′ untranslated utr region Search Results


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  • 99
    Millipore 3 untranslated region 3 utr cdna library
    3 Untranslated Region 3 Utr Cdna Library, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/3 untranslated region 3 utr cdna library/product/Millipore
    Average 99 stars, based on 9 article reviews
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    3 untranslated region 3 utr cdna library - by Bioz Stars, 2020-03
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    89
    Genecopoeia 3 untranslated region utr
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    3 Untranslated Region Utr, supplied by Genecopoeia, used in various techniques. Bioz Stars score: 89/100, based on 48 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/3 untranslated region utr/product/Genecopoeia
    Average 89 stars, based on 48 article reviews
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    3 untranslated region utr - by Bioz Stars, 2020-03
    89/100 stars
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    78
    Roche untranslated regions utr library
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Regions Utr Library, supplied by Roche, used in various techniques. Bioz Stars score: 78/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    untranslated regions utr library - by Bioz Stars, 2020-03
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    89
    BGI Shenzhen untranslated regions utrs
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Regions Utrs, supplied by BGI Shenzhen, used in various techniques. Bioz Stars score: 89/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/untranslated regions utrs/product/BGI Shenzhen
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    untranslated regions utrs - by Bioz Stars, 2020-03
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    79
    Roche untranslated regions utrs
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Regions Utrs, supplied by Roche, used in various techniques. Bioz Stars score: 79/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/untranslated regions utrs/product/Roche
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    96
    Thermo Fisher untranslated region utr
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Region Utr, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 96/100, based on 65 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    83
    TaKaRa untranslated regions utrs
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Regions Utrs, supplied by TaKaRa, used in various techniques. Bioz Stars score: 83/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    untranslated regions utrs - by Bioz Stars, 2020-03
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    90
    5 PRIME untranslated region utr
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Region Utr, supplied by 5 PRIME, used in various techniques. Bioz Stars score: 90/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    80
    GenScript untranslated regions utrs
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Regions Utrs, supplied by GenScript, used in various techniques. Bioz Stars score: 80/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/untranslated regions utrs/product/GenScript
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    Unigene untranslated regions utrs
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Regions Utrs, supplied by Unigene, used in various techniques. Bioz Stars score: 78/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    untranslated regions utrs - by Bioz Stars, 2020-03
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    79
    Horizon Discovery untranslated regions utrs
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Regions Utrs, supplied by Horizon Discovery, used in various techniques. Bioz Stars score: 79/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 79 stars, based on 2 article reviews
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    untranslated regions utrs - by Bioz Stars, 2020-03
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    88
    GenScript 5 untraslated regions utr
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    5 Untraslated Regions Utr, supplied by GenScript, used in various techniques. Bioz Stars score: 88/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/5 untraslated regions utr/product/GenScript
    Average 88 stars, based on 8 article reviews
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    5 untraslated regions utr - by Bioz Stars, 2020-03
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    89
    Vigene Biosciences txnrd1 3 untranslated region utr
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Txnrd1 3 Untranslated Region Utr, supplied by Vigene Biosciences, used in various techniques. Bioz Stars score: 89/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/txnrd1 3 untranslated region utr/product/Vigene Biosciences
    Average 89 stars, based on 4 article reviews
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    82
    5 PRIME untranslated region utr variant
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Region Utr Variant, supplied by 5 PRIME, used in various techniques. Bioz Stars score: 82/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Illumina Inc 3 untranslated region utr
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    3 Untranslated Region Utr, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 91/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/3 untranslated region utr/product/Illumina Inc
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    78
    Thermo Fisher untranslated region utr dsrna
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Region Utr Dsrna, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 78/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/untranslated region utr dsrna/product/Thermo Fisher
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    80
    ATUM untranslated region 5 utr
    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
    Untranslated Region 5 Utr, supplied by ATUM, used in various techniques. Bioz Stars score: 80/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    untranslated region 5 utr - by Bioz Stars, 2020-03
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    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
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    Regulatory role of miR-133a in diabetic hearts. miR-133a targets <t>3′UTR</t> of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.
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    Variation in isoform preference may alter <t>microRNA</t> targeting of the choline acetyltransferase gene Sc-cha-1 between strains of S. carpocapsae. a Diagrammatic depiction of isoform structure between predicted variants (not to scale); white boxes indicate <t>UTRs,</t> red boxes indicate exons. b Graph indicating relative percentage abundance of L596_g14764.t2 across S. carpocapsae strains ( n = 6 independent libraries per strain). One way ANOVA and Tukey’s multiple comparison tests were conducted using Graphpad Prism 7.02. P
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    SMAD7 is a direct target of hsa-miR-21-5p. ( A ) The <t>3′-UTR</t> sequences of SAMD7 is cloned at the 3′ end of luciferase reporter gene in the pMirTarget plasmid. The predicted binding site of hsa-miR-21-5p on the region of 3′-UTR sequence of SMAD7 (SMAD7 3′-UTR) was shown. The “seed sequences” were indicated by lowercase; ( B ) Luciferase reporter assay. HEK293 cells were transfected with mimic-miR-21-5p or mimic control while transfection of pMirTarget plasmid or SMAD7 3′-UTR plasmid. *** p
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    miR-23a modulates the expression of RKIP via direct interaction with the <t>3′UTR.</t> A, sequence of the human RKIP 3′UTR (hsa RKIP ) showing the two miR-23a–binding sites (bs1-2). Matching regions are highlighted by lines. Alteration of bs1 by either deletion ( RKIP Del) or mutation ( RKIP Mut) is displayed. B, HEK-293 cells were transfected with either miR-23a mimic (white bars) or unspecific control (Cntrl, black bars) together with luciferase reporter clones, containing (i) wild-type RKIP 3′UTR ( RKIP 3′UTR), (ii) RKIP Del, or (iii) RKIP Mut. pCS2-RFP was included in all transfections to compensate for different transfection efficiencies. Graphs represent the mean RFP-compensated luciferase activity of three independent experiments ± SD; values are given as x -fold expression of the respective control-transfected setting.
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    miR-23a modulates the expression of RKIP via direct interaction with the <t>3′UTR.</t> A, sequence of the human RKIP 3′UTR (hsa RKIP ) showing the two miR-23a–binding sites (bs1-2). Matching regions are highlighted by lines. Alteration of bs1 by either deletion ( RKIP Del) or mutation ( RKIP Mut) is displayed. B, HEK-293 cells were transfected with either miR-23a mimic (white bars) or unspecific control (Cntrl, black bars) together with luciferase reporter clones, containing (i) wild-type RKIP 3′UTR ( RKIP 3′UTR), (ii) RKIP Del, or (iii) RKIP Mut. pCS2-RFP was included in all transfections to compensate for different transfection efficiencies. Graphs represent the mean RFP-compensated luciferase activity of three independent experiments ± SD; values are given as x -fold expression of the respective control-transfected setting.
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    Image Search Results


