guinea pig anti glur2 glua2 extracellular antibody  (Alomone Labs)


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    Structured Review

    Alomone Labs guinea pig anti glur2 glua2 extracellular antibody
    Validation of differentially expressed genes using qRT-PCR. ( A–E ) qPCR verification of the expression of genes involved in biological process identified as enriched by GO analysis compared with WT control. (F) Fold change expression of Ca 2+ -permeable AMPAR subunit Gria1 , Gria3 and Gria4 mRNAs, relative to WT motor neurons at E12.5. (G) Relative expression of Adarb1 mRNA in SOD1 G93A motor neurons at E12.5. ( H ) Schema showing the position of the fully complementary miR-124 target site at the 5′-end of the mouse <t>Gria2</t> , 3′-UTR. The seed region of miR-124 is shown. Data represent mean ± SEM, unpaired student t -test, n = 5–7 biological replicates, * P
    Guinea Pig Anti Glur2 Glua2 Extracellular Antibody, 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/guinea pig anti glur2 glua2 extracellular antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    guinea pig anti glur2 glua2 extracellular antibody - by Bioz Stars, 2022-12
    94/100 stars

    Images

    1) Product Images from "α-Amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor and RNA processing gene dysregulation are early determinants of selective motor neuron vulnerability in a mouse model of amyotrophic lateral sclerosis"

    Article Title: α-Amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor and RNA processing gene dysregulation are early determinants of selective motor neuron vulnerability in a mouse model of amyotrophic lateral sclerosis

    Journal: Brain Communications

    doi: 10.1093/braincomms/fcac081

    Validation of differentially expressed genes using qRT-PCR. ( A–E ) qPCR verification of the expression of genes involved in biological process identified as enriched by GO analysis compared with WT control. (F) Fold change expression of Ca 2+ -permeable AMPAR subunit Gria1 , Gria3 and Gria4 mRNAs, relative to WT motor neurons at E12.5. (G) Relative expression of Adarb1 mRNA in SOD1 G93A motor neurons at E12.5. ( H ) Schema showing the position of the fully complementary miR-124 target site at the 5′-end of the mouse Gria2 , 3′-UTR. The seed region of miR-124 is shown. Data represent mean ± SEM, unpaired student t -test, n = 5–7 biological replicates, * P
    Figure Legend Snippet: Validation of differentially expressed genes using qRT-PCR. ( A–E ) qPCR verification of the expression of genes involved in biological process identified as enriched by GO analysis compared with WT control. (F) Fold change expression of Ca 2+ -permeable AMPAR subunit Gria1 , Gria3 and Gria4 mRNAs, relative to WT motor neurons at E12.5. (G) Relative expression of Adarb1 mRNA in SOD1 G93A motor neurons at E12.5. ( H ) Schema showing the position of the fully complementary miR-124 target site at the 5′-end of the mouse Gria2 , 3′-UTR. The seed region of miR-124 is shown. Data represent mean ± SEM, unpaired student t -test, n = 5–7 biological replicates, * P

    Techniques Used: Quantitative RT-PCR, Real-time Polymerase Chain Reaction, Expressing

    Expression of GluA2 in spinal cords of embryonic SOD1 G93A mice. Cross-sections of lumbar spinal cord from WT (HB9:GFP; WT) and SOD1 G93A (SOD1 G93A ; HB9:GFP) mice at (A–J) E12.5 and ( K–T ) E17.5. Double-immunolabelling for GFP, GluA2 and NeuN (Neuronal nuclei). Plots represent quantification analysis of GluA2 signal intensity in HB9:GFP motor neurons at ( U ) E12.5 and ( V ) E17.5. Data represent mean ± SEM, unpaired student t -test performed on n = 4 biological replicates, ∼50 neurons analysed per biological replicate, * P
    Figure Legend Snippet: Expression of GluA2 in spinal cords of embryonic SOD1 G93A mice. Cross-sections of lumbar spinal cord from WT (HB9:GFP; WT) and SOD1 G93A (SOD1 G93A ; HB9:GFP) mice at (A–J) E12.5 and ( K–T ) E17.5. Double-immunolabelling for GFP, GluA2 and NeuN (Neuronal nuclei). Plots represent quantification analysis of GluA2 signal intensity in HB9:GFP motor neurons at ( U ) E12.5 and ( V ) E17.5. Data represent mean ± SEM, unpaired student t -test performed on n = 4 biological replicates, ∼50 neurons analysed per biological replicate, * P

