atx  (Alomone Labs)


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    Structured Review

    Alomone Labs atx
    Atx, 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/atx/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    atx - by Bioz Stars, 2022-09
    93/100 stars

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    Alomone Labs atx ii
    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 <t>(ATX-II-30nM,</t> n = 28 in three independent experiments, G). All agents caused significant APD 90 prolongation (right) and development of EADs and triggered beats (lower). ∗ p
    Atx Ii, 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/atx ii/product/Alomone Labs
    Average 94 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    atx ii - by Bioz Stars, 2022-09
    94/100 stars
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    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

    Journal: Stem Cell Reports

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

    doi: 10.1016/j.stemcr.2015.08.009

    Figure Lengend 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

    Article Snippet: E4031 (500 nM), ATX-II (30 nM; both from Alomone labs), ouabain (0.5–1 μM), sotalol (20 μM), isoproterenol (1 μM), and erythromycin (30 μM) were dissolved in H2O, while chromanol 293B (30 μM), cisapride (100 nM; all from Sigma), and nilotinib (1 μM; Adooq Bioscience) were dissolved in DMSO.

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

    nNa v inhibition reduces LQT-associated VT. (a) Representative ECG recordings in CASQ-null mice after catecholamine challenge (black ECG) composed of epinephrine (1.5 mg/kg) and caffeine (120 mg/kg) injected intraperitoneally, which induced a narrow-QRS complex VT exhibiting beat-to-beat alternations in the polarity of QRS. Addition of BayK (1 mg/kg; orange ECG) or ATX-II (30 µg/kg; red ECG) resulted in a typical short-long-short initiating ventricular cycle leading to a wide-QRS complex polymorphic VT that resembled human TdP. A subset of mice 10 min after exposure to BayK or ATX-II and 10 min before catecholamine challenge were pretreated with either 4,9-ah-TTX (750 µg/kg; blue ECGs) or riluzole (Ril; 15 mg/kg). (b) VT incidence (%) in CASQ-null mice exposed to catecholamine challenge without (black bars) and with BayK (orange bars) or ATX-II (red bars) during Na + channel blockade with 4,9-ah-TTX or Ril (green bars). Number of mice from independent experiments is specified in the bar graph. VT was defined as three or more premature ectopies. (c) TdP-like VT incidence (%) in CASQ-null mice exposed to catecholamine challenge without (black bars) and with BayK (orange bars) or ATX-II (red bars) during Na + channel blockade with 4,9-ah-TTX or Ril (green bars). TdP-like VT was defined as three or more premature wide-QRS ectopies. Significance between the treatment groups was determined with Fisher’s exact test.

    Journal: The Journal of General Physiology

    Article Title: Tetrodotoxin-sensitive Navs contribute to early and delayed afterdepolarizations in long QT arrhythmia models

    doi: 10.1085/jgp.201711909

    Figure Lengend Snippet: nNa v inhibition reduces LQT-associated VT. (a) Representative ECG recordings in CASQ-null mice after catecholamine challenge (black ECG) composed of epinephrine (1.5 mg/kg) and caffeine (120 mg/kg) injected intraperitoneally, which induced a narrow-QRS complex VT exhibiting beat-to-beat alternations in the polarity of QRS. Addition of BayK (1 mg/kg; orange ECG) or ATX-II (30 µg/kg; red ECG) resulted in a typical short-long-short initiating ventricular cycle leading to a wide-QRS complex polymorphic VT that resembled human TdP. A subset of mice 10 min after exposure to BayK or ATX-II and 10 min before catecholamine challenge were pretreated with either 4,9-ah-TTX (750 µg/kg; blue ECGs) or riluzole (Ril; 15 mg/kg). (b) VT incidence (%) in CASQ-null mice exposed to catecholamine challenge without (black bars) and with BayK (orange bars) or ATX-II (red bars) during Na + channel blockade with 4,9-ah-TTX or Ril (green bars). Number of mice from independent experiments is specified in the bar graph. VT was defined as three or more premature ectopies. (c) TdP-like VT incidence (%) in CASQ-null mice exposed to catecholamine challenge without (black bars) and with BayK (orange bars) or ATX-II (red bars) during Na + channel blockade with 4,9-ah-TTX or Ril (green bars). TdP-like VT was defined as three or more premature wide-QRS ectopies. Significance between the treatment groups was determined with Fisher’s exact test.

    Article Snippet: Briefly, after baseline recording (5 min), a subset of animals received either intraperitoneal ATX-II (30 µg/kg; Alomone Labs) or BayK (1 mg/kg; Tocris).

