HY-R04608 Search Results


rad51 ssdna-1  (MedChemExpress)
N/A
RAD51 SSDNA-1 is a chemically synthesized miRNA mimic that mimics endogenous miRNAs and upregulates miRNA activity for gain-of-function studies.
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mir 1183 inhibitor  (MedChemExpress)
95
MedChemExpress mir 1183 inhibitor
DDX11-AS1 competitively <t>binds</t> <t>miR-1183</t> through competing endogenous RNA (ceRNA) mechanism. ( A ) In silico analysis of the binding site of miR-1183 within DDX11-AS1 sequence. ( B ) Correlation between DDX11-AS1 and miR-1183 expression in clinical glioma samples ( n = 32). ( C , D ) The expression level of miR-1183 in glioma cells with DDX11-AS1 ( C ) knockdown or ( D ) overexpression ( n = 6). ( E ) The relative luciferase activity was examined in U87 glioma cells co-transfected with DDX11-AS1 wild-type (WT) or DDX11-AS1 mutant (MUT) and miR-1183 mimics or the miR-NC. ( F , G ) RIP assay in ( F ) U87 and ( G ) U251 glioma cells. ( H ) Binding of miR-1183 and miR-NC to DDX11-AS1 in the RNA pull-down assay (GAPDH as control). ( I ) RNA FISH for DDX11-AS1 and miR-1183 in human glioma sample. Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test
Mir 1183 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/HY-R04608/MicroRNA+Mimic+Negative+Control/pmc12494103-52-33-37
Average 95 stars, based on 1 article reviews
mir 1183 inhibitor - by Bioz Stars, 2026-10
95/100 stars
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Image Search Results


DDX11-AS1 competitively binds miR-1183 through competing endogenous RNA (ceRNA) mechanism. ( A ) In silico analysis of the binding site of miR-1183 within DDX11-AS1 sequence. ( B ) Correlation between DDX11-AS1 and miR-1183 expression in clinical glioma samples ( n = 32). ( C , D ) The expression level of miR-1183 in glioma cells with DDX11-AS1 ( C ) knockdown or ( D ) overexpression ( n = 6). ( E ) The relative luciferase activity was examined in U87 glioma cells co-transfected with DDX11-AS1 wild-type (WT) or DDX11-AS1 mutant (MUT) and miR-1183 mimics or the miR-NC. ( F , G ) RIP assay in ( F ) U87 and ( G ) U251 glioma cells. ( H ) Binding of miR-1183 and miR-NC to DDX11-AS1 in the RNA pull-down assay (GAPDH as control). ( I ) RNA FISH for DDX11-AS1 and miR-1183 in human glioma sample. Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: DDX11-AS1 competitively binds miR-1183 through competing endogenous RNA (ceRNA) mechanism. ( A ) In silico analysis of the binding site of miR-1183 within DDX11-AS1 sequence. ( B ) Correlation between DDX11-AS1 and miR-1183 expression in clinical glioma samples ( n = 32). ( C , D ) The expression level of miR-1183 in glioma cells with DDX11-AS1 ( C ) knockdown or ( D ) overexpression ( n = 6). ( E ) The relative luciferase activity was examined in U87 glioma cells co-transfected with DDX11-AS1 wild-type (WT) or DDX11-AS1 mutant (MUT) and miR-1183 mimics or the miR-NC. ( F , G ) RIP assay in ( F ) U87 and ( G ) U251 glioma cells. ( H ) Binding of miR-1183 and miR-NC to DDX11-AS1 in the RNA pull-down assay (GAPDH as control). ( I ) RNA FISH for DDX11-AS1 and miR-1183 in human glioma sample. Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Article Snippet: All cell cultures underwent validation via short tandem repeat profiling and confirmed absence of mycoplasma contamination. miR-1183 mimics (catalog #HY-R00073; MCE, Monmouth Junction, NJ, USA), miRNA negative controls (miR-NC; catalog #HY-R04602; MCE) and miR-1183 inhibitor (catalog #HY-RI00073; MCE) were acquired from MCE.

