Increased ventral (V) compared to dorsal (D) Kir4.1 protein by western blot from mouse lumbar spinal cord at P30 (n = 4 mice, mean ± SEM, Welch’s t test). (F) Left: fold change of Kir4.1 mRNA levels between ventral and dorsal samples from cultured (n = 6 mice, mean ± SEM, one-sample t test) neonatal mouse spinal cord AS. Right: FACS-purified AS from P5 Aldh1l1-GFP + (n = 3 mice, mean ± SEM, one-sample t test) mouse spinal cord. (G) Kir4.1 mRNA levels in P5 Aldh1l1-GFP + FACS-purified AS compared to Aldh1l1-GFP − non-AS cells from mouse ventral spinal cord (n = 3 mice, mean ± SEM, one-sample t test). (H) Kir4.1 protein is preferentially found around larger MMP-9 + FαMNs (white arrowheads) compared to smaller MMP-9 − SαMNs (yellow arrowheads) at P30 (scale bar, 50 μm). (I) Quantification of Kir4.1 signal intensity around individual MMP-9 + or MMP-9 − MN (n = 4 mice, >100 MN counts/animal, boxplot, Mann-Whitney test). (J) Kir4.1 loss in AS from VGLUT1 KO animals at P26. VGLUT1 KO mice were crossed with EAAT2-td-Tomato reporter for AS visualization. (K) Quantification of Kir4.1 immunofluorescence intensity per AS (EAAT2-td-tomato + ) (n = 2 mice, >50 AS counts/animal, boxplot, Mann-Whitney test; scale bar, 40 μm, insert: 20 μm). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and the black line denoting the median value. " title="Kir4.1 Upregulation in Ventral Horn AS around Large FαMN ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Kir4.1 Upregulation in Ventral Horn AS around Large FαMN MNs (A and B) Kir4.1 mRNA is enriched in spinal cord compared to other CNS regions in humans (A) and mice ( Kasukawa et al., 2011 ) (B). Data are represented as mean ± SEM. (C and D) Perineuronal enrichment of Kir4.1 expression in human and mouse ventral spinal cord. (C) KIR4.1 is expressed around SMI32 + neurons in adult human ventral spinal cord (scale bars, 1 mm, left; 50 μm, right). Representative image of n = 3 control human spinal cord. Patient data are provided in . (D) Kir4.1 is expressed around ChAT + MNs in mouse ventral lumbar spinal cord at P16 (scale bars, 200 μm, left; 50 μm, right). Dotted line denotes gray/white matter boundary. WM, white matter. Arrowheads denote Kir4.1 enrichment around ventral horn neurons. High-resolution images are single-plane confocal images. (E) Increased ventral (V) compared to dorsal (D) Kir4.1 protein by western blot from mouse lumbar spinal cord at P30 (n = 4 mice, mean ± SEM, Welch’s t test). (F) Left: fold change of Kir4.1 mRNA levels between ventral and dorsal samples from cultured (n = 6 mice, mean ± SEM, one-sample t test) neonatal mouse spinal cord AS. Right: FACS-purified AS from P5 Aldh1l1-GFP + (n = 3 mice, mean ± SEM, one-sample t test) mouse spinal cord. (G) Kir4.1 mRNA levels in P5 Aldh1l1-GFP + FACS-purified AS compared to Aldh1l1-GFP − non-AS cells from mouse ventral spinal cord (n = 3 mice, mean ± SEM, one-sample t test). (H) Kir4.1 protein is preferentially found around larger MMP-9 + FαMNs (white arrowheads) compared to smaller MMP-9 − SαMNs (yellow arrowheads) at P30 (scale bar, 50 μm). (I) Quantification of Kir4.1 signal intensity around individual MMP-9 + or MMP-9 − MN (n = 4 mice, >100 MN counts/animal, boxplot, Mann-Whitney test). (J) Kir4.1 loss in AS from VGLUT1 KO animals at P26. VGLUT1 KO mice were crossed with EAAT2-td-Tomato reporter for AS visualization. (K) Quantification of Kir4.1 immunofluorescence intensity per AS (EAAT2-td-tomato + ) (n = 2 mice, >50 AS counts/animal, boxplot, Mann-Whitney test; scale bar, 40 μm, insert: 20 μm). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and the black line denoting the median value.

    Techniques Used: Expressing, Western Blot, Cell Culture, Purification, MANN-WHITNEY, Immunofluorescence

