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Thermo Fisher
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Rockland Immunochemicals
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Cusabio
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Proteintech
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R&D Systems
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Biorbyt
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Image Search Results
Journal: International Journal of Molecular Sciences
Article Title: Effective Restoration of Gastric and Esophageal Tissues in an In Vitro Model of GERD: Mucoadhesive and Protective Properties of Xyloglucan, Pea Proteins, and Polyacrylic Acid
doi: 10.3390/ijms26094409
Figure Lengend Snippet: Evaluation of barrier integrity of GTL-16 cells. ( A ) TEER (transepithelial electrical resistance) value measured using EVOM3 at different timepoints (from 1 h to 4 h); ( B – D ) analysis of TJ measured by Enzyme-Linked Immunosorbent Assay (ELISA) test (Claudin-1, ZO-1, and occludin, respectively) at 4 h. HCl = positive control, cells in GERD condition induced by HCl; Control = negative control, untreated cells. Data are expressed as means ± SD (%) of 5 independent experiments. * p < 0.05 vs. negative control; φ p < 0.05 vs. positive control. HCl: hydrochloric acid; TEER: trans-epithelial electrical resistance; XXPA: combination of xyloglucan, pea protein, and polyacrylic acid; ZO-1: Zonula Occludens-1.
Article Snippet: Fibronectin quantification was determined using the
Techniques: Enzyme-linked Immunosorbent Assay, Positive Control, Control, Negative Control
Journal: International Journal of Molecular Sciences
Article Title: Effective Restoration of Gastric and Esophageal Tissues in an In Vitro Model of GERD: Mucoadhesive and Protective Properties of Xyloglucan, Pea Proteins, and Polyacrylic Acid
doi: 10.3390/ijms26094409
Figure Lengend Snippet: Adhesion study on GTL-16 cells. ( A ) Vitronectin and ( B ) fibronectin analysis measured by Enzyme-Linked Immunosorbent Assay (ELISA) test at 4 h. HCl = positive control, cells in GERD condition induced by HCl; Control = negative control, untreated cells. Data are expressed as means ± SD (%) of 5 independent experiments. * p < 0.05 vs. negative control; φ p < 0.05 vs. positive control. HCl: hydrochloric acid; XXPA: combination of xyloglucan, pea protein, and polyacrylic acid.
Article Snippet: Fibronectin quantification was determined using the
Techniques: Enzyme-linked Immunosorbent Assay, Positive Control, Control, Negative Control
Journal: Molecules
Article Title: Vincamine Ameliorates Epithelial-Mesenchymal Transition in Bleomycin-Induced Pulmonary Fibrosis in Rats; Targeting TGF-β/MAPK/Snai1 Pathway
doi: 10.3390/molecules28124665
Figure Lengend Snippet: Effect of vincamine on fibronectin ( A ), N-cadherin ( B ), and collagen ( C ) levels in lung tissues. Bars represent mean ± SD. Significant difference was analyzed by one-way ANOVA test followed by post hoc Dunnett test, where * p < 0.001, compared to sham group, and # p < 0.001, compared to BLM-induced group.
Article Snippet: In lung tissue homogenates, levels of fibronectin, N-cadherin, and collagen were also assessed, according to the manufacturer’s instructions, utilizing
Techniques:
Journal: Molecules (Basel, Switzerland)
Article Title: Effects of the Calix[4]arene Derivative Compound OTX008 on High Glucose-Stimulated ARPE-19 Cells: Focus on Galectin-1/TGF-β/EMT Pathway.
doi: 10.3390/molecules27154785
Figure Lengend Snippet: Figure 7. EMT markers in ARPE-19 cells. (A) ACTA2 and (B) Fn1 mRNA and protein levels. ACTA2 and Fn1 relative mRNA levels are reported as 2ˆ−∆∆Ct ± SD and quantized by using GAPDH as control. ACTA2 and Fn1 protein levels are reported as ng/mL ± SD of 9 observations per group (three independent experiments, each done in triplicate). ** p < 0.01 vs. NG; ◦p < 0.05 and ◦◦p < 0.01 vs. HG; NG, normal glucose (5 mM) + vehicle; M, mannitol (30 mM); HG, high glucose (35 mM) + vehicle; OTX 2.5, OTX 2.5 µM; OTX 5, OTX 5 µM; OTX 10, OTX 10 µM.
