mn pubchem cid Search Results


mn pubchem cid  (Addgene inc)
90
Addgene inc mn pubchem cid
Mn Pubchem Cid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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selective p2x7r antagonist jnj 47965567  (Tocris)
94
Tocris selective p2x7r antagonist jnj 47965567
Schematic diagram of experimental study design showing treatment groups, examined factors and chronogram This in vivo experimental system replicates aspects of the human manic behavior in mice, which is used to investigate the molecular basis of mania. Hereafter, the circle indicates WT mice, the square indicates IL-1αβKO mice, and the rhombus indicates P2X7KO mice in the experiments shown in the figures. In addition, the color of the treatment groups is consistently the same. AMPH, d-amphetamine, BDNF, brain-derived neurotrophic factor, DA, dopamine, IFN, interferon, IL, interleukin; IL-1αβKO, interleukin-1α/β knockout mice, NA, noradrenaline, OFT, open field test, P2X7KO, <t>P2X7</t> <t>receptor</t> knockout mice, SBE, beta cyclodextrin sulfobutyl ether, TBARS, thiobarbituric acid reactive substances, TNF, tumor necrosis factor, VAL, valproic acid sodium salt, WT, wild-type mice, 5-HT, serotonin.
Selective P2x7r Antagonist Jnj 47965567, supplied by Tocris, 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/product/mn+pubchem+cid/pmc10914489-276-45-55?v=Tocris
Average 94 stars, based on 1 article reviews
selective p2x7r antagonist jnj 47965567 - by Bioz Stars, 2026-08
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jzl184  (Tocris)
95
Tocris jzl184
Schematic diagram of experimental study design showing treatment groups, examined factors and chronogram This in vivo experimental system replicates aspects of the human manic behavior in mice, which is used to investigate the molecular basis of mania. Hereafter, the circle indicates WT mice, the square indicates IL-1αβKO mice, and the rhombus indicates P2X7KO mice in the experiments shown in the figures. In addition, the color of the treatment groups is consistently the same. AMPH, d-amphetamine, BDNF, brain-derived neurotrophic factor, DA, dopamine, IFN, interferon, IL, interleukin; IL-1αβKO, interleukin-1α/β knockout mice, NA, noradrenaline, OFT, open field test, P2X7KO, <t>P2X7</t> <t>receptor</t> knockout mice, SBE, beta cyclodextrin sulfobutyl ether, TBARS, thiobarbituric acid reactive substances, TNF, tumor necrosis factor, VAL, valproic acid sodium salt, WT, wild-type mice, 5-HT, serotonin.
Jzl184, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mn+pubchem+cid/pm28890367-52-46-49?v=Tocris
Average 95 stars, based on 1 article reviews
jzl184 - by Bioz Stars, 2026-08
95/100 stars
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Image Search Results


Schematic diagram of experimental study design showing treatment groups, examined factors and chronogram This in vivo experimental system replicates aspects of the human manic behavior in mice, which is used to investigate the molecular basis of mania. Hereafter, the circle indicates WT mice, the square indicates IL-1αβKO mice, and the rhombus indicates P2X7KO mice in the experiments shown in the figures. In addition, the color of the treatment groups is consistently the same. AMPH, d-amphetamine, BDNF, brain-derived neurotrophic factor, DA, dopamine, IFN, interferon, IL, interleukin; IL-1αβKO, interleukin-1α/β knockout mice, NA, noradrenaline, OFT, open field test, P2X7KO, P2X7 receptor knockout mice, SBE, beta cyclodextrin sulfobutyl ether, TBARS, thiobarbituric acid reactive substances, TNF, tumor necrosis factor, VAL, valproic acid sodium salt, WT, wild-type mice, 5-HT, serotonin.

