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(A) The volcano plot of the differentially expressed genes (DEGs) in mature 7 d grown epithelium in comparison to developing 2 d grown epithelium. MAPK-signaling -associated genes highlighted in red. (B) Ingenuity pathway analysis (IPA) pathway generator -derived map presenting affected nuclear mechanotransduction and NE -associated components and their downstream actors. Red and green indicate up- and down-regulation, respectively. Purple lines indicate statistically significantly affected components (Abs(log2FC)) >1 and pAdj <0.05). (C) ClusterProfiler KEGG pathway over-representation “MAPK signaling pathway” analysis of the 7 d -grown mature epithelium showing significantly affected biological processes in the 7-d grown mature epithelium in comparison to the 2 d-grown epithelium. (D) IPA pathway generator -derived map showing affected components of MAPK-signaling. Red indicates up-regulated, and green indicates down-regulated. Purple lines indicate statistically significantly affected components (Abs(log2FC)) >1 and pAdj <0.05). (E) STRING analysis of MAPK-associated DEGs in the 7 d grown epithelium, indicating functional enrichment in three clusters within interconnected networks. (F) Transcription factor (TF) motif analysis of transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) of 2 d and 7 d grown cells indicates global decreased accessibility of TF motifs, highlighting significant suppression of MAPK/ERK-associated motifs in the mature epithelium. Box-and-whiskers plots presenting (G) intracellular normalized fluorescence intensity distribution, and (H) nucleo-cytoplasmic ratio of activated phosphorylated <t>ERK1/2</t> <t>(phospho-ERK,</t> <t>p44/42</t> MAPK) at 2, 4, and 7 d post-seeding. One-way ANOVA with Dunnett’s multiple comparisons test indicates statistical significance, n=three independent biological replicates. Box-and-whisker plots represent the 25 th –75 th percentiles as boxes, the median as a line within the box, and whiskers indicating the minimum and maximum values.
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Figure 5. Intermittent LDIR activates ERK and <t>p38MAPK</t> pathways in 5-FU chemotherapy. In order to inhibit the function of ERK and p38MAPK, 10 µM PD98059 and SB203580 were added to the cell culture media at 2 h prior to 5-FU chemotherapy. (A) Western blotting of the MEK/ERK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (B) Relative band density of western blotting. (C) Western blotting of the p38MAPK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (D) Relative band density of western blotting. (E) ERK pathway inhibitors could not reverse the intermittent LDIR induced cell proliferation inhibition. (F) p38MAPK pathway inhibitors neutralized the intermittent LDIR induced cell proliferation inhibition. L, LDIR; IL, intermittent LDIR; NS, not significant. **p<0.01 as compared with the single dose LDIR group.
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Figure 5. Intermittent LDIR activates ERK and <t>p38MAPK</t> pathways in 5-FU chemotherapy. In order to inhibit the function of ERK and p38MAPK, 10 µM PD98059 and SB203580 were added to the cell culture media at 2 h prior to 5-FU chemotherapy. (A) Western blotting of the MEK/ERK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (B) Relative band density of western blotting. (C) Western blotting of the p38MAPK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (D) Relative band density of western blotting. (E) ERK pathway inhibitors could not reverse the intermittent LDIR induced cell proliferation inhibition. (F) p38MAPK pathway inhibitors neutralized the intermittent LDIR induced cell proliferation inhibition. L, LDIR; IL, intermittent LDIR; NS, not significant. **p<0.01 as compared with the single dose LDIR group.
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Figure 5. Intermittent LDIR activates ERK and <t>p38MAPK</t> pathways in 5-FU chemotherapy. In order to inhibit the function of ERK and p38MAPK, 10 µM PD98059 and SB203580 were added to the cell culture media at 2 h prior to 5-FU chemotherapy. (A) Western blotting of the MEK/ERK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (B) Relative band density of western blotting. (C) Western blotting of the p38MAPK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (D) Relative band density of western blotting. (E) ERK pathway inhibitors could not reverse the intermittent LDIR induced cell proliferation inhibition. (F) p38MAPK pathway inhibitors neutralized the intermittent LDIR induced cell proliferation inhibition. L, LDIR; IL, intermittent LDIR; NS, not significant. **p<0.01 as compared with the single dose LDIR group.
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Cell Signaling Technology Inc extracellular signal related kinase erk 1 2
Figure 5. Intermittent LDIR activates ERK and <t>p38MAPK</t> pathways in 5-FU chemotherapy. In order to inhibit the function of ERK and p38MAPK, 10 µM PD98059 and SB203580 were added to the cell culture media at 2 h prior to 5-FU chemotherapy. (A) Western blotting of the MEK/ERK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (B) Relative band density of western blotting. (C) Western blotting of the p38MAPK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (D) Relative band density of western blotting. (E) ERK pathway inhibitors could not reverse the intermittent LDIR induced cell proliferation inhibition. (F) p38MAPK pathway inhibitors neutralized the intermittent LDIR induced cell proliferation inhibition. L, LDIR; IL, intermittent LDIR; NS, not significant. **p<0.01 as compared with the single dose LDIR group.
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Figure 5. Intermittent LDIR activates ERK and <t>p38MAPK</t> pathways in 5-FU chemotherapy. In order to inhibit the function of ERK and p38MAPK, 10 µM PD98059 and SB203580 were added to the cell culture media at 2 h prior to 5-FU chemotherapy. (A) Western blotting of the MEK/ERK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (B) Relative band density of western blotting. (C) Western blotting of the p38MAPK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (D) Relative band density of western blotting. (E) ERK pathway inhibitors could not reverse the intermittent LDIR induced cell proliferation inhibition. (F) p38MAPK pathway inhibitors neutralized the intermittent LDIR induced cell proliferation inhibition. L, LDIR; IL, intermittent LDIR; NS, not significant. **p<0.01 as compared with the single dose LDIR group.
Fn Ab45688, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Figure 5. Intermittent LDIR activates ERK and <t>p38MAPK</t> pathways in 5-FU chemotherapy. In order to inhibit the function of ERK and p38MAPK, 10 µM PD98059 and SB203580 were added to the cell culture media at 2 h prior to 5-FU chemotherapy. (A) Western blotting of the MEK/ERK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (B) Relative band density of western blotting. (C) Western blotting of the p38MAPK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (D) Relative band density of western blotting. (E) ERK pathway inhibitors could not reverse the intermittent LDIR induced cell proliferation inhibition. (F) p38MAPK pathway inhibitors neutralized the intermittent LDIR induced cell proliferation inhibition. L, LDIR; IL, intermittent LDIR; NS, not significant. **p<0.01 as compared with the single dose LDIR group.
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Image Search Results


