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ms2 gfp fusion protein  (Proteintech)


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    Proteintech ms2 gfp fusion protein
    a , b The half-life of EN2 mRNA were determined by qRT-PCR in LINC00973 knockdown or overexpressed Cal27 and HN6 cells with time-course Actinomycin D exposure. c Experimental design of AGO2-RIP was depicted by schematic diagram (left panel). Endogenous LINC00973 was assessed by qRT-PCR in cell lyses immunoprecipitated with either AGO2 antibody or mouse IgG (right panel). d , e The putative miRNA candidates with high EN2 mRNA binding affinity were computed by TargetScan webtool ( https://www.targetscan.org/vert_80/ ), while LINC00973 sponged miRNAs (top10) were predicted by DIANA tool kits ( http://diana.imis.athena-innovation.gr/DianaTools/index.php ). Six overlapped miRNA candidates were identified ( d ). Only miR-6756-3p expression were shown with significant upregulation followed by LINC00973 silencing in both Cal27 and HN6 cells ( e ). f The expression of miR-6756-3p in 50 HNSCC clinical samples and paired normal counterparts were determined by qRT-PCR. Paired Wilcoxon rank-sum test. g Kaplan-Meier analyses of OS and DSS stratified by median miR-6756-3p expression in 50 in-house samples Log-rank test. h , i Schematic diagram depicted the experimental design of MS2-RIP assays to detect the direct binding between LINC00973 and miR-6756-3p in HNSCC ( h ). The <t>LINC00973-MS2-GFP</t> complex was pulled down by anti-GFP antibody and the interacted miR-6756-3p were assessed by qRT-PCR in Cal27, HN6, and HEK293T cells ( i ). j The sequence alignment displayed the binding sequence between miR-6756-3p and LINC00973 [LINC00973 (WT)] or 3’UTR of EN2 [3’UTR EN2 (WT)]. The miR-6756-3p binding site mutated LINC00973 and EN2 transcripts [LINC00973 (MT) or 3’UTR EN2 (MT)] were showed below. k , l Cal27 and HN6 cells transfected with LINC00973/3’UTR EN2 wild type or miR-6756-3p binding site mutated pmirGLO luciferase reporter vectors and treated with miR-6756-3p or control mimics. The luciferase activated was measured. m The expression levels of EN2 were measured by qRT-PCR in Cal27 and HN6 treated with sh-LINC00973-1 lentivirus or in combination with miR-6756-3p inhibitor (inhibitor). n The correlations between EN2, LINC00973, and miR-6756-3p expression in HNSCC clinical samples were estimated by using Spearman’s correlation. o Schematic illustration of the regulatory model of LINC00973 decoys miR-6756-3p to stabilize EN2 mRNA. Data were presented as mean ± SD, # P ≥ 0.05, * P < 0.05, ** P < 0.01, Student’s t test.
    Ms2 Gfp Fusion Protein, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1550 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ms2+gfp+fusion+protein/pmc12848070-97-18-12?v=Proteintech
    Average 96 stars, based on 1550 article reviews
    ms2 gfp fusion protein - by Bioz Stars, 2026-07
    96/100 stars

    Images

    1) Product Images from "A novel super-enhancer-driven lncRNA LINC00973 governs head and neck squamous cell carcinoma progression through EN2"

    Article Title: A novel super-enhancer-driven lncRNA LINC00973 governs head and neck squamous cell carcinoma progression through EN2

