PAR-1 for the course of neurodegeneration.
The large number of kinases that phosphorylate the microtubule binding protein tau has posed a challenge to understanding their individual roles in turning this protein into a killer of neurons. A study in this issue of Cell (Nishimura et al., 2004) uses an elegant fusion of loss-of-function genetics and transgenic overexpression to make the case that the PAR-1 kinase stands at the head of a temporally ordered series of tau phosphorylations.
Fortini
Mark E
ME
National Cancer Institute, Molecular Genetics Section, Building 560, Room 22-12, Fort Detrick, Frederick, MD 21702, USA.
D000818:Animals; D030801:Animals, Genetically Modified; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism*; D004331:Drosophila melanogaster / Q000235:genetics / Q000502:physiology; D006801:Humans; D019636:Neurodegenerative Diseases / Q000235:genetics / Q000378:metabolism*; D009474:Neurons / Q000502:physiology*; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D016875:tau Proteins / Q000378:metabolism*
D029742:Caenorhabditis elegans Proteins; D016875:tau Proteins; D017346:Protein Serine-Threonine Kinases