tissue microarrays (Proteintech)
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Tissue Microarrays, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/antibody+microarray/ALY+Antibody/pmc12827963-124-6-20
Average 93 stars, based on 28 article reviews
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1) Product Images from "Multi-omics analysis reveals that ALYREF-mediated m 5 C modification promotes platinum resistance in ovarian cancer via the NSUN2/ALYREF/LGR4 axis"
Article Title: Multi-omics analysis reveals that ALYREF-mediated m 5 C modification promotes platinum resistance in ovarian cancer via the NSUN2/ALYREF/LGR4 axis
Journal: Cell Death & Disease
doi: 10.1038/s41419-025-08310-8
Figure Legend Snippet: A Schematic diagram of the ALYREF m 5 C methylation binding site mutation. B m 5 C-RIP and qRT-PCR assays detecting the influence of ALYREF on the m 5 C methylation level of LGR4 mRNA. C qPCR detection of LGR4 RNA expression in the influence of ALYREF. D Western blot analysis of LGR4 protein expression in ALYREF-overexpressing A2780/DDP and SKOV3/DDP cells, and in cells with mutated ALYREF binding sites. E Actinomycin D assay assessing the impact of ALYREF on LGR4 mRNA stability. F Representative images of IHC staining of LGR4 expression levels in tissue microarrays. G Correlation analysis between ALYREF and LGR4 protein expression levels. H Schematic representation of the subcutaneous tumor model in cisplatin-resistant ovarian cancer-bearing mice by Generic Diagramming Platform (GDP) . I Final diameter and weight of the subcutaneous tumors. Data are displayed as mean ± SD; *: p < 0.05. **: p < 0.01. ***: p < 0.001. ****: p < 0.0001.
Techniques Used: Methylation, Binding Assay, Mutagenesis, Quantitative RT-PCR, RNA Expression, Western Blot, Expressing, Immunohistochemistry
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Incubation:Article Title: Multi-omics analysis reveals that ALYREF-mediated m 5 C modification promotes platinum resistance in ovarian cancer via the NSUN2/ALYREF/LGR4 axis Article Snippet: To get rid of endogenous peroxidase activity, tissue sections were treated with 3% hydrogen peroxide, followed by blocking with 10% goat serum (C0265; Beyotime, China) for 1 h at room temperature. .. Following a rinse with PBS, the tissue microarrays were incubated at 4 °C for 16 h with Article Title: Nsun2-mediated m5C methylation of Ncor1 exacerbates sepsis-induced cardiomyopathy by promoting mitochondrial dysfunction. Article Snippet: Sepsis-induced cardiomyopathy (SIC) is a severe complication of sepsis characterized by mitochondrial dysfunction and impaired myocardial contractility, yet its molecular pathogenesis remains incompletely understood.. In this study, we demonstrate that excessive mitochondrial fission plays a pivotal role in SIC, contributing to inflammation, oxidative stress, and cardiomyocyte apoptosis.. Pharmacological inhibition of mitochondrial fission using Mdivi-1 alleviated these pathological changes both in vivo and in vitro. Article Title: Targeting NSUN5-mediated m5C-RNA modification overcomes sunitinib resistance in renal cell carcinoma by suppressing Fibronectin/PI3K/AKT signaling Article Snippet: Cells were subjected to lysis utilizing RIPA buffer (Beyotime, China) with the addition of protease inhibitors PMSF (MedChemExpress [MCE], China), and quantification of protein concentrations was performed employing the bicinchoninic acid (BCA) assay (Beyotime). .. Proteins were separated by 10% SDS-PAGE, transferred onto PVDF membranes, and incubated overnight at 4 °C with different primary antibodies, including anti-NSUN5 (1:2000; #ab121633; RRID: AB_11129930; Abcam, USA), anti-PI3K (1:2000; #ab302958; Abcam), anti-AKT (1:5000; #4691T; Cell Signaling Technology [CST], USA), anti-p-AKT (1:5000; #4060T; RRID: AB_2315049; CST), anti-pPI3K (1:2000; #4228T; CST), anti-FN1 (1:10000; #15613-1-AP; RRID: AB_2105691; Proteintech, China), Immunoprecipitation:Article Title: Nsun2-mediated m5C methylation of Ncor1 exacerbates sepsis-induced cardiomyopathy by promoting mitochondrial dysfunction. Article Snippet: Sepsis-induced cardiomyopathy (SIC) is a severe complication of sepsis characterized by mitochondrial dysfunction and impaired myocardial contractility, yet its molecular pathogenesis remains incompletely understood.. In this study, we demonstrate that excessive mitochondrial fission plays a pivotal role in SIC, contributing to inflammation, oxidative stress, and cardiomyocyte apoptosis.. Pharmacological inhibition of mitochondrial fission using Mdivi-1 alleviated these pathological changes both in vivo and in vitro. Control:Article Title: Nsun2-mediated m5C methylation of Ncor1 exacerbates sepsis-induced cardiomyopathy by promoting mitochondrial dysfunction. Article Snippet: Sepsis-induced cardiomyopathy (SIC) is a severe complication of sepsis characterized by mitochondrial dysfunction and impaired myocardial contractility, yet its molecular pathogenesis remains incompletely understood.. In this study, we demonstrate that excessive mitochondrial fission plays a pivotal role in SIC, contributing to inflammation, oxidative stress, and cardiomyocyte apoptosis.. Pharmacological inhibition of mitochondrial fission using Mdivi-1 alleviated these pathological changes both in vivo and in vitro. Magnetic Beads:Article Title: Nsun2-mediated m5C methylation of Ncor1 exacerbates sepsis-induced cardiomyopathy by promoting mitochondrial dysfunction. Article Snippet: Sepsis-induced cardiomyopathy (SIC) is a severe complication of sepsis characterized by mitochondrial dysfunction and impaired myocardial contractility, yet its molecular pathogenesis remains incompletely understood.. In this study, we demonstrate that excessive mitochondrial fission plays a pivotal role in SIC, contributing to inflammation, oxidative stress, and cardiomyocyte apoptosis.. Pharmacological inhibition of mitochondrial fission using Mdivi-1 alleviated these pathological changes both in vivo and in vitro. Cell-Signaling:Article Title: Targeting NSUN5-mediated m5C-RNA modification overcomes sunitinib resistance in renal cell carcinoma by suppressing Fibronectin/PI3K/AKT signaling Article Snippet: Cells were subjected to lysis utilizing RIPA buffer (Beyotime, China) with the addition of protease inhibitors PMSF (MedChemExpress [MCE], China), and quantification of protein concentrations was performed employing the bicinchoninic acid (BCA) assay (Beyotime). .. Proteins were separated by 10% SDS-PAGE, transferred onto PVDF membranes, and incubated overnight at 4 °C with different primary antibodies, including anti-NSUN5 (1:2000; #ab121633; RRID: AB_11129930; Abcam, USA), anti-PI3K (1:2000; #ab302958; Abcam), anti-AKT (1:5000; #4691T; Cell Signaling Technology [CST], USA), anti-p-AKT (1:5000; #4060T; RRID: AB_2315049; CST), anti-pPI3K (1:2000; #4228T; CST), anti-FN1 (1:10000; #15613-1-AP; RRID: AB_2105691; Proteintech, China), |
