Review



pcmv myc n expression vector  (TaKaRa)


Bioz Verified Symbol TaKaRa is a verified supplier
Bioz Manufacturer Symbol TaKaRa manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 96

    Structured Review

    TaKaRa pcmv myc n expression vector
    Pcmv Myc N Expression Vector, supplied by TaKaRa, used in various techniques. Bioz Stars score: 96/100, based on 752 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pcmv+myc+n+expression+vector/pCMV-Myc+Vector+Set/pm39565137-72-38-41
    Average 96 stars, based on 752 article reviews
    pcmv myc n expression vector - by Bioz Stars, 2026-09
    96/100 stars

    Images

    Related Articles

    Amplification:

    Article Title: YB1 protects cardiac myocytes against H 2 O 2 -induced injury via suppression of PIAS3 mRNA and phosphorylation of STAT3
    Article Snippet: .. The PIAS3 gene was amplified from cDNA from H9c2 cells by PCR, using forward primer, 5′-GGAATTCGGATGGCGGAGCTGGGCGAA-3′ and reverse primer, 5′-GGGGTACCTCAGTCCAAGGAAATGC-3′, cloned into the pCMV-Myc-N-expression vector (Clontech Laboratories, Inc.) and sequenced. siRNAs (100 nM) or plasmids (2 μg) were transfected into H9c2 cells, using Exfect Transfection Reagent (Vazyme), according to the manufacturer's instructions. ..

    Article Title: Minute virus of mice NS1 redirects casein kinase 2 specificity to suppress the ATR DNA damage response pathway during infection.
    Article Snippet: During infection the autonomous parvovirus minute virus of mice (MVM) generates extensive DNA damage which facilitates virus replication and induces a cellular DNA damage response (DDR) driven by the ataxia telangiectasia mutated (ATM) kinase.. Atypically, the ataxia telangiectasia and Rad-3-related (ATR) DDR pathway remains inactive.. Upon DNA damage ATR is normally recruited to single-stranded DNA sequences formed at genomic DNA damage sites, and while within a multiprotein complex activates, via phosphorylation, the key DDR regulator checkpoint kinase 1 (Chk1).

    Article Title: YB1 protects cardiac myocytes against H2O2‑induced injury via suppression of PIAS3 mRNA and phosphorylation of STAT3.
    Article Snippet: .. The PIAS3 gene was amplified from cdna from H9c2 cells by Pcr, using forward primer, 5'-GGa aTT cGG aTG GcG GaG cTG GGc Gaa-3' and reverse primer, 5'-GGG GTa ccT caG Tcc aaG Gaa aTG c-3', cloned into the pcMV-Myc-n-expression vector (clontech laboratories, inc.) and sequenced. sirnas (100 nM) or plasmids (2 μg) were transfected into H9c2 cells, using exfect Transfection reagent (Vazyme), according to the manufacturer's instructions. at 24 h post-transfection, cells were processed for further analysis. ..

    Polymerase Chain Reaction:

    Article Title: YB1 protects cardiac myocytes against H 2 O 2 -induced injury via suppression of PIAS3 mRNA and phosphorylation of STAT3
    Article Snippet: .. The PIAS3 gene was amplified from cDNA from H9c2 cells by PCR, using forward primer, 5′-GGAATTCGGATGGCGGAGCTGGGCGAA-3′ and reverse primer, 5′-GGGGTACCTCAGTCCAAGGAAATGC-3′, cloned into the pCMV-Myc-N-expression vector (Clontech Laboratories, Inc.) and sequenced. siRNAs (100 nM) or plasmids (2 μg) were transfected into H9c2 cells, using Exfect Transfection Reagent (Vazyme), according to the manufacturer's instructions. ..

    Article Title: Minute virus of mice NS1 redirects casein kinase 2 specificity to suppress the ATR DNA damage response pathway during infection.
    Article Snippet: During infection the autonomous parvovirus minute virus of mice (MVM) generates extensive DNA damage which facilitates virus replication and induces a cellular DNA damage response (DDR) driven by the ataxia telangiectasia mutated (ATM) kinase.. Atypically, the ataxia telangiectasia and Rad-3-related (ATR) DDR pathway remains inactive.. Upon DNA damage ATR is normally recruited to single-stranded DNA sequences formed at genomic DNA damage sites, and while within a multiprotein complex activates, via phosphorylation, the key DDR regulator checkpoint kinase 1 (Chk1).

