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What’s Inside This whitepaper introduces Ribo96, a 96-well platform developed by EIRNABio to support large-scale studies of translation. It explains how researchers can generate and interpret translatomic data across many conditions using low-input samples and automation-compatible workflows. You’ll learn about: The design and function of the Ribo96 platform Applications in studying translational control, drug response […]

Gene expression is the process by which genetic information is used to make the proteins which carry out the biological functions essential to all life. Interrogation of this process at a global level facilitates early-stage drug discovery and allows signatures of disease susceptibility to be elucidated. This type of analysis is typically carried out at the level of transcription

Numerous diseases, ranging from cancer to neurodegenerative disorders, exhibit dysregulated translation as a central feature of their pathogenesis. Translation, the process by which mRNA is translated into functional proteins, is finely regulated to maintain cellular homeostasis. However, aberrant translation can lead to the production of harmful proteins, disruption of cellular processes, and ultimately disease onset and progression. Traditional approaches such

Dysregulated translation lies at the heart of numerous pathological conditions, including cancer, neurodegenerative disorders, and infectious diseases. Unravelling the specific genes, pathways, and regulatory mechanisms driving aberrant translation offers promising avenues for therapeutic intervention. Identifying whether lead compounds for disease targets impact global translational signatures is a useful first step in understanding their pharmacological effects and potential therapeutic efficacy.  Polysome

Ribosome stalling (also known as ribosome pausing) occurs physiologically across most of the transcriptome and is known to facilitate co-translational folding of the nascent peptide chain. Prolonged stalling, however, can also lead to ribosome collisions arising due to transcript mutations or defective nascent peptides, ultimately resulting in both the transcript and the nascent polypeptide being targeted for degradation. Global