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p gl3 myb  (Addgene inc)


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    Addgene inc p gl3 myb
    Effect of miR-150 inhibition and restoration on MYB expression in low- and high-dose DHT-treated prostate cancer cells. A and B , LNCaP and C4-2 cells were transfected with negative control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h, followed by low and high doses treatment of DHT for another 24 h. MYB expression was analyzed by Western blotting. β-actin was used as a loading control. C and D , cells were transfected with negative control miRNA mimic (miR-NC) or miR-150 mimic (miR-150) for 24 h, followed by DHT (1.0 nM) treatment for 24 h and MYB expression analysis. E – G , prostate cancer cells were transfected with a luciferase reporter plasmid carrying MYB-3ʹUTR-WT (WT) sequence containing a putative-binding site for miR-150 or MYB-3ʹUTR-Mut (Mutant) where miR-150 binding site is mutated. Cells were also cotransfected with Renilla luciferase plasmid (pRL/TK) to control transfection efficiency. After 24 h, cells received treatment with low and high doses of DHT, and luciferase activity was examined after 24 h of incubation. The data is presented as normalized luciferase activity (mean ± SD), ∗ p = < 0.05. H and I , LNCaP and C4-2 cells were cotransfected with <t>pGL3-MYB-3′UTR</t> WT or pGL3-MYB-3′UTR mutant (Mut) luciferase along with either control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h. Thereafter, cells were treated with low and high DHT doses for 24 h. Luciferase activity was examined, and the data presented as the normalized luciferase activity (mean ± SD), ∗ p = < 0.05, n.s. not significant. DHT, dihydrotestosterone.
    P Gl3 Myb, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p gl3 myb/product/Addgene inc
    Average 93 stars, based on 5 article reviews
    p gl3 myb - by Bioz Stars, 2026-03
    93/100 stars

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    1) Product Images from "Biphasic transcriptional and posttranscriptional regulation of MYB by androgen signaling mediates its growth control in prostate cancer"

    Article Title: Biphasic transcriptional and posttranscriptional regulation of MYB by androgen signaling mediates its growth control in prostate cancer

    Journal: The Journal of Biological Chemistry

    doi: 10.1016/j.jbc.2022.102725

    Effect of miR-150 inhibition and restoration on MYB expression in low- and high-dose DHT-treated prostate cancer cells. A and B , LNCaP and C4-2 cells were transfected with negative control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h, followed by low and high doses treatment of DHT for another 24 h. MYB expression was analyzed by Western blotting. β-actin was used as a loading control. C and D , cells were transfected with negative control miRNA mimic (miR-NC) or miR-150 mimic (miR-150) for 24 h, followed by DHT (1.0 nM) treatment for 24 h and MYB expression analysis. E – G , prostate cancer cells were transfected with a luciferase reporter plasmid carrying MYB-3ʹUTR-WT (WT) sequence containing a putative-binding site for miR-150 or MYB-3ʹUTR-Mut (Mutant) where miR-150 binding site is mutated. Cells were also cotransfected with Renilla luciferase plasmid (pRL/TK) to control transfection efficiency. After 24 h, cells received treatment with low and high doses of DHT, and luciferase activity was examined after 24 h of incubation. The data is presented as normalized luciferase activity (mean ± SD), ∗ p = < 0.05. H and I , LNCaP and C4-2 cells were cotransfected with pGL3-MYB-3′UTR WT or pGL3-MYB-3′UTR mutant (Mut) luciferase along with either control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h. Thereafter, cells were treated with low and high DHT doses for 24 h. Luciferase activity was examined, and the data presented as the normalized luciferase activity (mean ± SD), ∗ p = < 0.05, n.s. not significant. DHT, dihydrotestosterone.
    Figure Legend Snippet: Effect of miR-150 inhibition and restoration on MYB expression in low- and high-dose DHT-treated prostate cancer cells. A and B , LNCaP and C4-2 cells were transfected with negative control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h, followed by low and high doses treatment of DHT for another 24 h. MYB expression was analyzed by Western blotting. β-actin was used as a loading control. C and D , cells were transfected with negative control miRNA mimic (miR-NC) or miR-150 mimic (miR-150) for 24 h, followed by DHT (1.0 nM) treatment for 24 h and MYB expression analysis. E – G , prostate cancer cells were transfected with a luciferase reporter plasmid carrying MYB-3ʹUTR-WT (WT) sequence containing a putative-binding site for miR-150 or MYB-3ʹUTR-Mut (Mutant) where miR-150 binding site is mutated. Cells were also cotransfected with Renilla luciferase plasmid (pRL/TK) to control transfection efficiency. After 24 h, cells received treatment with low and high doses of DHT, and luciferase activity was examined after 24 h of incubation. The data is presented as normalized luciferase activity (mean ± SD), ∗ p = < 0.05. H and I , LNCaP and C4-2 cells were cotransfected with pGL3-MYB-3′UTR WT or pGL3-MYB-3′UTR mutant (Mut) luciferase along with either control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h. Thereafter, cells were treated with low and high DHT doses for 24 h. Luciferase activity was examined, and the data presented as the normalized luciferase activity (mean ± SD), ∗ p = < 0.05, n.s. not significant. DHT, dihydrotestosterone.

