antibodies against kir6 1  (Alomone Labs)


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    Structured Review

    Alomone Labs antibodies against kir6 1
    Nico ameliorated LPS-induced ALI and inflammation. (a) Nico increased LPS-induced <t>Kir6.1</t> and Kir6.2 downregulation in the lung. (b, c) Lung sections stained with H E showed severe injury in the LPS group which was attenuated by Nico pretreatment. The data revealed a high score for the LPS-treated group which was decreased in the Nico-pretreated group. (d) Nico pretreatment significantly reduced LPS-induced protein leakage in BALF. (e, f) Nico alleviated LPS-induced increments of MPO activities in BALF and lung homogenate. (g, h) Nico prevented the production of TNF- α and IL-1 β in lung homogenate. Data were shown as mean ± SEM ( n = 6 − 8). Statistically significant differences: ∗ P
    Antibodies Against Kir6 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against kir6 1/product/Alomone Labs
    Average 91 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    antibodies against kir6 1 - by Bioz Stars, 2022-11
    91/100 stars

    Images

    1) Product Images from "Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways"

    Article Title: Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2019/4957646

    Nico ameliorated LPS-induced ALI and inflammation. (a) Nico increased LPS-induced Kir6.1 and Kir6.2 downregulation in the lung. (b, c) Lung sections stained with H E showed severe injury in the LPS group which was attenuated by Nico pretreatment. The data revealed a high score for the LPS-treated group which was decreased in the Nico-pretreated group. (d) Nico pretreatment significantly reduced LPS-induced protein leakage in BALF. (e, f) Nico alleviated LPS-induced increments of MPO activities in BALF and lung homogenate. (g, h) Nico prevented the production of TNF- α and IL-1 β in lung homogenate. Data were shown as mean ± SEM ( n = 6 − 8). Statistically significant differences: ∗ P
    Figure Legend Snippet: Nico ameliorated LPS-induced ALI and inflammation. (a) Nico increased LPS-induced Kir6.1 and Kir6.2 downregulation in the lung. (b, c) Lung sections stained with H E showed severe injury in the LPS group which was attenuated by Nico pretreatment. The data revealed a high score for the LPS-treated group which was decreased in the Nico-pretreated group. (d) Nico pretreatment significantly reduced LPS-induced protein leakage in BALF. (e, f) Nico alleviated LPS-induced increments of MPO activities in BALF and lung homogenate. (g, h) Nico prevented the production of TNF- α and IL-1 β in lung homogenate. Data were shown as mean ± SEM ( n = 6 − 8). Statistically significant differences: ∗ P

    Techniques Used: Staining

    2) Product Images from "Cytochrome P450 epoxygenase-derived epoxyeicosatrienoic acids contribute to insulin sensitivity in mice and in humans"

    Article Title: Cytochrome P450 epoxygenase-derived epoxyeicosatrienoic acids contribute to insulin sensitivity in mice and in humans

    Journal: Diabetologia

    doi: 10.1007/s00125-017-4260-0

    Cyp2c44 disruption impairs K ATP -mediated vascular relaxation. ( a ) Mesenteric resistance artery endothelium-independent vasodilation in response to the ATP-sensitive potassium channel opener pinacidil was impaired in Cyp2c44 −/− mice (black circles) compared with WT controls (white circles). ( b ) After administration of the K ATP channel blocker glibenclamide (Glib.), the plasma insulin response was diminished in Cyp2c44 −/− mice compared with WT mice. ( c , d ) Western blots for the K ATP channel subunits Kir6.1 ( c ) and Kir6.2 ( d ) in skeletal muscle demonstrated similar expression. * p
    Figure Legend Snippet: Cyp2c44 disruption impairs K ATP -mediated vascular relaxation. ( a ) Mesenteric resistance artery endothelium-independent vasodilation in response to the ATP-sensitive potassium channel opener pinacidil was impaired in Cyp2c44 −/− mice (black circles) compared with WT controls (white circles). ( b ) After administration of the K ATP channel blocker glibenclamide (Glib.), the plasma insulin response was diminished in Cyp2c44 −/− mice compared with WT mice. ( c , d ) Western blots for the K ATP channel subunits Kir6.1 ( c ) and Kir6.2 ( d ) in skeletal muscle demonstrated similar expression. * p

