Abstract
Several EF-hand recoverin mutants were obtained and their abilities to bind to photoreceptor membranes and to inhibit rhodopsin kinase were determined. The mutants with the 'spoiled' 2nd, 3rd or (2nd+3rd) EF-hand structures did not act upon the kinase activity in the microM range of Ca2+ concentrations. Mutations of the 4th EF hand, which 'repaired' its Ca2+-binding activity, resulted in recoverin with three 'working' Ca2+-binding sites. The latter mutant inhibited rhodopsin kinase even more effectively than the wild-type recoverin, containing two working Ca2+-binding structures.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Binding Sites
-
Calcium / metabolism
-
Calcium-Binding Proteins / chemistry
-
Calcium-Binding Proteins / genetics*
-
Calcium-Binding Proteins / metabolism*
-
Cattle
-
Eye Proteins*
-
G-Protein-Coupled Receptor Kinase 1
-
Hippocalcin
-
Lipoproteins*
-
Mutagenesis, Site-Directed
-
Mutation*
-
Nerve Tissue Proteins*
-
Phenotype
-
Phosphorylation
-
Protein Kinase Inhibitors*
-
Protein Kinases*
-
Protein Structure, Secondary
-
Recoverin
-
Retina
-
Rod Cell Outer Segment / metabolism*
Substances
-
Calcium-Binding Proteins
-
Eye Proteins
-
Lipoproteins
-
Nerve Tissue Proteins
-
Protein Kinase Inhibitors
-
Recoverin
-
Hippocalcin
-
Protein Kinases
-
G-Protein-Coupled Receptor Kinase 1
-
Calcium