    AS Kir4.1 Is Required for Maintenance of FαMN Size (A) Left: breeding scheme. AS-Kir4.1cKO and cre-negative control animals were bred with ChAT-GFP mice for MN visualization. Right: total FαMN (ChAT + /MMP-9 + /NeuN + ), SαMN (ChAT + /MMP-9 − /NeuN + ), and γMN (ChAT + /MMP-9 − /NeuN − ) numbers are equivalent in AS-Kir4.1cKO and cre-negative control mice at the indicated ages (n = 3 mice/group, mean ± SEM, lumbar spinal cord, Welch’s t test). (B, D, and F) Representative images of lumbar MNs at P14 (B), P30 (D), and 6 months (F). Arrowheads denote example FαMNs (scale bar, 50 μm). (C, E, and G) Quantification of MN size at P14 (C), P30 (E), and 6 months (G) (n = 3 mice/group, >100 MN counts/animal, boxplot, Mann-Whitney test). (H) Schematic of retrograde labeling of MN pools using intramuscular injection of fluorescent cholera toxin subunit B (CTSB) in the tibialis anterior (TA) muscle. (I) Representative images of retrograde-labeled ventral horn MNs in AS-Kir4.1cKO and cre-negative control mice. Arrowheads denote example putative FαMNs (scale bar, 50 μm). (J) Quantification of ChAT-GFP + CTSB + MN soma area from (G) (n = 3 mice/group, >50 MN counts/animal, boxplot, Mann-Whitney test). ∗ p < 0.05, ∗∗∗ p < 0.001. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and black line denoting the median value.
    Figure Legend Snippet: AS Kir4.1 Is Required for Maintenance of FαMN Size (A) Left: breeding scheme. AS-Kir4.1cKO and cre-negative control animals were bred with ChAT-GFP mice for MN visualization. Right: total FαMN (ChAT + /MMP-9 + /NeuN + ), SαMN (ChAT + /MMP-9 − /NeuN + ), and γMN (ChAT + /MMP-9 − /NeuN − ) numbers are equivalent in AS-Kir4.1cKO and cre-negative control mice at the indicated ages (n = 3 mice/group, mean ± SEM, lumbar spinal cord, Welch’s t test). (B, D, and F) Representative images of lumbar MNs at P14 (B), P30 (D), and 6 months (F). Arrowheads denote example FαMNs (scale bar, 50 μm). (C, E, and G) Quantification of MN size at P14 (C), P30 (E), and 6 months (G) (n = 3 mice/group, >100 MN counts/animal, boxplot, Mann-Whitney test). (H) Schematic of retrograde labeling of MN pools using intramuscular injection of fluorescent cholera toxin subunit B (CTSB) in the tibialis anterior (TA) muscle. (I) Representative images of retrograde-labeled ventral horn MNs in AS-Kir4.1cKO and cre-negative control mice. Arrowheads denote example putative FαMNs (scale bar, 50 μm). (J) Quantification of ChAT-GFP + CTSB + MN soma area from (G) (n = 3 mice/group, >50 MN counts/animal, boxplot, Mann-Whitney test). ∗ p < 0.05, ∗∗∗ p < 0.001. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and black line denoting the median value.

    Techniques Used: Negative Control, MANN-WHITNEY, Labeling, Injection

    AS Kir4.1 Is Required for FαMN Function, Fast-Twitch Muscle Fiber Size, and Peak Force (A) Breeding scheme and electrophysiology recording schematic. (B) Two representative current steps at 3× rheobase (RB). (C–E) Rheobase (C), input resistance (D), and steady-state (SS) firing frequency (at 3× rheobase) (E) demonstrate altered intrinsic electrophysiological deficits in MNs from AS-Kir4.1cKO-ChAT-GFP animals at P12–P15 (n = 12 control MNs, n = 14 AS-Kir4.1cKO MNs from at least 3 animals per group, boxplot, Mann-Whitney test). (F) Input resistance versus rheobase scatterplot shows shift in electrophysiological properties from fast-like to slow-like in AS-Kir4.1cKO compared to control MNs. (G) Cross sections of TA muscle fibers immunolabeled for marker of fast-twitch muscle (myosin type 2) and laminin in P30 AS-Kir4.1cKO and cre-negative control animals (scale bar, 50 μm). (H) Quantification of TA muscle fiber cross-sectional area (n = 3 mice/group, >100 muscle fibers/animal, boxplot, Mann-Whitney test). (I–K) Abnormal muscle strength behavior in AS-Kir4.1cKO mice. Adult AS-Kir4.1cKO animals generate less peak force (>P50, n = 14–15 mice/group, boxplot, Welch’s t test) (I). AS-Kir4.1cKO animals have slower front and hindlimb movements as assessed by gait analysis with the catwalk behavioral test. Swing speed corresponds to the limb speed while in the air (same animals as in I, boxplot, Welch’s t test) (J). AS-Kir4.1cKO animals display a shorter latency to fall on the accelerating rotarod at P30–P35 (n ≥ 7 mice/group, mean ± SEM, two-way ANOVA, Bonferroni post hoc test) (K). Mice performed three trials (T, T2, and T3) per day on 3 consecutive days (D1, D2, and D3). ∗ p < 0.05, ∗∗ p < 0.01. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and black line denoting the median value.
    Figure Legend Snippet: AS Kir4.1 Is Required for FαMN Function, Fast-Twitch Muscle Fiber Size, and Peak Force (A) Breeding scheme and electrophysiology recording schematic. (B) Two representative current steps at 3× rheobase (RB). (C–E) Rheobase (C), input resistance (D), and steady-state (SS) firing frequency (at 3× rheobase) (E) demonstrate altered intrinsic electrophysiological deficits in MNs from AS-Kir4.1cKO-ChAT-GFP animals at P12–P15 (n = 12 control MNs, n = 14 AS-Kir4.1cKO MNs from at least 3 animals per group, boxplot, Mann-Whitney test). (F) Input resistance versus rheobase scatterplot shows shift in electrophysiological properties from fast-like to slow-like in AS-Kir4.1cKO compared to control MNs. (G) Cross sections of TA muscle fibers immunolabeled for marker of fast-twitch muscle (myosin type 2) and laminin in P30 AS-Kir4.1cKO and cre-negative control animals (scale bar, 50 μm). (H) Quantification of TA muscle fiber cross-sectional area (n = 3 mice/group, >100 muscle fibers/animal, boxplot, Mann-Whitney test). (I–K) Abnormal muscle strength behavior in AS-Kir4.1cKO mice. Adult AS-Kir4.1cKO animals generate less peak force (>P50, n = 14–15 mice/group, boxplot, Welch’s t test) (I). AS-Kir4.1cKO animals have slower front and hindlimb movements as assessed by gait analysis with the catwalk behavioral test. Swing speed corresponds to the limb speed while in the air (same animals as in I, boxplot, Welch’s t test) (J). AS-Kir4.1cKO animals display a shorter latency to fall on the accelerating rotarod at P30–P35 (n ≥ 7 mice/group, mean ± SEM, two-way ANOVA, Bonferroni post hoc test) (K). Mice performed three trials (T, T2, and T3) per day on 3 consecutive days (D1, D2, and D3). ∗ p < 0.05, ∗∗ p < 0.01. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and black line denoting the median value.