    Techniques Used: Mouse Assay, Western Blot, Expressing

    3) Product Images from "Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway"

    Article Title: Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13006

    The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.
    Figure Legend Snippet: The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Negative Control, Western Blot, Staining, Marker

    4) Product Images from "Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway"

    Article Title: Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13006

    The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.
    Figure Legend Snippet: The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Negative Control, Western Blot, Staining, Marker

    5) Product Images from "Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway"

    Article Title: Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13006

    The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.
    Figure Legend Snippet: The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Negative Control, Western Blot, Staining, Marker

    6) Product Images from "Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway"

    Article Title: Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13006

    The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.
    Figure Legend Snippet: The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Negative Control, Western Blot, Staining, Marker

    7) Product Images from "Role of Kir6.2 subunits of ATP-sensitive potassium channels in endotoxemia-induced cardiac dysfunction"

    Article Title: Role of Kir6.2 subunits of ATP-sensitive potassium channels in endotoxemia-induced cardiac dysfunction

    Journal: Cardiovascular Diabetology

    doi: 10.1186/1475-2840-12-75

    Unchanged Kir6.1 subunits expression in heart tissues in Kir6.2 −/− mice. Data are expressed as means ± SEM (n=3 per group).
    Figure Legend Snippet: Unchanged Kir6.1 subunits expression in heart tissues in Kir6.2 −/− mice. Data are expressed as means ± SEM (n=3 per group).

    Techniques Used: Expressing, Mouse Assay

    8) Product Images from "Diabetes mellitus reduces the function and expression of ATP-dependent K+ channels in cardiac mitochondria"

    Article Title: Diabetes mellitus reduces the function and expression of ATP-dependent K+ channels in cardiac mitochondria

    Journal: Life sciences

    doi: 10.1016/j.lfs.2012.11.019

    Diabetes mellitus reduces Kir6.1 expression in SSM
    Figure Legend Snippet: Diabetes mellitus reduces Kir6.1 expression in SSM

    Techniques Used: Expressing

    9) Product Images from "High blood pressure associates with the remodelling of inward rectifier K+ channels in mice mesenteric vascular smooth muscle cells"

    Article Title: High blood pressure associates with the remodelling of inward rectifier K+ channels in mice mesenteric vascular smooth muscle cells

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2012.236190

    Expression of Kir2.1, Kir4.1, Kir6.1 and SUR2 proteins in BPN and BPH mesenteric VSMCs
    Figure Legend Snippet: Expression of Kir2.1, Kir4.1, Kir6.1 and SUR2 proteins in BPN and BPH mesenteric VSMCs

    Techniques Used: Expressing

    10) Product Images from "Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis"

    Article Title: Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-8-149

    Western blotting show expression of both Kir6.1 and Kir6.2 K ATP channel pore-forming subunits in unstimulated and LPS/IFNγ-stimulated BV-2 cells (A, left) and microglial primary cultures (A, Right). Staining for the microglial cell membrane marker CD11b (B and E) and the K ATP channel subunits Kir 6.1 (C) or Kir 6.2 (F) showed colocalization in BV-2 microglia, indicating the expression of the K ATP channel at the cytoplasmic membrane (D and G, white arrows) . Control: unstimulated cells; L+I: cells stimulated with LPS and IFNγ. Scale bar = 30 μm.
    Figure Legend Snippet: Western blotting show expression of both Kir6.1 and Kir6.2 K ATP channel pore-forming subunits in unstimulated and LPS/IFNγ-stimulated BV-2 cells (A, left) and microglial primary cultures (A, Right). Staining for the microglial cell membrane marker CD11b (B and E) and the K ATP channel subunits Kir 6.1 (C) or Kir 6.2 (F) showed colocalization in BV-2 microglia, indicating the expression of the K ATP channel at the cytoplasmic membrane (D and G, white arrows) . Control: unstimulated cells; L+I: cells stimulated with LPS and IFNγ. Scale bar = 30 μm.