    Clone Assay:

    Article Title: YB1 protects cardiac myocytes against H 2 O 2 -induced injury via suppression of PIAS3 mRNA and phosphorylation of STAT3
    Article Snippet: .. The PIAS3 gene was amplified from cDNA from H9c2 cells by PCR, using forward primer, 5′-GGAATTCGGATGGCGGAGCTGGGCGAA-3′ and reverse primer, 5′-GGGGTACCTCAGTCCAAGGAAATGC-3′, cloned into the pCMV-Myc-N-expression vector (Clontech Laboratories, Inc.) and sequenced. siRNAs (100 nM) or plasmids (2 μg) were transfected into H9c2 cells, using Exfect Transfection Reagent (Vazyme), according to the manufacturer's instructions. ..

    Article Title: YB1 protects cardiac myocytes against H2O2‑induced injury via suppression of PIAS3 mRNA and phosphorylation of STAT3.
    Article Snippet: .. The PIAS3 gene was amplified from cdna from H9c2 cells by Pcr, using forward primer, 5'-GGa aTT cGG aTG GcG GaG cTG GGc Gaa-3' and reverse primer, 5'-GGG GTa ccT caG Tcc aaG Gaa aTG c-3', cloned into the pcMV-Myc-n-expression vector (clontech laboratories, inc.) and sequenced. sirnas (100 nM) or plasmids (2 μg) were transfected into H9c2 cells, using exfect Transfection reagent (Vazyme), according to the manufacturer's instructions. at 24 h post-transfection, cells were processed for further analysis. ..

    Transfection:

    Article Title: YB1 protects cardiac myocytes against H 2 O 2 -induced injury via suppression of PIAS3 mRNA and phosphorylation of STAT3
    Article Snippet: .. The PIAS3 gene was amplified from cDNA from H9c2 cells by PCR, using forward primer, 5′-GGAATTCGGATGGCGGAGCTGGGCGAA-3′ and reverse primer, 5′-GGGGTACCTCAGTCCAAGGAAATGC-3′, cloned into the pCMV-Myc-N-expression vector (Clontech Laboratories, Inc.) and sequenced. siRNAs (100 nM) or plasmids (2 μg) were transfected into H9c2 cells, using Exfect Transfection Reagent (Vazyme), according to the manufacturer's instructions. ..

    Article Title: YB1 protects cardiac myocytes against H2O2‑induced injury via suppression of PIAS3 mRNA and phosphorylation of STAT3.
    Article Snippet: .. The PIAS3 gene was amplified from cdna from H9c2 cells by Pcr, using forward primer, 5'-GGa aTT cGG aTG GcG GaG cTG GGc Gaa-3' and reverse primer, 5'-GGG GTa ccT caG Tcc aaG Gaa aTG c-3', cloned into the pcMV-Myc-n-expression vector (clontech laboratories, inc.) and sequenced. sirnas (100 nM) or plasmids (2 μg) were transfected into H9c2 cells, using exfect Transfection reagent (Vazyme), according to the manufacturer's instructions. at 24 h post-transfection, cells were processed for further analysis. ..

    Expressing:

    Article Title: Minute virus of mice NS1 redirects casein kinase 2 specificity to suppress the ATR DNA damage response pathway during infection.
    Article Snippet: During infection the autonomous parvovirus minute virus of mice (MVM) generates extensive DNA damage which facilitates virus replication and induces a cellular DNA damage response (DDR) driven by the ataxia telangiectasia mutated (ATM) kinase.. Atypically, the ataxia telangiectasia and Rad-3-related (ATR) DDR pathway remains inactive.. Upon DNA damage ATR is normally recruited to single-stranded DNA sequences formed at genomic DNA damage sites, and while within a multiprotein complex activates, via phosphorylation, the key DDR regulator checkpoint kinase 1 (Chk1).

    Article Title: Grancalcin (GCA) modulates Toll-like receptor 9 (TLR9) mediated signaling through its direct interaction with TLR9.
    Article Snippet: .. All of the human GCA constructs were made by cutting and ligating at EcoRI and NotI into the pCMV-Myc-N expression vector (Clontech). ..

