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Tocris pf 184
a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with <t>IKKβ</t> inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.
Pf 184, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 184/product/Tocris
Average 86 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf 184 - by Bioz Stars, 2024-02
86/100 stars

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1) Product Images from "Therapy-induced APOBEC3A drives evolution of persistent cancer cells"

Article Title: Therapy-induced APOBEC3A drives evolution of persistent cancer cells

Journal: Nature

doi: 10.1038/s41586-023-06303-1

a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with IKKβ inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.
Figure Legend Snippet: a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with IKKβ inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.

Techniques Used: Expressing, Quantitative RT-PCR, Mutagenesis, MANN-WHITNEY, Comparison, Western Blot, Binding Assay

a, Chromatin accessibility profile of the APOBEC3 locus (chromosome 22) of PC9 cells treated with 300 nM gefitinib for 0 or 14 days (2 biological replicates), with expanded view of the A3A promoter region. Relative fold-change of peak accessibility in treated vs. non-treated control cells is shown. Transcription factors mapping to these peak regions were identified from the ENCODE database. b, Differential z-score (gefitinib vs. control) of global motif accessibility scores for each identified transcription factor family. c, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. (SCR = scrambled control siRNA) d, Expression of A3A in PC9 cells transfected scrambled or individual NFκB1 siRNAs. Cells were treated with osimertinib for 24 hours and mRNA expression was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). Knockdown efficacy was confirmed by western blot. e, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. f, Western blot of PC9 and MGH064–1 cells after treatment with TKI (osimertinib or lorlatinib) and IKKβ inhibitors (representative of 3 biological replicates).
Figure Legend Snippet: a, Chromatin accessibility profile of the APOBEC3 locus (chromosome 22) of PC9 cells treated with 300 nM gefitinib for 0 or 14 days (2 biological replicates), with expanded view of the A3A promoter region. Relative fold-change of peak accessibility in treated vs. non-treated control cells is shown. Transcription factors mapping to these peak regions were identified from the ENCODE database. b, Differential z-score (gefitinib vs. control) of global motif accessibility scores for each identified transcription factor family. c, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. (SCR = scrambled control siRNA) d, Expression of A3A in PC9 cells transfected scrambled or individual NFκB1 siRNAs. Cells were treated with osimertinib for 24 hours and mRNA expression was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). Knockdown efficacy was confirmed by western blot. e, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. f, Western blot of PC9 and MGH064–1 cells after treatment with TKI (osimertinib or lorlatinib) and IKKβ inhibitors (representative of 3 biological replicates).

Techniques Used: Expressing, Transfection, Quantitative RT-PCR, Western Blot


Structured Review

Tocris pf 184
a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with <t>IKKβ</t> inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.
Pf 184, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 184/product/Tocris
Average 86 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf 184 - by Bioz Stars, 2024-02
86/100 stars

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1) Product Images from "Therapy-induced APOBEC3A drives evolution of persistent cancer cells"

Article Title: Therapy-induced APOBEC3A drives evolution of persistent cancer cells

Journal: Nature

doi: 10.1038/s41586-023-06303-1

a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with IKKβ inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.
Figure Legend Snippet: a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with IKKβ inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.

Techniques Used: Expressing, Quantitative RT-PCR, Mutagenesis, MANN-WHITNEY, Comparison, Western Blot, Binding Assay

a, Chromatin accessibility profile of the APOBEC3 locus (chromosome 22) of PC9 cells treated with 300 nM gefitinib for 0 or 14 days (2 biological replicates), with expanded view of the A3A promoter region. Relative fold-change of peak accessibility in treated vs. non-treated control cells is shown. Transcription factors mapping to these peak regions were identified from the ENCODE database. b, Differential z-score (gefitinib vs. control) of global motif accessibility scores for each identified transcription factor family. c, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. (SCR = scrambled control siRNA) d, Expression of A3A in PC9 cells transfected scrambled or individual NFκB1 siRNAs. Cells were treated with osimertinib for 24 hours and mRNA expression was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). Knockdown efficacy was confirmed by western blot. e, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. f, Western blot of PC9 and MGH064–1 cells after treatment with TKI (osimertinib or lorlatinib) and IKKβ inhibitors (representative of 3 biological replicates).
Figure Legend Snippet: a, Chromatin accessibility profile of the APOBEC3 locus (chromosome 22) of PC9 cells treated with 300 nM gefitinib for 0 or 14 days (2 biological replicates), with expanded view of the A3A promoter region. Relative fold-change of peak accessibility in treated vs. non-treated control cells is shown. Transcription factors mapping to these peak regions were identified from the ENCODE database. b, Differential z-score (gefitinib vs. control) of global motif accessibility scores for each identified transcription factor family. c, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. (SCR = scrambled control siRNA) d, Expression of A3A in PC9 cells transfected scrambled or individual NFκB1 siRNAs. Cells were treated with osimertinib for 24 hours and mRNA expression was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). Knockdown efficacy was confirmed by western blot. e, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. f, Western blot of PC9 and MGH064–1 cells after treatment with TKI (osimertinib or lorlatinib) and IKKβ inhibitors (representative of 3 biological replicates).

