dnase  (Qiagen)


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    Name:
    RNase Free DNase Set
    Description:
    For DNase digestion during RNA purification Kit contents Qiagen RNase free DNase Set 50 preps For DNase Digestion During RNA Purification Silica gel Membrane Spin column Technology Efficiently Removes the Majority of the DNA Without DNase Treatment The Buffer is Also Well suited for Efficient DNase Digestion in Solution Includes 1500U RNase free DNase I RNase free Buffer RDD and RNase free Water
    Catalog Number:
    79254
    Price:
    108
    Category:
    RNase Free DNase Set
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    Structured Review

    Qiagen dnase
    RNase Free DNase Set
    For DNase digestion during RNA purification Kit contents Qiagen RNase free DNase Set 50 preps For DNase Digestion During RNA Purification Silica gel Membrane Spin column Technology Efficiently Removes the Majority of the DNA Without DNase Treatment The Buffer is Also Well suited for Efficient DNase Digestion in Solution Includes 1500U RNase free DNase I RNase free Buffer RDD and RNase free Water
    https://www.bioz.com/result/dnase/product/Qiagen
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    dnase - by Bioz Stars, 2021-03
    97/100 stars

    Images

    1) Product Images from "Transformation of accessible chromatin and 3D nucleome underlies lineage commitment of early T cells"

    Article Title: Transformation of accessible chromatin and 3D nucleome underlies lineage commitment of early T cells

    Journal: Immunity

    doi: 10.1016/j.immuni.2018.01.013

    BCL11B binding is associated with an increase in chromatin interaction (A) Expression of Bcl11b from HSPC to DP from RNA-Seq analysis. (B) UCSC genome browser image showing the distribution of ChIP-Seq read density across the genomic region enclosing the Id2 locus (in red) for BCL11B binding, an active histone modification H3K27ac (two independent experiments), and a repressive histone modification H3K27me3, all in DP cells. Top track: distribution of DNase-Seq read density; Yellow and pink rectangles: BCL11B binding sites enriched with H3K27ac and H3K27me3, respectively; K.Z.: a representative BCL11B Chip-Seq data from Dr. Zhao’s lab, NHLBI (two independent experiments); E.V.R.: a representative BCL11B ChIP-Seq data from Prof. Rothenberg’s lab, Cal Tech (two independent experiments). (C) Gene Ontology enrichment analysis for genes with promoters bound by BCL11B and marked by repressive histone modification H3K27me3 in DP cells. (D) Observed versus expected number of genes, sorted based on the status of BCL11B binding and H3K27me3 marker at promoters and expression change by Bcl11b deletion in DP cells. Blue and red arrow heads: gene set repressed and activated by BCL11B, respectively. (E) Empirical cumulative distribution of the fold change of the number of TAD PETs from DN2 to DP cells for TADs sorted into four equal size groups based on the BCL11B coverage, defined by the percentage of genomic region bound by BCL11B in DP cells. P -value by K.-S. test. (F) WashU genome browser showing the distribution of BCL11B ChIP-Seq reads in DPs and the distribution of intra-TAD PETs in DN2 and DP cells for a 360K bps genomic region in chromosome 11. Red rectangle: TAD enriched with BCL11B binding and showing an increase in intra-TAD PETs; Green lines: TAD boundaries.
    Figure Legend Snippet: BCL11B binding is associated with an increase in chromatin interaction (A) Expression of Bcl11b from HSPC to DP from RNA-Seq analysis. (B) UCSC genome browser image showing the distribution of ChIP-Seq read density across the genomic region enclosing the Id2 locus (in red) for BCL11B binding, an active histone modification H3K27ac (two independent experiments), and a repressive histone modification H3K27me3, all in DP cells. Top track: distribution of DNase-Seq read density; Yellow and pink rectangles: BCL11B binding sites enriched with H3K27ac and H3K27me3, respectively; K.Z.: a representative BCL11B Chip-Seq data from Dr. Zhao’s lab, NHLBI (two independent experiments); E.V.R.: a representative BCL11B ChIP-Seq data from Prof. Rothenberg’s lab, Cal Tech (two independent experiments). (C) Gene Ontology enrichment analysis for genes with promoters bound by BCL11B and marked by repressive histone modification H3K27me3 in DP cells. (D) Observed versus expected number of genes, sorted based on the status of BCL11B binding and H3K27me3 marker at promoters and expression change by Bcl11b deletion in DP cells. Blue and red arrow heads: gene set repressed and activated by BCL11B, respectively. (E) Empirical cumulative distribution of the fold change of the number of TAD PETs from DN2 to DP cells for TADs sorted into four equal size groups based on the BCL11B coverage, defined by the percentage of genomic region bound by BCL11B in DP cells. P -value by K.-S. test. (F) WashU genome browser showing the distribution of BCL11B ChIP-Seq reads in DPs and the distribution of intra-TAD PETs in DN2 and DP cells for a 360K bps genomic region in chromosome 11. Red rectangle: TAD enriched with BCL11B binding and showing an increase in intra-TAD PETs; Green lines: TAD boundaries.