    Activation Assay:

    Article Title: Minute virus of mice NS1 redirects casein kinase 2 specificity to suppress the ATR DNA damage response pathway during infection.
    Article Snippet: During infection the autonomous parvovirus minute virus of mice (MVM) generates extensive DNA damage which facilitates virus replication and induces a cellular DNA damage response (DDR) driven by the ataxia telangiectasia mutated (ATM) kinase.. Atypically, the ataxia telangiectasia and Rad-3-related (ATR) DDR pathway remains inactive.. Upon DNA damage ATR is normally recruited to single-stranded DNA sequences formed at genomic DNA damage sites, and while within a multiprotein complex activates, via phosphorylation, the key DDR regulator checkpoint kinase 1 (Chk1).

    Construct:

    Article Title: Minute virus of mice NS1 redirects casein kinase 2 specificity to suppress the ATR DNA damage response pathway during infection.
    Article Snippet: During infection the autonomous parvovirus minute virus of mice (MVM) generates extensive DNA damage which facilitates virus replication and induces a cellular DNA damage response (DDR) driven by the ataxia telangiectasia mutated (ATM) kinase.. Atypically, the ataxia telangiectasia and Rad-3-related (ATR) DDR pathway remains inactive.. Upon DNA damage ATR is normally recruited to single-stranded DNA sequences formed at genomic DNA damage sites, and while within a multiprotein complex activates, via phosphorylation, the key DDR regulator checkpoint kinase 1 (Chk1).

    Article Title: Grancalcin (GCA) modulates Toll-like receptor 9 (TLR9) mediated signaling through its direct interaction with TLR9.
    Article Snippet: .. All of the human GCA constructs were made by cutting and ligating at EcoRI and NotI into the pCMV-Myc-N expression vector (Clontech). ..

    Sequencing:

    Article Title: Minute virus of mice NS1 redirects casein kinase 2 specificity to suppress the ATR DNA damage response pathway during infection.
    Article Snippet: During infection the autonomous parvovirus minute virus of mice (MVM) generates extensive DNA damage which facilitates virus replication and induces a cellular DNA damage response (DDR) driven by the ataxia telangiectasia mutated (ATM) kinase.. Atypically, the ataxia telangiectasia and Rad-3-related (ATR) DDR pathway remains inactive.. Upon DNA damage ATR is normally recruited to single-stranded DNA sequences formed at genomic DNA damage sites, and while within a multiprotein complex activates, via phosphorylation, the key DDR regulator checkpoint kinase 1 (Chk1).

    Cloning:

    Article Title: Minute virus of mice NS1 redirects casein kinase 2 specificity to suppress the ATR DNA damage response pathway during infection.
    Article Snippet: During infection the autonomous parvovirus minute virus of mice (MVM) generates extensive DNA damage which facilitates virus replication and induces a cellular DNA damage response (DDR) driven by the ataxia telangiectasia mutated (ATM) kinase.. Atypically, the ataxia telangiectasia and Rad-3-related (ATR) DDR pathway remains inactive.. Upon DNA damage ATR is normally recruited to single-stranded DNA sequences formed at genomic DNA damage sites, and while within a multiprotein complex activates, via phosphorylation, the key DDR regulator checkpoint kinase 1 (Chk1).

    Plasmid Preparation:

    Article Title: Grancalcin (GCA) modulates Toll-like receptor 9 (TLR9) mediated signaling through its direct interaction with TLR9.
    Article Snippet: .. All of the human GCA constructs were made by cutting and ligating at EcoRI and NotI into the pCMV-Myc-N expression vector (Clontech). ..



    Similar Products

    96
    TaKaRa pcmv myc n expression vector
    Pcmv Myc N Expression Vector, supplied by TaKaRa, 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/pcmv+myc+n+expression+vector/pCMV-Myc+Vector+Set/pm39565137-72-38-41
    Average 96 stars, based on 1 article reviews
    pcmv myc n expression vector - by Bioz Stars, 2026-09
    96/100 stars
      Buy from Supplier

    90
    OriGene mycn expression vector pcmv xl4 mycn
    Mycn Expression Vector Pcmv Xl4 Mycn, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pcmv+myc+n+expression+vector/n-Myc+(MYCN)+(NM_005378)+Human+Untagged+Clone/pm32087738-67-0-9
    Average 90 stars, based on 1 article reviews
    mycn expression vector pcmv xl4 mycn - by Bioz Stars, 2026-09
    90/100 stars
      Buy from Supplier

