evp 4593 Search Results


evp 4593  (MedChemExpress)
94
MedChemExpress evp 4593
Evp 4593, supplied by MedChemExpress, 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/result/evp 4593/product/MedChemExpress
Average 94 stars, based on 1 article reviews
evp 4593 - by Bioz Stars, 2026-03
94/100 stars
  Buy from Supplier
nf-κb inhibitors sodium salicylate  (Millipore)
90
Millipore nf-κb inhibitors sodium salicylate
(A) Inhibition of NF-κB using various <t>chemical</t> <t>inhibitors</t> — BMS-345541 (100 nM), 6-amino-4-(4-phenoxyphenylethylamino) quinazoline <t>(QNZ;</t> 1 μM), or sodium salicylate (5 mM) — inhibited erlotinib-induced upregulation of TNF in HCC827 cells as determined by qPCR. Cells were treated with NF-κB inhibitors for 1 hour and then 100 nM erlotinib for 24 hours. (B) Expression of a dominant-negative (DN) IκBα super-repressor mutant blocks erlotinib-induced upregulation of TNF in HCC827 cells. (C) Mithramycin A (MMA) (1 μM), an inhibitor of Sp1, failed to inhibit erlotinib-induced TNF upregulation. (D and E) The same experiment as in A and B was conducted in A549 cells. Expression of the dominant-negative IκBα super-repressor mutant was detected by Western blot. The mutant protein migrates more slowly on electrophoretic gels. (F–H) siRNA knockdown of TNFR1 in NSCLC cells inhibits erlotinib-induced upregulation of TNF mRNA as detected by qPCR. Silencing of TNFR1 was confirmed by Western blot. (I and J) Inhibition of TNFR signaling using etanercept (100 μg/ml) results in a block of erlotinib-induced TNF upregulation in HCC827 and A549 cells. (K) ChIP was carried out to assess the recruitment of the NF-κB p65 subunit onto the TNF promoter using primers specific to NF-κB binding region 1 on the TNF promoter. There is a substantially increased p65 antibody enrichment (percentage of input, compared with rabbit IgG) on the TNF promoter in both HCC827 and A549 cells in response to erlotinib treatment for 24 hours. Data represent the mean ± SEM. n = 3 biologically independent experimental replicates. *P < 0.05, **P < 0.01, ***P < 0.001, #not statistically significant, by Student’s t test for comparing 2 indicated groups, or 1-way ANOVA, Dunnett’s method, for comparing multiple groups with the same control (A and D). Western blot results are representative of at least 3 independent replicates.
Nf κb Inhibitors Sodium Salicylate, supplied by Millipore, 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/result/nf-κb inhibitors sodium salicylate/product/Millipore
Average 90 stars, based on 1 article reviews
nf-κb inhibitors sodium salicylate - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier
evp4593  (Biosynth Carbosynth)
N/A
   Buy from Supplier
qnz (evp4593)  (Aladdin Scientific Corporation)
N/A
QNZ (EVP4593) shows potent inhibitory activity toward both NF-κB activation and TNF-α production with IC50 of 11 nM and 7 nM, respectively.An inhibitor of the transcription factor NFκB.
   Buy from Supplier
shrna clone set against human evpll  (Genecopoeia)
N/A
OmicsLink™ shRNA clone collections include lentiviral and non-viral vector-based shRNA constructs against genome-wide human, mouse and rat genes. shRNA of varying lengths (19 to 29 bases) were designed using a proprietary algorithm to make shRNA
   Buy from Supplier
sgrna/cas9 all-in-one expression clones targeting evpll  (Genecopoeia)
N/A
Transfect cells with our CRISPR plasmids with Cas9 and sgRNA for human, mouse, and rat. Search our database of more than 45,000 human, mouse, and rat genes for genome editing using CRISPR. sgRNA expression plasmids
   Buy from Supplier
h-tvevptydfvthsr-oh  (Biosynth Carbosynth)
N/A
   Buy from Supplier
mirna 3´utr target expression clone for human evpll  (Genecopoeia)
N/A
GeneCopoeia offers genome-wide human, mouse and rat microRNA (miRNA) 3′ UTR target clones in mammalian expression vectors. miRNA 3′ UTR target clones can be used for miRNA target identification and functional validation of predicted targets,
   Buy from Supplier

