atx ii  (Alomone Labs)


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    Structured Review

    Alomone Labs atx ii
    Reduction of MAPD 90 prolongation by Tetrodotoxin (TTX) and eleclazine (Elec) in hearts treated with Bay K <t>8644</t> alone and <t>ATX-II</t> plus Bay K 8644. ( a ) Representative recordings of MAPs recorded from the epicardium of the left ventricular wall in serially exposed to no drug (control, curve 1), ATX-II (3 nM, curve 2), ATX-II plus Bay K 8644 (200 nM, curve 3), ATX-II plus Bay K 8644 plus TTX (1 µM, curve 4), and ATX-II plus Bay K 8644 plus eleclazine (10 µM, curve 5). ( b ) Concentration-dependent decreases by TTX of epi-MAPD 90 and endo-MAPD 90 in the presence of 300 nM Bay K 8644 (n = 7). ( c ) Effect of TTX (1 µM) and eleclazine (10 µM) on the increase of Δ epi-MAPD 90 and Δ endo-epi MAPD 90 induced by Bay K 8644 in absence and presence of ATX-II. * P
    Atx Ii, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/atx ii/product/Alomone Labs
    Average 93 stars, based on 29 article reviews
    Price from $9.99 to $1999.99
    atx ii - by Bioz Stars, 2022-12
    93/100 stars

    Images

    1) Product Images from "Inhibition of late sodium current suppresses calcium-related ventricular arrhythmias by reducing the phosphorylation of CaMK-II and sodium channel expressions"

    Article Title: Inhibition of late sodium current suppresses calcium-related ventricular arrhythmias by reducing the phosphorylation of CaMK-II and sodium channel expressions

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-01056-0

    Reduction of MAPD 90 prolongation by Tetrodotoxin (TTX) and eleclazine (Elec) in hearts treated with Bay K 8644 alone and ATX-II plus Bay K 8644. ( a ) Representative recordings of MAPs recorded from the epicardium of the left ventricular wall in serially exposed to no drug (control, curve 1), ATX-II (3 nM, curve 2), ATX-II plus Bay K 8644 (200 nM, curve 3), ATX-II plus Bay K 8644 plus TTX (1 µM, curve 4), and ATX-II plus Bay K 8644 plus eleclazine (10 µM, curve 5). ( b ) Concentration-dependent decreases by TTX of epi-MAPD 90 and endo-MAPD 90 in the presence of 300 nM Bay K 8644 (n = 7). ( c ) Effect of TTX (1 µM) and eleclazine (10 µM) on the increase of Δ epi-MAPD 90 and Δ endo-epi MAPD 90 induced by Bay K 8644 in absence and presence of ATX-II. * P
    Figure Legend Snippet: Reduction of MAPD 90 prolongation by Tetrodotoxin (TTX) and eleclazine (Elec) in hearts treated with Bay K 8644 alone and ATX-II plus Bay K 8644. ( a ) Representative recordings of MAPs recorded from the epicardium of the left ventricular wall in serially exposed to no drug (control, curve 1), ATX-II (3 nM, curve 2), ATX-II plus Bay K 8644 (200 nM, curve 3), ATX-II plus Bay K 8644 plus TTX (1 µM, curve 4), and ATX-II plus Bay K 8644 plus eleclazine (10 µM, curve 5). ( b ) Concentration-dependent decreases by TTX of epi-MAPD 90 and endo-MAPD 90 in the presence of 300 nM Bay K 8644 (n = 7). ( c ) Effect of TTX (1 µM) and eleclazine (10 µM) on the increase of Δ epi-MAPD 90 and Δ endo-epi MAPD 90 induced by Bay K 8644 in absence and presence of ATX-II. * P

    Techniques Used: Concentration Assay

    TTX (at concentration of 1 µM) reduced the phosphorylation of CaMK II-δ and Na v 1.5 in hearts pretreated with Bay K 8644 (200 nM) in both absence and presence of ATX-II (3 nM). ( a ) Representative protein expression of p-CaMK II-δ, CaMK II-δ, p-Na v 1.5 and Na v 1.5 in rabbit left ventricular myocardium under conditions indicated. ( b ) and ( c ) The quantitative analysis of p-CaMK II-δ ( b ) and p-Na v 1.5 ( c ) protein expression. The corresponding intensity was normalized to expression in Ctrl. * P
    Figure Legend Snippet: TTX (at concentration of 1 µM) reduced the phosphorylation of CaMK II-δ and Na v 1.5 in hearts pretreated with Bay K 8644 (200 nM) in both absence and presence of ATX-II (3 nM). ( a ) Representative protein expression of p-CaMK II-δ, CaMK II-δ, p-Na v 1.5 and Na v 1.5 in rabbit left ventricular myocardium under conditions indicated. ( b ) and ( c ) The quantitative analysis of p-CaMK II-δ ( b ) and p-Na v 1.5 ( c ) protein expression. The corresponding intensity was normalized to expression in Ctrl. * P