    Techniques Used: MANN-WHITNEY, Immunolabeling, Marker, Negative Control

    Cell-Autonomous AS Kir4.1 Loss Does Not Alter MN Survival in ALS (A) Schematic of iPSC-derived AS from human SOD1D90A ALS patients and non-ALS controls (patient data are provided in ). (B) Representative images of iPSC-derived AS from human SOD1D90A ALS patients and non-ALS controls labeled with KIR4.1 and GFAP (scale bar, 40 μm). (C) KCNJ10 mRNA levels are downregulated in SOD1G90A iPSC-derived AS as compared to controls (n = 2–3 independent cultures, mean ± SEM, Mann-Whitney test). (D) Western blot of KIR4.1, ALDH1L1, and GFAP on iPSC-derived AS from human SOD1D90A ALS patients and non-ALS controls. (E) Quantification of KIR4.1, ALDH1L1, and GFAP protein levels from western blot in (D) (n = 3/group, mean ± SEM, Mann-Whitney test). (F) Breeding scheme used for the loss of function of AS Kir4.1 in SOD1G93A ( mSOD1 ) mutant background. (G) Representative images of ventral horn lumbar spinal cord at P80 from cre-negative control, mSOD1 , and mSOD1 ; AS-Kir4.1cKO ( mSOD1; cKO ) animals labeled with MN markers (scale bar, 50 μm). (H and I) Quantification of ChAT + NeuN + (H) and MMP-9 + NeuN + (I) MN numbers in cre-negative control, mSOD1 , and mSOD1; cKO animals (n = 4–7 mice/group, >100 MN counts/animal, mean ± SEM, Kruskal-Wallis test). ∗ p < 0.05, ∗∗ p < 0.01.
    Figure Legend Snippet: Cell-Autonomous AS Kir4.1 Loss Does Not Alter MN Survival in ALS (A) Schematic of iPSC-derived AS from human SOD1D90A ALS patients and non-ALS controls (patient data are provided in ). (B) Representative images of iPSC-derived AS from human SOD1D90A ALS patients and non-ALS controls labeled with KIR4.1 and GFAP (scale bar, 40 μm). (C) KCNJ10 mRNA levels are downregulated in SOD1G90A iPSC-derived AS as compared to controls (n = 2–3 independent cultures, mean ± SEM, Mann-Whitney test). (D) Western blot of KIR4.1, ALDH1L1, and GFAP on iPSC-derived AS from human SOD1D90A ALS patients and non-ALS controls. (E) Quantification of KIR4.1, ALDH1L1, and GFAP protein levels from western blot in (D) (n = 3/group, mean ± SEM, Mann-Whitney test). (F) Breeding scheme used for the loss of function of AS Kir4.1 in SOD1G93A ( mSOD1 ) mutant background. (G) Representative images of ventral horn lumbar spinal cord at P80 from cre-negative control, mSOD1 , and mSOD1 ; AS-Kir4.1cKO ( mSOD1; cKO ) animals labeled with MN markers (scale bar, 50 μm). (H and I) Quantification of ChAT + NeuN + (H) and MMP-9 + NeuN + (I) MN numbers in cre-negative control, mSOD1 , and mSOD1; cKO animals (n = 4–7 mice/group, >100 MN counts/animal, mean ± SEM, Kruskal-Wallis test). ∗ p < 0.05, ∗∗ p < 0.01.

    Techniques Used: Derivative Assay, Labeling, MANN-WHITNEY, Western Blot, Mutagenesis, Negative Control

    Kir4.1 Viral-Mediated Overexpression Is Sufficient to Increase MN Size (A and B) Left: schematic of intracerebroventricular injections in neonatal mice (P2–P3) of AAV-encoding Kir4.1-eGFP or control td-Tomato vectors for gain-of-function (GOF) experiments (A). Right: viral transduction of ventral spinal cord with AAV-td-Tomato or AAV-Kir4.1-eGFP quantified in (B) (n = 3–7 mice/group, mean ± SEM, Mann-Whitney test). (C) ChAT (right) and MMP-9 (left) immunofluorescent staining in the ventral spinal cord of AAV-td-Tomato and AAV-Kir4.1-eGFP-injected mice. (D and E) Quantifications of ChAT + (D) and MMP-9 + (E) MN soma area in P60 mice (2 months post injection) (n = 9–13 mice/group, 70–100 MNs counts/animal, boxplot, Mann-Whitney test, scale bar, 40 μm). (F) Example of MNs in contact (right) or not (left) with Kir4.1-overexpressing AS. (G) Ratio of soma area of MN contacting/non-contacting transduced AS (n = 9–13 mice/group, mean ± SEM, Mann-Whitney test). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and black line denoting the median value.
    Figure Legend Snippet: Kir4.1 Viral-Mediated Overexpression Is Sufficient to Increase MN Size (A and B) Left: schematic of intracerebroventricular injections in neonatal mice (P2–P3) of AAV-encoding Kir4.1-eGFP or control td-Tomato vectors for gain-of-function (GOF) experiments (A). Right: viral transduction of ventral spinal cord with AAV-td-Tomato or AAV-Kir4.1-eGFP quantified in (B) (n = 3–7 mice/group, mean ± SEM, Mann-Whitney test). (C) ChAT (right) and MMP-9 (left) immunofluorescent staining in the ventral spinal cord of AAV-td-Tomato and AAV-Kir4.1-eGFP-injected mice. (D and E) Quantifications of ChAT + (D) and MMP-9 + (E) MN soma area in P60 mice (2 months post injection) (n = 9–13 mice/group, 70–100 MNs counts/animal, boxplot, Mann-Whitney test, scale bar, 40 μm). (F) Example of MNs in contact (right) or not (left) with Kir4.1-overexpressing AS. (G) Ratio of soma area of MN contacting/non-contacting transduced AS (n = 9–13 mice/group, mean ± SEM, Mann-Whitney test). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Edges of boxplots denote interquartile range (25 th –75 th percentile) with whiskers denoting 1.5 times the interquartile range and black line denoting the median value.

