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wt5260 083850 transposase 837  (ATCC)


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    Structured Review

    ATCC wt5260 083850 transposase 837
    Wt5260 083850 Transposase 837, supplied by ATCC, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 91 stars, based on 1 article reviews
    wt5260 083850 transposase 837 - by Bioz Stars, 2026-05
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    Santa Cruz Biotechnology post kainic acid induced status epilepticus
    Figure 3 RTA 408 rescues total glutathione and ATP levels following <t>kainic</t> acid-induces status <t>epilepticus</t> in vivo. (A) Total (oxidized and reduced forms of glutathione) were measured in the cortex and hippocampus of sham rats (sham; n = 7 for cortex and n = 6 for hippocampus), and from treated rats 7 days following kainic acid-induced status epilepticus (2 h), followed by vehicle (10% DMSO/saline kainic acid + vehicle; n = 5), RTA 408 groups at doses: 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 6), 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). (B) ATP levels measured in the same animals (sham; n = 6), vehicle (kainic acid + vehicle; n = 5), RTA 408 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 5), RTA 408 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and RTA 408 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). Data are expressed as mean SEM. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 versus kainic acid group, by one-way ANOVA with Bonferroni post hoc test. In A, cortex: F(4,24) = 18.197, P 5 0.001; hippocampus: F(4,22) = 101.409, P 5 0.001; In B, cortex: F(4,21) = 11.738, P 5 0.001; hippocampus: F(4,21) = 20.262, P 5 0.001. KA = kainic acid.
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    Santa Cruz Biotechnology référence catalogue
    Figure 3 RTA 408 rescues total glutathione and ATP levels following <t>kainic</t> acid-induces status <t>epilepticus</t> in vivo. (A) Total (oxidized and reduced forms of glutathione) were measured in the cortex and hippocampus of sham rats (sham; n = 7 for cortex and n = 6 for hippocampus), and from treated rats 7 days following kainic acid-induced status epilepticus (2 h), followed by vehicle (10% DMSO/saline kainic acid + vehicle; n = 5), RTA 408 groups at doses: 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 6), 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). (B) ATP levels measured in the same animals (sham; n = 6), vehicle (kainic acid + vehicle; n = 5), RTA 408 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 5), RTA 408 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and RTA 408 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). Data are expressed as mean SEM. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 versus kainic acid group, by one-way ANOVA with Bonferroni post hoc test. In A, cortex: F(4,24) = 18.197, P 5 0.001; hippocampus: F(4,22) = 101.409, P 5 0.001; In B, cortex: F(4,21) = 11.738, P 5 0.001; hippocampus: F(4,21) = 20.262, P 5 0.001. KA = kainic acid.
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    Santa Cruz Biotechnology sc 200454a
    Figure 3 RTA 408 rescues total glutathione and ATP levels following <t>kainic</t> acid-induces status <t>epilepticus</t> in vivo. (A) Total (oxidized and reduced forms of glutathione) were measured in the cortex and hippocampus of sham rats (sham; n = 7 for cortex and n = 6 for hippocampus), and from treated rats 7 days following kainic acid-induced status epilepticus (2 h), followed by vehicle (10% DMSO/saline kainic acid + vehicle; n = 5), RTA 408 groups at doses: 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 6), 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). (B) ATP levels measured in the same animals (sham; n = 6), vehicle (kainic acid + vehicle; n = 5), RTA 408 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 5), RTA 408 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and RTA 408 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). Data are expressed as mean SEM. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 versus kainic acid group, by one-way ANOVA with Bonferroni post hoc test. In A, cortex: F(4,24) = 18.197, P 5 0.001; hippocampus: F(4,22) = 101.409, P 5 0.001; In B, cortex: F(4,21) = 11.738, P 5 0.001; hippocampus: F(4,21) = 20.262, P 5 0.001. KA = kainic acid.
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    Image Search Results


    Figure 3 RTA 408 rescues total glutathione and ATP levels following kainic acid-induces status epilepticus in vivo. (A) Total (oxidized and reduced forms of glutathione) were measured in the cortex and hippocampus of sham rats (sham; n = 7 for cortex and n = 6 for hippocampus), and from treated rats 7 days following kainic acid-induced status epilepticus (2 h), followed by vehicle (10% DMSO/saline kainic acid + vehicle; n = 5), RTA 408 groups at doses: 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 6), 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). (B) ATP levels measured in the same animals (sham; n = 6), vehicle (kainic acid + vehicle; n = 5), RTA 408 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 5), RTA 408 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and RTA 408 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). Data are expressed as mean SEM. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 versus kainic acid group, by one-way ANOVA with Bonferroni post hoc test. In A, cortex: F(4,24) = 18.197, P 5 0.001; hippocampus: F(4,22) = 101.409, P 5 0.001; In B, cortex: F(4,21) = 11.738, P 5 0.001; hippocampus: F(4,21) = 20.262, P 5 0.001. KA = kainic acid.

