RIC-3 expression and splicing regulate nAChR functional expression.

Background: The nicotinic acetylcholine receptors form a large and diverse family of acetylcholine gated ion channels having diverse roles in the central nervous system. Maturation of nicotinic acetylcholine receptors is a complex and inefficient process requiring assistance from multiple cellular factors including RIC-3, a functionally conserved endoplasmic reticulum-resident protein and nicotinic acetylcholine receptor-specific chaperone. In mammals and in Drosophila melanogaster RIC-3 is alternatively spliced to produce multiple isoforms.

Regulation of osteoclastogenesis by integrated signals from toll-like receptors.

A variety of pathogen-derived molecules have been shown to cause bone loss by enhancing osteoclast differentiation through activation of toll-like receptors (TLRs). The pathogen-derived molecules (TLR-ligands) modulate osteoclastogenesis in a complex manner: inhibition of the osteoclast differentiation factor RANKL in early precursors and osteoclastogenesis stimulation in RANKL-primed cells. Since organisms may be challenged by several TLR ligands at a time, we investigated osteoclastogenesis modulation by simultaneous challenge with different TLR ligands.