    Regulatory role of miR-133a in diabetic hearts. miR-133a targets 3′UTR of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.

    Journal: Diabetes

    Article Title: Lack of miR-133a Decreases Contractility of Diabetic Hearts: A Role for Novel Cross Talk Between Tyrosine Aminotransferase and Tyrosine Hydroxylase

    doi: 10.2337/db16-0023

    Figure Lengend Snippet: Regulatory role of miR-133a in diabetic hearts. miR-133a targets 3′UTR of TAT. A : The binding sequence of miR-133a with TAT 3′UTR in rat. B : The plasmid clone of TAT 3′UTR used for luciferase (Luc) reporter assay. The mutant plasmid is identical except the miR-133a binding site is deleted. CMV, cytomegalovirus; hLuc, humanized firefly luciferase; hRLuc, humanized renilla luciferase; SV40, simian vacuolating virus 40. The luciferase reporter assay results with TAT 3′UTR ( C ) and mutant TAT 3′UTR ( D ). miR, miR-133a; scm, scrambled. The relative luciferase activity is measured in CATH.a cells treated with 3′UTR and increasing doses of miR-133a. The values are mean ± SEM ( n = 6). E : miR-133a regulates contractility by targeting TAT in diabetic hearts. Schematic shows that the reduced level of miR-133a upregulates TAT in diabetic hearts. Elevated TAT inhibits TH, which decreases the cardiac NE (c-NE) level. It results in inactivation of β 1 -AR and β 2 -AR that decreases contractility in diabetic hearts. However, treatment with miR-133a mimic increases the miR-133a level in the diabetic heart that decreases TAT by binding to its 3′UTR. Decreased TAT increases the level of TH, which induces c-NE biosynthesis. The elevated level of c-NE induces β-AR and improves the contractility of diabetic hearts.