Techniques: In Silico, Binding Assay, Sequencing, Expressing, Knockdown, Over Expression, Luciferase, Activity Assay, Transfection, Mutagenesis, Pull Down Assay, Control

DDX11-AS1 promotes glioma cell proliferation and migration by targeting miR-1183. Glioma cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed by miR-1183 inhibitor treatment were used. ( A , B ) CCK-8 assays of ( A ) U87 and ( B ) U251 glioma cells ( n = 6). ( C , D ) Colony formation assays of ( C ) U87 and ( D ) U251 glioma cells ( n = 6). ( E ) Scratch wound healing assay of U87 and U251 glioma cells. ( F ) Transwell assay of U87 and U251 glioma cells. The right panel is the quantified data depicting migrated cell number ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: DDX11-AS1 promotes glioma cell proliferation and migration by targeting miR-1183. Glioma cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed by miR-1183 inhibitor treatment were used. ( A , B ) CCK-8 assays of ( A ) U87 and ( B ) U251 glioma cells ( n = 6). ( C , D ) Colony formation assays of ( C ) U87 and ( D ) U251 glioma cells ( n = 6). ( E ) Scratch wound healing assay of U87 and U251 glioma cells. ( F ) Transwell assay of U87 and U251 glioma cells. The right panel is the quantified data depicting migrated cell number ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Article Snippet: All cell cultures underwent validation via short tandem repeat profiling and confirmed absence of mycoplasma contamination. miR-1183 mimics (catalog #HY-R00073; MCE, Monmouth Junction, NJ, USA), miRNA negative controls (miR-NC; catalog #HY-R04602; MCE) and miR-1183 inhibitor (catalog #HY-RI00073; MCE) were acquired from MCE.

Techniques: Migration, Transfection, CCK-8 Assay, Wound Healing Assay, Transwell Assay

E2F7 is a target of miR-1183. ( A ) The bioinformatics analysis tools were used to predict the binding site of miR-1183 in E2F7. ( B ) Correlation between miR-1183 and E2F7 expression. ( C ) Luciferase activity in U87 cells co-transfected with miR-1183 and WT/MUT E2F7 reporter constructs ( n = 6). ( D – G ) U87 and U251 cells transfected with miR-1183, miR-NC or E2F7-overexpression vectors were used; ( D , E ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6); ( F , G ) CCK-8 assay of ( F ) U87 and ( G ) U251 cells ( n = 6); ( H , I ) U87 and U251 cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed with miR-1183 inhibitor treatment were used. ( H ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6). ( I ) Immunoblotting assays detected E2F7 and GAPDH in U87 and U251 cells. The bar chart quantifies relative E2F7 protein abundance normalized to GAPDH ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: E2F7 is a target of miR-1183. ( A ) The bioinformatics analysis tools were used to predict the binding site of miR-1183 in E2F7. ( B ) Correlation between miR-1183 and E2F7 expression. ( C ) Luciferase activity in U87 cells co-transfected with miR-1183 and WT/MUT E2F7 reporter constructs ( n = 6). ( D – G ) U87 and U251 cells transfected with miR-1183, miR-NC or E2F7-overexpression vectors were used; ( D , E ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6); ( F , G ) CCK-8 assay of ( F ) U87 and ( G ) U251 cells ( n = 6); ( H , I ) U87 and U251 cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed with miR-1183 inhibitor treatment were used. ( H ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6). ( I ) Immunoblotting assays detected E2F7 and GAPDH in U87 and U251 cells. The bar chart quantifies relative E2F7 protein abundance normalized to GAPDH ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Article Snippet: All cell cultures underwent validation via short tandem repeat profiling and confirmed absence of mycoplasma contamination. miR-1183 mimics (catalog #HY-R00073; MCE, Monmouth Junction, NJ, USA), miRNA negative controls (miR-NC; catalog #HY-R04602; MCE) and miR-1183 inhibitor (catalog #HY-RI00073; MCE) were acquired from MCE.

Techniques: Binding Assay, Expressing, Luciferase, Activity Assay, Transfection, Construct, Over Expression, Quantitative RT-PCR, CCK-8 Assay, Western Blot, Quantitative Proteomics