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 4 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 4 article reviews
    Price from $9.99 to $1999.99
    antibodies against kir6 1 - by Bioz Stars, 2022-08
    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 "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

    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

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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 1 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 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against kir6 1 - by Bioz Stars, 2022-08
    91/100 stars
      Buy from Supplier

    94
    Alomone Labs primary antibodies against kir6 2
    Distribution and localization of <t>Kir6.2</t> immunoreactivity (ir) in the SCN. ( A ) Distribution of the Kir6.2 (A1–3) and AVP (A4-6) immunoreactivity in the rostral (A1, A4), middle (A2, A5), and caudal (A3, A6) sections of the SCN. Scale bar: 200 µm. ( B ) Selective colocalization of Kir6.2-ir with AVP-ir (B1–3) but not with VIP-ir (B4–6). Note the colocalization of Kir6.2-ir and AVP-ir in and around the soma (B2) and in varicosities along the process (marked by arrowheads, B3). Note the reciprocal apposition of VIP-ir bouton-like swellings against a Kir6.2-ir soma (B5) and Kir6.2-ir bouton-like swellings against VIP-ir somata (B6). Note also bouton-like swellings (yellow) double-stained with Kir6.2 (green) and AVP (red) apposing Hoechst-stained cells (blue) in the ventrolateral region of the SCN (B7). Scale bar: 100 µm (B1, B4); 10 µm (B2, B3, B5–7). ( C ) Lack of colocalization of Kir6.2-ir with markers for three afferent inputs SERT-ir (C1, C2), vGluT2-ir (C3, C4), NPY-ir (C5, C6). Insets: co-distribution of SERT-ir, vGluT2-ir, and NPY-ir with Kir6.2-stained somata in the ventromedial region of the mid-SCN section. Scale bar: 100 µm (C1, C3, C5); 10 µm (C2, C4, C6, insets). OC: optic chiasm. 3 V: third ventricle. Asterisks mark Hoechst-stained nuclei.
    Primary Antibodies Against Kir6 2, 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/primary antibodies against kir6 2/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    primary antibodies against kir6 2 - by Bioz Stars, 2022-08
    94/100 stars
      Buy from Supplier

    Image Search Results


    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

    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: After blocking, the transferred membranes were incubated with primary antibodies against Kir6.1 (Alomone Labs, Jerusalem, Israel), Kir6.2 (Abcam, Cambridge, UK), SUR1 (Abcam), SUR2a (Santa Cruz), SUR2b (Santa Cruz), calcium/calmodulin‐dependent protein kinase II (CaMKII) (Santa Cruz), phospho‐CaMKII (P‐CaMKII) (Santa Cruz), Akt (Cell Signaling Technology, Danvers, MA, USA), phospho‐Akt (P‐Akt) (Cell Signaling Technology), eNOS (Santa Cruz), phospho‐eNOS (P‐eNOS) (Ser1177; Santa Cruz) and GAPDH (Santa Cruz).

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

    Distribution and localization of Kir6.2 immunoreactivity (ir) in the SCN. ( A ) Distribution of the Kir6.2 (A1–3) and AVP (A4-6) immunoreactivity in the rostral (A1, A4), middle (A2, A5), and caudal (A3, A6) sections of the SCN. Scale bar: 200 µm. ( B ) Selective colocalization of Kir6.2-ir with AVP-ir (B1–3) but not with VIP-ir (B4–6). Note the colocalization of Kir6.2-ir and AVP-ir in and around the soma (B2) and in varicosities along the process (marked by arrowheads, B3). Note the reciprocal apposition of VIP-ir bouton-like swellings against a Kir6.2-ir soma (B5) and Kir6.2-ir bouton-like swellings against VIP-ir somata (B6). Note also bouton-like swellings (yellow) double-stained with Kir6.2 (green) and AVP (red) apposing Hoechst-stained cells (blue) in the ventrolateral region of the SCN (B7). Scale bar: 100 µm (B1, B4); 10 µm (B2, B3, B5–7). ( C ) Lack of colocalization of Kir6.2-ir with markers for three afferent inputs SERT-ir (C1, C2), vGluT2-ir (C3, C4), NPY-ir (C5, C6). Insets: co-distribution of SERT-ir, vGluT2-ir, and NPY-ir with Kir6.2-stained somata in the ventromedial region of the mid-SCN section. Scale bar: 100 µm (C1, C3, C5); 10 µm (C2, C4, C6, insets). OC: optic chiasm. 3 V: third ventricle. Asterisks mark Hoechst-stained nuclei.