Article Snippet: Competitive ELISA tests were used to quantify the cellular levels of human AP4S1 (My Biosource, MBS7206462), ACTA2 (or α-SMA) (antibodies-online, ABIN6953406), and
Techniques: Control
Journal: Cancers
Article Title: ROCK2 Confers Acquired Gemcitabine Resistance in Pancreatic Cancer Cells by Upregulating Transcription Factor ZEB1
doi: 10.3390/cancers11121881
Figure Lengend Snippet: Primer for PCR assay.
Article Snippet:
Techniques:
Journal: Oncology Research
Article Title: The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling
doi: 10.32604/or.2025.072084
Figure Lengend Snippet: Establishment and characterization of GC (Gemcitabine and Cisplatin)-resistant bladder cancer cell lines and identification of resistance-related proteins. ( A ) GC-resistant T24-R and UC3-R cell lines were generated by gradually increasing GC concentrations. Created in BioRender ( https://BioRender.com ). ( B ) Dose-response curves and calculated half-maximal inhibitory concentration (IC50) values for cisplatin (upper panel) and gemcitabine (lower panel) in parental (T24, UC3) and GC-resistant (T24-R, UC3-R) cell lines. Data are presented as the mean ± SD from at least three independent experiments. ( C ) Apoptosis rates of parental and resistant cell lines after treatment with cisplatin, as determined by flow cytometry. Data are presented as the mean ± SD ( n ≥ 3). ( D ) Transcriptomic and proteomic analyses identified FN1 (Fibronectin), EEF1A2 (Eukaryotic Translation Elongation Factor 1 Alpha 2), MRC2 (Mannose Receptor C-Type 2), RAB6B (RAB6B, Member RAS Oncogene Family), THBS1 (Thrombospondin 1), DYSF (Dysferlin), TMOD1 (Tropomodulin 1), NES (Nestin), and APOE (Apolipoprotein E) as overexpressed in GC-resistant cells. ( E ) RT-qPCR (Reverse Transcription Quantitative Polymerase Chain Reaction) and Western blot confirmed FN1 overexpression in T24-R and UC3-R. ( F ) FN1 staining was stronger in GC-resistant bladder cancer tissues (Chemotherapy Sensitive Group: n = 6; Chemotherapy Resistant Group: n = 6). For all panels, a t -test was used for comparisons between two groups, and one-way ANOVA was used for comparisons among multiple groups. Statistical significance was set at p < 0.05. ns, not significant, * p < 0.05, ** p < 0.01
Article Snippet: The resulting sample was subsequently analyzed using the
Techniques: Generated, Concentration Assay, Flow Cytometry, Quantitative RT-PCR, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Over Expression, Staining
Journal: Oncology Research
Article Title: The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling
doi: 10.32604/or.2025.072084
Figure Lengend Snippet: ITGB4 is critical for FN1-mediated chemotherapy resistance in bladder cancer cells. ( A ) Differential expression analysis revealed that ITGB4 (highlighted by the red box) was significantly overexpressed in T24-R cells compared to T24, suggesting a role in FN1-mediated resistance. ( B ) Structural modeling shows multiple binding sites between FN1 (blue ribbon) and ITGB4 (green ribbon). ( C ) The interaction between FN1 and ITGB4 had a binding score of −318.75 with a confidence score of 96%, indicating a stable interaction. ( D ) The Co-IP experiment confirmed that there is a mutual binding interaction between FN1 and ITGB4. ( E ) Adding rFN1 to resistant strains increased FAK (Y397) phosphorylation and inhibited apoptosis, whereas ITGB4 silencing reversed these effects, highlighting the dependency of FN1-mediated resistance on ITGB4 expression and activation. For panels ( A , C , E ), a t -test was used for comparisons between two groups, and one-way ANOVA was used for comparisons among multiple groups
Article Snippet: The resulting sample was subsequently analyzed using the
Techniques: Quantitative Proteomics, Binding Assay, Co-Immunoprecipitation Assay, Phospho-proteomics, Expressing, Activation Assay
Journal: Oncology Research
Article Title: The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling
doi: 10.32604/or.2025.072084