    Techniques Used: Over Expression, Transduction, MANN-WHITNEY, Staining, Injection

    AS Kir4.1 Regulates MN Size through PI3K/mTOR/pS6 Pathway (A and C) Immunofluorescence co-staining of mTOR downstream effector pS6 and MMP-9 + MNs in P30 AS-Kir4.1cKO LOF mice (A) and in P60 AAV-Kir4.1 GOF mice (C). (B and D) Quantification of pS6 fluorescence intensity per MMP-9 + MN (B, LOF: n = 3 mice/group, 80 MNs counts/animal; D, GOF: n = 5 mice/group, 200 MN counts/animal, boxplot, Mann-Whitney test, scale bar, 25 μm). (E) Rapamycin treatment in AAV-Kir4.1 GOF mice. (F) Immunofluorescent co-staining of ChAT (left) and MMP-9 (right) in vehicle-treated AAV-td-Tomato and AAV-Kir4.1-eGFP mice (top two panels) or rapamycin-treated AAV-Kir4.1-eGFP mice (lower panel). (G and H) Quantification of ChAT + (G) and MMP-9 + (H) MN size in vehicle-treated AAV-td-Tomato and AAV-Kir4.1-eGFP and rapamycin-treated AAV-Kir4.1-eGFP mice (n = 3–4 mice/group, 100 MN counts/animal, boxplot, Kruskal-Wallis test, scale bar, 30 μm). (I) Incubation of acute spinal cord slices in solutions with high K + concentration. (J) Detection of ChAT-GFP + MNs in the ventral horn of P14 mice after 2 hr incubation in 3 mM KCl, 12 mM KCl, or 5 mM mannitol ACSF. (K) Quantification of MN soma area in the corresponding conditions (n = 4 mice/group, average 250 MN counts/animal, mean ± SEM, Kruskal-Wallis test, scale bar, 25 μm).
    Figure Legend Snippet: AS Kir4.1 Regulates MN Size through PI3K/mTOR/pS6 Pathway (A and C) Immunofluorescence co-staining of mTOR downstream effector pS6 and MMP-9 + MNs in P30 AS-Kir4.1cKO LOF mice (A) and in P60 AAV-Kir4.1 GOF mice (C). (B and D) Quantification of pS6 fluorescence intensity per MMP-9 + MN (B, LOF: n = 3 mice/group, 80 MNs counts/animal; D, GOF: n = 5 mice/group, 200 MN counts/animal, boxplot, Mann-Whitney test, scale bar, 25 μm). (E) Rapamycin treatment in AAV-Kir4.1 GOF mice. (F) Immunofluorescent co-staining of ChAT (left) and MMP-9 (right) in vehicle-treated AAV-td-Tomato and AAV-Kir4.1-eGFP mice (top two panels) or rapamycin-treated AAV-Kir4.1-eGFP mice (lower panel). (G and H) Quantification of ChAT + (G) and MMP-9 + (H) MN size in vehicle-treated AAV-td-Tomato and AAV-Kir4.1-eGFP and rapamycin-treated AAV-Kir4.1-eGFP mice (n = 3–4 mice/group, 100 MN counts/animal, boxplot, Kruskal-Wallis test, scale bar, 30 μm). (I) Incubation of acute spinal cord slices in solutions with high K + concentration. (J) Detection of ChAT-GFP + MNs in the ventral horn of P14 mice after 2 hr incubation in 3 mM KCl, 12 mM KCl, or 5 mM mannitol ACSF. (K) Quantification of MN soma area in the corresponding conditions (n = 4 mice/group, average 250 MN counts/animal, mean ± SEM, Kruskal-Wallis test, scale bar, 25 μm).

    Techniques Used: Immunofluorescence, Staining, Fluorescence, MANN-WHITNEY, Incubation, Concentration Assay

    AS-Encoded Kir4.1 Is Required for FαMN Function and Peak Force Generation AS Kir4.1 deletion leads to decreased FαMN size with mTOR downregulation, loss of fast-firing MN frequency, and decrease in fast-twitch muscle fiber size and peak strength without affecting MN survival.
    Figure Legend Snippet: AS-Encoded Kir4.1 Is Required for FαMN Function and Peak Force Generation AS Kir4.1 deletion leads to decreased FαMN size with mTOR downregulation, loss of fast-firing MN frequency, and decrease in fast-twitch muscle fiber size and peak strength without affecting MN survival.

