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tRNA m7G TRAC-Sequencing and m3C HAC-Sequencing

TRAC-seq and HAC-seq are designed for precise detection of individual RNA modifications at single-nucleotide resolution. By combining selective chemical/enzymatic treatment with next-generation sequencing, these methods convert specific RNA modifications into characteristic reverse transcription signatures, enabling accurate identification and site-specific mapping of target modifications across the transcriptome. Their high sensitivity and nucleotide-level precision make them powerful […]

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Turnkey Solutions for tRNA Research

tRNAs are abundant small RNAs essential for delivering amino acids and decoding genetic codons during protein translation. Beyond this canonical role, tRNAs actively regulate translation and disease processes through changes in tRNA expression, modification, and charging, three key determinants of tRNA function. Altered tRNA expression can reshape codon-dependent translation, while tRNA modifications (e.g., m7G, m1A)

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RNA G-Quadruplex (rG4) – What it is, why it matters, how to study it

What is RNA G-Quadruplex (rG4)?   RNA G-quadruplexes (rG4s) are non-canonical secondary structures originated from guanine-rich RNA sequences, where  four guanines are arranged together by Hoogsteen hydrogen bonding in a planar G-quartet and the quartets are stacked forming a stable four-stranded conformation. Monovalent cations, particularly K⁺, greatly enhance the rG4 stability (Fig. 1). rG4s are evolutionarily

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Why Study Circular RNA?

  Introduction Circular RNA (circRNA) is a novel type of RNA that, unlike linear RNA, forms a covalently closed continuous loop, and is highly represented in the eukaryotic transcriptome. Most of these circRNAs are generated from exonic sequences, are conserved across species, and often show tissue/developmental-stage-specific expression. Circular RNAs are more stable than linear RNAs

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Epigenetic and Epitranscriptomic Regulation of DoG RNAs

Dysregulation of H3K36 tri-methylation In clear cell renal cell carcinoma (ccRCC), read-through transcription and DoG formation are extensive due to defective transcription termination and consequent aberrant splicing [1]. Notably, H3K36 methyl transferase gene SETD2 is frequently mutated. SETD2 knockout in ccRCC cells induced read-through transcription[1]. Read-through transcription has also been observed in a variety of cancers, underlining this transcription

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DoG RNAs Modulate Gene Transcription in Diseases

The functional roles of read-through transcription and DoG RNAs are currently the focus of active research, with several proposed mechanisms highlighting their involvement in gene regulation. DoG RNAs mediate transcriptional interference in cell senescence DoGs can act as antisense RNAs to control the gene expression of convergent protein-coding genes. In senescent cells, a family of

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What Are DoG RNAs?

Downstream-of-gene (DoG) RNAs are RNA transcripts that arise downstream of ~10% of host genes and are continuous with their upstream RNAs [1]. DoGs are defined as having a minimal length of 5 kb beyond the polyadenylation signal (PAS) at transcription end site (TES), with maximal length up to 200 kb in mammalian cells [1]. Due

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DoG-derived Chimera RNAs and Circular RNAs in Cancers and Diseases

DoG-derived chimera RNAs A chimeraRNA is produced by Cis-Splicing between Adjacent Genes (cis-SAGe) when RNA polymerase II skips the stop signals, generating a read-through pre-transcript of two neighboring genes (Fig. 1). It is estimated that ~5% of the tandem gene pairs in the human genome can be transcribed into single precursor RNAs and eventually spliced into chimeric RNAs.

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Arraystar rG4 Microarray – The Gold Standard of Profiling in vivo rG4s

The identification and quantification of RNA G-quadruplex (rG4) in vivo is an essential step to study rG4 in cell biology and human diseases. Next-generation sequencing (NGS)-based techniques, such as G4RP-seq [1], BG4 uvRIP-seq, and DMS-seq plus RT Stop profiling[2], have been employed to investigate in rG4 vivo landscapes across the transcriptome and to assess quantitative

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Overview of Cancer Metabolism

Cancer metabolism is one of the core hallmarks of cancer [1, 2]. Mainly driven by oncogenic signaling pathways and by amplified or alternatively spliced metabolic enzymes, the characteristic and profound metabolic alteration allows cancer cells to accommodate metabolic demands to sustain growth, proliferation, and survival in nutrient fluctuating environment [3, 4](Fig. 1). Enhanced uptake of

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