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miRNAs function by binding to the 3' untranslated region (3'-UTR) of target mRNAs, leading to mRNA degradation or translational repression. With over 2600 miRNAs identified in humans, a single miRNA has the potential to regulate hundreds of genes, indicating their widespread influence on gene expression.
Creative Biogene offers a comprehensive 3'UTR lentiviral vector library targeting all human genes, featuring a choice of GFP or luciferase reporter genes. These constructs incorporate 3'-UTR sequences obtained from public gene sequence databases, cloned downstream of a reporter gene in a lentiviral vector under the control of the CMV promoter. Creative Biogene's 3'UTR lentiviral vector library provides researchers with a powerful platform for exploring miRNA-mediated gene regulation and its implications in diverse biological contexts.
Key Features of Our 3'UTR Virus
Our 3'UTR Virus platform enables efficient investigation of miRNA-mediated gene regulation, facilitating comprehensive studies on cellular processes and disease mechanisms. Leveraging our advanced technology and extensive library targeting all human genes, researchers can explore miRNA binding requirements with ease and accuracy:
Case Study 1
The role of cellular senescence as a tumor suppression mechanism highlights the importance of investigating gene expression regulation during senescence, providing insights into cancer therapy. Researchers aimed to elucidate the role of the 3'UTR Virus vector in investigating the regulatory mechanisms of gene expression during cellular senescence, with implications for cancer therapy. By studying alternative polyadenylation (APA) and its impact on the HN1 gene, they found that APA of HN1 correlated with cancer and senescence, influencing its stability and protein production. Manipulating HN1 expression induced senescence-associated phenotypes, and patients with higher HN1 expression exhibited lower survival rates in various carcinomas. Notably, modulating the splicing factor HNRNPA1 affected HN1 APA and senescence-associated phenotypes, indicating the HNRNPA1-HN1 axis as a potential target for cancer treatment. This study underscores the importance of understanding gene regulation in senescence and its implications for cancer therapy.
Figure 1. Researchers investigated the downstream effects of HN1 transcripts with shorter (HN1-S) and longer (HN1-L) 3' UTRs on gene expression, respectively, using 3'UTR Virus vectors. (Jia Q, et al., 2019)
Case Study 2
In colorectal cancer (CRC), PLAGL2 or POFUT1 promote tumorigenesis and exhibit significant positive correlations, yet the mechanism driving their co-expression and functional implications remain unclear. Researchers investigated the co-expression mechanism and functional implications of PLAGL2 and POFUT1 in colorectal cancer (CRC). Clinical data and TCGA dataset analysis confirmed their significant positive correlation (r = 0.91, p < .0001). Employing luciferase reporter assays, bidirectional promoter vectors, and 3'UTR expression, they elucidated an evolutionarily conserved bidirectional promoter responsible for their co-expression. Furthermore, in vitro and in vivo assays demonstrated their synergistic oncogenic effects in CRC, particularly in maintaining colorectal cancer stem cell (CSC) stemness via the Wnt and Notch pathways. Mutational analysis of shared transcription factor binding sites confirmed the regulatory role of the bidirectional promoter. This study uncovers the oncogenic potential of the PLAGL2-POFUT1 bidirectional promoter pair, offering novel therapeutic targets for CRC intervention.
Figure 2. Lentiviral vectors carrying PLAGL2, POFUT1, and various cDNA constructs, including PLAGL2–3'UTR1 and PLAGL2–3'UTR2, were utilized, along with lentiviral shRNA targeting human PLAGL2 and POFUT1. (Li D, et al., 2019)
Q: How do these 3'UTR Virus products assist in validating the interaction between miRNA and target genes?
A: Our 3'UTR Virus platform enables researchers to effectively validate the interaction between miRNA and target genes by observing the reduction in reporter gene expression to confirm whether such interaction occurs.
Q: How are these products utilized to analyze the expression of endogenous miRNA?
A: By transfecting the 3'UTR reporter vector into the cell line of interest, along with miRNA inhibitors, one can observe whether the interaction between miRNA and the UTR of the Reporter Vector is reduced or abolished, facilitating the analysis of endogenous miRNA expression.
Q: How do these products aid in studying the binding requirements of miRNA?
A: By employing 3'UTR mutant reporters, researchers can determine the significance of a locus for miRNA binding. Mutating the locus and observing whether reporter gene expression is affected allows for the exploration of miRNA binding requirements.
Q: How are 3'UTR reporter cell lines utilized for stable expression of the 3'UTR reporter construct?
A: Our products offer cell lines for stable expression of the 3'UTR reporter construct from HEK293 cells, providing researchers with a more stable and reliable expression system to facilitate their research endeavors.
| Cat.No. | Product Name | Price |
|---|---|---|
| MiUTR4H-TG00003 | A2ML1 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00005 | A4GNT miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00008 | AADACL2 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00011 | AANAT miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00017 | AATK miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00018 | ABAT miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00027 | ABCA13 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00047 | ABCG4 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00050 | ABHD5 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00060 | ABRA miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00072 | ACAP2 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00075 | ACBD5 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00079 | ACER3 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00088 | ACOT11 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG00089 | ACOT12 miRNA 3'UTR clone | Inquiry |
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