(A) The volcano plot of the differentially expressed genes (DEGs) in mature 7 d grown epithelium in comparison to developing 2 d grown epithelium. MAPK-signaling -associated genes highlighted in red. (B) Ingenuity pathway analysis (IPA) pathway generator -derived map presenting affected nuclear mechanotransduction and NE -associated components and their downstream actors. Red and green indicate up- and down-regulation, respectively. Purple lines indicate statistically significantly affected components (Abs(log2FC)) >1 and pAdj <0.05). (C) ClusterProfiler KEGG pathway over-representation “MAPK signaling pathway” analysis of the 7 d -grown mature epithelium showing significantly affected biological processes in the 7-d grown mature epithelium in comparison to the 2 d-grown epithelium. (D) IPA pathway generator -derived map showing affected components of MAPK-signaling. Red indicates up-regulated, and green indicates down-regulated. Purple lines indicate statistically significantly affected components (Abs(log2FC)) >1 and pAdj <0.05). (E) STRING analysis of MAPK-associated DEGs in the 7 d grown epithelium, indicating functional enrichment in three clusters within interconnected networks. (F) Transcription factor (TF) motif analysis of transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) of 2 d and 7 d grown cells indicates global decreased accessibility of TF motifs, highlighting significant suppression of MAPK/ERK-associated motifs in the mature epithelium. Box-and-whiskers plots presenting (G) intracellular normalized fluorescence intensity distribution, and (H) nucleo-cytoplasmic ratio of activated phosphorylated ERK1/2 (phospho-ERK, p44/42 MAPK) at 2, 4, and 7 d post-seeding. One-way ANOVA with Dunnett’s multiple comparisons test indicates statistical significance, n=three independent biological replicates. Box-and-whisker plots represent the 25 th –75 th percentiles as boxes, the median as a line within the box, and whiskers indicating the minimum and maximum values.