    Techniques Used: Western Blot, Expressing, Staining, Marker

    11) Product Images from "Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis"

    Article Title: Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-8-149

    Western blotting show expression of both Kir6.1 and Kir6.2 K ATP  channel pore-forming subunits in unstimulated and LPS/IFNγ-stimulated BV-2 cells (A, left) and microglial primary cultures (A, Right). Staining for the microglial cell membrane marker CD11b (B and E) and the K ATP  channel subunits Kir 6.1 (C) or Kir 6.2 (F) showed colocalization in BV-2 microglia, indicating the expression of the K ATP  channel at the cytoplasmic membrane (D and G, white arrows) . Control: unstimulated cells; L+I: cells stimulated with LPS and IFNγ. Scale bar = 30 μm.
    Figure Legend Snippet: Western blotting show expression of both Kir6.1 and Kir6.2 K ATP channel pore-forming subunits in unstimulated and LPS/IFNγ-stimulated BV-2 cells (A, left) and microglial primary cultures (A, Right). Staining for the microglial cell membrane marker CD11b (B and E) and the K ATP channel subunits Kir 6.1 (C) or Kir 6.2 (F) showed colocalization in BV-2 microglia, indicating the expression of the K ATP channel at the cytoplasmic membrane (D and G, white arrows) . Control: unstimulated cells; L+I: cells stimulated with LPS and IFNγ. Scale bar = 30 μm.

    Techniques Used: Western Blot, Expressing, Staining, Marker

    12) Product Images from "Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis"

    Article Title: Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-8-149

    Western blotting show expression of both Kir6.1 and Kir6.2 K ATP channel pore-forming subunits in unstimulated and LPS/IFNγ-stimulated BV-2 cells (A, left) and microglial primary cultures (A, Right). Staining for the microglial cell membrane marker CD11b (B and E) and the K ATP channel subunits Kir 6.1 (C) or Kir 6.2 (F) showed colocalization in BV-2 microglia, indicating the expression of the K ATP channel at the cytoplasmic membrane (D and G, white arrows) . Control: unstimulated cells; L+I: cells stimulated with LPS and IFNγ. Scale bar = 30 μm.
    Figure Legend Snippet: Western blotting show expression of both Kir6.1 and Kir6.2 K ATP channel pore-forming subunits in unstimulated and LPS/IFNγ-stimulated BV-2 cells (A, left) and microglial primary cultures (A, Right). Staining for the microglial cell membrane marker CD11b (B and E) and the K ATP channel subunits Kir 6.1 (C) or Kir 6.2 (F) showed colocalization in BV-2 microglia, indicating the expression of the K ATP channel at the cytoplasmic membrane (D and G, white arrows) . Control: unstimulated cells; L+I: cells stimulated with LPS and IFNγ. Scale bar = 30 μm.

    Techniques Used: Western Blot, Expressing, Staining, Marker

    13) Product Images from "Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats"

    Article Title: Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats

    Journal: Acta Pharmacologica Sinica

    doi: 10.1038/aps.2010.195

    Expression of Kir6.1, Kir6.2 and SUR2 in both aorta and mesenteric artery in sinoaortic denervated and sham-operated rats. A and B, fold changes of mRNA level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =7). C and D, fold changes of protein level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =3). The representative images are from three independent experiments. Data are expressed as mean±SEM. b P
    Figure Legend Snippet: Expression of Kir6.1, Kir6.2 and SUR2 in both aorta and mesenteric artery in sinoaortic denervated and sham-operated rats. A and B, fold changes of mRNA level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =7). C and D, fold changes of protein level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =3). The representative images are from three independent experiments. Data are expressed as mean±SEM. b P

