Search results for GRK4

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Protein (1 results from a total of 1)

Identifier: R-HSA-6787795
Species: Homo sapiens
Compartment: photoreceptor disc membrane
Primary external reference: UniProt: GRK4: P32298

Reaction (1 results from a total of 1)

Identifier: R-HSA-2581474
Species: Homo sapiens
Compartment: cytosol, photoreceptor disc membrane
Activated rhodopsin (MII aka R*) must be deactivated to terminate the single photon response. Deactivation begins during the rising phase of the single photon response after MII binds rhodopsin kinase (GRK1), a serine/threonine protein kinase (Khani et al. 1996). GRK1 is activated by MII whereupon it phosphorylates MII at multiple serine and threonine sites on its C terminus. There are six serine and threonine residues that can be phosphorylated. Increasing phosphorylation progressively reduces the rate at which MII can activate transducin but full quenching requires the binding of arrestin (S-antigen or SAG, Yamaki et al. 1988) which binds to and sterically caps MII (Burns & Pugh 2010, Korenbrot 2012). GRK4-alpha (isoform 1) and GRK7 are also able to phosphorylate rhodopsin thereby deactivating it (Premont et al. 1996, Chen et al. 2001, Horner et al. 2005, Osawa et al. 2008).

A substantial fraction of rhodopsin kinase (GRK1) is bound to recoverin (RCVRN) in darkness, when internal Ca2+ levels are high. RCVRN is an EF-hand protein (Murakami et al. 1992) that functions as a myristoyl switch. With Ca2+ bound, the myristoyl group is exposed to attach RCVRN to the membrane. When Ca2+ levels drop with light exposure, Ca2+ dissociates from RCVRN and GRK1 is released. Higher levels of free GRK1 accelerate the phosphorylation and shutoff of photoexcited rhodopsin (MII).

Certain mutations in GRK1 cause Oguchi type 2 disease, a rare, recessive form of congenital stationary night blindness (https://sph.uth.edu/retnet/).
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