    Techniques Used: Binding Assay, Expressing, RNA Sequencing Assay, Chromatin Immunoprecipitation, Modification, Marker

    Related Articles

    Real-time Polymerase Chain Reaction:

    Article Title: Cadherin-23 Mediates Heterotypic Cell-Cell Adhesion between Breast Cancer Epithelial Cells and Fibroblasts
    Article Snippet: RT-PCR, immunoblotting and adhesion assays were performed as described above. .. qPCR Confluent monocultures of MCF-7s and NBFs were trypsinized and ∼20×104 cells were used for mRNA isolation (RNEasy with RNAse-Free DNase set, Qiagen). qPCR was performed using the QuantiFast SYBR Green RT-PCR kit (Qiagen) on a LightCycler 480 (Roche, Indianapolis, IN). ..

    Isolation:

    Article Title: Cadherin-23 Mediates Heterotypic Cell-Cell Adhesion between Breast Cancer Epithelial Cells and Fibroblasts
    Article Snippet: RT-PCR, immunoblotting and adhesion assays were performed as described above. .. qPCR Confluent monocultures of MCF-7s and NBFs were trypsinized and ∼20×104 cells were used for mRNA isolation (RNEasy with RNAse-Free DNase set, Qiagen). qPCR was performed using the QuantiFast SYBR Green RT-PCR kit (Qiagen) on a LightCycler 480 (Roche, Indianapolis, IN). ..

    SYBR Green Assay:

    Article Title: Cadherin-23 Mediates Heterotypic Cell-Cell Adhesion between Breast Cancer Epithelial Cells and Fibroblasts
    Article Snippet: RT-PCR, immunoblotting and adhesion assays were performed as described above. .. qPCR Confluent monocultures of MCF-7s and NBFs were trypsinized and ∼20×104 cells were used for mRNA isolation (RNEasy with RNAse-Free DNase set, Qiagen). qPCR was performed using the QuantiFast SYBR Green RT-PCR kit (Qiagen) on a LightCycler 480 (Roche, Indianapolis, IN). ..

    Reverse Transcription Polymerase Chain Reaction:

    Article Title: Cadherin-23 Mediates Heterotypic Cell-Cell Adhesion between Breast Cancer Epithelial Cells and Fibroblasts
    Article Snippet: RT-PCR, immunoblotting and adhesion assays were performed as described above. .. qPCR Confluent monocultures of MCF-7s and NBFs were trypsinized and ∼20×104 cells were used for mRNA isolation (RNEasy with RNAse-Free DNase set, Qiagen). qPCR was performed using the QuantiFast SYBR Green RT-PCR kit (Qiagen) on a LightCycler 480 (Roche, Indianapolis, IN). ..

    Purification:

    Article Title: Enhanced methods for unbiased deep sequencing of Lassa and Ebola RNA viruses from clinical and biological samples
    Article Snippet: .. The complementary DNA probes were removed by bringing the reaction up to 75 μL and treating with RNase-free DNase kit (Qiagen) according to the manufacturer’s protocol. rRNA-depleted samples were purified using 2.2× volumes AMPure RNA clean beads (Beckman Coulter Genomics) and eluted into 10 μL water for cDNA synthesis. .. Illumina library construction and sequencing For the experiments in this study, selectively-depleted EBOV and LASV RNA were fragmented for 4 minutes at 85° C using NEBNext Fragmentation buffer (New England Biolabs).

    Article Title: Dual-functional peptide with defective interfering genes effectively protects mice against avian and seasonal influenza
    Article Snippet: Viral RNA was extracted by Viral RNA Mini Kit (QIAGEN, Cat# 52906, USA) according to the manufacturer’s instructions. .. Extracted RNA were treated with DNase I (QIAGEN, Cat# 79254, USA) according to the manufacturer’s protocol and purified by RNeasy Mini Kit (QIAGEN, Cat# 74106, USA) to exclude plasmid DNA contamination. .. Real-time RT-qPCR was performed as we described previously .