    Techniques Used:


    Figure Legend Snippet:

    Techniques Used: Plasmid Preparation, Recombinant, SYBR Green Assay, Mutagenesis, Software

    rabbit polyclonal  (Alomone Labs)


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    anti kir4 1 rabbit polyclonal antibody  (Alomone Labs)


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    Alomone Labs anti kir4 1 rabbit polyclonal antibody
    Anti Kir4 1 Rabbit Polyclonal Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs rabbit polyclonal

    Rabbit Polyclonal, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    RACK1 KO in astrocytes leads to higher levels of <t>Kir4.1</t> in astrocyte somata and PAPs (A) Generation of a mouse line with RACK1 KO in astrocytes (RACK1 cKO). Shown is a schematic of the RACK1 fl/fl and Aldh1l1-Cre/ERT2 alleles. Deletion of exon 2 in Gnb2l1 (the gene coding for RACK1) is induced in astrocytes by tamoxifen injection; this results in a frameshift and premature termination of Gnb2l1 translation. Primers are indicated by red arrows. (B) PCR assays for Gnb2l1 KO in brain DNA from RACK1 fl/fl or Aldh1l1-CreERT2: RACK1 fl/fl tamoxifen-injected mice (RACK1 cKO). The 898-bp band corresponds to the floxed allele ( <xref ref-type=Table S4 ). The 672-bp band corresponds to the exon 2-deleted allele. (C) Confocal images of RACK1 immunofluorescence (red) in the hippocampus in RACK1 fl/fl and RACK1 cKO mice. Astrocytes are co-immunolabeled for GFAP (green). Some astrocytes are indicated by white arrowheads. Nuclei are stained with DAPI. The bottom panel gives a higher-magnification view of the boxed areas in the RACK1 fl/fl and RACK1 cKO images, which shows that RACK1 is specifically depleted in astrocytes ( ∗ ) and is still expressed by neurons (°). Scale bars, 20 μm. (D), Western blot detection and analysis of Kir4.1 and GLT-1 in protein extracts from whole brain, hippocampus, whole-brain synaptogliosomes, hippocampal synaptogliosomes, or whole-brain microvessels purified from RACK1 fl/fl or RACK1 cKO mice. The position of molecular weight markers is indicated on the right. Signals were normalized against that of stain-free membranes except for the experiment on purified microvessels, where histone 3 was used. The data are quoted as the mean ± SD (N = 5 samples per genotype, 1 mouse per sample); two-tailed unpaired t test or Mann-Whitney test. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 and Figure S2 . " width="250" height="auto" />
    Rabbit Polyclonal Anti Kir4 1 Extracellular, 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
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    92
    Alomone Labs anti kir4 1 rabbit polyclonal antibody
    RACK1 KO in astrocytes leads to higher levels of <t>Kir4.1</t> in astrocyte somata and PAPs (A) Generation of a mouse line with RACK1 KO in astrocytes (RACK1 cKO). Shown is a schematic of the RACK1 fl/fl and Aldh1l1-Cre/ERT2 alleles. Deletion of exon 2 in Gnb2l1 (the gene coding for RACK1) is induced in astrocytes by tamoxifen injection; this results in a frameshift and premature termination of Gnb2l1 translation. Primers are indicated by red arrows. (B) PCR assays for Gnb2l1 KO in brain DNA from RACK1 fl/fl or Aldh1l1-CreERT2: RACK1 fl/fl tamoxifen-injected mice (RACK1 cKO). The 898-bp band corresponds to the floxed allele ( <xref ref-type=Table S4 ). The 672-bp band corresponds to the exon 2-deleted allele. (C) Confocal images of RACK1 immunofluorescence (red) in the hippocampus in RACK1 fl/fl and RACK1 cKO mice. Astrocytes are co-immunolabeled for GFAP (green). Some astrocytes are indicated by white arrowheads. Nuclei are stained with DAPI. The bottom panel gives a higher-magnification view of the boxed areas in the RACK1 fl/fl and RACK1 cKO images, which shows that RACK1 is specifically depleted in astrocytes ( ∗ ) and is still expressed by neurons (°). Scale bars, 20 μm. (D), Western blot detection and analysis of Kir4.1 and GLT-1 in protein extracts from whole brain, hippocampus, whole-brain synaptogliosomes, hippocampal synaptogliosomes, or whole-brain microvessels purified from RACK1 fl/fl or RACK1 cKO mice. The position of molecular weight markers is indicated on the right. Signals were normalized against that of stain-free membranes except for the experiment on purified microvessels, where histone 3 was used. The data are quoted as the mean ± SD (N = 5 samples per genotype, 1 mouse per sample); two-tailed unpaired t test or Mann-Whitney test. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 and Figure S2 . " width="250" height="auto" />
    Anti Kir4 1 Rabbit Polyclonal Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti kir4 1 rabbit polyclonal antibody - by Bioz Stars, 2023-09
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    Image Search Results


    Journal: eLife

    Article Title: Megalencephalic leukoencephalopathy with subcortical cysts is a developmental disorder of the gliovascular unit

    doi: 10.7554/eLife.71379

    Figure Lengend Snippet:

    Article Snippet: Antibody , Kir 4.1 extracellular (rabbit polyclonal) , Alomone Labs , APC-165 , Immunofluorescence (1:200).

