qnz Search Results


morpholinyl quinazoline s  (Enamine Ltd)
92
Enamine Ltd morpholinyl quinazoline s
Morpholinyl Quinazoline S, supplied by Enamine Ltd, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/qnz/us11608344-654-144-149?v=Enamine+Ltd
Average 92 stars, based on 1 article reviews
morpholinyl quinazoline s - by Bioz Stars, 2026-07
92/100 stars
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n 2 methoxyphenyl methyl n methyl  (Enamine Ltd)
93
Enamine Ltd n 2 methoxyphenyl methyl n methyl
N 2 Methoxyphenyl Methyl N Methyl, supplied by Enamine Ltd, 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/product/qnz/pm38719475-47-25-30?v=Enamine+Ltd
Average 93 stars, based on 1 article reviews
n 2 methoxyphenyl methyl n methyl - by Bioz Stars, 2026-07
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qnz46  (Tocris)
94
Tocris qnz46
(A) Bath application of the GluN2D antagonist DQP-1105 (30 µM) completely abolished homosynaptic NMDAR-LTP at MPP-GC synapses (control: 149.1 ± 8.1 %, p < 0.001, n = 7, paired t-test; DQP-1105: 95.6 ± 8.8 %, p = 0.65, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (B) Induction of heterosynaptic NMDAR-LTP at LPP-GC synapses was also blocked in the presence of 30 µM DQP-1105 (control: 147.8 ± 9.1 %, p < 0.01, n = 7, paired t-test; DQP-1105: 99.1 ± 2.2 %, p = 0.71, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (C, D) Bath application of DQP-1105 or <t>QNZ46</t> had no effect on basal NMDAR synaptic transmission at either MPP-GC (C, 100.2 ± 5.9 %, p = 0.98, n = 9, paired t-test) or LPP-GC synapses (D, 103.4 ± 7.7 %, p = 0.67, n = 9, paired t-test). Application of D-APV abolished these EPSCs, confirming these responses were mediated by NMDARs (C, MPP: 5.3 ± 1.6 %, p < 0.0001, n = 5, paired t-test; D, LPP: 9.0 ± 3.7 %, p < 0.001). (E, F) Pre-post pairing LTP induction protocol was delivered at MPP inputs. Bath application of either DQP-1105 (30 µM) or QNZ46 (30 µM) 30 min after NMDAR-LTP induction substantially reduced both homosynaptic (E, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) and heterosynaptic (F, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) NMDAR-EPSC amplitude. Numbers in parentheses indicate the number of cells. Summary data represent mean ± s.e.m.
Qnz46, 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/qnz/bio_rxiv__2022__01__12__476040-52-5-12?v=Tocris
Average 94 stars, based on 1 article reviews
qnz46 - by Bioz Stars, 2026-07
94/100 stars
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factor kappa b nf κb pathway inhibitor n4  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology factor kappa b nf κb pathway inhibitor n4
(A) Bath application of the GluN2D antagonist DQP-1105 (30 µM) completely abolished homosynaptic NMDAR-LTP at MPP-GC synapses (control: 149.1 ± 8.1 %, p < 0.001, n = 7, paired t-test; DQP-1105: 95.6 ± 8.8 %, p = 0.65, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (B) Induction of heterosynaptic NMDAR-LTP at LPP-GC synapses was also blocked in the presence of 30 µM DQP-1105 (control: 147.8 ± 9.1 %, p < 0.01, n = 7, paired t-test; DQP-1105: 99.1 ± 2.2 %, p = 0.71, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (C, D) Bath application of DQP-1105 or <t>QNZ46</t> had no effect on basal NMDAR synaptic transmission at either MPP-GC (C, 100.2 ± 5.9 %, p = 0.98, n = 9, paired t-test) or LPP-GC synapses (D, 103.4 ± 7.7 %, p = 0.67, n = 9, paired t-test). Application of D-APV abolished these EPSCs, confirming these responses were mediated by NMDARs (C, MPP: 5.3 ± 1.6 %, p < 0.0001, n = 5, paired t-test; D, LPP: 9.0 ± 3.7 %, p < 0.001). (E, F) Pre-post pairing LTP induction protocol was delivered at MPP inputs. Bath application of either DQP-1105 (30 µM) or QNZ46 (30 µM) 30 min after NMDAR-LTP induction substantially reduced both homosynaptic (E, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) and heterosynaptic (F, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) NMDAR-EPSC amplitude. Numbers in parentheses indicate the number of cells. Summary data represent mean ± s.e.m.
Factor Kappa B Nf κb Pathway Inhibitor N4, supplied by Santa Cruz Biotechnology, 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/product/qnz/pmc07927934-396-2-9?v=Santa+Cruz+Biotechnology
Average 93 stars, based on 1 article reviews
factor kappa b nf κb pathway inhibitor n4 - by Bioz Stars, 2026-07
93/100 stars
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qnz  (Selleck Chemicals)
94
Selleck Chemicals qnz
