PAR-1 for the course of neurodegeneration

Mark E Fortini

doi:10.1016/s0092-8674(04)00207-7

PAR-1 for the course of neurodegeneration

Cell. 2004 Mar 5;116(5):631-2. doi: 10.1016/s0092-8674(04)00207-7.

Author

Mark E Fortini¹

Affiliation

¹ National Cancer Institute, Molecular Genetics Section, Building 560, Room 22-12, Fort Detrick, Frederick, MD 21702, USA.

PMID: 15006343
DOI: 10.1016/s0092-8674(04)00207-7

Abstract

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.

Publication types

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MeSH terms

Animals
Animals, Genetically Modified
Caenorhabditis elegans Proteins / genetics
Caenorhabditis elegans Proteins / metabolism*
Drosophila melanogaster / genetics
Drosophila melanogaster / physiology
Humans
Neurodegenerative Diseases / genetics
Neurodegenerative Diseases / metabolism*
Neurons / physiology*
Phosphorylation
Protein Serine-Threonine Kinases / genetics
Protein Serine-Threonine Kinases / metabolism*
tau Proteins / metabolism*

Substances

Caenorhabditis elegans Proteins
tau Proteins
Protein Serine-Threonine Kinases