    Techniques Used: Expressing, Mouse Assay

    Expression of GRIA2 and ADAR2 in iPSC motor neurons derived from ALS patients with SOD1 mutations and healthy control lines. Representative images of iPSC mature motor neurons derived from ( A–E ) healthy control line and ( F–J ) SOD1 I114T line, immunolabelled with ChAT, GluA2 and TUJ1, counterstained with Hoechst. ( K ) Plot represents quantification analysis of GluA2 signal intensity in iPSC motor neurons. Data represent mean ± SEM, unpaired student t -test performed on n = 3 biological replicates, 50 neurons analysed per biological replicate. (L) Fold change expression of GRIA2 in SOD1 lines, compared with healthy control line determined by qRT-PCR. ( M ) Fold change expression of ADAR2 in SOD1 lines, compared with healthy control line determined by qRT-PCR. Data represent mean ± SEM, n = 3 biological replicates, one-way ANOVA with Dunnett's multiple comparison test, * P
    Figure Legend Snippet: Expression of GRIA2 and ADAR2 in iPSC motor neurons derived from ALS patients with SOD1 mutations and healthy control lines. Representative images of iPSC mature motor neurons derived from ( A–E ) healthy control line and ( F–J ) SOD1 I114T line, immunolabelled with ChAT, GluA2 and TUJ1, counterstained with Hoechst. ( K ) Plot represents quantification analysis of GluA2 signal intensity in iPSC motor neurons. Data represent mean ± SEM, unpaired student t -test performed on n = 3 biological replicates, 50 neurons analysed per biological replicate. (L) Fold change expression of GRIA2 in SOD1 lines, compared with healthy control line determined by qRT-PCR. ( M ) Fold change expression of ADAR2 in SOD1 lines, compared with healthy control line determined by qRT-PCR. Data represent mean ± SEM, n = 3 biological replicates, one-way ANOVA with Dunnett's multiple comparison test, * P

