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tissue microarrays  (Proteintech)


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    Structured Review

    Proteintech tissue microarrays
    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 <t>microarrays.</t> 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.
    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
    tissue microarrays - by Bioz Stars, 2026-11
    93/100 stars

    Images

    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

    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.
    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

    Related Articles

    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 anti-ALYREF antibody (16690-1-AP; Proteintech, China) and anti-LGR4 antibody (20150-1-AP; Proteintech, China), each at a 1:300 dilution. .. The Secondary antibody (GB23303; Servicebio, China) and DAB chromogen (G1212; Servicebio, China) were utilized for secondary antibody incubation and staining of the tissue microarray.

    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), antiALYREF (1:1000; #16690-1-AP; RRID: AB_2878300; Proteintech), anti-YBX1 (1:10000; #20339-1-AP; RRID: AB_10665424; Proteintech), anti-FAK (1:10000; #12636-1-AP; RRID: AB_2173668; Proteintech), anti-p-FAK Cell Death and Disease (1:1000; #83933-1-AP; RRID:AB_3671514; Proteintech), anti-NOP2 (1:1000; #10448-1-AP; RRID:AB_2282772; Proteintech), anti-NSUN2 (1:10000; #20854-1-AP; RRID:AB_10693629; Proteintech), anti-NSUN3 (1:1000; #16560-1-AP; RRID:AB_3085496; Proteintech), anti-NSUN4 (1:1000; #29786-1-AP; RRID:AB_2935480; Proteintech), anti-NSUN6 (1:1000; #17240-1-AP; RRID:AB_2878367; Proteintech), anti-DNMT1 (1:1000; #24206-1- AP; RRID:AB_2879457; Proteintech), anti-DNMT3A (1:10000; #20954-1-AP; RRID:AB_10733339; Proteintech), anti-DNMT3B (1:1000; #26971-1-AP; RRID:AB_2880705; Proteintech), and anti-GAPDH (1:25000; #60004-1-Ig; RRID: AB_2107436; Proteintech). .. The membranes were then subjected to incubation with secondary antibodies, followed by imaging conducted with a Multifunction Imager (GE Amersham Imager 600, USA).

    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), antiALYREF (1:1000; #16690-1-AP; RRID: AB_2878300; Proteintech), anti-YBX1 (1:10000; #20339-1-AP; RRID: AB_10665424; Proteintech), anti-FAK (1:10000; #12636-1-AP; RRID: AB_2173668; Proteintech), anti-p-FAK Cell Death and Disease (1:1000; #83933-1-AP; RRID:AB_3671514; Proteintech), anti-NOP2 (1:1000; #10448-1-AP; RRID:AB_2282772; Proteintech), anti-NSUN2 (1:10000; #20854-1-AP; RRID:AB_10693629; Proteintech), anti-NSUN3 (1:1000; #16560-1-AP; RRID:AB_3085496; Proteintech), anti-NSUN4 (1:1000; #29786-1-AP; RRID:AB_2935480; Proteintech), anti-NSUN6 (1:1000; #17240-1-AP; RRID:AB_2878367; Proteintech), anti-DNMT1 (1:1000; #24206-1- AP; RRID:AB_2879457; Proteintech), anti-DNMT3A (1:10000; #20954-1-AP; RRID:AB_10733339; Proteintech), anti-DNMT3B (1:1000; #26971-1-AP; RRID:AB_2880705; Proteintech), and anti-GAPDH (1:25000; #60004-1-Ig; RRID: AB_2107436; Proteintech). .. The membranes were then subjected to incubation with secondary antibodies, followed by imaging conducted with a Multifunction Imager (GE Amersham Imager 600, USA).



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    Proteintech tissue microarrays
    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 <t>microarrays.</t> 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.
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    Image Search Results


    ( A ) Experimental workflow used for phosphoproteomic analysis of F508del-CFBE41o- cells treated with control peptide (CP) or PI3Kγ MP (25 μM, 30 minutes). A phospho-specific microarray, containing 875 phosphosite-specific and 451 pan-specific antibodies, was used. Thirty-six proteins showing phosphorylation changes exceeding ±60% compared with the control (expressed as percentage CFC, i.e., percentage fold-change compared with control) were selected for downstream analysis. ( B and C ) Panther Gene Ontology (GO) slim-term enrichment analysis of proteins with altered phosphorylation after PI3Kγ MP treatment. Significantly enriched GO terms (FDR < 0.05) were categorized under ( B ) biological processes and ( C ) cellular components. ( D ) Reactome pathway enrichment analysis of differentially phosphorylated proteins after PI3Kγ MP treatment. Lines represent the top 20 pathways; x axis shows the –log 10 (FDR). Color intensity reflects fold enrichment, and circle size indicates the number of proteins; color intensity (yellow to red) indicates increasing fold enrichment. The full phospho-array protein list served as background reference. ( E ) Proteins with CFC greater than 60% (green) or less than −60% (red). A CFC of 100% corresponds to a 2-fold increase in signal intensity after PI3Kγ MP treatment relative to CP.

    Journal: JCI Insight

    Article Title: Targeting PI3K γ anchoring enhances CFTR membrane localization and modulator efficacy via PKD1

    doi: 10.1172/jci.insight.198846

    Figure Lengend Snippet: ( A ) Experimental workflow used for phosphoproteomic analysis of F508del-CFBE41o- cells treated with control peptide (CP) or PI3Kγ MP (25 μM, 30 minutes). A phospho-specific microarray, containing 875 phosphosite-specific and 451 pan-specific antibodies, was used. Thirty-six proteins showing phosphorylation changes exceeding ±60% compared with the control (expressed as percentage CFC, i.e., percentage fold-change compared with control) were selected for downstream analysis. ( B and C ) Panther Gene Ontology (GO) slim-term enrichment analysis of proteins with altered phosphorylation after PI3Kγ MP treatment. Significantly enriched GO terms (FDR < 0.05) were categorized under ( B ) biological processes and ( C ) cellular components. ( D ) Reactome pathway enrichment analysis of differentially phosphorylated proteins after PI3Kγ MP treatment. Lines represent the top 20 pathways; x axis shows the –log 10 (FDR). Color intensity reflects fold enrichment, and circle size indicates the number of proteins; color intensity (yellow to red) indicates increasing fold enrichment. The full phospho-array protein list served as background reference. ( E ) Proteins with CFC greater than 60% (green) or less than −60% (red). A CFC of 100% corresponds to a 2-fold increase in signal intensity after PI3Kγ MP treatment relative to CP.

    Article Snippet: After treatment with 25 μM PI3Kγ MP or an equimolar amount of CP for 30 minutes, F508del-CFBE41o- cells were lysed as described above, and protein samples were frozen at –80°C before being subjected to an antibody microarray (KAM-1325 array) and data analysis, which was performed at Kinexus.

    Techniques: Control, Microarray, Phospho-proteomics

    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.

    Journal: Cell Death & Disease

    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

    doi: 10.1038/s41419-025-08310-8

    Figure Lengend 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.

    Article Snippet: Following a rinse with PBS, the tissue microarrays were incubated at 4 °C for 16 h with anti-ALYREF antibody (16690-1-AP; Proteintech, China) and anti-LGR4 antibody (20150-1-AP; Proteintech, China), each at a 1:300 dilution.

    Techniques: Methylation, Binding Assay, Mutagenesis, Quantitative RT-PCR, RNA Expression, Western Blot, Expressing, Immunohistochemistry