Figure Lengend Snippet: FN1 silencing enhances cisplatin-induced apoptosis in bladder cancer cells. ( A ) FN1 knockdown efficiency in T24-R and UC3-R cells was confirmed by Western blot analysis. ( B ) FN1 knockdown efficiency in T24-R and UC3-R cells was confirmed by RT-qPCR analysis. ( C ) Silencing FN1 significantly increased apoptosis in the resistant cell lines by TUNEL staining. ( D ) Silencing FN1 reduced the IC50 of cisplatin in the resistant cell lines by CCK-8 assay. ( E ) In resistant cells, FN1 knockdown induced the expression of pro-apoptotic mediators, including BAX and cleaved-caspase-3, but suppressed levels of the anti-apoptotic protein Bcl-2. ( F ) Cell apoptosis rates were quantified by flow cytometry. For all panels, a t-test was used for comparisons between two groups, and one-way ANOVA was used for comparisons among multiple groups. Statistical significance was set at p < 0.05. ns, not significant, * p < 0.05, ** p < 0.01
Article Snippet: The resulting sample was subsequently analyzed using the
Techniques: Knockdown, Western Blot, Quantitative RT-PCR, TUNEL Assay, Staining, CCK-8 Assay, Expressing, Flow Cytometry
Journal: Oncology Research
Article Title: The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling
doi: 10.32604/or.2025.072084
Figure Lengend Snippet: FN1 silencing inhibits tumor growth in vivo , enhancing cisplatin sensitivity. ( A ) Representative images of tumors from each treatment group. ( B ) Tumor volume growth curves over time measured in the T24-R xenograft model. ( C ) Apoptosis in tumor tissues was detected by TUNEL staining. ( D ) Immunohistochemical analysis showed decreased FN1 expression in tumor sections from the FN1 knockdown group. For all panels, a t -test was used for comparisons between two groups, and one-way ANOVA was used for comparisons among multiple groups. Statistical significance was set at p < 0.05. * p < 0.05, *** p < 0.001
Article Snippet: The resulting sample was subsequently analyzed using the
Techniques: In Vivo, TUNEL Assay, Staining, Immunohistochemical staining, Expressing, Knockdown
Journal: Oncology Research
Article Title: The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling
doi: 10.32604/or.2025.072084
Figure Lengend Snippet: FN1 regulates FAK (Y397) phosphorylation and mediates cisplatin resistance in bladder cancer cells. ( A ) Silencing FN1 in resistant cell lines reduced the phosphorylation of FAK (Y397) as detected by Western blot. ( B ) T24 and UC3 parental and resistant cells were treated with a fixed dose of cisplatin along with a gradient of rFN1 for 48 h. Phosphorylation of FAK (Y397) was assessed by Western blot. Resistant cells (T24-R, UC3-R) showed sensitivity to rFN1 at lower concentrations under cisplatin stress. ( C ) Silencing FN1 in resistant cell lines reduced the phosphorylation of FAK (Y397) as detected by immunofluorescence. ( D ) rFN1 addition increased resistance index in resistant strains. ( E ) The addition of rFN1 reduced apoptosis in resistant strains. For all panels, a t -test was used for comparisons between two groups, and one-way ANOVA was used for comparisons among multiple groups. Statistical significance was set at p < 0.05. ns, not significant, * p < 0.05, *** p < 0.001
Article Snippet: The resulting sample was subsequently analyzed using the
Techniques: Phospho-proteomics, Western Blot, Immunofluorescence
Journal: Tissue Engineering Part A
Article Title: A Strategy to Enhance Secretion of Extracellular Matrix Components by Stem Cells: Relevance to Tissue Engineering
doi: 10.1089/ten.tea.2017.0060
Figure Lengend Snippet: Figure 7: Immunostaining of Fibronectin and Collagen. Immunofluorescence staining of
Article Snippet: The RIPA solubilized samples were diluted at 1:40 dilution with ELISA sample diluent, followed by
Techniques: Immunostaining, Immunofluorescence, Staining
Journal: Tissue Engineering Part A
Article Title: A Strategy to Enhance Secretion of Extracellular Matrix Components by Stem Cells: Relevance to Tissue Engineering
doi: 10.1089/ten.tea.2017.0060
Figure Lengend Snippet: Figure 9: Concentration dependent stimulation of fibronectin by hADSCs. A) KTTKS (P0),
Article Snippet: The RIPA solubilized samples were diluted at 1:40 dilution with ELISA sample diluent, followed by
Techniques: Concentration Assay