(A) Bath application of the GluN2D antagonist DQP-1105 (30 µM) completely abolished homosynaptic NMDAR-LTP at MPP-GC synapses (control: 149.1 ± 8.1 %, p < 0.001, n = 7, paired t-test; DQP-1105: 95.6 ± 8.8 %, p = 0.65, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (B) Induction of heterosynaptic NMDAR-LTP at LPP-GC synapses was also blocked in the presence of 30 µM DQP-1105 (control: 147.8 ± 9.1 %, p < 0.01, n = 7, paired t-test; DQP-1105: 99.1 ± 2.2 %, p = 0.71, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (C, D) Bath application of DQP-1105 or <t>QNZ46</t> had no effect on basal NMDAR synaptic transmission at either MPP-GC (C, 100.2 ± 5.9 %, p = 0.98, n = 9, paired t-test) or LPP-GC synapses (D, 103.4 ± 7.7 %, p = 0.67, n = 9, paired t-test). Application of D-APV abolished these EPSCs, confirming these responses were mediated by NMDARs (C, MPP: 5.3 ± 1.6 %, p < 0.0001, n = 5, paired t-test; D, LPP: 9.0 ± 3.7 %, p < 0.001). (E, F) Pre-post pairing LTP induction protocol was delivered at MPP inputs. Bath application of either DQP-1105 (30 µM) or QNZ46 (30 µM) 30 min after NMDAR-LTP induction substantially reduced both homosynaptic (E, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) and heterosynaptic (F, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) NMDAR-EPSC amplitude. Numbers in parentheses indicate the number of cells. Summary data represent mean ± s.e.m.
Qnz, supplied by Selleck Chemicals, 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/qnz/pm38886378-312-36-40?v=Selleck+Chemicals
Average 94 stars, based on 1 article reviews
qnz - by Bioz Stars, 2026-07
94/100 stars
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nfκb activation inhibitor  (Biosynth Carbosynth)
89
Biosynth Carbosynth nfκb activation inhibitor
PGE2 upregulates uPA and MMP-9 via JNK1/2 signaling pathway in human LoVo colon cancer cells . (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 μM), SB203580 (p38 MAPK inhibitor, 1 μM), SP600125 (JNK1/2 inhibitor, 1 μM) or QNZ <t>(NFκB</t> inhibitor, 1 μM) for 1 h and followed by PGE2 (10 -6 M) administration for 24 h, and then were harvested for immunoblotting assays. (B) LoVo cells cultured in DMEM were treated with PGE2 (10 -6 M) for various periods (15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. Total protein of cell extracts was separated by 12% SDS-PAGE, transferred to PVDF membranes, and immunoblotted with antibodies against uPA, MMP-9 (A) , phospho-JNK1/2 and JNK1/2 (B) proteins. Equal loading was assessed with an anti-α-tubulin antibody. **, p < 0.01 versus control (mean ± SE, n = 3).
Nfκb Activation Inhibitor, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 89/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/qnz/pmc03179949-33-3-9?v=Biosynth+Carbosynth
Average 89 stars, based on 1 article reviews
nfκb activation inhibitor - by Bioz Stars, 2026-07
89/100 stars
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nf κb activation inhibitor  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology nf κb activation inhibitor
PGE2 upregulates uPA and MMP-9 via JNK1/2 signaling pathway in human LoVo colon cancer cells . (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 μM), SB203580 (p38 MAPK inhibitor, 1 μM), SP600125 (JNK1/2 inhibitor, 1 μM) or QNZ <t>(NFκB</t> inhibitor, 1 μM) for 1 h and followed by PGE2 (10 -6 M) administration for 24 h, and then were harvested for immunoblotting assays. (B) LoVo cells cultured in DMEM were treated with PGE2 (10 -6 M) for various periods (15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. Total protein of cell extracts was separated by 12% SDS-PAGE, transferred to PVDF membranes, and immunoblotted with antibodies against uPA, MMP-9 (A) , phospho-JNK1/2 and JNK1/2 (B) proteins. Equal loading was assessed with an anti-α-tubulin antibody. **, p < 0.01 versus control (mean ± SE, n = 3).
Nf κb Activation Inhibitor, supplied by Santa Cruz Biotechnology, 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/qnz/pmc04454663-49-27-10?v=Santa+Cruz+Biotechnology
Average 90 stars, based on 1 article reviews
nf κb activation inhibitor - by Bioz Stars, 2026-07
90/100 stars
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bipiperidin 10 yl n cycloheptyl 6 7 dimethoxy 4 quinazolinamine dihydrochloride  (Santa Cruz Biotechnology)
86
Santa Cruz Biotechnology bipiperidin 10 yl n cycloheptyl 6 7 dimethoxy 4 quinazolinamine dihydrochloride