    Chloramphenicol Acetyltransferase Assay:

    Article Title: Transformation of accessible chromatin and 3D nucleome underlies lineage commitment of early T cells
    Article Snippet: Three thousand cells were sorted into 700μl of QIAzol Lysis Reagent (miRNAeasy Micro Kit (QIAGEN, Cat#217084). .. Total RNA was extracted and on-column digestion with DNase (QIAGEN, Cat79254) was performed, followed by elution with 10μl of RNase-free water. .. Total RNA from 1K cells was reverse transcribed by SuperScript II (Invitrogen, Cat#18064-014) with oligo-dT and LNA-containing TSO primers in a final reaction volume of 10μl using the condition: 42°C for 90min, 10 cycles of 50°C 2min to 42°C 2min, 70°C for 15min and hold at 4°C. cDNA was pre-amplified by PCR using KAPA HiFi HotStart ReadyMix (KAPABIOSYSTEMS Cat#KK2602) with IS PCR for 12 cycles in 25μl.

    Plasmid Preparation:

    Article Title: Dual-functional peptide with defective interfering genes effectively protects mice against avian and seasonal influenza
    Article Snippet: Viral RNA was extracted by Viral RNA Mini Kit (QIAGEN, Cat# 52906, USA) according to the manufacturer’s instructions. .. Extracted RNA were treated with DNase I (QIAGEN, Cat# 79254, USA) according to the manufacturer’s protocol and purified by RNeasy Mini Kit (QIAGEN, Cat# 74106, USA) to exclude plasmid DNA contamination. .. Real-time RT-qPCR was performed as we described previously .

    Polyacrylamide Gel Electrophoresis:

    Article Title: Optimization of a Method for the Simultaneous Extraction of Polar and Non-Polar Oxylipin Metabolites, DNA, RNA, Small RNA, and Protein from a Single Small Tissue Sample
    Article Snippet: .. The following steps were taken from the manual of the AllPrep DNA/RNA/Protein Mini Kit (step 4 on page 31 to step 24, as well as Appendix E1–E4 on page 52; December 2014 version), RNeasy MinElute Cleanup Kit (Supplementary protocol RY38; November 2008 version), as well as RNase-Free DNase Set (June 2018 version). ..

    Incubation:

    Article Title: In Vivo Occupancy of Mitochondrial Single-Stranded DNA Binding Protein Supports the Strand Displacement Mode of DNA Replication
    Article Snippet: In vitro priming on ssDNA oligonucleotides The reaction mixture contained 100 fmol ssDNA oligonucleotide, 10 mM Tris-HCl [pH 8.0], 25 mM MgCl2 , 1 mM DTT, 100 µg/ml BSA, 400 µM ATP, 150 µM CTP, 10 µM GTP, 150 µM UTP, (α-32P) 2 µci GTP, 4 units RNase inhibitor (Amersham Biosciences), 500 fmol of POLRMT and 1 pmol of mtSSB (if added). .. After 30 min incubation at 32 °C, 12 units of RNase free DNase I (Qiagen) was added. .. Reactions were processed as previously described for in vitro transcription reactions and analyzed on a 25% polyacrylamide gel containing 3 M urea in 1× TBE.