    Techniques Used: Expressing, Derivative Assay, Quantitative RT-PCR

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    Alomone Labs guinea pig anti glur2 glua2 extracellular antibody
    Validation of differentially expressed genes using qRT-PCR. ( A–E ) qPCR verification of the expression of genes involved in biological process identified as enriched by GO analysis compared with WT control. (F) Fold change expression of Ca 2+ -permeable AMPAR subunit Gria1 , Gria3 and Gria4 mRNAs, relative to WT motor neurons at E12.5. (G) Relative expression of Adarb1 mRNA in SOD1 G93A motor neurons at E12.5. ( H ) Schema showing the position of the fully complementary miR-124 target site at the 5′-end of the mouse <t>Gria2</t> , 3′-UTR. The seed region of miR-124 is shown. Data represent mean ± SEM, unpaired student t -test, n = 5–7 biological replicates, * P
    Guinea Pig Anti Glur2 Glua2 Extracellular Antibody, 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/guinea pig anti glur2 glua2 extracellular antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    94
    Alomone Labs guinea pig anti nav1 5 scn5a antibody
    <t>NaV1.5</t> protein level is significantly reduced in patient-specific DMD iPSC-CMs. (a) Representative Western blot for each antibody used. The bands within the blue rectangles at ∼250 KDa and below 50 KDa correspond to <t>NaV1.5</t> and Kir2.1, respectively. About 50K cells were collected to quantify total NaV1.5, Kir2.1 and actinin levels in control, heterozygous and hemizygous DMD cells. (b) Scatter plots of NaV1.5 and Kir2.1 detected in control, female and DMD iPSC-CMs. NaV1.5 and Kir2.1 protein levels were normalized to actinin (loading control). (c) Representative Western blot after biotinylation and protein precipitation with streptavidin magnetic beads. (d) Scatter plots of biotinylated NaV1.5 and Kir2.1 from control, female , and DMD iPSC-CMs. Fifty μg of biotinylated protein was loaded. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. *** P
    Guinea Pig Anti Nav1 5 Scn5a Antibody, 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/guinea pig anti nav1 5 scn5a antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    93
    Alomone Labs guinea pig anti kv1 3 kcna3 extracellular antibody
    Comparison of stroke severity in WT versus <t>Kv1.3</t> −/− mice. (A) Infarct area and deficit score in 16‐week‐old WT ( n = 10) were compared to Kv1.3 −/− ( n = 14) male mice ( p
    Guinea Pig Anti Kv1 3 Kcna3 Extracellular Antibody, 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
    https://www.bioz.com/result/guinea pig anti kv1 3 kcna3 extracellular antibody/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    guinea pig anti kv1 3 kcna3 extracellular antibody - by Bioz Stars, 2022-12
    93/100 stars
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    Image Search Results


    Validation of differentially expressed genes using qRT-PCR. ( A–E ) qPCR verification of the expression of genes involved in biological process identified as enriched by GO analysis compared with WT control. (F) Fold change expression of Ca 2+ -permeable AMPAR subunit Gria1 , Gria3 and Gria4 mRNAs, relative to WT motor neurons at E12.5. (G) Relative expression of Adarb1 mRNA in SOD1 G93A motor neurons at E12.5. ( H ) Schema showing the position of the fully complementary miR-124 target site at the 5′-end of the mouse Gria2 , 3′-UTR. The seed region of miR-124 is shown. Data represent mean ± SEM, unpaired student t -test, n = 5–7 biological replicates, * P

    Journal: Brain Communications

    Article Title: α-Amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor and RNA processing gene dysregulation are early determinants of selective motor neuron vulnerability in a mouse model of amyotrophic lateral sclerosis

    doi: 10.1093/braincomms/fcac081

    Figure Lengend Snippet: Validation of differentially expressed genes using qRT-PCR. ( A–E ) qPCR verification of the expression of genes involved in biological process identified as enriched by GO analysis compared with WT control. (F) Fold change expression of Ca 2+ -permeable AMPAR subunit Gria1 , Gria3 and Gria4 mRNAs, relative to WT motor neurons at E12.5. (G) Relative expression of Adarb1 mRNA in SOD1 G93A motor neurons at E12.5. ( H ) Schema showing the position of the fully complementary miR-124 target site at the 5′-end of the mouse Gria2 , 3′-UTR. The seed region of miR-124 is shown. Data represent mean ± SEM, unpaired student t -test, n = 5–7 biological replicates, * P

    Article Snippet: Primary antibodies were as follows: chicken anti-GFP (1:1000; Abcam; AB13970), rabbit anti-NeuN (1:1000; Abcam; AB104225), goat anti-ChAT (1:500; Abcam; AB34419) and guinea pig anti-AMPA receptor 2 subunit (GluA2) (1:500; Alomone Labs; AGP-073).