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-025-08380-8

    a , b The half-life of EN2 mRNA were determined by qRT-PCR in LINC00973 knockdown or overexpressed Cal27 and HN6 cells with time-course Actinomycin D exposure. c Experimental design of AGO2-RIP was depicted by schematic diagram (left panel). Endogenous LINC00973 was assessed by qRT-PCR in cell lyses immunoprecipitated with either AGO2 antibody or mouse IgG (right panel). d , e The putative miRNA candidates with high EN2 mRNA binding affinity were computed by TargetScan webtool ( https://www.targetscan.org/vert_80/ ), while LINC00973 sponged miRNAs (top10) were predicted by DIANA tool kits ( http://diana.imis.athena-innovation.gr/DianaTools/index.php ). Six overlapped miRNA candidates were identified ( d ). Only miR-6756-3p expression were shown with significant upregulation followed by LINC00973 silencing in both Cal27 and HN6 cells ( e ). f The expression of miR-6756-3p in 50 HNSCC clinical samples and paired normal counterparts were determined by qRT-PCR. Paired Wilcoxon rank-sum test. g Kaplan-Meier analyses of OS and DSS stratified by median miR-6756-3p expression in 50 in-house samples Log-rank test. h , i Schematic diagram depicted the experimental design of MS2-RIP assays to detect the direct binding between LINC00973 and miR-6756-3p in HNSCC ( h ). The LINC00973-MS2-GFP complex was pulled down by anti-GFP antibody and the interacted miR-6756-3p were assessed by qRT-PCR in Cal27, HN6, and HEK293T cells ( i ). j The sequence alignment displayed the binding sequence between miR-6756-3p and LINC00973 [LINC00973 (WT)] or 3’UTR of EN2 [3’UTR EN2 (WT)]. The miR-6756-3p binding site mutated LINC00973 and EN2 transcripts [LINC00973 (MT) or 3’UTR EN2 (MT)] were showed below. k , l Cal27 and HN6 cells transfected with LINC00973/3’UTR EN2 wild type or miR-6756-3p binding site mutated pmirGLO luciferase reporter vectors and treated with miR-6756-3p or control mimics. The luciferase activated was measured. m The expression levels of EN2 were measured by qRT-PCR in Cal27 and HN6 treated with sh-LINC00973-1 lentivirus or in combination with miR-6756-3p inhibitor (inhibitor). n The correlations between EN2, LINC00973, and miR-6756-3p expression in HNSCC clinical samples were estimated by using Spearman’s correlation. o Schematic illustration of the regulatory model of LINC00973 decoys miR-6756-3p to stabilize EN2 mRNA. Data were presented as mean ± SD, # P ≥ 0.05, * P < 0.05, ** P < 0.01, Student’s t test.
    Figure Legend Snippet: a , b The half-life of EN2 mRNA were determined by qRT-PCR in LINC00973 knockdown or overexpressed Cal27 and HN6 cells with time-course Actinomycin D exposure. c Experimental design of AGO2-RIP was depicted by schematic diagram (left panel). Endogenous LINC00973 was assessed by qRT-PCR in cell lyses immunoprecipitated with either AGO2 antibody or mouse IgG (right panel). d , e The putative miRNA candidates with high EN2 mRNA binding affinity were computed by TargetScan webtool ( https://www.targetscan.org/vert_80/ ), while LINC00973 sponged miRNAs (top10) were predicted by DIANA tool kits ( http://diana.imis.athena-innovation.gr/DianaTools/index.php ). Six overlapped miRNA candidates were identified ( d ). Only miR-6756-3p expression were shown with significant upregulation followed by LINC00973 silencing in both Cal27 and HN6 cells ( e ). f The expression of miR-6756-3p in 50 HNSCC clinical samples and paired normal counterparts were determined by qRT-PCR. Paired Wilcoxon rank-sum test. g Kaplan-Meier analyses of OS and DSS stratified by median miR-6756-3p expression in 50 in-house samples Log-rank test. h , i Schematic diagram depicted the experimental design of MS2-RIP assays to detect the direct binding between LINC00973 and miR-6756-3p in HNSCC ( h ). The LINC00973-MS2-GFP complex was pulled down by anti-GFP antibody and the interacted miR-6756-3p were assessed by qRT-PCR in Cal27, HN6, and HEK293T cells ( i ). j The sequence alignment displayed the binding sequence between miR-6756-3p and LINC00973 [LINC00973 (WT)] or 3’UTR of EN2 [3’UTR EN2 (WT)]. The miR-6756-3p binding site mutated LINC00973 and EN2 transcripts [LINC00973 (MT) or 3’UTR EN2 (MT)] were showed below. k , l Cal27 and HN6 cells transfected with LINC00973/3’UTR EN2 wild type or miR-6756-3p binding site mutated pmirGLO luciferase reporter vectors and treated with miR-6756-3p or control mimics. The luciferase activated was measured. m The expression levels of EN2 were measured by qRT-PCR in Cal27 and HN6 treated with sh-LINC00973-1 lentivirus or in combination with miR-6756-3p inhibitor (inhibitor). n The correlations between EN2, LINC00973, and miR-6756-3p expression in HNSCC clinical samples were estimated by using Spearman’s correlation. o Schematic illustration of the regulatory model of LINC00973 decoys miR-6756-3p to stabilize EN2 mRNA. Data were presented as mean ± SD, # P ≥ 0.05, * P < 0.05, ** P < 0.01, Student’s t test.