    Journal: Scientific Reports

    Article Title: KATP Channels Mediate Differential Metabolic Responses to Glucose Shortage of the Dorsomedial and Ventrolateral Oscillators in the Central Clock

    doi: 10.1038/s41598-017-00699-3

    Figure Lengend Snippet: Distribution and localization of Kir6.2 immunoreactivity (ir) in the SCN. ( A ) Distribution of the Kir6.2 (A1–3) and AVP (A4-6) immunoreactivity in the rostral (A1, A4), middle (A2, A5), and caudal (A3, A6) sections of the SCN. Scale bar: 200 µm. ( B ) Selective colocalization of Kir6.2-ir with AVP-ir (B1–3) but not with VIP-ir (B4–6). Note the colocalization of Kir6.2-ir and AVP-ir in and around the soma (B2) and in varicosities along the process (marked by arrowheads, B3). Note the reciprocal apposition of VIP-ir bouton-like swellings against a Kir6.2-ir soma (B5) and Kir6.2-ir bouton-like swellings against VIP-ir somata (B6). Note also bouton-like swellings (yellow) double-stained with Kir6.2 (green) and AVP (red) apposing Hoechst-stained cells (blue) in the ventrolateral region of the SCN (B7). Scale bar: 100 µm (B1, B4); 10 µm (B2, B3, B5–7). ( C ) Lack of colocalization of Kir6.2-ir with markers for three afferent inputs SERT-ir (C1, C2), vGluT2-ir (C3, C4), NPY-ir (C5, C6). Insets: co-distribution of SERT-ir, vGluT2-ir, and NPY-ir with Kir6.2-stained somata in the ventromedial region of the mid-SCN section. Scale bar: 100 µm (C1, C3, C5); 10 µm (C2, C4, C6, insets). OC: optic chiasm. 3 V: third ventricle. Asterisks mark Hoechst-stained nuclei.

    Article Snippet: For immunohistochemical staining, sections (20 µm) were treated with 0.3% H2 O2 for 15 min to quench endogenous peroxidase, and then incubated overnight at 4 °C in PBS containing 2% serum, 0.3% Triton X-100, and primary antibodies against Kir6.2 (rabbit anti-Kir6.2; 1:5000; APC-020; Alomone Labs, Jerusalem, Israel) and AVP (rabbit anti-AVP; 1:3000; AB1565; Millipore, Temecula, CA, USA) .

    Techniques: Staining

    Kir6.2/SUR1 combination of K ATP channels in the SCN neurones. ( A ) RT-PCR analysis indicating the expression of mRNA for pore-forming Kir6.2 and sulfonylurea subunits 1 in the SCN. Positive controls were performed using cDNA from rat brain. The expected PCR product sizes for Kir6.1, Kir6.2, SUR1, and SUR2 were 411, 385, 388, and 501 bp, respectively. Negative controls were performed using RT products with omission of reverse transcriptase (RT-) to examine the contamination of genomic DNA. ( B ) Cell-attached recordings showing the effects of the sulfonylurea on spontaneous firing of the SCN neurones (ZT 4–15). Firing responses of a representative cell to 200 μM tolbutamide (top left panel), 200 μM diazoxide (top middle panel), and 0.1 μM glibenclamide (top right panel). Note the lack of recovery of spontaneous firing after washout of glibenclamide. Daytime recordings (ZT 7). Bottom left panel: summary of experiments showing a moderate increase in firing rate by tolbutamide. Baseline spontaneous firing rate: 2.7 ± 0.3 Hz ( n = 50). Bottom right panel: summary of experiments showing a decrease in firing rate by diazoxide. Baseline spontaneous firing rate: 3.0 ± 0.3 Hz ( n = 17). * P

    Journal: Scientific Reports

    Article Title: KATP Channels Mediate Differential Metabolic Responses to Glucose Shortage of the Dorsomedial and Ventrolateral Oscillators in the Central Clock

    doi: 10.1038/s41598-017-00699-3

    Figure Lengend Snippet: Kir6.2/SUR1 combination of K ATP channels in the SCN neurones. ( A ) RT-PCR analysis indicating the expression of mRNA for pore-forming Kir6.2 and sulfonylurea subunits 1 in the SCN. Positive controls were performed using cDNA from rat brain. The expected PCR product sizes for Kir6.1, Kir6.2, SUR1, and SUR2 were 411, 385, 388, and 501 bp, respectively. Negative controls were performed using RT products with omission of reverse transcriptase (RT-) to examine the contamination of genomic DNA. ( B ) Cell-attached recordings showing the effects of the sulfonylurea on spontaneous firing of the SCN neurones (ZT 4–15). Firing responses of a representative cell to 200 μM tolbutamide (top left panel), 200 μM diazoxide (top middle panel), and 0.1 μM glibenclamide (top right panel). Note the lack of recovery of spontaneous firing after washout of glibenclamide. Daytime recordings (ZT 7). Bottom left panel: summary of experiments showing a moderate increase in firing rate by tolbutamide. Baseline spontaneous firing rate: 2.7 ± 0.3 Hz ( n = 50). Bottom right panel: summary of experiments showing a decrease in firing rate by diazoxide. Baseline spontaneous firing rate: 3.0 ± 0.3 Hz ( n = 17). * P

    Article Snippet: For immunohistochemical staining, sections (20 µm) were treated with 0.3% H2 O2 for 15 min to quench endogenous peroxidase, and then incubated overnight at 4 °C in PBS containing 2% serum, 0.3% Triton X-100, and primary antibodies against Kir6.2 (rabbit anti-Kir6.2; 1:5000; APC-020; Alomone Labs, Jerusalem, Israel) and AVP (rabbit anti-AVP; 1:3000; AB1565; Millipore, Temecula, CA, USA) .

    Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Polymerase Chain Reaction