    Techniques Used: Concentration Assay, Expressing

    TTX and eleclazine (Elec) abolished ventricular arrhythmias induced by Bay K 8644 both in absence ( a ) and presence ( b ) of ATX-II. Representative recordings of MAPs (upper records in each panel) and ECG (lower records in each panel) were recorded simultaneously in control, Bay K 8644 (200 and 300 nM, a ) or ATX-II-treated hearts ( b ) before and after treatment with TTX. Arrows indicate an episode of VT. The incidence of all ventricular arrhythmias and VT are presented in panel c. * P
    Figure Legend Snippet: TTX and eleclazine (Elec) abolished ventricular arrhythmias induced by Bay K 8644 both in absence ( a ) and presence ( b ) of ATX-II. Representative recordings of MAPs (upper records in each panel) and ECG (lower records in each panel) were recorded simultaneously in control, Bay K 8644 (200 and 300 nM, a ) or ATX-II-treated hearts ( b ) before and after treatment with TTX. Arrows indicate an episode of VT. The incidence of all ventricular arrhythmias and VT are presented in panel c. * P

    Techniques Used:

    Prolongation of left ventricular monophasic action potential duration (MAPD 90 ) by Bay K 8644 in the absence and presence of ATX-II. ( a ) and ( b ) Representative recordings of MAPs recorded from the epi- ( a ) and endo- ( b ) myocardium of the left ventricular wall in serially exposed to no drug (control), ATX-II (3 nM), Bay K 8644 (200 nM), and ATX-II (3 nM) plus Bay K 8644 (200 nM). ( c ) and ( d ) Concentration-dependent increases by Bay K 8644 of left ventricular epi- ( c ) and endo- ( d ) MAPD 90 in absence (n = 11) and presence (n = 7) of ATX-II. * P
    Figure Legend Snippet: Prolongation of left ventricular monophasic action potential duration (MAPD 90 ) by Bay K 8644 in the absence and presence of ATX-II. ( a ) and ( b ) Representative recordings of MAPs recorded from the epi- ( a ) and endo- ( b ) myocardium of the left ventricular wall in serially exposed to no drug (control), ATX-II (3 nM), Bay K 8644 (200 nM), and ATX-II (3 nM) plus Bay K 8644 (200 nM). ( c ) and ( d ) Concentration-dependent increases by Bay K 8644 of left ventricular epi- ( c ) and endo- ( d ) MAPD 90 in absence (n = 11) and presence (n = 7) of ATX-II. * P

    Techniques Used: Concentration Assay

    2) Product Images from "Monitoring Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes with Genetically Encoded Calcium and Voltage Fluorescent Reporters"

    Article Title: Monitoring Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes with Genetically Encoded Calcium and Voltage Fluorescent Reporters

    Journal: Stem Cell Reports

    doi: 10.1016/j.stemcr.2015.08.009

    ArcLight Expression and Imaging (A) Lentiviral transduction of the hiPSC-CMs led to robust ArcLight expression, manifested by cyclic changes in the cell fluorescence with reduced intensity during depolarization. Scale bars, 20 μm. (B and C) Optical APs derived from line-scan imaging of ArcLight-expressing hiPSC-CMs. (D) Optical APs revealing ventricular-, atrial-, and nodal-like AP morphologies. (E–G) Changes in AP morphologies (top-left images, red signals depict post-treatment tracings), following the application of blockers of the fast (E4031, 500 nM, n = 27 in three independent experiments, E) and slow (Chromanol293B, 30 μM, n = 29 in three independent experiments, F) components of the delayed rectifier potassium currents and activator of the late-sodium current (ATX-II-30nM, n = 28 in three independent experiments, G). All agents caused significant APD 90 prolongation (right) and development of EADs and triggered beats (lower). ∗ p
    Figure Legend Snippet: ArcLight Expression and Imaging (A) Lentiviral transduction of the hiPSC-CMs led to robust ArcLight expression, manifested by cyclic changes in the cell fluorescence with reduced intensity during depolarization. Scale bars, 20 μm. (B and C) Optical APs derived from line-scan imaging of ArcLight-expressing hiPSC-CMs. (D) Optical APs revealing ventricular-, atrial-, and nodal-like AP morphologies. (E–G) Changes in AP morphologies (top-left images, red signals depict post-treatment tracings), following the application of blockers of the fast (E4031, 500 nM, n = 27 in three independent experiments, E) and slow (Chromanol293B, 30 μM, n = 29 in three independent experiments, F) components of the delayed rectifier potassium currents and activator of the late-sodium current (ATX-II-30nM, n = 28 in three independent experiments, G). All agents caused significant APD 90 prolongation (right) and development of EADs and triggered beats (lower). ∗ p

    Techniques Used: Expressing, Imaging, Transduction, Fluorescence, Derivative Assay

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    Alomone Labs atxii
    Atxii, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/atxii/product/Alomone Labs
    Average 94 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    atxii - by Bioz Stars, 2022-12
    94/100 stars
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