    Techniques: Quantitative RT-PCR, Real-time Polymerase Chain Reaction, Expressing

    Expression of GluA2 in spinal cords of embryonic SOD1 G93A mice. Cross-sections of lumbar spinal cord from WT (HB9:GFP; WT) and SOD1 G93A (SOD1 G93A ; HB9:GFP) mice at (A–J) E12.5 and ( K–T ) E17.5. Double-immunolabelling for GFP, GluA2 and NeuN (Neuronal nuclei). Plots represent quantification analysis of GluA2 signal intensity in HB9:GFP motor neurons at ( U ) E12.5 and ( V ) E17.5. Data represent mean ± SEM, unpaired student t -test performed on n = 4 biological replicates, ∼50 neurons analysed per biological replicate, * P

    Journal: Brain Communications

    Article Title: α-Amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor and RNA processing gene dysregulation are early determinants of selective motor neuron vulnerability in a mouse model of amyotrophic lateral sclerosis

    doi: 10.1093/braincomms/fcac081

    Figure Lengend Snippet: Expression of GluA2 in spinal cords of embryonic SOD1 G93A mice. Cross-sections of lumbar spinal cord from WT (HB9:GFP; WT) and SOD1 G93A (SOD1 G93A ; HB9:GFP) mice at (A–J) E12.5 and ( K–T ) E17.5. Double-immunolabelling for GFP, GluA2 and NeuN (Neuronal nuclei). Plots represent quantification analysis of GluA2 signal intensity in HB9:GFP motor neurons at ( U ) E12.5 and ( V ) E17.5. Data represent mean ± SEM, unpaired student t -test performed on n = 4 biological replicates, ∼50 neurons analysed per biological replicate, * P

    Article Snippet: Primary antibodies were as follows: chicken anti-GFP (1:1000; Abcam; AB13970), rabbit anti-NeuN (1:1000; Abcam; AB104225), goat anti-ChAT (1:500; Abcam; AB34419) and guinea pig anti-AMPA receptor 2 subunit (GluA2) (1:500; Alomone Labs; AGP-073).

    Techniques: Expressing, Mouse Assay

    Expression of GRIA2 and ADAR2 in iPSC motor neurons derived from ALS patients with SOD1 mutations and healthy control lines. Representative images of iPSC mature motor neurons derived from ( A–E ) healthy control line and ( F–J ) SOD1 I114T line, immunolabelled with ChAT, GluA2 and TUJ1, counterstained with Hoechst. ( K ) Plot represents quantification analysis of GluA2 signal intensity in iPSC motor neurons. Data represent mean ± SEM, unpaired student t -test performed on n = 3 biological replicates, 50 neurons analysed per biological replicate. (L) Fold change expression of GRIA2 in SOD1 lines, compared with healthy control line determined by qRT-PCR. ( M ) Fold change expression of ADAR2 in SOD1 lines, compared with healthy control line determined by qRT-PCR. Data represent mean ± SEM, n = 3 biological replicates, one-way ANOVA with Dunnett's multiple comparison test, * P

    Journal: Brain Communications

    Article Title: α-Amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor and RNA processing gene dysregulation are early determinants of selective motor neuron vulnerability in a mouse model of amyotrophic lateral sclerosis

    doi: 10.1093/braincomms/fcac081

    Figure Lengend Snippet: Expression of GRIA2 and ADAR2 in iPSC motor neurons derived from ALS patients with SOD1 mutations and healthy control lines. Representative images of iPSC mature motor neurons derived from ( A–E ) healthy control line and ( F–J ) SOD1 I114T line, immunolabelled with ChAT, GluA2 and TUJ1, counterstained with Hoechst. ( K ) Plot represents quantification analysis of GluA2 signal intensity in iPSC motor neurons. Data represent mean ± SEM, unpaired student t -test performed on n = 3 biological replicates, 50 neurons analysed per biological replicate. (L) Fold change expression of GRIA2 in SOD1 lines, compared with healthy control line determined by qRT-PCR. ( M ) Fold change expression of ADAR2 in SOD1 lines, compared with healthy control line determined by qRT-PCR. Data represent mean ± SEM, n = 3 biological replicates, one-way ANOVA with Dunnett's multiple comparison test, * P

    Article Snippet: Primary antibodies were as follows: chicken anti-GFP (1:1000; Abcam; AB13970), rabbit anti-NeuN (1:1000; Abcam; AB104225), goat anti-ChAT (1:500; Abcam; AB34419) and guinea pig anti-AMPA receptor 2 subunit (GluA2) (1:500; Alomone Labs; AGP-073).