    Techniques: Sequencing, Western Blot, Immunofluorescence, Transduction

    RACK1 KO in astrocytes leads to higher levels of Kir4.1 in astrocyte somata and PAPs (A) Generation of a mouse line with RACK1 KO in astrocytes (RACK1 cKO). Shown is a schematic of the RACK1 fl/fl and Aldh1l1-Cre/ERT2 alleles. Deletion of exon 2 in Gnb2l1 (the gene coding for RACK1) is induced in astrocytes by tamoxifen injection; this results in a frameshift and premature termination of Gnb2l1 translation. Primers are indicated by red arrows. (B) PCR assays for Gnb2l1 KO in brain DNA from RACK1 fl/fl or Aldh1l1-CreERT2: RACK1 fl/fl tamoxifen-injected mice (RACK1 cKO). The 898-bp band corresponds to the floxed allele ( <xref ref-type=Table S4 ). The 672-bp band corresponds to the exon 2-deleted allele. (C) Confocal images of RACK1 immunofluorescence (red) in the hippocampus in RACK1 fl/fl and RACK1 cKO mice. Astrocytes are co-immunolabeled for GFAP (green). Some astrocytes are indicated by white arrowheads. Nuclei are stained with DAPI. The bottom panel gives a higher-magnification view of the boxed areas in the RACK1 fl/fl and RACK1 cKO images, which shows that RACK1 is specifically depleted in astrocytes ( ∗ ) and is still expressed by neurons (°). Scale bars, 20 μm. (D), Western blot detection and analysis of Kir4.1 and GLT-1 in protein extracts from whole brain, hippocampus, whole-brain synaptogliosomes, hippocampal synaptogliosomes, or whole-brain microvessels purified from RACK1 fl/fl or RACK1 cKO mice. The position of molecular weight markers is indicated on the right. Signals were normalized against that of stain-free membranes except for the experiment on purified microvessels, where histone 3 was used. The data are quoted as the mean ± SD (N = 5 samples per genotype, 1 mouse per sample); two-tailed unpaired t test or Mann-Whitney test. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 and Figure S2 . " width="100%" height="100%">

    Journal: Cell Reports

    Article Title: The ribosome-associated protein RACK1 represses Kir4.1 translation in astrocytes and influences neuronal activity

    doi: 10.1016/j.celrep.2023.112456

    Figure Lengend Snippet: RACK1 KO in astrocytes leads to higher levels of Kir4.1 in astrocyte somata and PAPs (A) Generation of a mouse line with RACK1 KO in astrocytes (RACK1 cKO). Shown is a schematic of the RACK1 fl/fl and Aldh1l1-Cre/ERT2 alleles. Deletion of exon 2 in Gnb2l1 (the gene coding for RACK1) is induced in astrocytes by tamoxifen injection; this results in a frameshift and premature termination of Gnb2l1 translation. Primers are indicated by red arrows. (B) PCR assays for Gnb2l1 KO in brain DNA from RACK1 fl/fl or Aldh1l1-CreERT2: RACK1 fl/fl tamoxifen-injected mice (RACK1 cKO). The 898-bp band corresponds to the floxed allele ( Table S4 ). The 672-bp band corresponds to the exon 2-deleted allele. (C) Confocal images of RACK1 immunofluorescence (red) in the hippocampus in RACK1 fl/fl and RACK1 cKO mice. Astrocytes are co-immunolabeled for GFAP (green). Some astrocytes are indicated by white arrowheads. Nuclei are stained with DAPI. The bottom panel gives a higher-magnification view of the boxed areas in the RACK1 fl/fl and RACK1 cKO images, which shows that RACK1 is specifically depleted in astrocytes ( ∗ ) and is still expressed by neurons (°). Scale bars, 20 μm. (D), Western blot detection and analysis of Kir4.1 and GLT-1 in protein extracts from whole brain, hippocampus, whole-brain synaptogliosomes, hippocampal synaptogliosomes, or whole-brain microvessels purified from RACK1 fl/fl or RACK1 cKO mice. The position of molecular weight markers is indicated on the right. Signals were normalized against that of stain-free membranes except for the experiment on purified microvessels, where histone 3 was used. The data are quoted as the mean ± SD (N = 5 samples per genotype, 1 mouse per sample); two-tailed unpaired t test or Mann-Whitney test. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 and Figure S2 .

    Article Snippet: Rabbit polyclonal anti-KIR4.1 extracellular , Alomone labs , Cat#APC-165; RRID: AB_2341043.

    Techniques: Injection, Immunofluorescence, Immunolabeling, Staining, Western Blot, Purification, Molecular Weight, Two Tailed Test, MANN-WHITNEY

    Absence of RACK1 in astrocytes leads to higher Kir4.1-mediated astrocytic inward K + currents and cell volumes (A) Schematic of electrode positions used to record astrocyte whole-cell currents evoked by Schaffer collateral (SC) stimulation in the CA1 region of hippocampal slices. (B) Left: representative traces of astrocytic whole-cell currents induced by 150-ms voltage steps (from −200 mV to +100 mV, 10-mV steps; black traces at the bottom) in RACK1 fl/fl and RACK1 cKO mice before (black and pink) and after (blue) application of a KIR 4.1 antagonist (VU). Scale bars, 50 ms, 5 nA. Right: current-voltage (I-V) plot in RACK1 fl/fl (white filled dots) and in RACK1 cKO (pink-filled dots) mice before (black) and after (blue) application of VU (N = 7 and 10 astrocytes for RACK1 fl/fl and RACK1 cKO mice, respectively; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons) The data are quoted as the mean ± SD. (C) Left: representative astrocytic Kir4.1 (VU-sensitive) currents induced by SC stimulation (10 Hz, 1 s) in RACK1 fl/fl (black) and RACK1 cKO (pink) mice. Scale bars, 200 ms, 50 pA. Right: quantification of astrocytic Kir4.1 current peak amplitude after each stimulus during SC stimulation (10 Hz, 1 s) in RACK1 fl/fl (white filled dots) and RACK1 cKO (pink filled dots) mice (N = 6 and 5 astrocytes for RACK1 fl/fl and RACK1 cKO mice, respectively; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons). The data are quoted as the mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Illustration of the imaging method with a representative raw confocal image of an isolated RACK1 fl/fl CA1 astrocyte expressing tdTomato. (E–G) Imaris analysis: filament tracing (E), convex hull volume (F), and a 3D Sholl analysis (G). (H) Mean territory volume and filament length of RACK1 fl/fl and RACK1 cKO astrocytes. Shown is a histogram of the data, presented as the mean ± SD (N = 4 mice per genotype, 45 astrocytes); two-tailed t test. The data are quoted as the mean ± SD. (I) A Sholl analysis of the ramification complexity of RACK1 fl/fl and RACK1 cKO astrocytes. Two-way analysis of variance. ∗ p < 0.05, ∗∗ p < 0.01. The data are quoted as the mean ± SD. The raw data are presented in <xref ref-type=Table S3 . " width="100%" height="100%">