Journal: iScience

Article Title: P2X7 receptor inhibition alleviates mania-like behavior independently of interleukin-1β

doi: 10.1016/j.isci.2024.109284

Figure Lengend Snippet: Schematic diagram of experimental study design showing treatment groups, examined factors and chronogram This in vivo experimental system replicates aspects of the human manic behavior in mice, which is used to investigate the molecular basis of mania. Hereafter, the circle indicates WT mice, the square indicates IL-1αβKO mice, and the rhombus indicates P2X7KO mice in the experiments shown in the figures. In addition, the color of the treatment groups is consistently the same. AMPH, d-amphetamine, BDNF, brain-derived neurotrophic factor, DA, dopamine, IFN, interferon, IL, interleukin; IL-1αβKO, interleukin-1α/β knockout mice, NA, noradrenaline, OFT, open field test, P2X7KO, P2X7 receptor knockout mice, SBE, beta cyclodextrin sulfobutyl ether, TBARS, thiobarbituric acid reactive substances, TNF, tumor necrosis factor, VAL, valproic acid sodium salt, WT, wild-type mice, 5-HT, serotonin.

Article Snippet: The following chemicals were used: the CNS stimulant d-amphetamine hemisulfate salt (AMPH, PubChem CID: 24891028, Cat# A5880, Sigma-Aldrich, St. Louis, MO, US), the histone deacetylase inhibitor valproic acid sodium salt (VAL, PubChem CID: 16760703, Cat# P4543, Sigma-Aldrich, St. Louis, MO, US), the brain-penetrant potent and selective P2X7R antagonist JNJ-47965567 (JNJ, PubChem CID: 66553218, Cat# 5299, Tocris, Minneapolis, MN, US) and its vehicle beta cyclodextrin sulfobutyl ether (SBE, PubChem CID: 131634907, flat, Cat# RC-0C7-100, Captisol, San Diego, CA, US), the potent NLRP3 inflammasome inhibitor, MCC950 (MCC, PubChem CID: 91826093, CRID3 sodium salt, Cat# 5479, Tocris, Minneapolis, MN, US), the IL-1 receptor antagonist (IL-1Ra) anakinra (ANA, Kineret, Swedish Orphan Biovitrum AB, SOBI, Stockholm, Sweden).

Techniques: In Vivo, Derivative Assay, Knock-Out

Social and aggressive behavior of mice (A and B) Duration and number of social contacts (sniffing, allogrooming, following) between resident and intruder mice during the test session (duration: genotype: F[2,21] = 7.4790, p = 0.003527; number: F[1,21] = 5.8926, p = 0.009304). (C and D) Duration and number of aggressive contacts (aggressive grooming, upright posture, boxing, chasing, tail rattling, clinch, wrestling, dominant posture, keeping down) of resident mice on an intruder during the session (number: F[2,21] = 7.4509, p = 0.003586). (E, F, and G) Analysis of latency to first attack (E) and number of attacks (F). (G) Aggression score of mice (the ratio of aggressive interactions out of total aggressive + non-aggressive interactions). Values are presented as means ± SEM of n = 8 mice per group. One-way ANOVA (A (square root transformation), B, C, D, G) followed by Tukey’s multiple comparison post hoc test and Kruskal-Wallis test with multiple comparisons (E, F): $ p < 0.05, $$ p < 0.01 compared to WT residents; & p < 0.05 compared IL-1αβKO residents. IL-1αβKO, interleukin-1α/β knockout mice, P2X7KO, P2X7 receptor knockout mice, WT, wild-type mice.

Journal: iScience

Article Title: P2X7 receptor inhibition alleviates mania-like behavior independently of interleukin-1β

doi: 10.1016/j.isci.2024.109284

Figure Lengend Snippet: Social and aggressive behavior of mice (A and B) Duration and number of social contacts (sniffing, allogrooming, following) between resident and intruder mice during the test session (duration: genotype: F[2,21] = 7.4790, p = 0.003527; number: F[1,21] = 5.8926, p = 0.009304). (C and D) Duration and number of aggressive contacts (aggressive grooming, upright posture, boxing, chasing, tail rattling, clinch, wrestling, dominant posture, keeping down) of resident mice on an intruder during the session (number: F[2,21] = 7.4509, p = 0.003586). (E, F, and G) Analysis of latency to first attack (E) and number of attacks (F). (G) Aggression score of mice (the ratio of aggressive interactions out of total aggressive + non-aggressive interactions). Values are presented as means ± SEM of n = 8 mice per group. One-way ANOVA (A (square root transformation), B, C, D, G) followed by Tukey’s multiple comparison post hoc test and Kruskal-Wallis test with multiple comparisons (E, F): $ p < 0.05, $$ p < 0.01 compared to WT residents; & p < 0.05 compared IL-1αβKO residents. IL-1αβKO, interleukin-1α/β knockout mice, P2X7KO, P2X7 receptor knockout mice, WT, wild-type mice.