    Techniques: Expressing, Derivative Assay, Quantitative RT-PCR

    NaV1.5 protein level is significantly reduced in patient-specific DMD iPSC-CMs. (a) Representative Western blot for each antibody used. The bands within the blue rectangles at ∼250 KDa and below 50 KDa correspond to NaV1.5 and Kir2.1, respectively. About 50K cells were collected to quantify total NaV1.5, Kir2.1 and actinin levels in control, heterozygous and hemizygous DMD cells. (b) Scatter plots of NaV1.5 and Kir2.1 detected in control, female and DMD iPSC-CMs. NaV1.5 and Kir2.1 protein levels were normalized to actinin (loading control). (c) Representative Western blot after biotinylation and protein precipitation with streptavidin magnetic beads. (d) Scatter plots of biotinylated NaV1.5 and Kir2.1 from control, female , and DMD iPSC-CMs. Fifty μg of biotinylated protein was loaded. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. *** P

    Journal: bioRxiv

    Article Title: SNTA1 Gene Rescues Ion Channel Function in Cardiomyocytes Derived from Induced Pluripotent Stem Cells Reprogrammed from Muscular Dystrophy Patients with Arrhythmias

    doi: 10.1101/2022.01.25.477696

    Figure Lengend Snippet: NaV1.5 protein level is significantly reduced in patient-specific DMD iPSC-CMs. (a) Representative Western blot for each antibody used. The bands within the blue rectangles at ∼250 KDa and below 50 KDa correspond to NaV1.5 and Kir2.1, respectively. About 50K cells were collected to quantify total NaV1.5, Kir2.1 and actinin levels in control, heterozygous and hemizygous DMD cells. (b) Scatter plots of NaV1.5 and Kir2.1 detected in control, female and DMD iPSC-CMs. NaV1.5 and Kir2.1 protein levels were normalized to actinin (loading control). (c) Representative Western blot after biotinylation and protein precipitation with streptavidin magnetic beads. (d) Scatter plots of biotinylated NaV1.5 and Kir2.1 from control, female , and DMD iPSC-CMs. Fifty μg of biotinylated protein was loaded. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. *** P

    Article Snippet: Primary antibodies were used at different dilutions in block solution: Troponin I (#MAB1691, Millipore) was used at 1:500, Kir2.1 (#APC-026, Alomone) antibody was used at 1:200, Nav1.5 (#AGP-008, Alomone) was used at 1:200, Dystrophin MANDRA1 (#D8043, Sigma) was used at 1:100, and Phalloidin 488 (#A12379, Invitrogen) at 1:500 (it comes with a fluorophore conjugated so no secondary Ab incubation was needed, stains F-actin).

    Techniques: Western Blot, Magnetic Beads, Two Tailed Test, MANN-WHITNEY

    Electrophysiological analysis in Control 2 (human foreskin-derived BJ iPSC-CMs). ( a ) Representative AP trace of ventricular-like control BJ iPSC-CMs obtained at 1 Hz of pacing. Inset . First derivative with respect to time (dV/dt). ( b–f) Action potential properties. Recordings at 1 and 2 Hz were similar to those obtained from the healthy donor patient derived-iPSC-CMs (Control 1). ( g-i) Current traces, I/V curves, and normalized current densities for NaV1.5, CaV1.2, and Kir2.1 ion channels, respectively. Data obtained from the control BJ iPSC-CMs (Control 2) were similar to the other control iPSC-CMs.