Journal: bioRxiv

Article Title: Deep Invaginations of Nuclear Envelope Coordinate Spatial Organization of Chromatin in Epithelium

doi: 10.64898/2026.03.10.710762

Figure Lengend Snippet: (A) The volcano plot of the differentially expressed genes (DEGs) in mature 7 d grown epithelium in comparison to developing 2 d grown epithelium. MAPK-signaling -associated genes highlighted in red. (B) Ingenuity pathway analysis (IPA) pathway generator -derived map presenting affected nuclear mechanotransduction and NE -associated components and their downstream actors. Red and green indicate up- and down-regulation, respectively. Purple lines indicate statistically significantly affected components (Abs(log2FC)) >1 and pAdj <0.05). (C) ClusterProfiler KEGG pathway over-representation “MAPK signaling pathway” analysis of the 7 d -grown mature epithelium showing significantly affected biological processes in the 7-d grown mature epithelium in comparison to the 2 d-grown epithelium. (D) IPA pathway generator -derived map showing affected components of MAPK-signaling. Red indicates up-regulated, and green indicates down-regulated. Purple lines indicate statistically significantly affected components (Abs(log2FC)) >1 and pAdj <0.05). (E) STRING analysis of MAPK-associated DEGs in the 7 d grown epithelium, indicating functional enrichment in three clusters within interconnected networks. (F) Transcription factor (TF) motif analysis of transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) of 2 d and 7 d grown cells indicates global decreased accessibility of TF motifs, highlighting significant suppression of MAPK/ERK-associated motifs in the mature epithelium. Box-and-whiskers plots presenting (G) intracellular normalized fluorescence intensity distribution, and (H) nucleo-cytoplasmic ratio of activated phosphorylated ERK1/2 (phospho-ERK, p44/42 MAPK) at 2, 4, and 7 d post-seeding. One-way ANOVA with Dunnett’s multiple comparisons test indicates statistical significance, n=three independent biological replicates. Box-and-whisker plots represent the 25 th –75 th percentiles as boxes, the median as a line within the box, and whiskers indicating the minimum and maximum values.

Article Snippet: Active MAPK was detected by using a mouse monoclonal Ab identifying the phosphorylated p44/42 MAPK (1:400, ERK1/2, Thr202/Tyr204 [E10], #9106, Cell Signaling Technology, MA, USA).

Techniques: Comparison, Derivative Assay, Functional Assay, Next-Generation Sequencing, Fluorescence, Whisker Assay

Figure 5. Intermittent LDIR activates ERK and p38MAPK pathways in 5-FU chemotherapy. In order to inhibit the function of ERK and p38MAPK, 10 µM PD98059 and SB203580 were added to the cell culture media at 2 h prior to 5-FU chemotherapy. (A) Western blotting of the MEK/ERK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (B) Relative band density of western blotting. (C) Western blotting of the p38MAPK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (D) Relative band density of western blotting. (E) ERK pathway inhibitors could not reverse the intermittent LDIR induced cell proliferation inhibition. (F) p38MAPK pathway inhibitors neutralized the intermittent LDIR induced cell proliferation inhibition. L, LDIR; IL, intermittent LDIR; NS, not significant. **p<0.01 as compared with the single dose LDIR group.

Journal: Oncology reports

Article Title: Intermittent low dose irradiation enhances the effectiveness of radio- and chemo-therapy for human colorectal adenocarcinoma cell line HT-29.

doi: 10.3892/or.2017.5679

Figure Lengend Snippet: Figure 5. Intermittent LDIR activates ERK and p38MAPK pathways in 5-FU chemotherapy. In order to inhibit the function of ERK and p38MAPK, 10 µM PD98059 and SB203580 were added to the cell culture media at 2 h prior to 5-FU chemotherapy. (A) Western blotting of the MEK/ERK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (B) Relative band density of western blotting. (C) Western blotting of the p38MAPK pathway genes in HT-29 cells. β-actin was used as the internal control for blotting reaction. (D) Relative band density of western blotting. (E) ERK pathway inhibitors could not reverse the intermittent LDIR induced cell proliferation inhibition. (F) p38MAPK pathway inhibitors neutralized the intermittent LDIR induced cell proliferation inhibition. L, LDIR; IL, intermittent LDIR; NS, not significant. **p<0.01 as compared with the single dose LDIR group.

Article Snippet: The blots were blocked with 5% non-fat milk in TBST at 37 ̊C for 1 h. Then, blots were probed with monoclonal antibodies against ATM (1:500, Abcam, Shanghai, China), p53 (1:1,500, DO7, Santa Cruz Biotechnology, Santa Cruz, CA, USA), p21 (1:500, C-19, Santa Cruz Biotechnology), cyclin A (1:500, Santa Cruz Biotechnology), CDK2 (1:500, Santa Cruz Biotechnology), caspase-3 (1:1,000, Cell Signaling Technology, Beijing, China), cleaved caspase-3 (1:1,000, Cell Signaling Technology), ERK/phos-ERK (1:1,000, Cell Signaling Technology), p38/phos-p38 (1:1,000, Cell Signaling Technology) and β-actin (1:3,000, Santa Cruz Biotechnology) at 4 ̊C overnight.

Techniques: Cell Culture, Western Blot, Control, Inhibition