    Techniques Used: Expressing

    Representative images of Kir6.1, Kir6.2, and SUR2 expression in aorta (A–C) and mesenteric artery (D–F) from sinoaortic denervated (SAD) and sham-operated rats using laser scanning confocal microscopy. Aortic SUR2 expression was greater, while Kir6.1 was lower, in SAD rats than in sham-operated controls (A and C). In the mesenteric artery both SUR2 and Kir6.1 expression were markedly lower in SAD rats than controls (D and F). For both arteries, Kir6.2 expression was indistinguishable in sham-operated compared with SAD rats (B and E). Similar images were observed in vessels from at least 3 rats for each group. FITC,fluorescein isothiocyanate; DIC, differential interference contrast. The objective was ×20, scale bar: 50 μm.
    Figure Legend Snippet: Representative images of Kir6.1, Kir6.2, and SUR2 expression in aorta (A–C) and mesenteric artery (D–F) from sinoaortic denervated (SAD) and sham-operated rats using laser scanning confocal microscopy. Aortic SUR2 expression was greater, while Kir6.1 was lower, in SAD rats than in sham-operated controls (A and C). In the mesenteric artery both SUR2 and Kir6.1 expression were markedly lower in SAD rats than controls (D and F). For both arteries, Kir6.2 expression was indistinguishable in sham-operated compared with SAD rats (B and E). Similar images were observed in vessels from at least 3 rats for each group. FITC,fluorescein isothiocyanate; DIC, differential interference contrast. The objective was ×20, scale bar: 50 μm.

    Techniques Used: Expressing, Confocal Microscopy

    14) Product Images from "Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats"

    Article Title: Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats

    Journal: Acta Pharmacologica Sinica

    doi: 10.1038/aps.2010.195

    Representative images of Kir6.1, Kir6.2, and SUR2 expression in aorta (A–C) and mesenteric artery (D–F) from sinoaortic denervated (SAD) and sham-operated rats using laser scanning confocal microscopy. Aortic SUR2 expression was greater,
    Figure Legend Snippet: Representative images of Kir6.1, Kir6.2, and SUR2 expression in aorta (A–C) and mesenteric artery (D–F) from sinoaortic denervated (SAD) and sham-operated rats using laser scanning confocal microscopy. Aortic SUR2 expression was greater,

    Techniques Used: Expressing, Confocal Microscopy

    Expression of Kir6.1, Kir6.2 and SUR2 in both aorta and mesenteric artery in sinoaortic denervated and sham-operated rats. A and B, fold changes of mRNA level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =7). C and D, fold changes of protein
    Figure Legend Snippet: Expression of Kir6.1, Kir6.2 and SUR2 in both aorta and mesenteric artery in sinoaortic denervated and sham-operated rats. A and B, fold changes of mRNA level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =7). C and D, fold changes of protein

    Techniques Used: Expressing

    15) Product Images from "Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats"

    Article Title: Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats

    Journal: Acta Pharmacologica Sinica

    doi: 10.1038/aps.2010.195

    Representative images of Kir6.1, Kir6.2, and SUR2 expression in aorta (A–C) and mesenteric artery (D–F) from sinoaortic denervated (SAD) and sham-operated rats using laser scanning confocal microscopy. Aortic SUR2 expression was greater,
    Figure Legend Snippet: Representative images of Kir6.1, Kir6.2, and SUR2 expression in aorta (A–C) and mesenteric artery (D–F) from sinoaortic denervated (SAD) and sham-operated rats using laser scanning confocal microscopy. Aortic SUR2 expression was greater,

    Techniques Used: Expressing, Confocal Microscopy

    Expression of Kir6.1, Kir6.2 and SUR2 in both aorta and mesenteric artery in sinoaortic denervated and sham-operated rats. A and B, fold changes of mRNA level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =7). C and D, fold changes of protein
    Figure Legend Snippet: Expression of Kir6.1, Kir6.2 and SUR2 in both aorta and mesenteric artery in sinoaortic denervated and sham-operated rats. A and B, fold changes of mRNA level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =7). C and D, fold changes of protein

    Techniques Used: Expressing

    16) Product Images from "Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats"