    Journal: Cell Reports

    Article Title: The ribosome-associated protein RACK1 represses Kir4.1 translation in astrocytes and influences neuronal activity

    doi: 10.1016/j.celrep.2023.112456

    Figure Lengend Snippet: Absence of RACK1 in astrocytes leads to higher Kir4.1-mediated astrocytic inward K + currents and cell volumes (A) Schematic of electrode positions used to record astrocyte whole-cell currents evoked by Schaffer collateral (SC) stimulation in the CA1 region of hippocampal slices. (B) Left: representative traces of astrocytic whole-cell currents induced by 150-ms voltage steps (from −200 mV to +100 mV, 10-mV steps; black traces at the bottom) in RACK1 fl/fl and RACK1 cKO mice before (black and pink) and after (blue) application of a KIR 4.1 antagonist (VU). Scale bars, 50 ms, 5 nA. Right: current-voltage (I-V) plot in RACK1 fl/fl (white filled dots) and in RACK1 cKO (pink-filled dots) mice before (black) and after (blue) application of VU (N = 7 and 10 astrocytes for RACK1 fl/fl and RACK1 cKO mice, respectively; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons) The data are quoted as the mean ± SD. (C) Left: representative astrocytic Kir4.1 (VU-sensitive) currents induced by SC stimulation (10 Hz, 1 s) in RACK1 fl/fl (black) and RACK1 cKO (pink) mice. Scale bars, 200 ms, 50 pA. Right: quantification of astrocytic Kir4.1 current peak amplitude after each stimulus during SC stimulation (10 Hz, 1 s) in RACK1 fl/fl (white filled dots) and RACK1 cKO (pink filled dots) mice (N = 6 and 5 astrocytes for RACK1 fl/fl and RACK1 cKO mice, respectively; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons). The data are quoted as the mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Illustration of the imaging method with a representative raw confocal image of an isolated RACK1 fl/fl CA1 astrocyte expressing tdTomato. (E–G) Imaris analysis: filament tracing (E), convex hull volume (F), and a 3D Sholl analysis (G). (H) Mean territory volume and filament length of RACK1 fl/fl and RACK1 cKO astrocytes. Shown is a histogram of the data, presented as the mean ± SD (N = 4 mice per genotype, 45 astrocytes); two-tailed t test. The data are quoted as the mean ± SD. (I) A Sholl analysis of the ramification complexity of RACK1 fl/fl and RACK1 cKO astrocytes. Two-way analysis of variance. ∗ p < 0.05, ∗∗ p < 0.01. The data are quoted as the mean ± SD. The raw data are presented in Table S3 .

    Article Snippet: Rabbit polyclonal anti-KIR4.1 extracellular , Alomone labs , Cat#APC-165; RRID: AB_2341043.

    Techniques: Imaging, Isolation, Expressing, Two Tailed Test

    Absence of RACK1 in astrocytes alters network population activity and neuronal responses to intense stimulation (A) Schematic of electrode positions used to record field excitatory postsynaptic potentials (fEPSPs) evoked by SC stimulation in the CA1 region of hippocampal slices. (B) Input-output curves for basal synaptic transmission. Left: representative recordings in RACK1 fl/fl mice (black) and RACK1 cKO mice before (pink) and after (blue) application of a Kir 4.1 antagonist (VU). Scale bars, 10 ms, 0.5 mV. Right: quantification of the fEPSP slope for different fiber volley amplitudes after SC stimulation. The data are quoted as the mean ± SD. RACK1 fl/fl: n = 5 slices from 4 mice; p = 0.0087; RACK1 cKO: n = 5 slices from 5 mice; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons. (C) Top: a representative recording of fEPSPs evoked by repetitive stimulation (10 Hz, 30 s) of CA1 SCs in RACK1 fl/fl mice under control conditions. Scale bars, 5 s, 0.2 mV. Bottom: enlarged view of fEPSPs evoked by the first 10 stimuli. Scale bars, 200 ms, 0.2 mV. (D) Changes in the fEPSP slope induced by 10-Hz stimulation relative to responses measured before the onset of stimulation (baseline responses) in RACK1 fl/fl mice (white filled dots) and in RACK1 cKO mice (pink-filled dots) before (black) and after (blue) application of VU. The data are quoted as the mean ± SD. RACK1 fl/fl: n = 5 from 5 mice; RACK1 cKO: n = 6 slices from 4 mice; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons. (E) Schematic (left) and picture (right) of a hippocampal slice placed on a multielectrode array (MEA). Scale bar, 200 μm. (F) Representative MEA recordings of burst activity induced in hippocampal slices of RACK1 fl/fl (black) and RACK1 cKO (pink) mice by incubation in Mg 2+ -free ACSF containing 6 mM KCl. The expanded recordings of the bursts (surrounded by gray rectangles) are shown on the right. Scale bars, 10 s (left)/200 ms (right), 50 μV. (G) Quantification of burst frequency (top) and burst duration (bottom) in RACK1 fl/fl (white) and RACK1 cKO (pink) hippocampal slices. The data are quoted as the mean ± SD. n = 15 slices from 5 mice for RACK1 fl/fl and n = 18 slices from 6 mice for RACK1 cKO; unpaired t test. (H) Representative MEA recordings of hippocampal bursting activity in RACK1 fl/fl (top) and RACK1 cKO (bottom) slices in control (Ct) and during 25-min treatment with the Kir4.1 blocker VU0134992 (VU). The corresponding time-frequency plots are shown under the traces. Scale bar, 20 s/2 min, 50 μV. (I) Quantification of VU’s effect on burst frequency (top) and duration (bottom) in RACK1 fl/fl (white) and RACK1 cKO (pink) hippocampal slices (RACK1 fl/fl: n = 15 slices from 5 mice for burst frequency and duration, respectively; RACK1 cKO: n = 18 slices from 6 mice for burst frequency and duration; paired t test. The data are quoted as the mean ± SD. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in <xref ref-type=Table S3 . " width="100%" height="100%">

