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Structured Review

Abbott Laboratories iks channels
Iks Channels, supplied by Abbott Laboratories, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/iks+channels/iks+channels/10__7554_slash_elife__85773-81-14-26
Average 90 stars, based on 1 article reviews
iks channels - by Bioz Stars, 2026-09
90/100 stars

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Related Articles

Mutagenesis:

Article Title: Mechanistic insights into robust cardiac IKs potassium channel activation by aromatic polyunsaturated fatty acid analogues
Article Snippet: .. The additional mutation Q234R is necessary to preserve the voltage dependence of activation in IKs channels with the R231Q mutation (Liin et al., 2018; Panaghie and Abbott, 2007; Wu et al., 2010). ..

Activation Assay:

Article Title: Mechanistic insights into robust cardiac IKs potassium channel activation by aromatic polyunsaturated fatty acid analogues
Article Snippet: .. The additional mutation Q234R is necessary to preserve the voltage dependence of activation in IKs channels with the R231Q mutation (Liin et al., 2018; Panaghie and Abbott, 2007; Wu et al., 2010). ..



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Fig. 2 Extracellular histones are not cytotoxic to mouse brain endothelial cells or native cerebrovascular endothelium. a Cytotoxic effect of histones (10, 25, 50, 100, and 250 μg/mL) on brain endothelial cells assessed by PI uptake and analyzed by flow cytometry after 3 h treatment. (Top) Histograms showing percentage of total PI uptake in brain endothelial cells exposed to different histone concentrations as representative from one experiment. (Bottom) Summary data showing histone-induced cytotoxicity expressed as percentage cell viability relative to vehicle- treated cells after exposure of histones. Mean ± S.E.M. of 6–8 experiments. b TEER measurements of brain endothelial cell monolayers treated with vehicle (saline) or histones (10, 25, 50, and 100 μg/mL) in the presence of the pan caspase inhibitor ZVAD-fmk (100 μM; 1 h treatment). Mean ± S.E.M. Treatments were done in triplicate with three independent biological replicates. c Representative traces illustrating lumen diameter responses in a cannulated posterior cerebral artery pressurized to 60 mmHg isolated from a saline and a histone-injected mouse. Endothelial- dependent dilations were assessed by SK/IK channel activation using <t>NS309</t> (0.1–1 μM). d Summary data showing percent dilation to NS309 relative to passive (0 calcium) in arteries isolated from saline- and histone-treated mice. Data are presented as means ± S.E.M
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Fig. 2 Extracellular histones are not cytotoxic to mouse brain endothelial cells or native cerebrovascular endothelium. a Cytotoxic effect of histones (10, 25, 50, 100, and 250 μg/mL) on brain endothelial cells assessed by PI uptake and analyzed by flow cytometry after 3 h treatment. (Top) Histograms showing percentage of total PI uptake in brain endothelial cells exposed to different histone concentrations as representative from one experiment. (Bottom) Summary data showing histone-induced cytotoxicity expressed as percentage cell viability relative to vehicle- treated cells after exposure of histones. Mean ± S.E.M. of 6–8 experiments. b TEER measurements of brain endothelial cell monolayers treated with vehicle (saline) or histones (10, 25, 50, and 100 μg/mL) in the presence of the pan caspase inhibitor ZVAD-fmk (100 μM; 1 h treatment). Mean ± S.E.M. Treatments were done in triplicate with three independent biological replicates. c Representative traces illustrating lumen diameter responses in a cannulated posterior cerebral artery pressurized to 60 mmHg isolated from a saline and a histone-injected mouse. Endothelial- dependent dilations were assessed by SK/IK channel activation using NS309 (0.1–1 μM). d Summary data showing percent dilation to NS309 relative to passive (0 calcium) in arteries isolated from saline- and histone-treated mice. Data are presented as means ± S.E.M

Journal: Journal of neuroinflammation

Article Title: Site-specific opening of the blood-brain barrier by extracellular histones.

doi: 10.1186/s12974-020-01950-x

Figure Lengend Snippet: Fig. 2 Extracellular histones are not cytotoxic to mouse brain endothelial cells or native cerebrovascular endothelium. a Cytotoxic effect of histones (10, 25, 50, 100, and 250 μg/mL) on brain endothelial cells assessed by PI uptake and analyzed by flow cytometry after 3 h treatment. (Top) Histograms showing percentage of total PI uptake in brain endothelial cells exposed to different histone concentrations as representative from one experiment. (Bottom) Summary data showing histone-induced cytotoxicity expressed as percentage cell viability relative to vehicle- treated cells after exposure of histones. Mean ± S.E.M. of 6–8 experiments. b TEER measurements of brain endothelial cell monolayers treated with vehicle (saline) or histones (10, 25, 50, and 100 μg/mL) in the presence of the pan caspase inhibitor ZVAD-fmk (100 μM; 1 h treatment). Mean ± S.E.M. Treatments were done in triplicate with three independent biological replicates. c Representative traces illustrating lumen diameter responses in a cannulated posterior cerebral artery pressurized to 60 mmHg isolated from a saline and a histone-injected mouse. Endothelial- dependent dilations were assessed by SK/IK channel activation using NS309 (0.1–1 μM). d Summary data showing percent dilation to NS309 relative to passive (0 calcium) in arteries isolated from saline- and histone-treated mice. Data are presented as means ± S.E.M

Article Snippet: Endothelial cell function was determined by measuring the dilatory response to activation of endothelial SK/IK channels with NS309 (Tocris Biosciences; catalog no. 3895) [25, 26].

Techniques: Flow Cytometry, Saline, Isolation, Injection, Activation Assay