    Article Title: Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats

    Journal: Acta Pharmacologica Sinica

    doi: 10.1038/aps.2010.195

    Expression of Kir6.1, Kir6.2 and SUR2 in both aorta and mesenteric artery in sinoaortic denervated and sham-operated rats. A and B, fold changes of mRNA level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =7). C and D, fold changes of protein level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =3). The representative images are from three independent experiments. Data are expressed as mean±SEM. b P
    Figure Legend Snippet: Expression of Kir6.1, Kir6.2 and SUR2 in both aorta and mesenteric artery in sinoaortic denervated and sham-operated rats. A and B, fold changes of mRNA level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =7). C and D, fold changes of protein level (Kir6.1, Kir6.2, and SUR2) in aorta and mesenteric artery ( n =3). The representative images are from three independent experiments. Data are expressed as mean±SEM. b P

    Techniques Used: Expressing

    Representative images of Kir6.1, Kir6.2, and SUR2 expression in aorta (A–C) and mesenteric artery (D–F) from sinoaortic denervated (SAD) and sham-operated rats using laser scanning confocal microscopy. Aortic SUR2 expression was greater, while Kir6.1 was lower, in SAD rats than in sham-operated controls (A and C). In the mesenteric artery both SUR2 and Kir6.1 expression were markedly lower in SAD rats than controls (D and F). For both arteries, Kir6.2 expression was indistinguishable in sham-operated compared with SAD rats (B and E). Similar images were observed in vessels from at least 3 rats for each group. FITC,fluorescein isothiocyanate; DIC, differential interference contrast. The objective was ×20, scale bar: 50 μm.
    Figure Legend Snippet: Representative images of Kir6.1, Kir6.2, and SUR2 expression in aorta (A–C) and mesenteric artery (D–F) from sinoaortic denervated (SAD) and sham-operated rats using laser scanning confocal microscopy. Aortic SUR2 expression was greater, while Kir6.1 was lower, in SAD rats than in sham-operated controls (A and C). In the mesenteric artery both SUR2 and Kir6.1 expression were markedly lower in SAD rats than controls (D and F). For both arteries, Kir6.2 expression was indistinguishable in sham-operated compared with SAD rats (B and E). Similar images were observed in vessels from at least 3 rats for each group. FITC,fluorescein isothiocyanate; DIC, differential interference contrast. The objective was ×20, scale bar: 50 μm.

    Techniques Used: Expressing, Confocal Microscopy

    17) Product Images from "The ATP-sensitive K+-channel (KATP) controls early left-right patterning in Xenopus and chick embryos"

    Article Title: The ATP-sensitive K+-channel (KATP) controls early left-right patterning in Xenopus and chick embryos

    Journal: Developmental biology

    doi: 10.1016/j.ydbio.2010.07.011

    Immunolocalization of Xenopus Kir6.1 and SUR2A
    Figure Legend Snippet: Immunolocalization of Xenopus Kir6.1 and SUR2A

    Techniques Used:

    18) Product Images from "The ATP-sensitive K+-channel (KATP) controls early left-right patterning in Xenopus and chick embryos"

    Article Title: The ATP-sensitive K+-channel (KATP) controls early left-right patterning in Xenopus and chick embryos

    Journal: Developmental biology

    doi: 10.1016/j.ydbio.2010.07.011

    Immunolocalization of Xenopus Kir6.1 and SUR2A
    Figure Legend Snippet: Immunolocalization of Xenopus Kir6.1 and SUR2A

    Techniques Used:

    19) Product Images from "ATP-Sensitive Potassium Channel-Mediated Lactate Effect on Orexin Neurons: Implications for Brain Energetics during Arousal"

    Article Title: ATP-Sensitive Potassium Channel-Mediated Lactate Effect on Orexin Neurons: Implications for Brain Energetics during Arousal

