superscriptiii reverse transcriptase Thermo Fisher Search Results


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  • 99
    Thermo Fisher superscriptii rnase h reverse transcriptase
    Superscriptii Rnase H Reverse Transcriptase, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 228 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/superscriptii rnase h reverse transcriptase/product/Thermo Fisher
    Average 99 stars, based on 228 article reviews
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    92
    Thermo Fisher superscriptii reverse transcriptase
    40S ribosomal subunits bind to the 5′ UTR of TCV and scan to initiate translation. (A) TCV 5′ sequence showing the location of the 5′ TE (bracket) and mutations used for this analysis. Single filled circles denote reverse transcriptase-mediated stop sites in the presence of bound 40S subunits, with the double circles at U71 denoting the stop site found in the presence of both 40S subunits and 80S ribosomes. Open circles are new stop sites found using template containing the m0 mutations. (B) 40S ribosomal subunits bind to the 5′ UTR of TCV. Salt-washed 40S ribosomal subunits were added to radiolabeled wt and mutant 5′ UTR RNA fragments and binding affinity determined using filter binding assays. Standard deviations from three experiments are shown. (C) Toeprints with purified ribosomes and 40S ribosomal subunits. Salt-washed 80S ribosomes and 40S ribosomal subunits were mixed with RNA containing the 5′ 120 nt of TCV gRNA, and toeprints were determined by reverse transcription with <t>SuperScriptIII.</t> U and A, sequencing ladders; 0, no added ribosomes. Arrowheads denote locations of new polymerase stop sites in the presence of 40S subunits or 80S ribosomes. (D) Out-of-frame initiation codons upstream or downstream of the 5′ TE downregulate translation in vivo . Single-luciferase constructs containing the TCV 5′ UTR and 3′ UTR+ and mutations shown below the sequence in panel A were assayed for translation in protoplasts. Standard deviations in three independent experiments are shown.
    Superscriptii Reverse Transcriptase, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 26187 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/superscriptii reverse transcriptase/product/Thermo Fisher
    Average 92 stars, based on 26187 article reviews
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    85
    Thermo Fisher superscriptiii transcriptase
    40S ribosomal subunits bind to the 5′ UTR of TCV and scan to initiate translation. (A) TCV 5′ sequence showing the location of the 5′ TE (bracket) and mutations used for this analysis. Single filled circles denote reverse transcriptase-mediated stop sites in the presence of bound 40S subunits, with the double circles at U71 denoting the stop site found in the presence of both 40S subunits and 80S ribosomes. Open circles are new stop sites found using template containing the m0 mutations. (B) 40S ribosomal subunits bind to the 5′ UTR of TCV. Salt-washed 40S ribosomal subunits were added to radiolabeled wt and mutant 5′ UTR RNA fragments and binding affinity determined using filter binding assays. Standard deviations from three experiments are shown. (C) Toeprints with purified ribosomes and 40S ribosomal subunits. Salt-washed 80S ribosomes and 40S ribosomal subunits were mixed with RNA containing the 5′ 120 nt of TCV gRNA, and toeprints were determined by reverse transcription with <t>SuperScriptIII.</t> U and A, sequencing ladders; 0, no added ribosomes. Arrowheads denote locations of new polymerase stop sites in the presence of 40S subunits or 80S ribosomes. (D) Out-of-frame initiation codons upstream or downstream of the 5′ TE downregulate translation in vivo . Single-luciferase constructs containing the TCV 5′ UTR and 3′ UTR+ and mutations shown below the sequence in panel A were assayed for translation in protoplasts. Standard deviations in three independent experiments are shown.
    Superscriptiii Transcriptase, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 49 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher transcriptase rt buffer
    40S ribosomal subunits bind to the 5′ UTR of TCV and scan to initiate translation. (A) TCV 5′ sequence showing the location of the 5′ TE (bracket) and mutations used for this analysis. Single filled circles denote reverse transcriptase-mediated stop sites in the presence of bound 40S subunits, with the double circles at U71 denoting the stop site found in the presence of both 40S subunits and 80S ribosomes. Open circles are new stop sites found using template containing the m0 mutations. (B) 40S ribosomal subunits bind to the 5′ UTR of TCV. Salt-washed 40S ribosomal subunits were added to radiolabeled wt and mutant 5′ UTR RNA fragments and binding affinity determined using filter binding assays. Standard deviations from three experiments are shown. (C) Toeprints with purified ribosomes and 40S ribosomal subunits. Salt-washed 80S ribosomes and 40S ribosomal subunits were mixed with RNA containing the 5′ 120 nt of TCV gRNA, and toeprints were determined by reverse transcription with <t>SuperScriptIII.</t> U and A, sequencing ladders; 0, no added ribosomes. Arrowheads denote locations of new polymerase stop sites in the presence of 40S subunits or 80S ribosomes. (D) Out-of-frame initiation codons upstream or downstream of the 5′ TE downregulate translation in vivo . Single-luciferase constructs containing the TCV 5′ UTR and 3′ UTR+ and mutations shown below the sequence in panel A were assayed for translation in protoplasts. Standard deviations in three independent experiments are shown.
    Transcriptase Rt Buffer, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 68 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Thermo Fisher transcriptase superscriptii
    40S ribosomal subunits bind to the 5′ UTR of TCV and scan to initiate translation. (A) TCV 5′ sequence showing the location of the 5′ TE (bracket) and mutations used for this analysis. Single filled circles denote reverse transcriptase-mediated stop sites in the presence of bound 40S subunits, with the double circles at U71 denoting the stop site found in the presence of both 40S subunits and 80S ribosomes. Open circles are new stop sites found using template containing the m0 mutations. (B) 40S ribosomal subunits bind to the 5′ UTR of TCV. Salt-washed 40S ribosomal subunits were added to radiolabeled wt and mutant 5′ UTR RNA fragments and binding affinity determined using filter binding assays. Standard deviations from three experiments are shown. (C) Toeprints with purified ribosomes and 40S ribosomal subunits. Salt-washed 80S ribosomes and 40S ribosomal subunits were mixed with RNA containing the 5′ 120 nt of TCV gRNA, and toeprints were determined by reverse transcription with <t>SuperScriptIII.</t> U and A, sequencing ladders; 0, no added ribosomes. Arrowheads denote locations of new polymerase stop sites in the presence of 40S subunits or 80S ribosomes. (D) Out-of-frame initiation codons upstream or downstream of the 5′ TE downregulate translation in vivo . Single-luciferase constructs containing the TCV 5′ UTR and 3′ UTR+ and mutations shown below the sequence in panel A were assayed for translation in protoplasts. Standard deviations in three independent experiments are shown.
    Transcriptase Superscriptii, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/transcriptase superscriptii/product/Thermo Fisher
    Average 92 stars, based on 22 article reviews
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    Image Search Results