PGE2 upregulates uPA and MMP-9 via JNK1/2 signaling pathway in human LoVo colon cancer cells . (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 μM), SB203580 (p38 MAPK inhibitor, 1 μM), SP600125 (JNK1/2 inhibitor, 1 μM) or QNZ <t>(NFκB</t> inhibitor, 1 μM) for 1 h and followed by PGE2 (10 -6 M) administration for 24 h, and then were harvested for immunoblotting assays. (B) LoVo cells cultured in DMEM were treated with PGE2 (10 -6 M) for various periods (15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. Total protein of cell extracts was separated by 12% SDS-PAGE, transferred to PVDF membranes, and immunoblotted with antibodies against uPA, MMP-9 (A) , phospho-JNK1/2 and JNK1/2 (B) proteins. Equal loading was assessed with an anti-α-tubulin antibody. **, p < 0.01 versus control (mean ± SE, n = 3).
Bipiperidin 10 Yl N Cycloheptyl 6 7 Dimethoxy 4 Quinazolinamine Dihydrochloride, supplied by Santa Cruz Biotechnology, 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/product/qnz/pm24582560-57-6-10?v=Santa+Cruz+Biotechnology
Average 86 stars, based on 1 article reviews
bipiperidin 10 yl n cycloheptyl 6 7 dimethoxy 4 quinazolinamine dihydrochloride - by Bioz Stars, 2026-07
86/100 stars
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chloro 3 pyridyl scheme 5  (BOC Sciences)
90
BOC Sciences chloro 3 pyridyl scheme 5
PGE2 upregulates uPA and MMP-9 via JNK1/2 signaling pathway in human LoVo colon cancer cells . (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 μM), SB203580 (p38 MAPK inhibitor, 1 μM), SP600125 (JNK1/2 inhibitor, 1 μM) or QNZ <t>(NFκB</t> inhibitor, 1 μM) for 1 h and followed by PGE2 (10 -6 M) administration for 24 h, and then were harvested for immunoblotting assays. (B) LoVo cells cultured in DMEM were treated with PGE2 (10 -6 M) for various periods (15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. Total protein of cell extracts was separated by 12% SDS-PAGE, transferred to PVDF membranes, and immunoblotted with antibodies against uPA, MMP-9 (A) , phospho-JNK1/2 and JNK1/2 (B) proteins. Equal loading was assessed with an anti-α-tubulin antibody. **, p < 0.01 versus control (mean ± SE, n = 3).
Chloro 3 Pyridyl Scheme 5, supplied by BOC Sciences, 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/qnz/pm31293165-59-166-140?v=BOC+Sciences
Average 90 stars, based on 1 article reviews
chloro 3 pyridyl scheme 5 - by Bioz Stars, 2026-07
90/100 stars
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qnz  (Enzo Biochem)
90
Enzo Biochem qnz
PGE2 upregulates uPA and MMP-9 via JNK1/2 signaling pathway in human LoVo colon cancer cells . (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 μM), SB203580 (p38 MAPK inhibitor, 1 μM), SP600125 (JNK1/2 inhibitor, 1 μM) or QNZ <t>(NFκB</t> inhibitor, 1 μM) for 1 h and followed by PGE2 (10 -6 M) administration for 24 h, and then were harvested for immunoblotting assays. (B) LoVo cells cultured in DMEM were treated with PGE2 (10 -6 M) for various periods (15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. Total protein of cell extracts was separated by 12% SDS-PAGE, transferred to PVDF membranes, and immunoblotted with antibodies against uPA, MMP-9 (A) , phospho-JNK1/2 and JNK1/2 (B) proteins. Equal loading was assessed with an anti-α-tubulin antibody. **, p < 0.01 versus control (mean ± SE, n = 3).
Qnz, supplied by Enzo Biochem, 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/qnz/us10112978-428-0-1?v=Enzo+Biochem
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qnz - by Bioz Stars, 2026-07
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nf-κb inhibitor ppm-18  (ApexBio)
90
ApexBio nf-κb inhibitor ppm-18
PGE2 upregulates uPA and MMP-9 via JNK1/2 signaling pathway in human LoVo colon cancer cells . (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 μM), SB203580 (p38 MAPK inhibitor, 1 μM), SP600125 (JNK1/2 inhibitor, 1 μM) or QNZ <t>(NFκB</t> inhibitor, 1 μM) for 1 h and followed by PGE2 (10 -6 M) administration for 24 h, and then were harvested for immunoblotting assays. (B) LoVo cells cultured in DMEM were treated with PGE2 (10 -6 M) for various periods (15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. Total protein of cell extracts was separated by 12% SDS-PAGE, transferred to PVDF membranes, and immunoblotted with antibodies against uPA, MMP-9 (A) , phospho-JNK1/2 and JNK1/2 (B) proteins. Equal loading was assessed with an anti-α-tubulin antibody. **, p < 0.01 versus control (mean ± SE, n = 3).
Nf κb Inhibitor Ppm 18, supplied by ApexBio, 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/qnz/pm37032340-48-6-12?v=ApexBio
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nf-κb inhibitor ppm-18 - by Bioz Stars, 2026-07
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Image Search Results