    Journal: Brain : a journal of neurology

    Article Title: KEAP1 inhibition is neuroprotective and suppresses the development of epilepsy.

    doi: 10.1093/brain/awy071

    Figure Lengend Snippet: Figure 3 RTA 408 rescues total glutathione and ATP levels following kainic acid-induces status epilepticus in vivo. (A) Total (oxidized and reduced forms of glutathione) were measured in the cortex and hippocampus of sham rats (sham; n = 7 for cortex and n = 6 for hippocampus), and from treated rats 7 days following kainic acid-induced status epilepticus (2 h), followed by vehicle (10% DMSO/saline kainic acid + vehicle; n = 5), RTA 408 groups at doses: 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 6), 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). (B) ATP levels measured in the same animals (sham; n = 6), vehicle (kainic acid + vehicle; n = 5), RTA 408 17.5 mg/kg once daily for 3 days (kainic acid + RTA 17.5; n = 5), RTA 408 25 mg/kg once daily for 3 days (kainic acid + RTA 25; n = 5) and RTA 408 50 mg/kg once daily for 2 days (kainic acid + RTA 50; n = 6). Data are expressed as mean SEM. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 versus kainic acid group, by one-way ANOVA with Bonferroni post hoc test. In A, cortex: F(4,24) = 18.197, P 5 0.001; hippocampus: F(4,22) = 101.409, P 5 0.001; In B, cortex: F(4,21) = 11.738, P 5 0.001; hippocampus: F(4,21) = 20.262, P 5 0.001. KA = kainic acid.

    Article Snippet: One week or 15 weeks post kainic acid-induced status epilepticus, rats were perfused transcardially under terminal anaesthesia (pentobarbital sodium) with PBS (8 IU/ml), followed by 4% paraformaldehyde (PFA) in PBS (Santa Cruz Biotechnology).

    Techniques: In Vivo, Saline

    Figure 4 RTA 408 prevents neuronal cell death following kainic acid-induced status epilepticus in rats. (A) Representative images for CA1, CA3 and hilus of coronal sections from vehicle (10% DMSO/saline) treated and RTA 408 treated rats 15 weeks after status epilepticus (SE). Scale bar = 100 mM. (B–G) Cell densities in CA1, CA3 and hilus of sham (n = 6), and vehicle (n = 5) and RTA 408 (25 mg/kg/day for 3 days; n = 5) treated rats 1 week (B–D) and 15 weeks (E–G); in sham (n = 6), vehicle (n = 7), RTA 408 (25 mg/kg/day for 1 day; n = 5) and RTA 408 (25 mg/kg/day for 3 days; n = 7) following 2 h kainic acid induced status epilepticus. Data are expressed as mean SEM numbers of animals. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 compared to vehicle group by one-way ANOVA followed by Bonferroni post hoc test. (B) F(2,13) = 2.806, P = 0.097; (C) F(2,13) = 9.220, P = 0.003; (D) F(2,13) = 42.138, P 5 0.001; (E) F(2,13) = 20.536, P 5 0.001; (F) F(2,13) = 10.236, P 5 0.001; (G) F(2,13) = 24.550, P 5 0.001.

    Journal: Brain : a journal of neurology

    Article Title: KEAP1 inhibition is neuroprotective and suppresses the development of epilepsy.

    doi: 10.1093/brain/awy071

    Figure Lengend Snippet: Figure 4 RTA 408 prevents neuronal cell death following kainic acid-induced status epilepticus in rats. (A) Representative images for CA1, CA3 and hilus of coronal sections from vehicle (10% DMSO/saline) treated and RTA 408 treated rats 15 weeks after status epilepticus (SE). Scale bar = 100 mM. (B–G) Cell densities in CA1, CA3 and hilus of sham (n = 6), and vehicle (n = 5) and RTA 408 (25 mg/kg/day for 3 days; n = 5) treated rats 1 week (B–D) and 15 weeks (E–G); in sham (n = 6), vehicle (n = 7), RTA 408 (25 mg/kg/day for 1 day; n = 5) and RTA 408 (25 mg/kg/day for 3 days; n = 7) following 2 h kainic acid induced status epilepticus. Data are expressed as mean SEM numbers of animals. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 compared to vehicle group by one-way ANOVA followed by Bonferroni post hoc test. (B) F(2,13) = 2.806, P = 0.097; (C) F(2,13) = 9.220, P = 0.003; (D) F(2,13) = 42.138, P 5 0.001; (E) F(2,13) = 20.536, P 5 0.001; (F) F(2,13) = 10.236, P 5 0.001; (G) F(2,13) = 24.550, P 5 0.001.