    Journal: bioRxiv

    Article Title: SNTA1 Gene Rescues Ion Channel Function in Cardiomyocytes Derived from Induced Pluripotent Stem Cells Reprogrammed from Muscular Dystrophy Patients with Arrhythmias

    doi: 10.1101/2022.01.25.477696

    Figure Lengend Snippet: Electrophysiological analysis in Control 2 (human foreskin-derived BJ iPSC-CMs). ( a ) Representative AP trace of ventricular-like control BJ iPSC-CMs obtained at 1 Hz of pacing. Inset . First derivative with respect to time (dV/dt). ( b–f) Action potential properties. Recordings at 1 and 2 Hz were similar to those obtained from the healthy donor patient derived-iPSC-CMs (Control 1). ( g-i) Current traces, I/V curves, and normalized current densities for NaV1.5, CaV1.2, and Kir2.1 ion channels, respectively. Data obtained from the control BJ iPSC-CMs (Control 2) were similar to the other control iPSC-CMs.

    Article Snippet: Primary antibodies were used at different dilutions in block solution: Troponin I (#MAB1691, Millipore) was used at 1:500, Kir2.1 (#APC-026, Alomone) antibody was used at 1:200, Nav1.5 (#AGP-008, Alomone) was used at 1:200, Dystrophin MANDRA1 (#D8043, Sigma) was used at 1:100, and Phalloidin 488 (#A12379, Invitrogen) at 1:500 (it comes with a fluorophore conjugated so no secondary Ab incubation was needed, stains F-actin).

    Techniques: Derivative Assay

    SCN5A , KCNJ2 and CACNA1C mRNA expression in control, DMD, and female iPSC-CMs. (a) SCN5A mRNA expression was increased in iPSC-CMs from hemizygous and heterozygous DMD individuals (top), as well as in the human left ventricle heart tissue from a Becker MD individual compared to a healthy subject (bottom). (b) KCNJ2 mRNA levels were higher in both hemizygous and heterozygous iPSC-CMs (top), like those found in human left ventricle heart tissue from Becker DM patients (bottom) when compared to the corresponding control. (c) CACNA1C mRNA expression was not significant different among tested groups from either iPSC-CMs (top) or left ventricle tissues (bottom). mRNA levels were determined by qRT-PCR and calculated by the comparative Ct method (2 -ddCt ) normalized to the internal control 18s rRNA. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. ** P

    Journal: bioRxiv

    Article Title: SNTA1 Gene Rescues Ion Channel Function in Cardiomyocytes Derived from Induced Pluripotent Stem Cells Reprogrammed from Muscular Dystrophy Patients with Arrhythmias

    doi: 10.1101/2022.01.25.477696

    Figure Lengend Snippet: SCN5A , KCNJ2 and CACNA1C mRNA expression in control, DMD, and female iPSC-CMs. (a) SCN5A mRNA expression was increased in iPSC-CMs from hemizygous and heterozygous DMD individuals (top), as well as in the human left ventricle heart tissue from a Becker MD individual compared to a healthy subject (bottom). (b) KCNJ2 mRNA levels were higher in both hemizygous and heterozygous iPSC-CMs (top), like those found in human left ventricle heart tissue from Becker DM patients (bottom) when compared to the corresponding control. (c) CACNA1C mRNA expression was not significant different among tested groups from either iPSC-CMs (top) or left ventricle tissues (bottom). mRNA levels were determined by qRT-PCR and calculated by the comparative Ct method (2 -ddCt ) normalized to the internal control 18s rRNA. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. ** P

    Article Snippet: Primary antibodies were used at different dilutions in block solution: Troponin I (#MAB1691, Millipore) was used at 1:500, Kir2.1 (#APC-026, Alomone) antibody was used at 1:200, Nav1.5 (#AGP-008, Alomone) was used at 1:200, Dystrophin MANDRA1 (#D8043, Sigma) was used at 1:100, and Phalloidin 488 (#A12379, Invitrogen) at 1:500 (it comes with a fluorophore conjugated so no secondary Ab incubation was needed, stains F-actin).