Image Search Results


(A) Inhibition of NF-κB using various chemical inhibitors — BMS-345541 (100 nM), 6-amino-4-(4-phenoxyphenylethylamino) quinazoline (QNZ; 1 μM), or sodium salicylate (5 mM) — inhibited erlotinib-induced upregulation of TNF in HCC827 cells as determined by qPCR. Cells were treated with NF-κB inhibitors for 1 hour and then 100 nM erlotinib for 24 hours. (B) Expression of a dominant-negative (DN) IκBα super-repressor mutant blocks erlotinib-induced upregulation of TNF in HCC827 cells. (C) Mithramycin A (MMA) (1 μM), an inhibitor of Sp1, failed to inhibit erlotinib-induced TNF upregulation. (D and E) The same experiment as in A and B was conducted in A549 cells. Expression of the dominant-negative IκBα super-repressor mutant was detected by Western blot. The mutant protein migrates more slowly on electrophoretic gels. (F–H) siRNA knockdown of TNFR1 in NSCLC cells inhibits erlotinib-induced upregulation of TNF mRNA as detected by qPCR. Silencing of TNFR1 was confirmed by Western blot. (I and J) Inhibition of TNFR signaling using etanercept (100 μg/ml) results in a block of erlotinib-induced TNF upregulation in HCC827 and A549 cells. (K) ChIP was carried out to assess the recruitment of the NF-κB p65 subunit onto the TNF promoter using primers specific to NF-κB binding region 1 on the TNF promoter. There is a substantially increased p65 antibody enrichment (percentage of input, compared with rabbit IgG) on the TNF promoter in both HCC827 and A549 cells in response to erlotinib treatment for 24 hours. Data represent the mean ± SEM. n = 3 biologically independent experimental replicates. *P < 0.05, **P < 0.01, ***P < 0.001, #not statistically significant, by Student’s t test for comparing 2 indicated groups, or 1-way ANOVA, Dunnett’s method, for comparing multiple groups with the same control (A and D). Western blot results are representative of at least 3 independent replicates.

Journal: The Journal of Clinical Investigation

Article Title: TNF-driven adaptive response mediates resistance to EGFR inhibition in lung cancer

doi: 10.1172/JCI96148

Figure Lengend Snippet: (A) Inhibition of NF-κB using various chemical inhibitors — BMS-345541 (100 nM), 6-amino-4-(4-phenoxyphenylethylamino) quinazoline (QNZ; 1 μM), or sodium salicylate (5 mM) — inhibited erlotinib-induced upregulation of TNF in HCC827 cells as determined by qPCR. Cells were treated with NF-κB inhibitors for 1 hour and then 100 nM erlotinib for 24 hours. (B) Expression of a dominant-negative (DN) IκBα super-repressor mutant blocks erlotinib-induced upregulation of TNF in HCC827 cells. (C) Mithramycin A (MMA) (1 μM), an inhibitor of Sp1, failed to inhibit erlotinib-induced TNF upregulation. (D and E) The same experiment as in A and B was conducted in A549 cells. Expression of the dominant-negative IκBα super-repressor mutant was detected by Western blot. The mutant protein migrates more slowly on electrophoretic gels. (F–H) siRNA knockdown of TNFR1 in NSCLC cells inhibits erlotinib-induced upregulation of TNF mRNA as detected by qPCR. Silencing of TNFR1 was confirmed by Western blot. (I and J) Inhibition of TNFR signaling using etanercept (100 μg/ml) results in a block of erlotinib-induced TNF upregulation in HCC827 and A549 cells. (K) ChIP was carried out to assess the recruitment of the NF-κB p65 subunit onto the TNF promoter using primers specific to NF-κB binding region 1 on the TNF promoter. There is a substantially increased p65 antibody enrichment (percentage of input, compared with rabbit IgG) on the TNF promoter in both HCC827 and A549 cells in response to erlotinib treatment for 24 hours. Data represent the mean ± SEM. n = 3 biologically independent experimental replicates. *P < 0.05, **P < 0.01, ***P < 0.001, #not statistically significant, by Student’s t test for comparing 2 indicated groups, or 1-way ANOVA, Dunnett’s method, for comparing multiple groups with the same control (A and D). Western blot results are representative of at least 3 independent replicates.

Article Snippet: The NF-κB inhibitors BMS-345541, QNZ (EVP 4593), and sodium salicylate were obtained from MilliporeSigma.

Techniques: Inhibition, Expressing, Dominant Negative Mutation, Mutagenesis, Western Blot, Knockdown, Blocking Assay, Binding Assay, Control