Alteration of the G-quadruplex structure formed by GGGGCC repeat RNA through the direct interaction with RNA-binding proteins can suppress pathogenic repeat-associated non-AUG translation, leading to therapeutic effects on neurodegeneration in C9orf72-linked amyotrophic lateral sclerosis and frontotemporal dementia.

Mutational analysis in cell-based models of C9ORF72 ALS/FTD identifies canonical translation initiation codons (AUG) on the antisense CCCCGG transcript as initiation sites for synthesis of neurotoxic dipeptide repeat proteins.

A bacterial tRNA gene set rapidly evolves, compensating the loss of one tRNA type by large duplication events that increase the gene copy number of a second, different tRNA type.

Modulation of insulin signalling could be an effective therapeutic approach against hexanucleotide repeat expansion related to c9ALS/FTD neurodegenerative diseases.

The Ran GTPase plays a role in defining the physical properties of the nuclear pore complex transport channel by remodeling the binding interactions of importin-β with the nucleoporin Nup153 at the nuclear face of the pore.

Behavioral pharmacology and molecular biology reveal a translational control mechanism underlying auditory imprinting and structural plasticity that can be pharmacologically manipulated to reopen the critical period.

The p38 MAPK pathway functions downstream of a cell-size-sensing process to coordinate cell size/growth with G1 progression in animal cells.

β-catenin, a key effector of the Wnt signaling pathway, is transported into the nucleus via a direct interaction between its PY-NLS and TNPO1 offering new potential targets for cancer therapeutics.

Building on previous work (Fung et al., 2015), the structures of eight new nuclear export signal (NES) peptides bound to Exportin CRM1 are reported, revealing striking diversity in NES structures, a small conserved secondary structural element, and a CRM1 residue that functions as a selectivity filter.

The deletion of Ddx6 results in the translational upregulation, but not transcript stabilization, of microRNA targets in embryonic stem cells while largely phenocopying the overall impact of global microRNA loss.