    40S ribosomal subunits bind to the 5′ UTR of TCV and scan to initiate translation. (A) TCV 5′ sequence showing the location of the 5′ TE (bracket) and mutations used for this analysis. Single filled circles denote reverse transcriptase-mediated stop sites in the presence of bound 40S subunits, with the double circles at U71 denoting the stop site found in the presence of both 40S subunits and 80S ribosomes. Open circles are new stop sites found using template containing the m0 mutations. (B) 40S ribosomal subunits bind to the 5′ UTR of TCV. Salt-washed 40S ribosomal subunits were added to radiolabeled wt and mutant 5′ UTR RNA fragments and binding affinity determined using filter binding assays. Standard deviations from three experiments are shown. (C) Toeprints with purified ribosomes and 40S ribosomal subunits. Salt-washed 80S ribosomes and 40S ribosomal subunits were mixed with RNA containing the 5′ 120 nt of TCV gRNA, and toeprints were determined by reverse transcription with SuperScriptIII. U and A, sequencing ladders; 0, no added ribosomes. Arrowheads denote locations of new polymerase stop sites in the presence of 40S subunits or 80S ribosomes. (D) Out-of-frame initiation codons upstream or downstream of the 5′ TE downregulate translation in vivo . Single-luciferase constructs containing the TCV 5′ UTR and 3′ UTR+ and mutations shown below the sequence in panel A were assayed for translation in protoplasts. Standard deviations in three independent experiments are shown.