Techniques Used: Expressing, Transfection, Quantitative RT-PCR, Western Blot


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Bio-Techne corporation pf 184
Pf 184, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 184/product/Bio-Techne corporation
Average 86 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf 184 - by Bioz Stars, 2024-02
86/100 stars

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Tocris iκb kinase β inhibitor pf 184
Activation of NF-κB and p38 pathways in naïve, M-triDAP- and LPS-tolerized macrophages after their reculture with medium (0), M-triDAP (M) or LPS (L). (A) Levels of TNF and IL-6 in macrophage supernatants after indicated stimulation sequences (3 to 9 experiments). Statistical analysis by repeated measures ANOVA with Tukey correction. * p < 0.05, n.s. = non-significant. (B) Immunoblotting for IκBα, phospho-p38, phospho-ERK1/2, phospho-JNK, total p38, total ERK1/2 and α-tubulin at indicated time points after 2 nd stimulation (one representative Western blot out of three) and corresponding densitometry data normalized to untreated macrophages at 15 min. (C) Effect of <t>IκB</t> <t>kinase</t> inhibitor on TNF , IL6 and IL1B mRNA expression in naïve and LPS-tolerized macrophages (RT-PCR). Cells were cultured without or with LPS for 24 h, washed, incubated without or with <t>PF</t> <t>184</t> (5 μM) for 15 min, whereafter recultured without or with LPS for 1 or 4 h. 3 experiments, bars denote means. *p < 0.05, **p < 0.01 for comparisons between cells treated or not with PF 184 in identical stimulation conditions (paired t-test).
Iκb Kinase β Inhibitor Pf 184, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/iκb kinase β inhibitor pf 184/product/Tocris
Average 86 stars, based on 1 article reviews
Price from $9.99 to $1999.99
iκb kinase β inhibitor pf 184 - by Bioz Stars, 2024-02
86/100 stars

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1) Product Images from "Inhibition of specific signaling pathways rather than epigenetic silencing of effector genes is the leading mechanism of innate tolerance"

Article Title: Inhibition of specific signaling pathways rather than epigenetic silencing of effector genes is the leading mechanism of innate tolerance

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2023.1006002

Activation of NF-κB and p38 pathways in naïve, M-triDAP- and LPS-tolerized macrophages after their reculture with medium (0), M-triDAP (M) or LPS (L). (A) Levels of TNF and IL-6 in macrophage supernatants after indicated stimulation sequences (3 to 9 experiments). Statistical analysis by repeated measures ANOVA with Tukey correction. * p < 0.05, n.s. = non-significant. (B) Immunoblotting for IκBα, phospho-p38, phospho-ERK1/2, phospho-JNK, total p38, total ERK1/2 and α-tubulin at indicated time points after 2 nd stimulation (one representative Western blot out of three) and corresponding densitometry data normalized to untreated macrophages at 15 min. (C) Effect of IκB kinase inhibitor on TNF , IL6 and IL1B mRNA expression in naïve and LPS-tolerized macrophages (RT-PCR). Cells were cultured without or with LPS for 24 h, washed, incubated without or with PF 184 (5 μM) for 15 min, whereafter recultured without or with LPS for 1 or 4 h. 3 experiments, bars denote means. *p < 0.05, **p < 0.01 for comparisons between cells treated or not with PF 184 in identical stimulation conditions (paired t-test).
Figure Legend Snippet: Activation of NF-κB and p38 pathways in naïve, M-triDAP- and LPS-tolerized macrophages after their reculture with medium (0), M-triDAP (M) or LPS (L). (A) Levels of TNF and IL-6 in macrophage supernatants after indicated stimulation sequences (3 to 9 experiments). Statistical analysis by repeated measures ANOVA with Tukey correction. * p < 0.05, n.s. = non-significant. (B) Immunoblotting for IκBα, phospho-p38, phospho-ERK1/2, phospho-JNK, total p38, total ERK1/2 and α-tubulin at indicated time points after 2 nd stimulation (one representative Western blot out of three) and corresponding densitometry data normalized to untreated macrophages at 15 min. (C) Effect of IκB kinase inhibitor on TNF , IL6 and IL1B mRNA expression in naïve and LPS-tolerized macrophages (RT-PCR). Cells were cultured without or with LPS for 24 h, washed, incubated without or with PF 184 (5 μM) for 15 min, whereafter recultured without or with LPS for 1 or 4 h. 3 experiments, bars denote means. *p < 0.05, **p < 0.01 for comparisons between cells treated or not with PF 184 in identical stimulation conditions (paired t-test).

