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Polycystin-1 and -2 — two integral membrane proteins that are mutated in polycystic kidney disease — regulate the cell cycle by preventing nuclear localization of the pro-proliferative helix-loop-helix (HLH) protein Id2. This novel mechanism for restraining Id proteins has important implications for our understanding of the nature of polycystic kidney disease and perhaps other proliferative disorders.
In myotonic dystrophy, a group of RNA-binding factors — the Muscleblind-like proteins — are sequestered by transcripts containing expanded trinucleotide repeats; this sequestration disrupts their proposed physiological function as regulators of alternative splicing. Now, exciting data suggest that Muscleblind-like proteins are also involved in the localization of integrin mRNA.
Neurotransmitter receptors must be targeted to the post-synaptic membrane to perform their function in synaptic transmission. Recent findings reveal a surprising role for heterotrimeric G proteins and their activator, Pins (Partner of Inscuteable), in this important protein targeting event.