    Article Snippet: miR-133a (cat #MmiR3445-MR03), scrambled miRNA (cat #CmiR0001-MR03), anti–miR-133a (cat #MmiR-AN0880-AM04), and TAT 3′-untranslated region (UTR) clones (WT 3′UTR: cat #RmiT048999-MT01; mutant 3′UTR: CS-RmiT048999-MT01-01) were purchased from GeneCopoeia, Rockville, MD.

    Techniques: Binding Assay, Sequencing, Plasmid Preparation, Luciferase, Reporter Assay, Mutagenesis, Activity Assay

    Variation in isoform preference may alter microRNA targeting of the choline acetyltransferase gene Sc-cha-1 between strains of S. carpocapsae. a Diagrammatic depiction of isoform structure between predicted variants (not to scale); white boxes indicate UTRs, red boxes indicate exons. b Graph indicating relative percentage abundance of L596_g14764.t2 across S. carpocapsae strains ( n = 6 independent libraries per strain). One way ANOVA and Tukey’s multiple comparison tests were conducted using Graphpad Prism 7.02. P

    Journal: BMC Genomics

    Article Title: Transcriptional variation and divergence of host-finding behaviour in Steinernema carpocapsae infective juveniles

    doi: 10.1186/s12864-019-6179-y

    Figure Lengend Snippet: Variation in isoform preference may alter microRNA targeting of the choline acetyltransferase gene Sc-cha-1 between strains of S. carpocapsae. a Diagrammatic depiction of isoform structure between predicted variants (not to scale); white boxes indicate UTRs, red boxes indicate exons. b Graph indicating relative percentage abundance of L596_g14764.t2 across S. carpocapsae strains ( n = 6 independent libraries per strain). One way ANOVA and Tukey’s multiple comparison tests were conducted using Graphpad Prism 7.02. P

    Article Snippet: MicroRNA target gene prediction Three and five prime UnTranslated Regions (UTRs) of computationally predicted S. carpocapsae genes were exported from wormbase parasite [ , ] using the biomart function.

    Techniques:

    Variation in isoform preference may alter microRNA targeting of the vesicular glutamine transporter gene Sc-vglu-2 between strains of S. carpocapsae. a Diagrammatic depiction of isoform structure between predicted variants (not to scale); white boxes indicate UTRs, red boxes indicate exons. b Graph indicating relative percentage abundance of L596_g5500.t2 across S. carpocapsae strains (n = 6 independent libraries per strain). One way ANOVA and Tukey’s multiple comparison tests were conducted using Graphpad Prism 7.02. P

    Journal: BMC Genomics

    Article Title: Transcriptional variation and divergence of host-finding behaviour in Steinernema carpocapsae infective juveniles

    doi: 10.1186/s12864-019-6179-y

    Figure Lengend Snippet: Variation in isoform preference may alter microRNA targeting of the vesicular glutamine transporter gene Sc-vglu-2 between strains of S. carpocapsae. a Diagrammatic depiction of isoform structure between predicted variants (not to scale); white boxes indicate UTRs, red boxes indicate exons. b Graph indicating relative percentage abundance of L596_g5500.t2 across S. carpocapsae strains (n = 6 independent libraries per strain). One way ANOVA and Tukey’s multiple comparison tests were conducted using Graphpad Prism 7.02. P

    Article Snippet: MicroRNA target gene prediction Three and five prime UnTranslated Regions (UTRs) of computationally predicted S. carpocapsae genes were exported from wormbase parasite [ , ] using the biomart function.