Techniques Used: Activation Assay, Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction, Cell Culture, Incubation


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Tocris pf 184
Pf 184, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 184/product/Tocris
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf 184 - by Bioz Stars, 2024-02
91/100 stars

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Tocris pf 184
Pf 184, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 184/product/Tocris
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf 184 - by Bioz Stars, 2024-02
91/100 stars

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Tocris pf 184
Pf 184, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 184/product/Tocris
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf 184 - by Bioz Stars, 2024-02
91/100 stars

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Tocris pf184
KEY RESOURCES TABLE
Pf184, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf184/product/Tocris
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf184 - by Bioz Stars, 2024-02
91/100 stars

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1) Product Images from "Interleukin-1β Induces mtDNA Release to Activate Innate Immune Signaling via cGAS-STING"

Article Title: Interleukin-1β Induces mtDNA Release to Activate Innate Immune Signaling via cGAS-STING

Journal: Molecular cell

doi: 10.1016/j.molcel.2019.02.038

KEY RESOURCES TABLE
Figure Legend Snippet: KEY RESOURCES TABLE

Techniques Used: Purification, Recombinant, Staining, Protease Inhibitor, Enzyme-linked Immunosorbent Assay, Clone Assay, Transfection, SYBR Green Assay, Western Blot


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Tocris pf184
Pf184, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf184/product/Tocris
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf184 - by Bioz Stars, 2024-02
91/100 stars

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Tocris pf184
Pf184, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf184/product/Tocris
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
pf184 - by Bioz Stars, 2024-02
91/100 stars

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    Tocris pf 184
    a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with <t>IKKβ</t> inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.
    Pf 184, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pf 184/product/Tocris
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pf 184 - by Bioz Stars, 2024-02
    86/100 stars
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    Bio-Techne corporation pf 184
    a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with <t>IKKβ</t> inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.
    Pf 184, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pf 184/product/Bio-Techne corporation
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    Tocris iκb kinase β inhibitor pf 184
    Activation of NF-κB and p38 pathways in naïve, M-triDAP- and LPS-tolerized macrophages after their reculture with medium (0), M-triDAP (M) or LPS (L). (A) Levels of TNF and IL-6 in macrophage supernatants after indicated stimulation sequences (3 to 9 experiments). Statistical analysis by repeated measures ANOVA with Tukey correction. * p < 0.05, n.s. = non-significant. (B) Immunoblotting for IκBα, phospho-p38, phospho-ERK1/2, phospho-JNK, total p38, total ERK1/2 and α-tubulin at indicated time points after 2 nd stimulation (one representative Western blot out of three) and corresponding densitometry data normalized to untreated macrophages at 15 min. (C) Effect of <t>IκB</t> <t>kinase</t> inhibitor on TNF , IL6 and IL1B mRNA expression in naïve and LPS-tolerized macrophages (RT-PCR). Cells were cultured without or with LPS for 24 h, washed, incubated without or with <t>PF</t> <t>184</t> (5 μM) for 15 min, whereafter recultured without or with LPS for 1 or 4 h. 3 experiments, bars denote means. *p < 0.05, **p < 0.01 for comparisons between cells treated or not with PF 184 in identical stimulation conditions (paired t-test).
    Iκb Kinase β Inhibitor Pf 184, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/iκb kinase β inhibitor pf 184/product/Tocris
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    iκb kinase β inhibitor pf 184 - by Bioz Stars, 2024-02
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    Tocris pf184
    KEY RESOURCES TABLE
    Pf184, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pf184/product/Tocris
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    pf184 - by Bioz Stars, 2024-02
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    Image Search Results


    a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with IKKβ inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.