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    Qiagen dnase
    BCL11B binding is associated with an increase in chromatin interaction (A) Expression of Bcl11b from HSPC to DP from <t>RNA-Seq</t> analysis. (B) UCSC genome browser image showing the distribution of ChIP-Seq read density across the genomic region enclosing the Id2 locus (in red) for BCL11B binding, an active histone modification H3K27ac (two independent experiments), and a repressive histone modification H3K27me3, all in DP cells. Top track: distribution of <t>DNase-Seq</t> read density; Yellow and pink rectangles: BCL11B binding sites enriched with H3K27ac and H3K27me3, respectively; K.Z.: a representative BCL11B Chip-Seq data from Dr. Zhao’s lab, NHLBI (two independent experiments); E.V.R.: a representative BCL11B ChIP-Seq data from Prof. Rothenberg’s lab, Cal Tech (two independent experiments). (C) Gene Ontology enrichment analysis for genes with promoters bound by BCL11B and marked by repressive histone modification H3K27me3 in DP cells. (D) Observed versus expected number of genes, sorted based on the status of BCL11B binding and H3K27me3 marker at promoters and expression change by Bcl11b deletion in DP cells. Blue and red arrow heads: gene set repressed and activated by BCL11B, respectively. (E) Empirical cumulative distribution of the fold change of the number of TAD PETs from DN2 to DP cells for TADs sorted into four equal size groups based on the BCL11B coverage, defined by the percentage of genomic region bound by BCL11B in DP cells. P -value by K.-S. test. (F) WashU genome browser showing the distribution of BCL11B ChIP-Seq reads in DPs and the distribution of intra-TAD PETs in DN2 and DP cells for a 360K bps genomic region in chromosome 11. Red rectangle: TAD enriched with BCL11B binding and showing an increase in intra-TAD PETs; Green lines: TAD boundaries.
    Dnase, supplied by Qiagen, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dnase/product/Qiagen
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    dnase - by Bioz Stars, 2021-03
    97/100 stars
      Buy from Supplier

    Image Search Results


    BCL11B binding is associated with an increase in chromatin interaction (A) Expression of Bcl11b from HSPC to DP from RNA-Seq analysis. (B) UCSC genome browser image showing the distribution of ChIP-Seq read density across the genomic region enclosing the Id2 locus (in red) for BCL11B binding, an active histone modification H3K27ac (two independent experiments), and a repressive histone modification H3K27me3, all in DP cells. Top track: distribution of DNase-Seq read density; Yellow and pink rectangles: BCL11B binding sites enriched with H3K27ac and H3K27me3, respectively; K.Z.: a representative BCL11B Chip-Seq data from Dr. Zhao’s lab, NHLBI (two independent experiments); E.V.R.: a representative BCL11B ChIP-Seq data from Prof. Rothenberg’s lab, Cal Tech (two independent experiments). (C) Gene Ontology enrichment analysis for genes with promoters bound by BCL11B and marked by repressive histone modification H3K27me3 in DP cells. (D) Observed versus expected number of genes, sorted based on the status of BCL11B binding and H3K27me3 marker at promoters and expression change by Bcl11b deletion in DP cells. Blue and red arrow heads: gene set repressed and activated by BCL11B, respectively. (E) Empirical cumulative distribution of the fold change of the number of TAD PETs from DN2 to DP cells for TADs sorted into four equal size groups based on the BCL11B coverage, defined by the percentage of genomic region bound by BCL11B in DP cells. P -value by K.-S. test. (F) WashU genome browser showing the distribution of BCL11B ChIP-Seq reads in DPs and the distribution of intra-TAD PETs in DN2 and DP cells for a 360K bps genomic region in chromosome 11. Red rectangle: TAD enriched with BCL11B binding and showing an increase in intra-TAD PETs; Green lines: TAD boundaries.

    Journal: Immunity

    Article Title: Transformation of accessible chromatin and 3D nucleome underlies lineage commitment of early T cells

    doi: 10.1016/j.immuni.2018.01.013

    Figure Lengend Snippet: BCL11B binding is associated with an increase in chromatin interaction (A) Expression of Bcl11b from HSPC to DP from RNA-Seq analysis. (B) UCSC genome browser image showing the distribution of ChIP-Seq read density across the genomic region enclosing the Id2 locus (in red) for BCL11B binding, an active histone modification H3K27ac (two independent experiments), and a repressive histone modification H3K27me3, all in DP cells. Top track: distribution of DNase-Seq read density; Yellow and pink rectangles: BCL11B binding sites enriched with H3K27ac and H3K27me3, respectively; K.Z.: a representative BCL11B Chip-Seq data from Dr. Zhao’s lab, NHLBI (two independent experiments); E.V.R.: a representative BCL11B ChIP-Seq data from Prof. Rothenberg’s lab, Cal Tech (two independent experiments). (C) Gene Ontology enrichment analysis for genes with promoters bound by BCL11B and marked by repressive histone modification H3K27me3 in DP cells. (D) Observed versus expected number of genes, sorted based on the status of BCL11B binding and H3K27me3 marker at promoters and expression change by Bcl11b deletion in DP cells. Blue and red arrow heads: gene set repressed and activated by BCL11B, respectively. (E) Empirical cumulative distribution of the fold change of the number of TAD PETs from DN2 to DP cells for TADs sorted into four equal size groups based on the BCL11B coverage, defined by the percentage of genomic region bound by BCL11B in DP cells. P -value by K.-S. test. (F) WashU genome browser showing the distribution of BCL11B ChIP-Seq reads in DPs and the distribution of intra-TAD PETs in DN2 and DP cells for a 360K bps genomic region in chromosome 11. Red rectangle: TAD enriched with BCL11B binding and showing an increase in intra-TAD PETs; Green lines: TAD boundaries.