Article Snippet: The following chemicals were used: the CNS stimulant d-amphetamine hemisulfate salt (AMPH, PubChem CID: 24891028, Cat# A5880, Sigma-Aldrich, St. Louis, MO, US), the histone deacetylase inhibitor valproic acid sodium salt (VAL, PubChem CID: 16760703, Cat# P4543, Sigma-Aldrich, St. Louis, MO, US), the brain-penetrant potent and selective P2X7R antagonist JNJ-47965567 (JNJ, PubChem CID: 66553218, Cat# 5299, Tocris, Minneapolis, MN, US) and its vehicle beta cyclodextrin sulfobutyl ether (SBE, PubChem CID: 131634907, flat, Cat# RC-0C7-100, Captisol, San Diego, CA, US), the potent NLRP3 inflammasome inhibitor, MCC950 (MCC, PubChem CID: 91826093, CRID3 sodium salt, Cat# 5479, Tocris, Minneapolis, MN, US), the IL-1 receptor antagonist (IL-1Ra) anakinra (ANA, Kineret, Swedish Orphan Biovitrum AB, SOBI, Stockholm, Sweden).

Techniques: Transformation Assay, Comparison, Knock-Out

The effect of genetic deletion of IL-1α/β and P2X7R on electrical- and AMPH-evoked [ 3 H]DA efflux in striatal slices [ 3 H]DA release was measured from superfused coronal striatal slices in response to electrical (40 V, 2 Hz, 1 ms, 2 min) and chemical (30 μM AMPH for 3 min) stimulation. JNJ shows the duration of administration to the perfusion solution. (A) [ 3 H]DA release in response to electrical (ES) and chemical (AMPH) stimulation. Repeated Measures ANOVA revealed a significant main effect for genotype and pretreatment over time (intercept: F[1,24] = 1645.308, p < 0.0000001; time × genotype × pretreatment: F[34,408] = 3.009, p < 0.0000001). The tritium content in the perfusate samples was expressed as percentage of basal levels and is shown as a function of time. Curves show the means ± SEM of the identical experiments. Blue lines and labels indicate the time of different type of stimulations. (B) Electric field stimulation evoked release of [ 3 H]DA (Factorial ANOVA, intercept: F[1,24] = 1295.984, p < 0.0000001. (C) Chemical stimulation evoked release of [ 3 H]DA (Factorial ANOVA, intercept: F[1,24] = 816.1452, p < 0.0000001). The tritium content in the perfusate samples was expressed as fractional release (FRS). (D) Tritium uptake of tissue in Bq/g (Kruskal-Wallis test: H(5,N = 30) = 18.00129, p = 0.0029). Values are presented as means ± SEM of n = 5 mice per group. Repeated Measures (A), Factorial ANOVA (B, C) followed by Tukey’s multiple comparison post hoc test, and Kruskal-Wallis test with multiple comparisons (D): # p < 0.05, ## p < 0.01 compared to non-JNJ-pre-perfused group in same genotype; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 compared to the same treatment group with WT; &&& p < 0.001 compared to the same treatment group with IL-1αβKO. AMPH, d-amphetamine stimulation, DA, dopamine, ES, electrical stimulation, IL-1αβKO, interleukin-1α/β knockout mice, JNJ, JNJ-47965567, P2X7KO, P2X7 receptor knockout mice, WT, wild-type mice, [ 3 H], tritium.

Journal: iScience

Article Title: P2X7 receptor inhibition alleviates mania-like behavior independently of interleukin-1β

