RNA-binding proteins (RBPs) are critical regulators of RNA metabolism. RBPs play a role in translational regulation and can influence the stability, function, transport, and cellular localization of RNA transcripts^[1]. RBPs can bind to both coding and non-coding untranslated RNA via single- or double-stranded RNA-binding motifs to form ribonucleic protein complexes (RNPs). The specific RBP binding domain and the individual RNA sequence determine RBP binding specificity. Single RBPs routinely bind several mRNA transcripts of proteins of similar function. In addition to transcriptional regulation, RNP function can also be attenuated by intra- or extracellular signals via post-translational modifications that affect their ability to sequester specific RNA sequences. More than 500 unique RBPs have been identified in the human genome.

In addition to binding RNA sequences, recent research has identified other roles for RBPs, including acting as substrates for kinases in DNA damage responses and influencing cell attachments through association with focal adhesion kinases^[2].

Several human diseases have been linked to genetic defects in RNA-binding proteins. For instance, loss of function of specific RBPs have been associated with spinal muscular atrophy and Fragile X Syndrome. Conversely, RBP gain of function has been associated with myotonic dystrophy and oculopharyngeal muscular dystrophy. Based on the potential influence of RBPs on cell cycle, growth, and proliferation, they are implicated in several different malignancies, including breast and prostate cancers^[3].

1. Glisovic et al. 2008. FEBS Lett. RNA-binding proteins and post-transcriptional gene regulation. 582(14):1977-86.
2. Lukong et al. 2008. Trends Genet. RNA-binding proteins in human genetic disease. 24(8):416-25.
3. Keene. 2007. Nature Reviews Genetics. RNA regulons: coordination of post-transcriptional events. 8, 533-543.