c2c12 cells Search Results


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CLS Cell Lines Service GmbH c2c12 cell line
C2c12 Cell Line, supplied by CLS Cell Lines Service GmbH, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Genecopoeia c2c12 myoblasts
C2c12 Myoblasts, supplied by Genecopoeia, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology c2c12 cells
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
C2c12 Cells, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Innovative Research Inc c2c12
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
C2c12, supplied by Innovative Research Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Dainippon Sumitomo mouse myoblastic c2c12 cells
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
Mouse Myoblastic C2c12 Cells, supplied by Dainippon Sumitomo, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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BioResource International Inc c2c12 cells
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
C2c12 Cells, supplied by BioResource International Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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KAC Co Ltd mouse c2c12 myoblasts
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
Mouse C2c12 Myoblasts, supplied by KAC Co Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Procell Inc skeletal muscle cell line c2c12 myotubes
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
Skeletal Muscle Cell Line C2c12 Myotubes, supplied by Procell Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Dawley Inc c2c12 myotubes
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
C2c12 Myotubes, supplied by Dawley Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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LGC Promochem c2c12 myogenic cell line
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
C2c12 Myogenic Cell Line, supplied by LGC Promochem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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European Collection of Authenticated Cell Cultures c2c12 cell line
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
C2c12 Cell Line, supplied by European Collection of Authenticated Cell Cultures, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Mediatech c2c12 cell line
miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) <t>C2C12</t> cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction
C2c12 Cell Line, supplied by Mediatech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) C2C12 cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction

Journal: Diabetologia

Article Title: MicroRNA-193b impairs muscle growth in mouse models of type 2 diabetes by targeting the PDK1/Akt signalling pathway

doi: 10.1007/s00125-021-05616-y

Figure Lengend Snippet: miR-193b decreases activation of Akt by inhibiting PDK1 expression. ( a ) Graphical representation of the conserved miR-193b binding motifs within the 3′-UTR of Pdk1 . Complementary sequences to the seed regions of miR-193b within the 3′-UTRs are conserved between human (Homo) and mouse (Mus) sequences. ( b , c ) C2C12 cells were treated with miR-193b mimic or control (Ctrl) RNA and qPCR analysis was used to determine the mRNA level of PDK1 ( n = 5). ** p < 0.01, *** p < 0.001 vs time 0 ( b ) or Ctrl RNA treatment alone ( c ), by one-way ANOVA with Bonferroni correction. ( d ) Luciferase (luc) activity of the reporter constructs containing either wild-type or mutated (MT) 3′-UTR of murine Pdk1 after treatment of C2C12 cells with miR-193b mimic or Ctrl RNA ( n = 5). *** p < 0.001 vs Ctrl RNA treatment alone in the 3′-UTR-transfected group, by one-way ANOVA with Bonferroni correction. ( e ) C2C12 cells were treated with miR-193b mimic (40 nmol/l) or miR-193b inhibitor (100 nmol/l) and the protein level of PDK1, Akt and p-Akt was detected by western blot analysis. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( f ) Pdk1 siRNA was transfected into C2C12 cells. Cells were then treated with miR-193b inhibitor or nontargeting negative Ctrl RNA and western blot analysis was used to determine the protein level of PDK1, Akt and p-Akt. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). ( g ) C2C12 cells were treated with DEX alone or with a combination of miR-193b inhibitor and DEX and the protein level of PDK1, Akt and p-Akt was detected by western blot. Quantification of the relative levels of PDK1 and p-Akt proteins is shown ( n = 3). In ( e – g ): * p < 0.05, ** p < 0.01, *** p < 0.001 vs untreated cells, by one-way ANOVA with Bonferroni correction

Article Snippet: C2C12 cells were transfected with 3′ untranslated region (UTR) luciferase reporter constructs ( Pdk1 3′-UTR or Pdk1 3′-UTR-mutant), miRNA (control RNA [catalogue no.: sc-36,869; Santa Cruz Biotechnology] or miR-193b-3p) and Renilla luciferase using Lipofectamine 3000 (Invitrogen).

Techniques: Activation Assay, Expressing, Binding Assay, Control, Luciferase, Activity Assay, Construct, Transfection, Western Blot