    Article Snippet: Total RNA was extracted and on-column digestion with DNase (QIAGEN, Cat#79254) was performed, followed by elution with 10μl of RNase-free water.

    Techniques: Binding Assay, Expressing, RNA Sequencing Assay, Chromatin Immunoprecipitation, Modification, Marker

    Suggested DNA/RNA co-extraction workflow for environmental samples, with stronger emphasis on thorough purification prior to all enzymatic steps (including DNase digestion). Optional steps are indicated by dotted arrows. Note that RNase digestion (between Extracts II and III) may be necessary for better results downstream, but may be omitted as a separate step (in the current study, RNase is present in the qPCR mix). (A) Pre-lysis inhibitor removal is only advisable if quick methods are used, or if mRNA is not the target molecule (lengthy inhibitor removal procedures compromise RNA integrity). (B) Various methods may be used, such as phenol/chloroform procedures or nucleic acid precipitation. (C) This purification step should target the removal of enzymatic-inhibitors (e.g., humic/fulvic acids and polyphenolics). (D) Purification of partially digested RNA extracts with residual genomic DNA aids in the removal of enduring inhibitors, prior to further digestion. (E) Stringent and well-documented quality control via rigorous and sensitive detection (preferably quantitative methods) is necessary to detect residual amplifiable gDNA prior to reverse transcription.

    Journal: Frontiers in Microbiology

    Article Title: Transparent DNA/RNA Co-extraction Workflow Protocol Suitable for Inhibitor-Rich Environmental Samples That Focuses on Complete DNA Removal for Transcriptomic Analyses

    doi: 10.3389/fmicb.2016.01588

    Figure Lengend Snippet: Suggested DNA/RNA co-extraction workflow for environmental samples, with stronger emphasis on thorough purification prior to all enzymatic steps (including DNase digestion). Optional steps are indicated by dotted arrows. Note that RNase digestion (between Extracts II and III) may be necessary for better results downstream, but may be omitted as a separate step (in the current study, RNase is present in the qPCR mix). (A) Pre-lysis inhibitor removal is only advisable if quick methods are used, or if mRNA is not the target molecule (lengthy inhibitor removal procedures compromise RNA integrity). (B) Various methods may be used, such as phenol/chloroform procedures or nucleic acid precipitation. (C) This purification step should target the removal of enzymatic-inhibitors (e.g., humic/fulvic acids and polyphenolics). (D) Purification of partially digested RNA extracts with residual genomic DNA aids in the removal of enduring inhibitors, prior to further digestion. (E) Stringent and well-documented quality control via rigorous and sensitive detection (preferably quantitative methods) is necessary to detect residual amplifiable gDNA prior to reverse transcription.

    Article Snippet: The following DNases were tested for their ability to remove amplifiable DNA from TNA samples: DNase I (Sigma), RNase-Free DNase Set (QIAGEN), RNase-Free DNase I (Epicentre Biotechnologies) and TURBO DNA-free DNase Kit (Ambion, Life Technologies).

    Techniques: Environmental Sampling, Purification, Real-time Polymerase Chain Reaction, Lysis

    Construction and antiviral activity of defective interfering genes (DIG). a The plasmid construction of DI-PB2, DI-PB1, and DI-PA. The indicated sequences of shortened viral polymerase gene PB2, PB1, and PA were inserted into phw2000, respectively. Dotted lines indicate the internal deletion of wild-type (WT) viral polymerase genes. b , c DI RNA expression in 293T and A549 cells. The plasmids of DI-PB2, DI-PB1, and DI-PA were co-transfected into cells with the indicated concentrations. At 24 h post transfection, DI RNAs were extracted from cells and digested by DNase I for RT-qPCR. Empty vector was used as a negative control for RT-qPCR. d Anti-A(H7N7) virus activity of individual plasmid of DI-PB2, DI-PB1, and DI-PA or three combined plasmid DIG (DIG-3, 0.6 μg per well). e , f Dose-dependent anti-A(H7N7) virus activity of DIG-3 in 293T and A549 cells. g Anti-A(H5N1) virus activity of DIG-3. Empty vector phw2000 and plasmids with DIG were individually transfected to cells. At 24 h post transfection, cells were infected with A(H7N7) or A(H5N1) virus at MOI = 0.005 and cell supernatants were collected at 40 h post infection. Viral titers in the supernatants were detected by plaque assay. Data were presented as mean ± SD of three independent experiments. * Indicates P

