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Literature summary extracted from

  • Chen, C.; Woodruff, M.; Chen, F.; Chen, Y.; Cilluffo, M.; Tranchina, D.; Fain, G.
    Modulation of mouse rod response decay by rhodopsin kinase and recoverin (2012), J. Neurosci., 32, 15998-16006.
    View publication on PubMedView publication on EuropePMC

Protein Variants

EC Number Protein Variants Comment Organism
2.7.11.14 S56L when studied ectopically in COS-7 cells, the S561L mutation cause GRK1 to be geranylgeranylated instead of farnesylated, with an apparent increase in membrane affinity but no effect on catalytic activity for light-activated rhodopsin In the RKS561L mouse retina, the expression of mutant S561L GRK1 is rod specific and confines exclusively to the outer segment layer Mus musculus

Organism

EC Number Organism UniProt Comment Textmining
2.7.11.14 Mus musculus
-
-
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
2.7.11.14 ATP + rhodopsin
-
 Mus musculus ADP + phosphorhodopsin
-
 ?

Synonyms

EC Number Synonyms Comment Organism
2.7.11.14 GRK1
-
 Mus musculus

General Information

EC Number General Information Comment Organism
2.7.11.14 malfunction a mouse line RKS561L is generated in which GRK1 is overexpressed (S56L mutant cDNA is used). Overexpressed GRK1 in RKS561L mice is located in the outer segment and greatly accelerates the rate of rhodopsin phosphorylation. Transgenic mice show that the light response amplitude is only modestly diminished, but the exponential decay constant of the response (tau REC) and the limiting time constant (tau D) are both highly significantly accelerated. It is concluded that GRK1 and recoverin, in addition to their role in phosphorylating rhodopsin, may also regulate light-activated phosphodiesterase decay and mediate the increase in temporal resolution of rods during light adaptation Mus musculus