    Techniques: Expressing, Quantitative RT-PCR, Two Tailed Test, MANN-WHITNEY

    Comparison of stroke severity in WT versus Kv1.3 −/− mice. (A) Infarct area and deficit score in 16‐week‐old WT ( n = 10) were compared to Kv1.3 −/− ( n = 14) male mice ( p

    Journal: Annals of Clinical and Translational Neurology

    Article Title: The potassium channel Kv1.3 as a therapeutic target for immunocytoprotection after reperfusion

    doi: 10.1002/acn3.51456

    Figure Lengend Snippet: Comparison of stroke severity in WT versus Kv1.3 −/− mice. (A) Infarct area and deficit score in 16‐week‐old WT ( n = 10) were compared to Kv1.3 −/− ( n = 14) male mice ( p

    Article Snippet: The immunofluorescence staining in Figure was performed with a polyclonal guinea pig anti‐Kv1.3 antibody (1:100, AGP‐005 from Alomone Labs) and the same polyclonal rabbit Iba‐1 (1;1000) and CD3 (1:250) antibodies listed above; Secondary Abs: Alexa Fluor® 546‐goat anti‐guinea pig IgG (1:1000, ab150185 from Abcam) and Alexa Fluor®488‐goat anti‐rabbit IgG (1:1500, ab150077 from Abcam).

    Techniques: Mouse Assay

    The Kv1.3 blocker PAP‐1 reduces infarction and improves neurological deficit in young and old WT female mice. (A) Infarct area and deficit score in vehicle ( n = 11) were compared to PAP‐1 (40 mg/kg; n = 15) treated 16‐week‐old female mice ( p = 0.007 for infarct, p = 0.016 for NES). (B) Infarct area and deficit score in vehicle ( n = 9) were compared to PAP‐1 (40 mg/kg; n = 9) treated 80‐week‐old female mice ( p = 0.032 for infarct, p = 0.003 for NES). Data are shown as whisker plots with data overlay. The boxes show mean ± SEM and the whiskers show confidence intervals.

    Journal: Annals of Clinical and Translational Neurology

    Article Title: The potassium channel Kv1.3 as a therapeutic target for immunocytoprotection after reperfusion

    doi: 10.1002/acn3.51456

    Figure Lengend Snippet: The Kv1.3 blocker PAP‐1 reduces infarction and improves neurological deficit in young and old WT female mice. (A) Infarct area and deficit score in vehicle ( n = 11) were compared to PAP‐1 (40 mg/kg; n = 15) treated 16‐week‐old female mice ( p = 0.007 for infarct, p = 0.016 for NES). (B) Infarct area and deficit score in vehicle ( n = 9) were compared to PAP‐1 (40 mg/kg; n = 9) treated 80‐week‐old female mice ( p = 0.032 for infarct, p = 0.003 for NES). Data are shown as whisker plots with data overlay. The boxes show mean ± SEM and the whiskers show confidence intervals.

    Article Snippet: The immunofluorescence staining in Figure was performed with a polyclonal guinea pig anti‐Kv1.3 antibody (1:100, AGP‐005 from Alomone Labs) and the same polyclonal rabbit Iba‐1 (1;1000) and CD3 (1:250) antibodies listed above; Secondary Abs: Alexa Fluor® 546‐goat anti‐guinea pig IgG (1:1000, ab150185 from Abcam) and Alexa Fluor®488‐goat anti‐rabbit IgG (1:1500, ab150077 from Abcam).

    Techniques: Mouse Assay, Whisker Assay

    Kv1.3 is expressed on microglia/macrophages and T cells in the infarct of an 80‐week‐old female mouse. (A) Sample immunofluorescence staining of 5‐ µ m thick paraffin sections from the 6‐mm slice of an 80‐week‐old female mouse on day 8 after tMCAO. (A) Kv1.3 staining colocalizes to Iba‐1 + cells. (B) Kv1.3 staining on smaller, CD3 + T cells (white arrowheads).