(A) Bath application of the GluN2D antagonist DQP-1105 (30 µM) completely abolished homosynaptic NMDAR-LTP at MPP-GC synapses (control: 149.1 ± 8.1 %, p < 0.001, n = 7, paired t-test; DQP-1105: 95.6 ± 8.8 %, p = 0.65, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (B) Induction of heterosynaptic NMDAR-LTP at LPP-GC synapses was also blocked in the presence of 30 µM DQP-1105 (control: 147.8 ± 9.1 %, p < 0.01, n = 7, paired t-test; DQP-1105: 99.1 ± 2.2 %, p = 0.71, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (C, D) Bath application of DQP-1105 or QNZ46 had no effect on basal NMDAR synaptic transmission at either MPP-GC (C, 100.2 ± 5.9 %, p = 0.98, n = 9, paired t-test) or LPP-GC synapses (D, 103.4 ± 7.7 %, p = 0.67, n = 9, paired t-test). Application of D-APV abolished these EPSCs, confirming these responses were mediated by NMDARs (C, MPP: 5.3 ± 1.6 %, p < 0.0001, n = 5, paired t-test; D, LPP: 9.0 ± 3.7 %, p < 0.001). (E, F) Pre-post pairing LTP induction protocol was delivered at MPP inputs. Bath application of either DQP-1105 (30 µM) or QNZ46 (30 µM) 30 min after NMDAR-LTP induction substantially reduced both homosynaptic (E, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) and heterosynaptic (F, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) NMDAR-EPSC amplitude. Numbers in parentheses indicate the number of cells. Summary data represent mean ± s.e.m.

