Gary Loughran

The paper investigates the StopGo/2A translational recoding mechanism using cryo-EM and bioinformatics, revealing structural and sequence features that enable this process in viruses.

The paper identifies a novel RNA stimulator that enhances +1 ribosomal frameshifting in yeast by promoting P-site tRNA re-pairing, revealing two distinct frameshifting mechanisms.

This study examines early transcriptional and translational changes in human T cells within four hours of activation, revealing dynamic gene expression and translation initiation patterns.

The paper identifies a programmed ribosomal frameshifting event in PLEKHM2 mRNA that generates a constitutively active protein domain essential for lysosome transport and cardiac function.

This study uses a small molecule inhibitor to rapidly and synchronously induce senescence-like features in human cells, enabling analysis of its core regulatory program without paracrine effects.

The paper determines the structure of the translating bacterial ribosome at 1.55 Å resolution using open access cryo-EM, enabling detailed analysis of ribosome polymorphism and drug design.

This study identifies HMGB1 as an RNA-binding protein that coordinates chromatin folding and RNA homeostasis in senescence through interactions with other RBPs and regulation of SASP-related transcripts.

This study presents the cryo-EM structure of the mammalian ribosome during SARS-CoV-2 RNA translation, revealing the pseudoknot structure that facilitates ribosomal frameshifting and identifies a compound that inhibits viral replication.

The paper shows tissue-specific stop codon readthrough in Drosophila kelch gene, with high-efficiency readthrough in CNS neurons and potential for extended neuronal proteome.

The paper identifies a novel protein, POLGARF, encoded by an overlapping reading frame in POLG mRNA, showing efficient CUG initiation and evolutionary origins via MIR transposition.

The paper challenges the evidence for -1 frameshifting in CCR5 mRNA, arguing that the frameshifting mechanism does not lead to premature termination codon formation or mRNA destabilization via NMD.

The paper develops a computational model to explain how a single upstream open reading frame (uORF) can upregulate downstream ORF translation during the Integrated Stress Response.