Evidence for functional and physical association between Caenorhabditis elegans SEL-10, a Cdc4p-related protein, and SEL-12 presenilin.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 9861048.
- Also identified by PMC identifier 28122.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Mutations in either of two human presenilin genes (PS1 and PS2) cause Alzheimer's disease. Here we describe genetic and physical interactions between Caenorhabditis elegans SEL-10, a member of the Cdc4p family of proteins, and SEL-12, a C. elegans presenilin. We show that loss of sel-10 activity can suppress the egg-laying defective phenotype associated with reducing sel-12 activity, and that SEL-10 can physically complex with SEL-12. Proteins of the Cdc4p family have been shown to target proteins for ubiquitin-mediated turnover. The functional and physical interaction between sel-10 and sel-12 therefore offers an approach to understanding how presenilin levels are normally regulated.
Medical subject headings
- Caenorhabditis elegans
- Caenorhabditis elegans Proteins
- Cell Cycle Proteins
- F-Box Proteins
- Helminth Proteins
- Membrane Proteins
- Ubiquitin-Protein Ligases