    Journal: Nature Communications

    Article Title: Dual-functional peptide with defective interfering genes effectively protects mice against avian and seasonal influenza

    doi: 10.1038/s41467-018-04792-7

    Figure Lengend Snippet: Construction and antiviral activity of defective interfering genes (DIG). a The plasmid construction of DI-PB2, DI-PB1, and DI-PA. The indicated sequences of shortened viral polymerase gene PB2, PB1, and PA were inserted into phw2000, respectively. Dotted lines indicate the internal deletion of wild-type (WT) viral polymerase genes. b , c DI RNA expression in 293T and A549 cells. The plasmids of DI-PB2, DI-PB1, and DI-PA were co-transfected into cells with the indicated concentrations. At 24 h post transfection, DI RNAs were extracted from cells and digested by DNase I for RT-qPCR. Empty vector was used as a negative control for RT-qPCR. d Anti-A(H7N7) virus activity of individual plasmid of DI-PB2, DI-PB1, and DI-PA or three combined plasmid DIG (DIG-3, 0.6 μg per well). e , f Dose-dependent anti-A(H7N7) virus activity of DIG-3 in 293T and A549 cells. g Anti-A(H5N1) virus activity of DIG-3. Empty vector phw2000 and plasmids with DIG were individually transfected to cells. At 24 h post transfection, cells were infected with A(H7N7) or A(H5N1) virus at MOI = 0.005 and cell supernatants were collected at 40 h post infection. Viral titers in the supernatants were detected by plaque assay. Data were presented as mean ± SD of three independent experiments. * Indicates P

    Article Snippet: Extracted RNA were treated with DNase I (QIAGEN, Cat# 79254, USA) according to the manufacturer’s protocol and purified by RNeasy Mini Kit (QIAGEN, Cat# 74106, USA) to exclude plasmid DNA contamination.

    Techniques: Activity Assay, Plasmid Preparation, RNA Expression, Transfection, Quantitative RT-PCR, Negative Control, Infection, Plaque Assay

    Neutral 2D-AGE analysis of mtDNA replication products. ( A ) Extracted DNA analyzed on 1% Agarose. ( B ) Purified DNA cut with HincII was analysed using 2D-AGE. A fragment (mtDNA 13636-1006 bp) spanning the OriH region was visualized with probe located in CYTB (14641-15590 bp). Upper panel; untreated DNA (containing both RNA and DNA), Middle panel; RNase A and RNase H treated DNA (containing only DNA); Lower panel, DNA treated with RNaseA and RNaseH remixed with the RNA still present after DNase I treatment. ( C ) Schematic illustration of how Y and bubble arcs are expected to run in 2D-AGE. The bubble arc observed here is dependent on RNA (indicated in red).

    Journal: PLoS Genetics

    Article Title: In Vivo Occupancy of Mitochondrial Single-Stranded DNA Binding Protein Supports the Strand Displacement Mode of DNA Replication

    doi: 10.1371/journal.pgen.1004832

    Figure Lengend Snippet: Neutral 2D-AGE analysis of mtDNA replication products. ( A ) Extracted DNA analyzed on 1% Agarose. ( B ) Purified DNA cut with HincII was analysed using 2D-AGE. A fragment (mtDNA 13636-1006 bp) spanning the OriH region was visualized with probe located in CYTB (14641-15590 bp). Upper panel; untreated DNA (containing both RNA and DNA), Middle panel; RNase A and RNase H treated DNA (containing only DNA); Lower panel, DNA treated with RNaseA and RNaseH remixed with the RNA still present after DNase I treatment. ( C ) Schematic illustration of how Y and bubble arcs are expected to run in 2D-AGE. The bubble arc observed here is dependent on RNA (indicated in red).

    Article Snippet: After 30 min incubation at 32 °C, 12 units of RNase free DNase I (Qiagen) was added.

    Techniques: Purification