    Article Snippet: One week or 15 weeks post kainic acid-induced status epilepticus, rats were perfused transcardially under terminal anaesthesia (pentobarbital sodium) with PBS (8 IU/ml), followed by 4% paraformaldehyde (PFA) in PBS (Santa Cruz Biotechnology).

    Techniques: Saline

    Figure 5 RTA 408 modifies seizure progression. (A) EEG sample traces recorded for status epilepticus (SE): an asterisk indicates the beginning of status epilepticus whereas an arrow indicates termination with diazepam. (B) Typical EEG example of a spontaneous seizure post status epilepticus, expanded in the right panel. Note the rhythmical high frequency discharges at the beginning of the seizure (2) when compared to baseline (1). This rhythmic fast activity increases in amplitude (3) and decreases in frequency (4) towards the end of the seizure thus fulfilling the criteria for EEG seizure activity. (C and D) Bar charts of mean frequency (SEM) of electrographically recorded seizures following kainic acid induced status epilepticus for control rats, treated with vehicle (10% DMSO/saline) once daily for 3 days (n = 9) and RTA 408-treated rats (RTA 408 25 mg/kg once daily for 3 days; n = 9) 1–12 weeks [C; F(1,192) = 5.828, P 5 0.05] and 13–15 weeks following the first spontaneous seizure [D; F(1,18) = 10.163, P 5 0.01]; animal numbers in D: n = 4 for both groups. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 by generalized log-linear mixed model followed by sequential Bonferroni post hoc test. (E) Probability distribution illustrating the probability of 0–10 seizures/day for each individual vehicle (n = 9) and RTA 408-treated rat (n = 9). (F) Bar chart summarizing mean SEM seizure probability across time; **P 5 0.01 probabilities of seizure free days were compared using Mann-Whitney U-test. (G) Seizure duration distribution for the same animals as in C, demonstrating no significant difference between vehicle or RTA408 treated animals. KA = kainic acid.

    Journal: Brain : a journal of neurology

    Article Title: KEAP1 inhibition is neuroprotective and suppresses the development of epilepsy.

    doi: 10.1093/brain/awy071

    Figure Lengend Snippet: Figure 5 RTA 408 modifies seizure progression. (A) EEG sample traces recorded for status epilepticus (SE): an asterisk indicates the beginning of status epilepticus whereas an arrow indicates termination with diazepam. (B) Typical EEG example of a spontaneous seizure post status epilepticus, expanded in the right panel. Note the rhythmical high frequency discharges at the beginning of the seizure (2) when compared to baseline (1). This rhythmic fast activity increases in amplitude (3) and decreases in frequency (4) towards the end of the seizure thus fulfilling the criteria for EEG seizure activity. (C and D) Bar charts of mean frequency (SEM) of electrographically recorded seizures following kainic acid induced status epilepticus for control rats, treated with vehicle (10% DMSO/saline) once daily for 3 days (n = 9) and RTA 408-treated rats (RTA 408 25 mg/kg once daily for 3 days; n = 9) 1–12 weeks [C; F(1,192) = 5.828, P 5 0.05] and 13–15 weeks following the first spontaneous seizure [D; F(1,18) = 10.163, P 5 0.01]; animal numbers in D: n = 4 for both groups. *P 5 0.05, **P 5 0.01 and ***P 5 0.001 by generalized log-linear mixed model followed by sequential Bonferroni post hoc test. (E) Probability distribution illustrating the probability of 0–10 seizures/day for each individual vehicle (n = 9) and RTA 408-treated rat (n = 9). (F) Bar chart summarizing mean SEM seizure probability across time; **P 5 0.01 probabilities of seizure free days were compared using Mann-Whitney U-test. (G) Seizure duration distribution for the same animals as in C, demonstrating no significant difference between vehicle or RTA408 treated animals. KA = kainic acid.

    Article Snippet: One week or 15 weeks post kainic acid-induced status epilepticus, rats were perfused transcardially under terminal anaesthesia (pentobarbital sodium) with PBS (8 IU/ml), followed by 4% paraformaldehyde (PFA) in PBS (Santa Cruz Biotechnology).

    Techniques: Activity Assay, Control, Saline, MANN-WHITNEY