    Techniques Used: Quantitative RT-PCR, Knockdown, Immunoprecipitation, Binding Assay, Expressing, Sequencing, Transfection, Luciferase, Control



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    ms2 gfp fusion protein  (Proteintech)
    96
    Proteintech ms2 gfp fusion protein
    a , b The half-life of EN2 mRNA were determined by qRT-PCR in LINC00973 knockdown or overexpressed Cal27 and HN6 cells with time-course Actinomycin D exposure. c Experimental design of AGO2-RIP was depicted by schematic diagram (left panel). Endogenous LINC00973 was assessed by qRT-PCR in cell lyses immunoprecipitated with either AGO2 antibody or mouse IgG (right panel). d , e The putative miRNA candidates with high EN2 mRNA binding affinity were computed by TargetScan webtool ( https://www.targetscan.org/vert_80/ ), while LINC00973 sponged miRNAs (top10) were predicted by DIANA tool kits ( http://diana.imis.athena-innovation.gr/DianaTools/index.php ). Six overlapped miRNA candidates were identified ( d ). Only miR-6756-3p expression were shown with significant upregulation followed by LINC00973 silencing in both Cal27 and HN6 cells ( e ). f The expression of miR-6756-3p in 50 HNSCC clinical samples and paired normal counterparts were determined by qRT-PCR. Paired Wilcoxon rank-sum test. g Kaplan-Meier analyses of OS and DSS stratified by median miR-6756-3p expression in 50 in-house samples Log-rank test. h , i Schematic diagram depicted the experimental design of MS2-RIP assays to detect the direct binding between LINC00973 and miR-6756-3p in HNSCC ( h ). The <t>LINC00973-MS2-GFP</t> complex was pulled down by anti-GFP antibody and the interacted miR-6756-3p were assessed by qRT-PCR in Cal27, HN6, and HEK293T cells ( i ). j The sequence alignment displayed the binding sequence between miR-6756-3p and LINC00973 [LINC00973 (WT)] or 3’UTR of EN2 [3’UTR EN2 (WT)]. The miR-6756-3p binding site mutated LINC00973 and EN2 transcripts [LINC00973 (MT) or 3’UTR EN2 (MT)] were showed below. k , l Cal27 and HN6 cells transfected with LINC00973/3’UTR EN2 wild type or miR-6756-3p binding site mutated pmirGLO luciferase reporter vectors and treated with miR-6756-3p or control mimics. The luciferase activated was measured. m The expression levels of EN2 were measured by qRT-PCR in Cal27 and HN6 treated with sh-LINC00973-1 lentivirus or in combination with miR-6756-3p inhibitor (inhibitor). n The correlations between EN2, LINC00973, and miR-6756-3p expression in HNSCC clinical samples were estimated by using Spearman’s correlation. o Schematic illustration of the regulatory model of LINC00973 decoys miR-6756-3p to stabilize EN2 mRNA. Data were presented as mean ± SD, # P ≥ 0.05, * P < 0.05, ** P < 0.01, Student’s t test.
    Ms2 Gfp Fusion Protein, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ms2+gfp+fusion+protein/pmc12848070-97-18-12?v=Proteintech
    Average 96 stars, based on 1 article reviews
    ms2 gfp fusion protein - by Bioz Stars, 2026-07
    96/100 stars
    		  Buy from Supplier

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    a , b The half-life of EN2 mRNA were determined by qRT-PCR in LINC00973 knockdown or overexpressed Cal27 and HN6 cells with time-course Actinomycin D exposure. c Experimental design of AGO2-RIP was depicted by schematic diagram (left panel). Endogenous LINC00973 was assessed by qRT-PCR in cell lyses immunoprecipitated with either AGO2 antibody or mouse IgG (right panel). d , e The putative miRNA candidates with high EN2 mRNA binding affinity were computed by TargetScan webtool ( https://www.targetscan.org/vert_80/ ), while LINC00973 sponged miRNAs (top10) were predicted by DIANA tool kits ( http://diana.imis.athena-innovation.gr/DianaTools/index.php ). Six overlapped miRNA candidates were identified ( d ). Only miR-6756-3p expression were shown with significant upregulation followed by LINC00973 silencing in both Cal27 and HN6 cells ( e ). f The expression of miR-6756-3p in 50 HNSCC clinical samples and paired normal counterparts were determined by qRT-PCR. Paired Wilcoxon rank-sum test. g Kaplan-Meier analyses of OS and DSS stratified by median miR-6756-3p expression in 50 in-house samples Log-rank test. h , i Schematic diagram depicted the experimental design of MS2-RIP assays to detect the direct binding between LINC00973 and miR-6756-3p in HNSCC ( h ). The LINC00973-MS2-GFP complex was pulled down by anti-GFP antibody and the interacted miR-6756-3p were assessed by qRT-PCR in Cal27, HN6, and HEK293T cells ( i ). j The sequence alignment displayed the binding sequence between miR-6756-3p and LINC00973 [LINC00973 (WT)] or 3’UTR of EN2 [3’UTR EN2 (WT)]. The miR-6756-3p binding site mutated LINC00973 and EN2 transcripts [LINC00973 (MT) or 3’UTR EN2 (MT)] were showed below. k , l Cal27 and HN6 cells transfected with LINC00973/3’UTR EN2 wild type or miR-6756-3p binding site mutated pmirGLO luciferase reporter vectors and treated with miR-6756-3p or control mimics. The luciferase activated was measured. m The expression levels of EN2 were measured by qRT-PCR in Cal27 and HN6 treated with sh-LINC00973-1 lentivirus or in combination with miR-6756-3p inhibitor (inhibitor). n The correlations between EN2, LINC00973, and miR-6756-3p expression in HNSCC clinical samples were estimated by using Spearman’s correlation. o Schematic illustration of the regulatory model of LINC00973 decoys miR-6756-3p to stabilize EN2 mRNA. Data were presented as mean ± SD, # P ≥ 0.05, * P < 0.05, ** P < 0.01, Student’s t test.