Journal: bioRxiv

Article Title: Heterosynaptic NMDA Receptor Plasticity in Hippocampal Dentate Granule Cells

doi: 10.1101/2022.01.12.476040

Figure Lengend Snippet: (A) Bath application of the GluN2D antagonist DQP-1105 (30 µM) completely abolished homosynaptic NMDAR-LTP at MPP-GC synapses (control: 149.1 ± 8.1 %, p < 0.001, n = 7, paired t-test; DQP-1105: 95.6 ± 8.8 %, p = 0.65, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (B) Induction of heterosynaptic NMDAR-LTP at LPP-GC synapses was also blocked in the presence of 30 µM DQP-1105 (control: 147.8 ± 9.1 %, p < 0.01, n = 7, paired t-test; DQP-1105: 99.1 ± 2.2 %, p = 0.71, n = 4, paired t-test, DQP-1105 vs control: p < 0.01, unpaired t-test). (C, D) Bath application of DQP-1105 or QNZ46 had no effect on basal NMDAR synaptic transmission at either MPP-GC (C, 100.2 ± 5.9 %, p = 0.98, n = 9, paired t-test) or LPP-GC synapses (D, 103.4 ± 7.7 %, p = 0.67, n = 9, paired t-test). Application of D-APV abolished these EPSCs, confirming these responses were mediated by NMDARs (C, MPP: 5.3 ± 1.6 %, p < 0.0001, n = 5, paired t-test; D, LPP: 9.0 ± 3.7 %, p < 0.001). (E, F) Pre-post pairing LTP induction protocol was delivered at MPP inputs. Bath application of either DQP-1105 (30 µM) or QNZ46 (30 µM) 30 min after NMDAR-LTP induction substantially reduced both homosynaptic (E, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) and heterosynaptic (F, DQP-1105 vs post-LTP: p < 0.05, unpaired t-test) NMDAR-EPSC amplitude. Numbers in parentheses indicate the number of cells. Summary data represent mean ± s.e.m.

Article Snippet: Cyclopiazonic acid, heparin, ryanodine, DQP-1105, QNZ46, D-APV, and MPEP were purchased from Tocris Biosciences.

Techniques: Control, Transmission Assay

PGE2 upregulates uPA and MMP-9 via JNK1/2 signaling pathway in human LoVo colon cancer cells . (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 μM), SB203580 (p38 MAPK inhibitor, 1 μM), SP600125 (JNK1/2 inhibitor, 1 μM) or QNZ (NFκB inhibitor, 1 μM) for 1 h and followed by PGE2 (10 -6 M) administration for 24 h, and then were harvested for immunoblotting assays. (B) LoVo cells cultured in DMEM were treated with PGE2 (10 -6 M) for various periods (15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. Total protein of cell extracts was separated by 12% SDS-PAGE, transferred to PVDF membranes, and immunoblotted with antibodies against uPA, MMP-9 (A) , phospho-JNK1/2 and JNK1/2 (B) proteins. Equal loading was assessed with an anti-α-tubulin antibody. **, p < 0.01 versus control (mean ± SE, n = 3).

Journal: Journal of Biomedical Science

Article Title: JNK suppression is essential for 17β-Estradiol inhibits prostaglandin E2-Induced uPA and MMP-9 expressions and cell migration in human LoVo colon cancer cells

doi: 10.1186/1423-0127-18-61

Figure Lengend Snippet: PGE2 upregulates uPA and MMP-9 via JNK1/2 signaling pathway in human LoVo colon cancer cells . (A) LoVo cells were pretreated with vehicle, LY294002 (Akt activation inhibitor), U0126 (ERK1/2 activation inhibitor, 1 μM), SB203580 (p38 MAPK inhibitor, 1 μM), SP600125 (JNK1/2 inhibitor, 1 μM) or QNZ (NFκB inhibitor, 1 μM) for 1 h and followed by PGE2 (10 -6 M) administration for 24 h, and then were harvested for immunoblotting assays. (B) LoVo cells cultured in DMEM were treated with PGE2 (10 -6 M) for various periods (15 min, 30 min, 1 h, 3 h, 6 h, 12 h and 24 h), and subsequently measured the phosphorylation/activation of proteins by immunoblotting assay. The fold ratio of p-JNK1/2 and JNK1/2 was measured. Total protein of cell extracts was separated by 12% SDS-PAGE, transferred to PVDF membranes, and immunoblotted with antibodies against uPA, MMP-9 (A) , phospho-JNK1/2 and JNK1/2 (B) proteins. Equal loading was assessed with an anti-α-tubulin antibody. **, p < 0.01 versus control (mean ± SE, n = 3).

Article Snippet: 6-Amino-4-(4-phenoxyphenylethylamino) quinazoline (QNZ), NFκB activation inhibitor was purchased from Peptides International (Louisville, Kentucky, USA).

Techniques: Activation Assay, Western Blot, Cell Culture, Phospho-proteomics, SDS Page, Control