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.5741-09.2010

    KATP channel composition in orexin neurons. A–C , Immunofluorescence labeling of orexin A (red) ( A ) and Kir6.1 (green) ( B ) displays colocalization ( C ). D–F , Immunofluorescence labeling of orexin A (red) ( D ) and Kir6.2 (green) ( E ) displays a lack of colocalization ( F ). G , Diazoxide induces an outward current in the presence of TTX. The arrows indicate the times of voltage ramp applications. H , Current–voltage relationship of the diazoxide-induced response, generated by subtracting the current response to voltage ramps in the baseline condition from that in the presence of diazoxide. The inset denotes the voltage ramp protocol used. I , Grouped data showing diazoxide (Dz) and pinacidil effects on orexin neurons. Diazoxide effect was significantly blocked by glibenclamide (Glib). J , Outward currents are also induced by postsynaptic dialysis with ATP-free internal solution (0 ATP) and CCCP. These currents are significantly blocked by glibenclamide. * p
    Figure Legend Snippet: KATP channel composition in orexin neurons. A–C , Immunofluorescence labeling of orexin A (red) ( A ) and Kir6.1 (green) ( B ) displays colocalization ( C ). D–F , Immunofluorescence labeling of orexin A (red) ( D ) and Kir6.2 (green) ( E ) displays a lack of colocalization ( F ). G , Diazoxide induces an outward current in the presence of TTX. The arrows indicate the times of voltage ramp applications. H , Current–voltage relationship of the diazoxide-induced response, generated by subtracting the current response to voltage ramps in the baseline condition from that in the presence of diazoxide. The inset denotes the voltage ramp protocol used. I , Grouped data showing diazoxide (Dz) and pinacidil effects on orexin neurons. Diazoxide effect was significantly blocked by glibenclamide (Glib). J , Outward currents are also induced by postsynaptic dialysis with ATP-free internal solution (0 ATP) and CCCP. These currents are significantly blocked by glibenclamide. * p

    Techniques Used: Immunofluorescence, Labeling, Generated

    20) Product Images from "Is Kir6.1 a subunit of mitoKATP?"

    Article Title: Is Kir6.1 a subunit of mitoKATP?

    Journal:

    doi: 10.1016/j.bbrc.2007.11.154

    Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes
    Figure Legend Snippet: Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes

    Techniques Used:

    Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody
    Figure Legend Snippet: Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody

    Techniques Used:

    21) Product Images from "Is Kir6.1 a subunit of mitoKATP?"

    Article Title: Is Kir6.1 a subunit of mitoKATP?

    Journal:

    doi: 10.1016/j.bbrc.2007.11.154

    Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes
    Figure Legend Snippet: Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes

    Techniques Used:

    Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody
    Figure Legend Snippet: Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody

    Techniques Used:

    22) Product Images from "Is Kir6.1 a subunit of mitoKATP?"

    Article Title: Is Kir6.1 a subunit of mitoKATP?

    Journal:

    doi: 10.1016/j.bbrc.2007.11.154

    Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes
    Figure Legend Snippet: Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes

    Techniques Used:

    Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody
    Figure Legend Snippet: Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody

    Techniques Used:

    23) Product Images from "Is Kir6.1 a subunit of mitoKATP?"

    Article Title: Is Kir6.1 a subunit of mitoKATP?

    Journal:

    doi: 10.1016/j.bbrc.2007.11.154

    Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes
    Figure Legend Snippet: Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes

    Techniques Used:

    Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody
    Figure Legend Snippet: Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody

    Techniques Used:

    24) Product Images from "Is Kir6.1 a subunit of mitoKATP?"

    Article Title: Is Kir6.1 a subunit of mitoKATP?

    Journal:

    doi: 10.1016/j.bbrc.2007.11.154

    Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes
    Figure Legend Snippet: Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes

    Techniques Used:

    Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody
    Figure Legend Snippet: Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody

    Techniques Used:

    25) Product Images from "Is Kir6.1 a subunit of mitoKATP?"

    Article Title: Is Kir6.1 a subunit of mitoKATP?

    Journal:

    doi: 10.1016/j.bbrc.2007.11.154

    Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes
    Figure Legend Snippet: Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes

    Techniques Used:

    Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody
    Figure Legend Snippet: Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody

    Techniques Used:

    26) Product Images from "Is Kir6.1 a subunit of mitoKATP?"

