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MrRNA-directed DNA methylation enables selective mutant oncogene silencing therapy without exogenous proteins [RRBS]

ABSTRACT: mrRNA-directed DNA methylation enables selective mutant oncogene silencing therapy without exogenous proteins [RRBS]

PROVIDER: PRJNA1309099 | ENA |

REPOSITORIES: ENA

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mrRNA-directed DNA methylation enables selective mutant oncogene silencing therapy without exogenous proteins

Project description:mrRNA-directed DNA methylation enables selective mutant oncogene silencing therapy without exogenous proteins

| PRJNA1303133 | ENA

mrRNA-directed DNA methylation enables selective mutant oncogene silencing therapy without exogenous proteins [RRBS]

Project description:The outcome of recent demethylation therapy is limited by the unspecific hypomethylation of oncogenes. The mechanism underlying differential DNA methylation distribution in the same topological domain remains unclear. Here, we established an efficient framework based on heterogeneity across pan-cancers to systemically characterize DNA methylation regulatory boxes (mrBoxes). Through plasmid-based functional motif interactome analysis assay, the role of mrBoxes on DNA methylation was validated. Moreover, the U1 small nuclear ribonucleoprotein A (SNPRA) was found to regulate the chromatin localization of DNMT1 to mrBox. In this process, long noncoding RNAs were identified to act as a bridge, connecting the targeted mrBox element and SNRPA/DNMT1 complex. Based on this regulatory model, we synthesized exogenous methylation-regulating RNA (mrRNA), which contains only the mrBox-recognizing and SNRPA/DNMT1 complex-binding motif. Furthermore, we developed a methylation-regulating therapy called “OncoMutation Silence”, which regulates the DNA methylation of mutated oncogenes through mrRNA. The efficacy and specificity of this therapy have been verified in tumors with KrasG12D mutation. Collectively, this study reveals mrBox-related regulatory model of DNA methylation, and provides mrRNA-based tumor therapy for silencing specific mutated oncogenes.

2025-08-26 | GSE306087 | GEO

mrRNA-directed DNA methylation enables selective mutant oncogene silencing therapy without exogenous proteins

2025-08-12 | GSE304877 | GEO

Replicative RNA enables directed evolution and Darwinian adaptation in mammalian cells

Project description:Replicative RNA enables directed evolution and Darwinian adaptation in mammalian cells

| PRJNA985713 | ENA

A Bivalent Molecular Glue Linking Lysine Acetyltransferases to Oncogene-directed Cell Death [RNA-seq]

Project description:A Bivalent Molecular Glue Linking Lysine Acetyltransferases to Oncogene-directed Cell Death [RNA-seq]

| PRJNA1213716 | ENA

A Bivalent Molecular Glue Linking Lysine Acetyltransferases to Oncogene-directed Cell Death [ChIP-seq]

Project description:A Bivalent Molecular Glue Linking Lysine Acetyltransferases to Oncogene-directed Cell Death [ChIP-seq]

| PRJNA1213717 | ENA

DNA epigenome editing using CRISPR-Cas SunTag-directed DNMT3A [RRBS]

Project description:We demonstrate that dCas9-SunTag-DNMT3A dramatically increased CpG methylation at the HOXA5 locus in human embryonic kidney 293T cells (HEK293T). Furthermore, using a single sgRNA, dCas9-SunTag-DNMT3A was able to methylate a 4.5 kb genomic region and repress HOXA5 gene expression. Reduced representation bisulfite sequencing (RRBS) and RNA-seq showed that dCas9-SunTag-DNMT3A methylated regions of interest with minimal impact on the global DNA methylome and transcriptome.

2017-08-22 | GSE97813 | GEO

Programmable Targeted RNA Degradation via dCas13d-Directed Chaperone-Mediated Autophagy (dCasCMA)

Project description:RNA-targeted degradation technologies offer significant promise for treating diseases by selectively disrupting gene expression. However, a robust method to specifically, efficiently, and programmability degrade targeted RNAs in mammalian cells is still in demand. Here, we present a versatile platform, dCas13d-directed chaperone-mediated autophagy (dCasCMA), which integrates the precise targeting capabilities of dCas13/CRISPR with the degradation efficiency of chaperone-mediated autophagy (CMA) to achieve efficient degradation of specific RNAs. By combining dCas13d with a CMA-targeting motif and customizable guide RNA (gRNA), the platform allows for accurate targeting of both exogenous and endogenous RNAs in cells. Moreover, the incorporation of multiplexed gRNA expression arrays enables the simultaneous degradation of multiple RNA targets during viral pathogenesis in live cells and in vivo. Our findings emphasize the platform’s modular design, which enables flexible combinations of dCCTM components with user-defined gRNA sequences. This versatility positions it as a promising tool for developing innovative therapies for various diseases.

2025-09-20 | GSE294475 | GEO

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (RRBS)

Project description:De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (RRBS)

| PRJNA573110 | ENA

UBC RRBS

Project description:UBC RRBS

2023-05-07 | OEX00023008 | NODE