    Journal: Annals of Clinical and Translational Neurology

    Article Title: The potassium channel Kv1.3 as a therapeutic target for immunocytoprotection after reperfusion

    doi: 10.1002/acn3.51456

    Figure Lengend Snippet: Kv1.3 is expressed on microglia/macrophages and T cells in the infarct of an 80‐week‐old female mouse. (A) Sample immunofluorescence staining of 5‐ µ m thick paraffin sections from the 6‐mm slice of an 80‐week‐old female mouse on day 8 after tMCAO. (A) Kv1.3 staining colocalizes to Iba‐1 + cells. (B) Kv1.3 staining on smaller, CD3 + T cells (white arrowheads).

    Article Snippet: The immunofluorescence staining in Figure was performed with a polyclonal guinea pig anti‐Kv1.3 antibody (1:100, AGP‐005 from Alomone Labs) and the same polyclonal rabbit Iba‐1 (1;1000) and CD3 (1:250) antibodies listed above; Secondary Abs: Alexa Fluor® 546‐goat anti‐guinea pig IgG (1:1000, ab150185 from Abcam) and Alexa Fluor®488‐goat anti‐rabbit IgG (1:1500, ab150077 from Abcam).

    Techniques: Immunofluorescence, Staining

    PAP‐1 treatment and Kv1.3 deletion reduce Iba‐1 and CD3 staining in 80‐week‐old female mice. Serial paraffin sections (5 µ m thick) cut at 4 mm and the 6 mm from 80‐week‐old female mice were stained for Iba‐1 and CD3. (A) Percentage of Iba‐1‐positive pixels in the infarcted hemisphere. Vehicle‐treated WT ( n = 9), PAP‐1‐treated WT ( n = 9, p = 0.120 for 4‐mm section; p = 0.014 for 6‐mm section), and Kv1.3 −/− ( n = 18, p = 0.011 for 4‐mm section; p = 0.007 for 6‐mm section). (B) Percentage of CD3‐positive pixels in the infarcted hemisphere. Vehicle‐treated WT ( n = 9), PAP‐1‐treated WT ( n = 9, p = 0.049 for 4‐mm section; p = 0.027 for 6‐mm section), and Kv1.3 −/− ( n = 18, p

    Journal: Annals of Clinical and Translational Neurology

    Article Title: The potassium channel Kv1.3 as a therapeutic target for immunocytoprotection after reperfusion

    doi: 10.1002/acn3.51456

    Figure Lengend Snippet: PAP‐1 treatment and Kv1.3 deletion reduce Iba‐1 and CD3 staining in 80‐week‐old female mice. Serial paraffin sections (5 µ m thick) cut at 4 mm and the 6 mm from 80‐week‐old female mice were stained for Iba‐1 and CD3. (A) Percentage of Iba‐1‐positive pixels in the infarcted hemisphere. Vehicle‐treated WT ( n = 9), PAP‐1‐treated WT ( n = 9, p = 0.120 for 4‐mm section; p = 0.014 for 6‐mm section), and Kv1.3 −/− ( n = 18, p = 0.011 for 4‐mm section; p = 0.007 for 6‐mm section). (B) Percentage of CD3‐positive pixels in the infarcted hemisphere. Vehicle‐treated WT ( n = 9), PAP‐1‐treated WT ( n = 9, p = 0.049 for 4‐mm section; p = 0.027 for 6‐mm section), and Kv1.3 −/− ( n = 18, p

    Article Snippet: The immunofluorescence staining in Figure was performed with a polyclonal guinea pig anti‐Kv1.3 antibody (1:100, AGP‐005 from Alomone Labs) and the same polyclonal rabbit Iba‐1 (1;1000) and CD3 (1:250) antibodies listed above; Secondary Abs: Alexa Fluor® 546‐goat anti‐guinea pig IgG (1:1000, ab150185 from Abcam) and Alexa Fluor®488‐goat anti‐rabbit IgG (1:1500, ab150077 from Abcam).

    Techniques: Staining, Mouse Assay