    Journal: Nature

    Article Title: Therapy-induced APOBEC3A drives evolution of persistent cancer cells

    doi: 10.1038/s41586-023-06303-1

    Figure Lengend Snippet: a, Expression of APOBECs by quantitative RT-PCR (3 biological replicates) in EGFR NSCLC cell lines. b, DDOST mRNA editing determined by ddPCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). c, DDOST mRNA editing in control (VEH) and osimertinib-treated EGFR-mutant xenograft MRD tumors (mean ± s.d. of 3–5 independent tumors, two-sided Mann Whitney test). d-e, DDOST (d) and transcriptome-wide editing of A3A hairpin motifs (e) in mRNA-seq reads from control and gefitinib-treated DTPs (5 biological replicates, bar: median, two-sided Mann Whitney test. NT, non-treated control). f-g, Individual (f) or aggregate (g) TKI-induced A3A and A3B expression in NSCLC cells (TRA, trametinib; g, bar: median, two-sided Student’s t-test). h, A3A expression in resistant EGFR NSCLC cells. i-j, A3A (YTCA) and A3B (RTCA) character (i) and A3A hairpin motif (j) mutations in MGH086 tumors. Reference tumors from the ICGC/PCAWG consortium are plotted for comparison as described in Extended Data Fig. 9 (A3A - red, A3B - blue, APOBEC < 2.5% - green). k, Chromatin accessibility of APOBEC3A locus in PC9 DTPs (2 biological replicate). l, TKI-induced A3A expression in PC9 cells after knockdown of NFκB pathway genes. m, Western blot of PC9 cells treated with osimertinib or TNFα (representative of three independent experiments). n, A3A expression in PC9 cells treated with TNFα. o, NFκB1 binding to A3A enhancer locus in TKI-treated NSCLC cells determined by ChIP-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). p-q TKI-induced A3A expression in PC9 cells after IKKα/β knockdown (p) or treatment with IKKβ inhibitors (q). mRNA expression (f, h, l, n, p-q) was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates); significant p values (l, n, p-q) were determined by two-sided Student’s t-test.

    Article Snippet: For cell culture studies, gefitinib (GEF: 1 st generation EGFR inhibitor), osimertinib (OSI: 3 rd generation EGFR inhibitor), lorlatinib (LOR: ALK inhibitor), trametinib (TRA: MEK inhibitor), GDC0941 (GDC: PI3K inhibitor), ARS1620 (KRAS G12C inhibitor), TPCA-1 (IKKβ inhibitor) (all from Selleck), AMG 510 (KRAS G12C inhibitor, Chemgood) and PF 184 (IKKβ inhibitor, Tocris Bioscience) were dissolved in DMSO to a final concentration of 10 mmol/L and stored at −20 °C.

    Techniques: Expressing, Quantitative RT-PCR, Mutagenesis, MANN-WHITNEY, Comparison, Western Blot, Binding Assay

    a, Chromatin accessibility profile of the APOBEC3 locus (chromosome 22) of PC9 cells treated with 300 nM gefitinib for 0 or 14 days (2 biological replicates), with expanded view of the A3A promoter region. Relative fold-change of peak accessibility in treated vs. non-treated control cells is shown. Transcription factors mapping to these peak regions were identified from the ENCODE database. b, Differential z-score (gefitinib vs. control) of global motif accessibility scores for each identified transcription factor family. c, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. (SCR = scrambled control siRNA) d, Expression of A3A in PC9 cells transfected scrambled or individual NFκB1 siRNAs. Cells were treated with osimertinib for 24 hours and mRNA expression was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). Knockdown efficacy was confirmed by western blot. e, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. f, Western blot of PC9 and MGH064–1 cells after treatment with TKI (osimertinib or lorlatinib) and IKKβ inhibitors (representative of 3 biological replicates).

    Journal: Nature

    Article Title: Therapy-induced APOBEC3A drives evolution of persistent cancer cells

    doi: 10.1038/s41586-023-06303-1

    Figure Lengend Snippet: a, Chromatin accessibility profile of the APOBEC3 locus (chromosome 22) of PC9 cells treated with 300 nM gefitinib for 0 or 14 days (2 biological replicates), with expanded view of the A3A promoter region. Relative fold-change of peak accessibility in treated vs. non-treated control cells is shown. Transcription factors mapping to these peak regions were identified from the ENCODE database. b, Differential z-score (gefitinib vs. control) of global motif accessibility scores for each identified transcription factor family. c, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. (SCR = scrambled control siRNA) d, Expression of A3A in PC9 cells transfected scrambled or individual NFκB1 siRNAs. Cells were treated with osimertinib for 24 hours and mRNA expression was determined by quantitative RT-PCR (mean ± s.d. of 3 biological replicates, two-sided Student’s t-test). Knockdown efficacy was confirmed by western blot. e, Knockdown efficacy of each SMARTPool siRNA in PC9 cells. f, Western blot of PC9 and MGH064–1 cells after treatment with TKI (osimertinib or lorlatinib) and IKKβ inhibitors (representative of 3 biological replicates).