    Techniques: Inhibition, Mouse Assay, Injection

    nNa v inhibition reduces LQT-associated VT. (a) Representative ECG recordings in CASQ-null mice after catecholamine challenge (black ECG) composed of epinephrine (1.5 mg/kg) and caffeine (120 mg/kg) injected intraperitoneally, which induced a narrow-QRS complex VT exhibiting beat-to-beat alternations in the polarity of QRS. Addition of BayK (1 mg/kg; orange ECG) or ATX-II (30 µg/kg; red ECG) resulted in a typical short-long-short initiating ventricular cycle leading to a wide-QRS complex polymorphic VT that resembled human TdP. A subset of mice 10 min after exposure to BayK or ATX-II and 10 min before catecholamine challenge were pretreated with either 4,9-ah-TTX (750 µg/kg; blue ECGs) or riluzole (Ril; 15 mg/kg). (b) VT incidence (%) in CASQ-null mice exposed to catecholamine challenge without (black bars) and with BayK (orange bars) or ATX-II (red bars) during Na + channel blockade with 4,9-ah-TTX or Ril (green bars). Number of mice from independent experiments is specified in the bar graph. VT was defined as three or more premature ectopies. (c) TdP-like VT incidence (%) in CASQ-null mice exposed to catecholamine challenge without (black bars) and with BayK (orange bars) or ATX-II (red bars) during Na + channel blockade with 4,9-ah-TTX or Ril (green bars). TdP-like VT was defined as three or more premature wide-QRS ectopies. Significance between the treatment groups was determined with Fisher’s exact test.

    Journal: The Journal of General Physiology

    Article Title: Tetrodotoxin-sensitive Navs contribute to early and delayed afterdepolarizations in long QT arrhythmia models

    doi: 10.1085/jgp.201711909

    Figure Lengend Snippet: nNa v inhibition reduces LQT-associated VT. (a) Representative ECG recordings in CASQ-null mice after catecholamine challenge (black ECG) composed of epinephrine (1.5 mg/kg) and caffeine (120 mg/kg) injected intraperitoneally, which induced a narrow-QRS complex VT exhibiting beat-to-beat alternations in the polarity of QRS. Addition of BayK (1 mg/kg; orange ECG) or ATX-II (30 µg/kg; red ECG) resulted in a typical short-long-short initiating ventricular cycle leading to a wide-QRS complex polymorphic VT that resembled human TdP. A subset of mice 10 min after exposure to BayK or ATX-II and 10 min before catecholamine challenge were pretreated with either 4,9-ah-TTX (750 µg/kg; blue ECGs) or riluzole (Ril; 15 mg/kg). (b) VT incidence (%) in CASQ-null mice exposed to catecholamine challenge without (black bars) and with BayK (orange bars) or ATX-II (red bars) during Na + channel blockade with 4,9-ah-TTX or Ril (green bars). Number of mice from independent experiments is specified in the bar graph. VT was defined as three or more premature ectopies. (c) TdP-like VT incidence (%) in CASQ-null mice exposed to catecholamine challenge without (black bars) and with BayK (orange bars) or ATX-II (red bars) during Na + channel blockade with 4,9-ah-TTX or Ril (green bars). TdP-like VT was defined as three or more premature wide-QRS ectopies. Significance between the treatment groups was determined with Fisher’s exact test.

    Article Snippet: Briefly, after baseline recording (5 min), a subset of animals received either intraperitoneal ATX-II (30 µg/kg; Alomone Labs) or BayK (1 mg/kg; Tocris).

    Techniques: Inhibition, Mouse Assay, Injection

    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

    Journal: Scientific Reports

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

    doi: 10.1038/s41598-017-01056-0

    Figure Lengend 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

    Article Snippet: To test the effects of Bay K 8644 in the presence of ATX-II (Alomone labs, Cat# STA-700, USA), hearts were perfused with ATX-II for 20 min and then exposed to Bay K 8644 and TTX.

    Techniques: 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

    Journal: Scientific Reports

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

    doi: 10.1038/s41598-017-01056-0

    Figure Lengend 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

    Article Snippet: To test the effects of Bay K 8644 in the presence of ATX-II (Alomone labs, Cat# STA-700, USA), hearts were perfused with ATX-II for 20 min and then exposed to Bay K 8644 and TTX.

    Techniques: 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

    Journal: Scientific Reports

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

    doi: 10.1038/s41598-017-01056-0

    Figure Lengend 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

    Article Snippet: To test the effects of Bay K 8644 in the presence of ATX-II (Alomone labs, Cat# STA-700, USA), hearts were perfused with ATX-II for 20 min and then exposed to Bay K 8644 and TTX.

    Techniques:

    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

    Journal: Scientific Reports

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

    doi: 10.1038/s41598-017-01056-0

    Figure Lengend 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

    Article Snippet: To test the effects of Bay K 8644 in the presence of ATX-II (Alomone labs, Cat# STA-700, USA), hearts were perfused with ATX-II for 20 min and then exposed to Bay K 8644 and TTX.

    Techniques: Concentration Assay