doi: 10.1016/j.isci.2024.109284

Figure Lengend Snippet: The effect of genetic deletion of IL-1α/β and P2X7R on electrical- and AMPH-evoked [ 3 H]DA efflux in striatal slices [ 3 H]DA release was measured from superfused coronal striatal slices in response to electrical (40 V, 2 Hz, 1 ms, 2 min) and chemical (30 μM AMPH for 3 min) stimulation. JNJ shows the duration of administration to the perfusion solution. (A) [ 3 H]DA release in response to electrical (ES) and chemical (AMPH) stimulation. Repeated Measures ANOVA revealed a significant main effect for genotype and pretreatment over time (intercept: F[1,24] = 1645.308, p < 0.0000001; time × genotype × pretreatment: F[34,408] = 3.009, p < 0.0000001). The tritium content in the perfusate samples was expressed as percentage of basal levels and is shown as a function of time. Curves show the means ± SEM of the identical experiments. Blue lines and labels indicate the time of different type of stimulations. (B) Electric field stimulation evoked release of [ 3 H]DA (Factorial ANOVA, intercept: F[1,24] = 1295.984, p < 0.0000001. (C) Chemical stimulation evoked release of [ 3 H]DA (Factorial ANOVA, intercept: F[1,24] = 816.1452, p < 0.0000001). The tritium content in the perfusate samples was expressed as fractional release (FRS). (D) Tritium uptake of tissue in Bq/g (Kruskal-Wallis test: H(5,N = 30) = 18.00129, p = 0.0029). Values are presented as means ± SEM of n = 5 mice per group. Repeated Measures (A), Factorial ANOVA (B, C) followed by Tukey’s multiple comparison post hoc test, and Kruskal-Wallis test with multiple comparisons (D): # p < 0.05, ## p < 0.01 compared to non-JNJ-pre-perfused group in same genotype; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 compared to the same treatment group with WT; &&& p < 0.001 compared to the same treatment group with IL-1αβKO. AMPH, d-amphetamine stimulation, DA, dopamine, ES, electrical stimulation, IL-1αβKO, interleukin-1α/β knockout mice, JNJ, JNJ-47965567, P2X7KO, P2X7 receptor knockout mice, WT, wild-type mice, [ 3 H], tritium.

Article Snippet: The following chemicals were used: the CNS stimulant d-amphetamine hemisulfate salt (AMPH, PubChem CID: 24891028, Cat# A5880, Sigma-Aldrich, St. Louis, MO, US), the histone deacetylase inhibitor valproic acid sodium salt (VAL, PubChem CID: 16760703, Cat# P4543, Sigma-Aldrich, St. Louis, MO, US), the brain-penetrant potent and selective P2X7R antagonist JNJ-47965567 (JNJ, PubChem CID: 66553218, Cat# 5299, Tocris, Minneapolis, MN, US) and its vehicle beta cyclodextrin sulfobutyl ether (SBE, PubChem CID: 131634907, flat, Cat# RC-0C7-100, Captisol, San Diego, CA, US), the potent NLRP3 inflammasome inhibitor, MCC950 (MCC, PubChem CID: 91826093, CRID3 sodium salt, Cat# 5479, Tocris, Minneapolis, MN, US), the IL-1 receptor antagonist (IL-1Ra) anakinra (ANA, Kineret, Swedish Orphan Biovitrum AB, SOBI, Stockholm, Sweden).

Techniques: Comparison, Knock-Out

Journal: iScience

Article Title: P2X7 receptor inhibition alleviates mania-like behavior independently of interleukin-1β

doi: 10.1016/j.isci.2024.109284

Figure Lengend Snippet:

Article Snippet: The following chemicals were used: the CNS stimulant d-amphetamine hemisulfate salt (AMPH, PubChem CID: 24891028, Cat# A5880, Sigma-Aldrich, St. Louis, MO, US), the histone deacetylase inhibitor valproic acid sodium salt (VAL, PubChem CID: 16760703, Cat# P4543, Sigma-Aldrich, St. Louis, MO, US), the brain-penetrant potent and selective P2X7R antagonist JNJ-47965567 (JNJ, PubChem CID: 66553218, Cat# 5299, Tocris, Minneapolis, MN, US) and its vehicle beta cyclodextrin sulfobutyl ether (SBE, PubChem CID: 131634907, flat, Cat# RC-0C7-100, Captisol, San Diego, CA, US), the potent NLRP3 inflammasome inhibitor, MCC950 (MCC, PubChem CID: 91826093, CRID3 sodium salt, Cat# 5479, Tocris, Minneapolis, MN, US), the IL-1 receptor antagonist (IL-1Ra) anakinra (ANA, Kineret, Swedish Orphan Biovitrum AB, SOBI, Stockholm, Sweden).

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Bicinchoninic Acid Protein Assay, Multiple Displacement Amplification, Double Knockout, Knock-Out, Software, FCAP Assay