    Article Title: Is Kir6.1 a subunit of mitoKATP?

    Journal:

    doi: 10.1016/j.bbrc.2007.11.154

    Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes
    Figure Legend Snippet: Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes

    Techniques Used:

    Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody
    Figure Legend Snippet: Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody

    Techniques Used:

    27) Product Images from "Is Kir6.1 a subunit of mitoKATP?"

    Article Title: Is Kir6.1 a subunit of mitoKATP?

    Journal:

    doi: 10.1016/j.bbrc.2007.11.154

    Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes
    Figure Legend Snippet: Detection of Kir6.1 Immunoreactivity in Mitochondrial Membranes

    Techniques Used:

    Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody
    Figure Legend Snippet: Mitochondrial Kir6.1-Immunoreactivity Revealed by a Second Antibody

    Techniques Used:

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    Alomone Labs antibodies against kir6 1
    Nico ameliorated LPS-induced ALI and inflammation. (a) Nico increased LPS-induced <t>Kir6.1</t> and Kir6.2 downregulation in the lung. (b, c) Lung sections stained with H E showed severe injury in the LPS group which was attenuated by Nico pretreatment. The data revealed a high score for the LPS-treated group which was decreased in the Nico-pretreated group. (d) Nico pretreatment significantly reduced LPS-induced protein leakage in BALF. (e, f) Nico alleviated LPS-induced increments of MPO activities in BALF and lung homogenate. (g, h) Nico prevented the production of TNF- α and IL-1 β in lung homogenate. Data were shown as mean ± SEM ( n = 6 − 8). Statistically significant differences: ∗ P
    Antibodies Against Kir6 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Nico ameliorated LPS-induced ALI and inflammation. (a) Nico increased LPS-induced Kir6.1 and Kir6.2 downregulation in the lung. (b, c) Lung sections stained with H E showed severe injury in the LPS group which was attenuated by Nico pretreatment. The data revealed a high score for the LPS-treated group which was decreased in the Nico-pretreated group. (d) Nico pretreatment significantly reduced LPS-induced protein leakage in BALF. (e, f) Nico alleviated LPS-induced increments of MPO activities in BALF and lung homogenate. (g, h) Nico prevented the production of TNF- α and IL-1 β in lung homogenate. Data were shown as mean ± SEM ( n = 6 − 8). Statistically significant differences: ∗ P

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways

    doi: 10.1155/2019/4957646

    Figure Lengend Snippet: Nico ameliorated LPS-induced ALI and inflammation. (a) Nico increased LPS-induced Kir6.1 and Kir6.2 downregulation in the lung. (b, c) Lung sections stained with H E showed severe injury in the LPS group which was attenuated by Nico pretreatment. The data revealed a high score for the LPS-treated group which was decreased in the Nico-pretreated group. (d) Nico pretreatment significantly reduced LPS-induced protein leakage in BALF. (e, f) Nico alleviated LPS-induced increments of MPO activities in BALF and lung homogenate. (g, h) Nico prevented the production of TNF- α and IL-1 β in lung homogenate. Data were shown as mean ± SEM ( n = 6 − 8). Statistically significant differences: ∗ P

    Article Snippet: Then, the transferred membranes were incubated with primary antibodies against Kir6.1 (Alomone Labs, Jerusalem, Israel), Kir6.2 (Abcam), NF-κ B p-p65/p65, p-iκ B-α /iκ B-α , p-p38/p38, p-ERK/ERK, p-JNK/JNK, intercellular adhesion molecule-1 (ICAM-1), cleaved-caspase-3 (c-caspase-3), caspase-9 (1 : 1000, Cell Signaling Technology), endothelial nitric oxide synthase (eNOS) (1 : 1000, Santa Cruz), inducible nitric oxide synthase (iNOS) (1 : 1000, Millipore), CCAAT/enhancer-binding protein homologous protein (CHOP), vascular cell adhesion molecule-1 (VCAM-1), VE-cadherin, Nox4 (1 : 1000), MnSOD (1 : 5000, Abcam), and β -actin (1 : 5000, Proteintech, Rosemont, USA) overnight.