    90
    Agilent technologies pcmv- myc -n-terminal epitope tagging mammalian expression vector
    Pcmv Myc N Terminal Epitope Tagging Mammalian Expression Vector, supplied by Agilent technologies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pcmv+myc+n+expression+vector/pmc05686498-67-13-18
    Average 90 stars, based on 1 article reviews
    pcmv- myc -n-terminal epitope tagging mammalian expression vector - by Bioz Stars, 2026-09
    90/100 stars
      Buy from Supplier

    86
    TaKaRa pcmv myc n dux4 expression vectors
    <t>DUX4</t> regulates the endogenous FRG1 gene in human muscle cells. ( A ) Control human muscle cells were electroporated with an expression vector either encoding DUX4 ( pCIneo-DUX4 ) or insertless ( pCIneo ). Expression levels of FRG1 are enhanced upon DUX4 overexpression. RFPL2 and TRIM48 , bona fide DUX4 targets, were used as positive controls and RPL13A as negative control (paired t -test, * P < 0.05, n = 3, mean ± SEM). N.d. is not detected. ( B ) FSHD human muscle cells were infected with retroviruses containing a non-targeting sequence (shNT) or a DUX4-targeting sequence (shDUX4). Upon DUX4 knockdown, FRG1 expression levels were reduced. RFPL2 and TRIM48 were used as positive control, while RPL13A was used as negative control (paired t -test, * P < 0.05, *** P < 0.001, n = 3, mean ± SEM). ( C ) Immunofluorescence for DUX4 and FRG1 in FSHD muscle cells. Scale bar is 10 μm.
    Pcmv Myc N Dux4 Expression Vectors, supplied by TaKaRa, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pcmv+myc+n+expression+vector/pmc04321439-215-10-8
    Average 86 stars, based on 1 article reviews
    pcmv myc n dux4 expression vectors - by Bioz Stars, 2026-09
    86/100 stars
      Buy from Supplier

    96
    TaKaRa n terminal myc tag expression vector pcmv myc
    <t>DUX4</t> regulates the endogenous FRG1 gene in human muscle cells. ( A ) Control human muscle cells were electroporated with an expression vector either encoding DUX4 ( pCIneo-DUX4 ) or insertless ( pCIneo ). Expression levels of FRG1 are enhanced upon DUX4 overexpression. RFPL2 and TRIM48 , bona fide DUX4 targets, were used as positive controls and RPL13A as negative control (paired t -test, * P < 0.05, n = 3, mean ± SEM). N.d. is not detected. ( B ) FSHD human muscle cells were infected with retroviruses containing a non-targeting sequence (shNT) or a DUX4-targeting sequence (shDUX4). Upon DUX4 knockdown, FRG1 expression levels were reduced. RFPL2 and TRIM48 were used as positive control, while RPL13A was used as negative control (paired t -test, * P < 0.05, *** P < 0.001, n = 3, mean ± SEM). ( C ) Immunofluorescence for DUX4 and FRG1 in FSHD muscle cells. Scale bar is 10 μm.
    N Terminal Myc Tag Expression Vector Pcmv Myc, supplied by TaKaRa, 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/pcmv+myc+n+expression+vector/pCMV-Myc+Vector+Set/pm15276230-41-12-17
    Average 96 stars, based on 1 article reviews
    n terminal myc tag expression vector pcmv myc - by Bioz Stars, 2026-09
    96/100 stars
      Buy from Supplier

    Image Search Results


    DUX4 regulates the endogenous FRG1 gene in human muscle cells. ( A ) Control human muscle cells were electroporated with an expression vector either encoding DUX4 ( pCIneo-DUX4 ) or insertless ( pCIneo ). Expression levels of FRG1 are enhanced upon DUX4 overexpression. RFPL2 and TRIM48 , bona fide DUX4 targets, were used as positive controls and RPL13A as negative control (paired t -test, * P < 0.05, n = 3, mean ± SEM). N.d. is not detected. ( B ) FSHD human muscle cells were infected with retroviruses containing a non-targeting sequence (shNT) or a DUX4-targeting sequence (shDUX4). Upon DUX4 knockdown, FRG1 expression levels were reduced. RFPL2 and TRIM48 were used as positive control, while RPL13A was used as negative control (paired t -test, * P < 0.05, *** P < 0.001, n = 3, mean ± SEM). ( C ) Immunofluorescence for DUX4 and FRG1 in FSHD muscle cells. Scale bar is 10 μm.