    Article Snippet: For cell culture studies, gefitinib (GEF: 1 st generation EGFR inhibitor), osimertinib (OSI: 3 rd generation EGFR inhibitor), lorlatinib (LOR: ALK inhibitor), trametinib (TRA: MEK inhibitor), GDC0941 (GDC: PI3K inhibitor), ARS1620 (KRAS G12C inhibitor), TPCA-1 (IKKβ inhibitor) (all from Selleck), AMG 510 (KRAS G12C inhibitor, Chemgood) and PF 184 (IKKβ inhibitor, Tocris Bioscience) were dissolved in DMSO to a final concentration of 10 mmol/L and stored at −20 °C.

    Techniques: Expressing, Transfection, Quantitative RT-PCR, Western Blot

    Activation of NF-κB and p38 pathways in naïve, M-triDAP- and LPS-tolerized macrophages after their reculture with medium (0), M-triDAP (M) or LPS (L). (A) Levels of TNF and IL-6 in macrophage supernatants after indicated stimulation sequences (3 to 9 experiments). Statistical analysis by repeated measures ANOVA with Tukey correction. * p < 0.05, n.s. = non-significant. (B) Immunoblotting for IκBα, phospho-p38, phospho-ERK1/2, phospho-JNK, total p38, total ERK1/2 and α-tubulin at indicated time points after 2 nd stimulation (one representative Western blot out of three) and corresponding densitometry data normalized to untreated macrophages at 15 min. (C) Effect of IκB kinase inhibitor on TNF , IL6 and IL1B mRNA expression in naïve and LPS-tolerized macrophages (RT-PCR). Cells were cultured without or with LPS for 24 h, washed, incubated without or with PF 184 (5 μM) for 15 min, whereafter recultured without or with LPS for 1 or 4 h. 3 experiments, bars denote means. *p < 0.05, **p < 0.01 for comparisons between cells treated or not with PF 184 in identical stimulation conditions (paired t-test).

    Journal: Frontiers in Immunology

    Article Title: Inhibition of specific signaling pathways rather than epigenetic silencing of effector genes is the leading mechanism of innate tolerance

    doi: 10.3389/fimmu.2023.1006002

    Figure Lengend Snippet: Activation of NF-κB and p38 pathways in naïve, M-triDAP- and LPS-tolerized macrophages after their reculture with medium (0), M-triDAP (M) or LPS (L). (A) Levels of TNF and IL-6 in macrophage supernatants after indicated stimulation sequences (3 to 9 experiments). Statistical analysis by repeated measures ANOVA with Tukey correction. * p < 0.05, n.s. = non-significant. (B) Immunoblotting for IκBα, phospho-p38, phospho-ERK1/2, phospho-JNK, total p38, total ERK1/2 and α-tubulin at indicated time points after 2 nd stimulation (one representative Western blot out of three) and corresponding densitometry data normalized to untreated macrophages at 15 min. (C) Effect of IκB kinase inhibitor on TNF , IL6 and IL1B mRNA expression in naïve and LPS-tolerized macrophages (RT-PCR). Cells were cultured without or with LPS for 24 h, washed, incubated without or with PF 184 (5 μM) for 15 min, whereafter recultured without or with LPS for 1 or 4 h. 3 experiments, bars denote means. *p < 0.05, **p < 0.01 for comparisons between cells treated or not with PF 184 in identical stimulation conditions (paired t-test).

    Article Snippet: IκB kinase β inhibitor (PF-184) was from Tocris (Bristol, UK), actinomycin D (ActD) from Sigma (St-Louis, MO).

    Techniques: Activation Assay, Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction, Cell Culture, Incubation

    KEY RESOURCES TABLE

    Journal: Molecular cell

    Article Title: Interleukin-1β Induces mtDNA Release to Activate Innate Immune Signaling via cGAS-STING

    doi: 10.1016/j.molcel.2019.02.038

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: PF184 , Tocris , Cat# 4238.

    Techniques: Purification, Recombinant, Staining, Protease Inhibitor, Enzyme-linked Immunosorbent Assay, Clone Assay, Transfection, SYBR Green Assay, Western Blot