    Journal: Cell Reports

    Article Title: The ribosome-associated protein RACK1 represses Kir4.1 translation in astrocytes and influences neuronal activity

    doi: 10.1016/j.celrep.2023.112456

    Figure Lengend Snippet: Absence of RACK1 in astrocytes alters network population activity and neuronal responses to intense stimulation (A) Schematic of electrode positions used to record field excitatory postsynaptic potentials (fEPSPs) evoked by SC stimulation in the CA1 region of hippocampal slices. (B) Input-output curves for basal synaptic transmission. Left: representative recordings in RACK1 fl/fl mice (black) and RACK1 cKO mice before (pink) and after (blue) application of a Kir 4.1 antagonist (VU). Scale bars, 10 ms, 0.5 mV. Right: quantification of the fEPSP slope for different fiber volley amplitudes after SC stimulation. The data are quoted as the mean ± SD. RACK1 fl/fl: n = 5 slices from 4 mice; p = 0.0087; RACK1 cKO: n = 5 slices from 5 mice; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons. (C) Top: a representative recording of fEPSPs evoked by repetitive stimulation (10 Hz, 30 s) of CA1 SCs in RACK1 fl/fl mice under control conditions. Scale bars, 5 s, 0.2 mV. Bottom: enlarged view of fEPSPs evoked by the first 10 stimuli. Scale bars, 200 ms, 0.2 mV. (D) Changes in the fEPSP slope induced by 10-Hz stimulation relative to responses measured before the onset of stimulation (baseline responses) in RACK1 fl/fl mice (white filled dots) and in RACK1 cKO mice (pink-filled dots) before (black) and after (blue) application of VU. The data are quoted as the mean ± SD. RACK1 fl/fl: n = 5 from 5 mice; RACK1 cKO: n = 6 slices from 4 mice; repeated-measures two-way ANOVA with Sidak’s correction for multiple comparisons. (E) Schematic (left) and picture (right) of a hippocampal slice placed on a multielectrode array (MEA). Scale bar, 200 μm. (F) Representative MEA recordings of burst activity induced in hippocampal slices of RACK1 fl/fl (black) and RACK1 cKO (pink) mice by incubation in Mg 2+ -free ACSF containing 6 mM KCl. The expanded recordings of the bursts (surrounded by gray rectangles) are shown on the right. Scale bars, 10 s (left)/200 ms (right), 50 μV. (G) Quantification of burst frequency (top) and burst duration (bottom) in RACK1 fl/fl (white) and RACK1 cKO (pink) hippocampal slices. The data are quoted as the mean ± SD. n = 15 slices from 5 mice for RACK1 fl/fl and n = 18 slices from 6 mice for RACK1 cKO; unpaired t test. (H) Representative MEA recordings of hippocampal bursting activity in RACK1 fl/fl (top) and RACK1 cKO (bottom) slices in control (Ct) and during 25-min treatment with the Kir4.1 blocker VU0134992 (VU). The corresponding time-frequency plots are shown under the traces. Scale bar, 20 s/2 min, 50 μV. (I) Quantification of VU’s effect on burst frequency (top) and duration (bottom) in RACK1 fl/fl (white) and RACK1 cKO (pink) hippocampal slices (RACK1 fl/fl: n = 15 slices from 5 mice for burst frequency and duration, respectively; RACK1 cKO: n = 18 slices from 6 mice for burst frequency and duration; paired t test. The data are quoted as the mean ± SD. ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001. The raw data are presented in Table S3 .

    Article Snippet: Rabbit polyclonal anti-KIR4.1 extracellular , Alomone labs , Cat#APC-165; RRID: AB_2341043.

    Techniques: Activity Assay, Transmission Assay, Incubation

    Journal: Cell Reports

    Article Title: The ribosome-associated protein RACK1 represses Kir4.1 translation in astrocytes and influences neuronal activity

    doi: 10.1016/j.celrep.2023.112456

    Figure Lengend Snippet:

    Article Snippet: Rabbit polyclonal anti-KIR4.1 extracellular , Alomone labs , Cat#APC-165; RRID: AB_2341043.

    Techniques: Transduction, Recombinant, Multiplex Assay, Mass Spectrometry, Software