    Journal: Journal of Virology

    Article Title: Ribosome Binding to a 5? Translational Enhancer Is Altered in the Presence of the 3? Untranslated Region in Cap-Independent Translation of Turnip Crinkle Virus ▿

    doi: 10.1128/JVI.00005-11

    Figure Lengend Snippet: 40S ribosomal subunits bind to the 5′ UTR of TCV and scan to initiate translation. (A) TCV 5′ sequence showing the location of the 5′ TE (bracket) and mutations used for this analysis. Single filled circles denote reverse transcriptase-mediated stop sites in the presence of bound 40S subunits, with the double circles at U71 denoting the stop site found in the presence of both 40S subunits and 80S ribosomes. Open circles are new stop sites found using template containing the m0 mutations. (B) 40S ribosomal subunits bind to the 5′ UTR of TCV. Salt-washed 40S ribosomal subunits were added to radiolabeled wt and mutant 5′ UTR RNA fragments and binding affinity determined using filter binding assays. Standard deviations from three experiments are shown. (C) Toeprints with purified ribosomes and 40S ribosomal subunits. Salt-washed 80S ribosomes and 40S ribosomal subunits were mixed with RNA containing the 5′ 120 nt of TCV gRNA, and toeprints were determined by reverse transcription with SuperScriptIII. U and A, sequencing ladders; 0, no added ribosomes. Arrowheads denote locations of new polymerase stop sites in the presence of 40S subunits or 80S ribosomes. (D) Out-of-frame initiation codons upstream or downstream of the 5′ TE downregulate translation in vivo . Single-luciferase constructs containing the TCV 5′ UTR and 3′ UTR+ and mutations shown below the sequence in panel A were assayed for translation in protoplasts. Standard deviations in three independent experiments are shown.

    Article Snippet: Reaction mixtures were incubated at 30°C for 30 min. To detect toeprints, primer extension with SuperScriptIII reverse transcriptase (Invitrogen) was performed as follows.

    Techniques: Sequencing, Mutagenesis, Binding Assay, Purification, In Vivo, Luciferase, Construct

    Multiple Chromatin Modifier Combinations Affect Resistance at a Single-Gene Level (A) Venn diagram shows the number of genes losing resistance upon four individual chromatin modifier treatments. (B) Example of digital signature of resistance obtained by differential gene expression analysis for a non-resistant ( G3pdh ) and three resistant ( Trap1A , Otx2 , and Sox2 ) genes. The digital signature indicates whether a gene is resistant (shown as 1 when the gene is differentially expressed in MEF-NT compared to ES-NT) or loses resistance (shown as 0, when the gene is not differentially expressed in MEF-NT compared to ES-NT) in each of the 12 conditions tested. The bar graphs show qRT-PCR analysis of gene expression (mean ± SEM of four samples of eight oocytes NT). (C) The numbers of genes for which a synergistic, neutral, adverse, or insensitive effect is observed when combining two chromatin modifier treatments are shown. (D) Venn diagram shows the number of genes sensitive to a histone modifier (Kdm4d, Kdm6b, or USP21) in nuclei with normal (WT) or hypomethylated DNA (Dnmt1N). (E) Loss of resistant gene sensitivity to Kdm6b in DNA-hypomethylated MEF correlates with loss of H3K27me3. The y axis indicates the number of genes that lose H3K27me3 in MEF with hypomethylated DNA compared to WT MEF. Resistant genes are split according to change in sensitivity to Kdm6b after NT when comparing WT MEF to MEF with hypomethylated DNA (red dot). The boxplot shows the background distribution of H3K27me3 change when sampling 10,000 times for a random set of genes of the same size as the resistant gene subset tested. The number in parentheses indicates a p value generated by calculating the proportion of the random background that has a more extreme value than the observed percentages from each of the three groups. (F) Heatmap illustrating the change in gene expression in normal (WT MEF nuclei) or hypomethylated DNA (Dnmt1N MEF nuclei) upon expression of histone modifiers. Ten clusters representing the main trend of gene expression change were selected based on k-means clustering of expression data from RNA-seq analysis (RPKM). The trend of change in gene expression in these ten clusters is shown in the heatmap as a Z score. See also Table S4 .

