ELP3 (Elongator Complex Protein 3) is a key subunit of the Elongator complex, a multi-protein assembly highly conserved across eukaryotes. Initially identified for its role in transcriptional elongation via interaction with RNA polymerase II, ELP3 is now recognized to possess dual functional domains: a histone acetyltransferase (HAT) domain implicated in chromatin remodeling and a radical S-adenosylmethionine (SAM) domain critical for catalytic activities. Beyond transcription, ELP3 plays essential roles in cytoplasmic processes, particularly tRNA modification. It facilitates the wobble uridine modification (U34) in tRNA, a step vital for translational fidelity and efficiency, thereby influencing protein synthesis rates and cellular stress responses.
Research links ELP3 dysfunction to neurodevelopmental and neurodegenerative disorders. Mutations or altered expression of ELP3 are associated with amyotrophic lateral sclerosis (ALS), intellectual disability, and autism spectrum disorders, likely due to impaired tRNA modification and disrupted neuronal protein homeostasis. In models like *Drosophila* and mice, ELP3 depletion causes axon degeneration and motor deficits, mirroring ALS pathology. Additionally, ELP3's HAT activity may regulate genes involved in neurodevelopment and synaptic plasticity.
Antibodies targeting ELP3 are widely used to study its expression, localization, and interactions in both physiological and disease contexts. These tools enable investigations into its roles in transcription, translation, and neurological disease mechanisms, making them critical for elucidating ELP3's multifaceted contributions to cellular and organismal health.