    Journal: Human Molecular Genetics

    Article Title: Direct interplay between two candidate genes in FSHD muscular dystrophy

    doi: 10.1093/hmg/ddu536

    Figure Lengend Snippet: DUX4 regulates the endogenous FRG1 gene in human muscle cells. ( A ) Control human muscle cells were electroporated with an expression vector either encoding DUX4 ( pCIneo-DUX4 ) or insertless ( pCIneo ). Expression levels of FRG1 are enhanced upon DUX4 overexpression. RFPL2 and TRIM48 , bona fide DUX4 targets, were used as positive controls and RPL13A as negative control (paired t -test, * P < 0.05, n = 3, mean ± SEM). N.d. is not detected. ( B ) FSHD human muscle cells were infected with retroviruses containing a non-targeting sequence (shNT) or a DUX4-targeting sequence (shDUX4). Upon DUX4 knockdown, FRG1 expression levels were reduced. RFPL2 and TRIM48 were used as positive control, while RPL13A was used as negative control (paired t -test, * P < 0.05, *** P < 0.001, n = 3, mean ± SEM). ( C ) Immunofluorescence for DUX4 and FRG1 in FSHD muscle cells. Scale bar is 10 μm.

    Article Snippet: Immortalized human control myoblasts were electroporated with pCMV-Myc-N (Clontech) and pCMV-Myc-N-DUX4 expression vectors.

    Techniques: Expressing, Plasmid Preparation, Over Expression, Negative Control, Infection, Sequencing, Positive Control, Immunofluorescence

    DUX4 associates to the FRG1 genomic area. ( A ) Schematic draw of the FRG1 genomic area. White boxes represent the exons of the FRG1 gene. ChIP-seq peak regions identified by Geng et al . are shown as boxes with stripes. The first peak ( FRG1 Peak1) is located inside the second intron, while the second peak ( FRG1 Peak2) is at the 3′ end of the gene. Black arrows represent the position of the primers employed for the ChIP-qPCR analysis. ( B ) Control human muscle cells were electroporated with an expression vector either encoding a Myc-tagged form of DUX4 ( pCMV-Myc-N-DUX4 ) or the corresponding empty vector ( pCMV-Myc-N ). DUX4 was immunoprecipitated with either α-Myc or α-DUX4, and the signal was detect showing enrichment at FRG1 Peak1 region. ( C ) DUX4 was present also in FRG1 Peak2 region as well as in the genomic region of the two positive controls ( D ) RFPL2 and ( E ) TRIM48 . One representative experiment out of three independent experiments is shown. Error bars indicate standard error of the mean.

    Journal: Human Molecular Genetics

    Article Title: Direct interplay between two candidate genes in FSHD muscular dystrophy

    doi: 10.1093/hmg/ddu536

    Figure Lengend Snippet: DUX4 associates to the FRG1 genomic area. ( A ) Schematic draw of the FRG1 genomic area. White boxes represent the exons of the FRG1 gene. ChIP-seq peak regions identified by Geng et al . are shown as boxes with stripes. The first peak ( FRG1 Peak1) is located inside the second intron, while the second peak ( FRG1 Peak2) is at the 3′ end of the gene. Black arrows represent the position of the primers employed for the ChIP-qPCR analysis. ( B ) Control human muscle cells were electroporated with an expression vector either encoding a Myc-tagged form of DUX4 ( pCMV-Myc-N-DUX4 ) or the corresponding empty vector ( pCMV-Myc-N ). DUX4 was immunoprecipitated with either α-Myc or α-DUX4, and the signal was detect showing enrichment at FRG1 Peak1 region. ( C ) DUX4 was present also in FRG1 Peak2 region as well as in the genomic region of the two positive controls ( D ) RFPL2 and ( E ) TRIM48 . One representative experiment out of three independent experiments is shown. Error bars indicate standard error of the mean.

