Analysis reveals that HuD’s TAP/NXF1-binding region drives translation in neurons, highlighting its role in neuronal differentiation.
The neuronal ELAV protein HuD is known to promote neuronal differentiation and stimulate cap‐dependent translation, but the underlying mechanism remains incompletely understood. Here, we identify a functional domain within the HuD linker that governs interaction with the nuclear export factor TAP/NXF1 and stimulates translation. Using a series of deletion mutants, we show that TAP/NXF1 binding is functionally separable from cytoplasmic localization, and that loss of this interaction correlates with impaired translation and neurite outgrowth. These findings reveal a critical subdomain within HuD that recruits TAP/NXF1 to promote translation and neuronal differentiation, establishing a mechanistic link between RNA export factors and ELAV‐mediated translational control.
No takes yet. Share an insight, caveat, or question.
Toshima et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: