Rory Johnson

This study uses CRISPR-Cas9 to identify functional exons in lncRNAs, finding most exons are non-functional and functionality is enriched at the 5' end.

The paper identifies 121 lncRNA driver mutations across 19 cancer types using 12,631 genomes, showing mutations disrupt RNA-binding protein interactions to promote oncogenesis.

The paper identifies TPL1 as a novel long noncoding RNA that drives triple-negative breast cancer hallmarks through multiple molecular mechanisms.

This paper identifies ADARreg, an elncRNA that modulates BCR signaling and immune evasion in lymphoma by altering RNA stability, localization, and editing, providing a potential therapeutic target.

The paper expands the lncRNA catalog using capture long-read RNA sequencing, significantly increasing the number of annotated transcripts in human and mouse genomes.

The paper introduces TransCistor, a framework to identify cis-regulatory lncRNAs with controlled false discovery rates, finding that only a minority of lncRNAs are cis-acting, primarily as activators.

The paper identifies mutated long noncoding RNAs (lncRNAs) as contributors to tumour cell fitness through experimental validation of their oncogenic effects.

The paper identifies 60 high-confidence oncogenic lncRNAs in NSCLC using CRISPR deletion screens and ASO validation, revealing therapeutic vulnerabilities.

The paper introduces MapToCleave, a method to profile miRNA biogenesis in living cells, showing that stable lower basal stems enhance processing and expression across species.

The paper identifies weak CEBPA binding in humans as a cause of slower B cell transdifferentiation compared to mice, linked to Alu repeat expansions.

The paper introduces a paired-guide RNA CRISPR-Cas9 system to identify protein-coding and lncRNA genes involved in human B-cell to macrophage transdifferentiation, identifying 26 potential novel genes.

The paper tracks transcriptomic and epigenomic changes during human pre-B cell to macrophage transdifferentiation, finding coordinated chromatin state transitions and gene activation patterns.

This paper shows that temporarily inhibiting DNA-PK increases CRISPR-Cas9 deletion efficiency by delaying NHEJ, improving experimental outcomes across multiple cell lines and guide RNAs.

The paper introduces the Cancer LncRNA Census (CLC), a curated resource of lncRNAs with causative roles in cancer, and shows their genomic and evolutionary features.

ActivePathways integrates multivariate omics data to identify enriched pathways, revealing cancer driver genes and prognostic pathways in breast cancer.

The paper identifies TE fragments associated with lncRNA nuclear enrichment and shows their role in subcellular localization.

The paper reanalyzes the CHESS database's new protein-coding predictions and finds most are false positives due to homology errors and lack of experimental evidence.

The paper identifies and characterizes coding and non-coding driver mutations across 2,500 cancer genomes, revealing new candidates and questioning previous findings.

The paper introduces RNA Capture Long Seq (CLS) to annotate full-length lncRNAs with high throughput and accuracy, doubling annotated complexity compared to short-read methods.

LncATLAS provides a database of lncRNA subcellular localization in human cells using RNA-seq data, offering tools to query and compare localization across cell types and organelles.

The paper identifies 15 high-confidence cancer driver lncRNAs across 1112 tumour genomes using a mutational pattern analysis approach.

CRISPETa is a scalable bioinformatic pipeline for designing paired CRISPR guide RNAs for genomic deletion, achieving ≥50% deletion efficiency in tested cases.

The paper traces the evolutionary history of selenophosphate synthetase (SPS) genes, showing how they duplicated and subfunctionalized to acquire distinct roles in metazoans.

This study maps cytoplasmic and ribosomal lncRNAs in human cells, revealing their association with polysomes and suggesting regulatory roles in translation.