    Techniques:

    SMAD7 is a direct target of hsa-miR-21-5p. ( A ) The 3′-UTR sequences of SAMD7 is cloned at the 3′ end of luciferase reporter gene in the pMirTarget plasmid. The predicted binding site of hsa-miR-21-5p on the region of 3′-UTR sequence of SMAD7 (SMAD7 3′-UTR) was shown. The “seed sequences” were indicated by lowercase; ( B ) Luciferase reporter assay. HEK293 cells were transfected with mimic-miR-21-5p or mimic control while transfection of pMirTarget plasmid or SMAD7 3′-UTR plasmid. *** p

    Journal: International Journal of Molecular Sciences

    Article Title: Dual Role of MiR-21-Mediated Signaling in HUVECs and Rat Surgical Flap under Normoxia and Hypoxia Condition

    doi: 10.3390/ijms18091917

    Figure Lengend Snippet: SMAD7 is a direct target of hsa-miR-21-5p. ( A ) The 3′-UTR sequences of SAMD7 is cloned at the 3′ end of luciferase reporter gene in the pMirTarget plasmid. The predicted binding site of hsa-miR-21-5p on the region of 3′-UTR sequence of SMAD7 (SMAD7 3′-UTR) was shown. The “seed sequences” were indicated by lowercase; ( B ) Luciferase reporter assay. HEK293 cells were transfected with mimic-miR-21-5p or mimic control while transfection of pMirTarget plasmid or SMAD7 3′-UTR plasmid. *** p

    Article Snippet: Reporter Assay The complete sequence of SMAD7 3′ untranslated region (UTR) was constructed into the pMirTarget vector (Origene, Rockville, MD, USA).

    Techniques: Clone Assay, Luciferase, Plasmid Preparation, Binding Assay, Sequencing, Reporter Assay, Transfection

    miR-23a modulates the expression of RKIP via direct interaction with the 3′UTR. A, sequence of the human RKIP 3′UTR (hsa RKIP ) showing the two miR-23a–binding sites (bs1-2). Matching regions are highlighted by lines. Alteration of bs1 by either deletion ( RKIP Del) or mutation ( RKIP Mut) is displayed. B, HEK-293 cells were transfected with either miR-23a mimic (white bars) or unspecific control (Cntrl, black bars) together with luciferase reporter clones, containing (i) wild-type RKIP 3′UTR ( RKIP 3′UTR), (ii) RKIP Del, or (iii) RKIP Mut. pCS2-RFP was included in all transfections to compensate for different transfection efficiencies. Graphs represent the mean RFP-compensated luciferase activity of three independent experiments ± SD; values are given as x -fold expression of the respective control-transfected setting.

    Journal: Cancer research

    Article Title: Increased Expression of miR-23a Mediates a Loss of Expression in the RAF Kinase Inhibitor Protein RKIP

    doi: 10.1158/0008-5472.CAN-15-3049

    Figure Lengend Snippet: miR-23a modulates the expression of RKIP via direct interaction with the 3′UTR. A, sequence of the human RKIP 3′UTR (hsa RKIP ) showing the two miR-23a–binding sites (bs1-2). Matching regions are highlighted by lines. Alteration of bs1 by either deletion ( RKIP Del) or mutation ( RKIP Mut) is displayed. B, HEK-293 cells were transfected with either miR-23a mimic (white bars) or unspecific control (Cntrl, black bars) together with luciferase reporter clones, containing (i) wild-type RKIP 3′UTR ( RKIP 3′UTR), (ii) RKIP Del, or (iii) RKIP Mut. pCS2-RFP was included in all transfections to compensate for different transfection efficiencies. Graphs represent the mean RFP-compensated luciferase activity of three independent experiments ± SD; values are given as x -fold expression of the respective control-transfected setting.

    Article Snippet: For luciferase reporter assays, HEK-293 were transfected with 0.25 ng/μl pCS2-red fluorescent protein (RFP), together with 0.125 ng/μL RKIP-3′-untranslated region (UTR)-pMirTarget (Origene) as well as with miR-23a mimics or scrambled control (both at a concentration of 20 nmol/L).

    Techniques: Expressing, Sequencing, Binding Assay, Mutagenesis, Transfection, Luciferase, Clone Assay, Activity Assay