Abstract
PHR proteins are large conserved ubiquitin E3 ligases whose functions were first discovered in 2000 through genetic studies in C. elegans and Drosophila. They are now widely shown to regulate a number of important steps during the development of the nervous system. Loss of function in the invertebrate PHR proteins, namely Drosophila Highwire and Caenorhabditis elegans RPM-1, results in dysregulation of synapses and axon patterning. Similar but more diverse effects have been reported for the vertebrate PHR proteins. A major function of PHR proteins is to negatively regulate the conserved Dual-Leucine Zipper MAP kinase through ubiquitin-mediated protein degradation. In addition, numerous binding partners of PHR proteins implicate their roles in a wide range of signal transduction pathways as well as in neurological and neurodegenerative diseases.
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