    Techniques: Staining

    Cyp2c44 disruption impairs K ATP -mediated vascular relaxation. ( a ) Mesenteric resistance artery endothelium-independent vasodilation in response to the ATP-sensitive potassium channel opener pinacidil was impaired in Cyp2c44 −/− mice (black circles) compared with WT controls (white circles). ( b ) After administration of the K ATP channel blocker glibenclamide (Glib.), the plasma insulin response was diminished in Cyp2c44 −/− mice compared with WT mice. ( c , d ) Western blots for the K ATP channel subunits Kir6.1 ( c ) and Kir6.2 ( d ) in skeletal muscle demonstrated similar expression. * p

    Journal: Diabetologia

    Article Title: Cytochrome P450 epoxygenase-derived epoxyeicosatrienoic acids contribute to insulin sensitivity in mice and in humans

    doi: 10.1007/s00125-017-4260-0

    Figure Lengend Snippet: Cyp2c44 disruption impairs K ATP -mediated vascular relaxation. ( a ) Mesenteric resistance artery endothelium-independent vasodilation in response to the ATP-sensitive potassium channel opener pinacidil was impaired in Cyp2c44 −/− mice (black circles) compared with WT controls (white circles). ( b ) After administration of the K ATP channel blocker glibenclamide (Glib.), the plasma insulin response was diminished in Cyp2c44 −/− mice compared with WT mice. ( c , d ) Western blots for the K ATP channel subunits Kir6.1 ( c ) and Kir6.2 ( d ) in skeletal muscle demonstrated similar expression. * p

    Article Snippet: SDS-PAGE and membranes were then incubated with anti-Kir6.1 (1:200 dilution; Alomone Labs, Jerusalem, Israel), anti-Kir6.2 (1:1000 dilution; Alomone Labs), anti-β-tubulin (1:2000 dilution; Cell Signaling Technology, Danvers, MA, USA), anti-pAkt (1:1000, Cell Signaling Technology) or anti-Akt (1:1000, Cell Signaling Technology) antibodies followed by horseradish peroxidase-conjugated secondary antibody (Cell Signaling Technology).

    Techniques: Mouse Assay, Western Blot, Expressing

    The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Activation of ATP‐sensitive potassium channels facilitates the function of human endothelial colony‐forming cells via Ca2+/Akt/ eNOS pathway

    doi: 10.1111/jcmm.13006

    Figure Lengend Snippet: The expression of K ATP subtypes in ECFC s. ( A ) RT ‐ PCR showed the expression of Kir6.1, Kir6.2 and SUR 2b, but not SUR 2a and SUR 1 in mRNA level. HPAEC s and mouse brain were used as positive controls, water (no template) as a negative control ( n = 3). ( B ) Western blotting confirmed the expression of Kir6.1 (48 kD), Kir6.2 (44 kD) and SUR 2b (140–150 kD), but not SUR 2a (140–150 kD) and SUR 1 (175 kD), using HPAEC s and mouse brain as positive controls ( n = 3). ( C ) Confocal images showed the subcellular localization of K ATP subunits in ECFC s co‐stained with a endothelial specific marker ( CD 31 or VE ‐cadherin), revealing the extensive distribution of Kir6.1, Kir6.2 and SUR 2b. DAPI staining for nuclear labelling ( n = 3), scale bar: 20 μm. M: marker, MB : mouse brain.

    Article Snippet: In brief, after fixation and blocking, ECFCs were permeabilized with 0.5% Triton X‐100 (Sigma‐Aldrich) in PBS, blocked with 5% BSA for 1 hr at room temperature and incubated with antibodies against Kir6.1 (Alomone Labs), Kir6.2 (Abcam), SUR2b (Santa Cruz), CD31 (Santa Cruz) and VE‐cadherin (Abcam) at 4°C overnight.

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Negative Control, Western Blot, Staining, Marker