    Journal: Cell Death & Disease

    Article Title: A novel super-enhancer-driven lncRNA LINC00973 governs head and neck squamous cell carcinoma progression through EN2

    doi: 10.1038/s41419-025-08380-8

    Figure Lengend Snippet: a , b The half-life of EN2 mRNA were determined by qRT-PCR in LINC00973 knockdown or overexpressed Cal27 and HN6 cells with time-course Actinomycin D exposure. c Experimental design of AGO2-RIP was depicted by schematic diagram (left panel). Endogenous LINC00973 was assessed by qRT-PCR in cell lyses immunoprecipitated with either AGO2 antibody or mouse IgG (right panel). d , e The putative miRNA candidates with high EN2 mRNA binding affinity were computed by TargetScan webtool ( https://www.targetscan.org/vert_80/ ), while LINC00973 sponged miRNAs (top10) were predicted by DIANA tool kits ( http://diana.imis.athena-innovation.gr/DianaTools/index.php ). Six overlapped miRNA candidates were identified ( d ). Only miR-6756-3p expression were shown with significant upregulation followed by LINC00973 silencing in both Cal27 and HN6 cells ( e ). f The expression of miR-6756-3p in 50 HNSCC clinical samples and paired normal counterparts were determined by qRT-PCR. Paired Wilcoxon rank-sum test. g Kaplan-Meier analyses of OS and DSS stratified by median miR-6756-3p expression in 50 in-house samples Log-rank test. h , i Schematic diagram depicted the experimental design of MS2-RIP assays to detect the direct binding between LINC00973 and miR-6756-3p in HNSCC ( h ). The LINC00973-MS2-GFP complex was pulled down by anti-GFP antibody and the interacted miR-6756-3p were assessed by qRT-PCR in Cal27, HN6, and HEK293T cells ( i ). j The sequence alignment displayed the binding sequence between miR-6756-3p and LINC00973 [LINC00973 (WT)] or 3’UTR of EN2 [3’UTR EN2 (WT)]. The miR-6756-3p binding site mutated LINC00973 and EN2 transcripts [LINC00973 (MT) or 3’UTR EN2 (MT)] were showed below. k , l Cal27 and HN6 cells transfected with LINC00973/3’UTR EN2 wild type or miR-6756-3p binding site mutated pmirGLO luciferase reporter vectors and treated with miR-6756-3p or control mimics. The luciferase activated was measured. m The expression levels of EN2 were measured by qRT-PCR in Cal27 and HN6 treated with sh-LINC00973-1 lentivirus or in combination with miR-6756-3p inhibitor (inhibitor). n The correlations between EN2, LINC00973, and miR-6756-3p expression in HNSCC clinical samples were estimated by using Spearman’s correlation. o Schematic illustration of the regulatory model of LINC00973 decoys miR-6756-3p to stabilize EN2 mRNA. Data were presented as mean ± SD, # P ≥ 0.05, * P < 0.05, ** P < 0.01, Student’s t test.

    Article Snippet: Immunoprecipitation was performed using an anti-GFP antibody (0.5 μg per sample, 50430-2-AP, Proteintech, China) to pull down the MS2-GFP fusion protein together with interacted LINC00973-MS2-12× transcripts and miRNAs.

    Techniques: Quantitative RT-PCR, Knockdown, Immunoprecipitation, Binding Assay, Expressing, Sequencing, Transfection, Luciferase, Control