    Article Snippet: Immortalized human control myoblasts were electroporated with pCMV-Myc-N (Clontech) and pCMV-Myc-N-DUX4 expression vectors.

    Techniques: ChIP-sequencing, Expressing, Plasmid Preparation, Immunoprecipitation

    FRG1 Peak1 region is sufficient for specific DUX4 transactivation. ( A ) Schematic representation of the constructs employed in luciferase assays. Genomic fragments of the FRG1 gene containing DUX4 putative binding sites were cloned upstream of the SV40 promoter, which controlled the expression of the Luciferase reporter gene. DUX4 core binding motifs within FRG1 genomic regions are reported. The three nucleotides of FRG1 Peak1 region that were mutated to generate FRG1 Peak1-mutated region are underlined. ( B ) FRG1 Peak1 region is able to transactivate the Luciferase reporter gene in the presence of DUX4, while the mutation in key DUX4 consensus sequence nucleotides abolishes the transactivation. DUX4 is not able to transactivate the Luciferase gene through FRG1 Peak2 region (paired t -test, * P < 0.05, n = 3, mean ± SEM).

    Journal: Human Molecular Genetics

    Article Title: Direct interplay between two candidate genes in FSHD muscular dystrophy

    doi: 10.1093/hmg/ddu536

    Figure Lengend Snippet: FRG1 Peak1 region is sufficient for specific DUX4 transactivation. ( A ) Schematic representation of the constructs employed in luciferase assays. Genomic fragments of the FRG1 gene containing DUX4 putative binding sites were cloned upstream of the SV40 promoter, which controlled the expression of the Luciferase reporter gene. DUX4 core binding motifs within FRG1 genomic regions are reported. The three nucleotides of FRG1 Peak1 region that were mutated to generate FRG1 Peak1-mutated region are underlined. ( B ) FRG1 Peak1 region is able to transactivate the Luciferase reporter gene in the presence of DUX4, while the mutation in key DUX4 consensus sequence nucleotides abolishes the transactivation. DUX4 is not able to transactivate the Luciferase gene through FRG1 Peak2 region (paired t -test, * P < 0.05, n = 3, mean ± SEM).

    Article Snippet: Immortalized human control myoblasts were electroporated with pCMV-Myc-N (Clontech) and pCMV-Myc-N-DUX4 expression vectors.

    Techniques: Construct, Luciferase, Binding Assay, Clone Assay, Expressing, Mutagenesis, Sequencing

    DUX4 directly binds to FRG1 Peak1. ( A ) In vitro translated DUX4 protein binds to the labelled FRG1 Peak1 probe containing the TAATTCAATCA core sequence. Competition with unlabelled FRG1 Peak1 probe abolishes DUX4 binding, while competition with an excess of unlabelled FRG1 Peak1-mutated region probe (mutated core sequence TA C TTC T AT G A) does not. ( B ) DUX4 incubation with TRIM48 Peak region probe produces a shifted band that indicates direct DNA–protein binding, while FRG1 Peak2 region probe, containing a partial DUX4 core motif (TAATGTA), is not bound by DUX4. One representative experiment out of three independent experiments is shown.

    Journal: Human Molecular Genetics

    Article Title: Direct interplay between two candidate genes in FSHD muscular dystrophy

    doi: 10.1093/hmg/ddu536

    Figure Lengend Snippet: DUX4 directly binds to FRG1 Peak1. ( A ) In vitro translated DUX4 protein binds to the labelled FRG1 Peak1 probe containing the TAATTCAATCA core sequence. Competition with unlabelled FRG1 Peak1 probe abolishes DUX4 binding, while competition with an excess of unlabelled FRG1 Peak1-mutated region probe (mutated core sequence TA C TTC T AT G A) does not. ( B ) DUX4 incubation with TRIM48 Peak region probe produces a shifted band that indicates direct DNA–protein binding, while FRG1 Peak2 region probe, containing a partial DUX4 core motif (TAATGTA), is not bound by DUX4. One representative experiment out of three independent experiments is shown.

    Article Snippet: Immortalized human control myoblasts were electroporated with pCMV-Myc-N (Clontech) and pCMV-Myc-N-DUX4 expression vectors.

    Techniques: In Vitro, Sequencing, Binding Assay, Incubation, Protein Binding