    Journal: Molecular Cell

    Article Title: Gene Resistance to Transcriptional Reprogramming following Nuclear Transfer Is Directly Mediated by Multiple Chromatin-Repressive Pathways

    doi: 10.1016/j.molcel.2017.01.030

    Figure Lengend Snippet: Multiple Chromatin Modifier Combinations Affect Resistance at a Single-Gene Level (A) Venn diagram shows the number of genes losing resistance upon four individual chromatin modifier treatments. (B) Example of digital signature of resistance obtained by differential gene expression analysis for a non-resistant ( G3pdh ) and three resistant ( Trap1A , Otx2 , and Sox2 ) genes. The digital signature indicates whether a gene is resistant (shown as 1 when the gene is differentially expressed in MEF-NT compared to ES-NT) or loses resistance (shown as 0, when the gene is not differentially expressed in MEF-NT compared to ES-NT) in each of the 12 conditions tested. The bar graphs show qRT-PCR analysis of gene expression (mean ± SEM of four samples of eight oocytes NT). (C) The numbers of genes for which a synergistic, neutral, adverse, or insensitive effect is observed when combining two chromatin modifier treatments are shown. (D) Venn diagram shows the number of genes sensitive to a histone modifier (Kdm4d, Kdm6b, or USP21) in nuclei with normal (WT) or hypomethylated DNA (Dnmt1N). (E) Loss of resistant gene sensitivity to Kdm6b in DNA-hypomethylated MEF correlates with loss of H3K27me3. The y axis indicates the number of genes that lose H3K27me3 in MEF with hypomethylated DNA compared to WT MEF. Resistant genes are split according to change in sensitivity to Kdm6b after NT when comparing WT MEF to MEF with hypomethylated DNA (red dot). The boxplot shows the background distribution of H3K27me3 change when sampling 10,000 times for a random set of genes of the same size as the resistant gene subset tested. The number in parentheses indicates a p value generated by calculating the proportion of the random background that has a more extreme value than the observed percentages from each of the three groups. (F) Heatmap illustrating the change in gene expression in normal (WT MEF nuclei) or hypomethylated DNA (Dnmt1N MEF nuclei) upon expression of histone modifiers. Ten clusters representing the main trend of gene expression change were selected based on k-means clustering of expression data from RNA-seq analysis (RPKM). The trend of change in gene expression in these ten clusters is shown in the heatmap as a Z score. See also Table S4 .

    Article Snippet: RT-qPCR Annealing of oligodT primers to the RNAs is performed by incubating at 65°C for 5min 12 μL of RNA mixed with 0.5 μL of 100 μM oligodT(15) and 0.5 μL of 10mM dNTPs followed by an incubation 5min on ice. cDNAs synthesis was performed by adding 4 μL of 5X second strand buffer, 1 μL 0.1M dTT, 1 μL H2 O, 0.5 μL RNase inhibitor, and 0.5 μL superscriptIII reverse transcriptase (InVitrogen, 18080093) to the RNA solution and incubating at 50°C for one hour.

    Techniques: Expressing, Quantitative RT-PCR, Sampling, Generated, RNA Sequencing Assay

    qRT-PCR validation of microarray results for a selected number of genes. cDNA was generated from total RNA independently prepared from small intestine epithelial cells isolated from three 3 month old Muc2 −/− mice and 3 age, and gender

    Journal: Cancer research

    Article Title: Interaction of Muc2 and Apc on Wnt signaling and in intestinal tumorigenesis: potential role of chronic inflammation

    doi: 10.1158/0008-5472.CAN-08-0598

    Figure Lengend Snippet: qRT-PCR validation of microarray results for a selected number of genes. cDNA was generated from total RNA independently prepared from small intestine epithelial cells isolated from three 3 month old Muc2 −/− mice and 3 age, and gender

    Article Snippet: RNA was reverse transcribed into cDNA (SuperScriptIII reverse transcriptase, Invitrogen).

    Techniques: Quantitative RT-PCR, Microarray, Generated, Isolation, Mouse Assay