    Techniques Used: Inhibition, Expressing, Transfection, Negative Control, Western Blot, Luciferase, Plasmid Preparation, Sequencing, Binding Assay, Mutagenesis, Activity Assay, Incubation



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    p gl3 myb  (Addgene inc)
    93
    Addgene inc p gl3 myb
    Effect of miR-150 inhibition and restoration on MYB expression in low- and high-dose DHT-treated prostate cancer cells. A and B , LNCaP and C4-2 cells were transfected with negative control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h, followed by low and high doses treatment of DHT for another 24 h. MYB expression was analyzed by Western blotting. β-actin was used as a loading control. C and D , cells were transfected with negative control miRNA mimic (miR-NC) or miR-150 mimic (miR-150) for 24 h, followed by DHT (1.0 nM) treatment for 24 h and MYB expression analysis. E – G , prostate cancer cells were transfected with a luciferase reporter plasmid carrying MYB-3ʹUTR-WT (WT) sequence containing a putative-binding site for miR-150 or MYB-3ʹUTR-Mut (Mutant) where miR-150 binding site is mutated. Cells were also cotransfected with Renilla luciferase plasmid (pRL/TK) to control transfection efficiency. After 24 h, cells received treatment with low and high doses of DHT, and luciferase activity was examined after 24 h of incubation. The data is presented as normalized luciferase activity (mean ± SD), ∗ p = < 0.05. H and I , LNCaP and C4-2 cells were cotransfected with <t>pGL3-MYB-3′UTR</t> WT or pGL3-MYB-3′UTR mutant (Mut) luciferase along with either control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h. Thereafter, cells were treated with low and high DHT doses for 24 h. Luciferase activity was examined, and the data presented as the normalized luciferase activity (mean ± SD), ∗ p = < 0.05, n.s. not significant. DHT, dihydrotestosterone.
    P Gl3 Myb, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p gl3 myb/product/Addgene inc
    Average 93 stars, based on 1 article reviews
    p gl3 myb - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier

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    Effect of miR-150 inhibition and restoration on MYB expression in low- and high-dose DHT-treated prostate cancer cells. A and B , LNCaP and C4-2 cells were transfected with negative control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h, followed by low and high doses treatment of DHT for another 24 h. MYB expression was analyzed by Western blotting. β-actin was used as a loading control. C and D , cells were transfected with negative control miRNA mimic (miR-NC) or miR-150 mimic (miR-150) for 24 h, followed by DHT (1.0 nM) treatment for 24 h and MYB expression analysis. E – G , prostate cancer cells were transfected with a luciferase reporter plasmid carrying MYB-3ʹUTR-WT (WT) sequence containing a putative-binding site for miR-150 or MYB-3ʹUTR-Mut (Mutant) where miR-150 binding site is mutated. Cells were also cotransfected with Renilla luciferase plasmid (pRL/TK) to control transfection efficiency. After 24 h, cells received treatment with low and high doses of DHT, and luciferase activity was examined after 24 h of incubation. The data is presented as normalized luciferase activity (mean ± SD), ∗ p = < 0.05. H and I , LNCaP and C4-2 cells were cotransfected with pGL3-MYB-3′UTR WT or pGL3-MYB-3′UTR mutant (Mut) luciferase along with either control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h. Thereafter, cells were treated with low and high DHT doses for 24 h. Luciferase activity was examined, and the data presented as the normalized luciferase activity (mean ± SD), ∗ p = < 0.05, n.s. not significant. DHT, dihydrotestosterone.

    Journal: The Journal of Biological Chemistry

    Article Title: Biphasic transcriptional and posttranscriptional regulation of MYB by androgen signaling mediates its growth control in prostate cancer

    doi: 10.1016/j.jbc.2022.102725

    Figure Lengend Snippet: Effect of miR-150 inhibition and restoration on MYB expression in low- and high-dose DHT-treated prostate cancer cells. A and B , LNCaP and C4-2 cells were transfected with negative control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h, followed by low and high doses treatment of DHT for another 24 h. MYB expression was analyzed by Western blotting. β-actin was used as a loading control. C and D , cells were transfected with negative control miRNA mimic (miR-NC) or miR-150 mimic (miR-150) for 24 h, followed by DHT (1.0 nM) treatment for 24 h and MYB expression analysis. E – G , prostate cancer cells were transfected with a luciferase reporter plasmid carrying MYB-3ʹUTR-WT (WT) sequence containing a putative-binding site for miR-150 or MYB-3ʹUTR-Mut (Mutant) where miR-150 binding site is mutated. Cells were also cotransfected with Renilla luciferase plasmid (pRL/TK) to control transfection efficiency. After 24 h, cells received treatment with low and high doses of DHT, and luciferase activity was examined after 24 h of incubation. The data is presented as normalized luciferase activity (mean ± SD), ∗ p = < 0.05. H and I , LNCaP and C4-2 cells were cotransfected with pGL3-MYB-3′UTR WT or pGL3-MYB-3′UTR mutant (Mut) luciferase along with either control-inhibitor (NC-Inh) or miR-150 inhibitor (miR150-Inh) for 24 h. Thereafter, cells were treated with low and high DHT doses for 24 h. Luciferase activity was examined, and the data presented as the normalized luciferase activity (mean ± SD), ∗ p = < 0.05, n.s. not significant. DHT, dihydrotestosterone.

    Article Snippet: WST-1 reagent was purchased from BioVision, Inc. MYB promoter-reporter construct (GLuc-ON MYB; HPRM34981-PG02), MYB mutant promoter-reporter construct (GLuc-ON MYB; HPRM34981-PG02-01), has-miR-150 WT and mutant (CS-HPRM54623-PG04-01 and CS-HPRM54623-PG04-02) were purchased from GeneCopoeia. p-GL3-MYB-3′UTR (Cat. # 25798) (Firefly Luciferase) ( ) was purchased from Addgene, p-GL3-MYB-3′ UTR-mutant (VB20819-12933men) was purchased from VectorBuilder, and pRL-Tk (Renilla Luciferase) plasmid constructs was purchased from Promega.

    Techniques: Inhibition, Expressing, Transfection, Negative Control, Western Blot, Luciferase, Plasmid Preparation, Sequencing, Binding Assay, Mutagenesis, Activity Assay, Incubation