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Gene analysis determined a novel GRK1 mutation c.923T>C, which caused Oguchi disease in all siblings. This mutation, was demonstrated by amino acid alignment analysis to be in a phylogenetically conserved region and resulted in an amino acid change from leucine to proline at position 308. Thus, the present study reports a novel missense mutation of GRK1 in the affected members of a consanguineous Turkish family.
AAMP (show AAMP Proteins) Regulates Endothelial Cell Migration and Angiogenesis Through RhoA (show RHOA Proteins)/Rho Kinase (show ROCK1 Proteins) Signaling.
In the Ca(2 (show CA2 Proteins)+)/NCS-1 (show NCS1 Proteins).D2R (show DRD2 Proteins) peptide complex, the C-terminal region adopts a 310 helix-turn-310 helix, whereas in the GRK1 peptide complex it forms an a-helix
Rho-kinase (show ROCK1 Proteins) activity exhibits distinct circadian variation associated with alterations in coronary vasomotor responses and autonomic activity in VSA patients.
The selective thinning of the inner retinal layers in patients with GRM6 (show GRM6 Proteins) mutations suggests either reduced bipolar or ganglion cell numbers or altered synaptic structure in the inner retina.
Defects in GRK1 or GRK7 (show GRK7 Proteins) cause patients to suffer from an inability to properly deactivate rhodopsin (show RHO Proteins) leading to problems with recovery and dark adaptation.
There are two genes that cause Oguchi disease: the G protein-coupled receptor kinase 1 gene and the S antigen (show SAG Proteins) gene. There is evidence that Oguchi disease and retinitis pigmentosa (RP) can coexist in the same family or even in the same individual
Phosphorylation of GRK1 and GRK7 by PKA occurs in the dark, when cAMP levels in photoreceptor cells are elevated.
The disease in the Pakistani family localizes to 13q34 and is caused by a novel deletion including Exon 3 of the GRK1 gene.
G protein-coupled receptor kinase site serine cluster has a role in beta2-adrenergic receptor internalization, desensitization, and beta-arrestin translocation
The C-terminal segment in GCAP2 (show GUCA1B Proteins) confers target selectivity, facilitates membrane binding and provides sensitivity of the membrane localization of the protein to phosphorylation by rhodopsin kinase.
The methylation status of GRK1 is affected by nucleotide binding and by the levels of free Ca2 (show CA2 Proteins) + via recoverin (show RCVRN Proteins).
crystalline dimer interface was disrupted with a L166K mutation and the structure of GRK1-L166K was determined in complex with Mg(2 (show MCOLN1 Proteins)+) . ATP to 2.5 A resolution
A novel rhodopsin-kinase-binding site within the C-terminal region of recoverin (show RCVRN Proteins).
similar to transducin (show GNAT1 Proteins) activation, rhodopsin (show RHO Proteins) phosphorylation by GRK1 and high affinity arrestin-1 (show SAG Proteins) binding only requires a rhodopsin (show RHO Proteins) monomer
Recoverin (show RCVRN Proteins) and rhodopsin kinase have roles in a Ca2 (show CA2 Proteins)+-dependent feedback loop in membrane rafts from rod outer segments
an interaction surface for the recoverin (show RCVRN Proteins) target rhodopsin kinase is constituted upon Ca2 (show CA2 Proteins)+ binding to the non-acylated mutant
Recoverin (show RCVRN Proteins) binds exclusively to an amphipathic peptide at the N terminus of rhodopsin kinase
Ca(2 (show CA2 Proteins)+)-bound recoverin (show RCVRN Proteins) is bound between rhodopsin (show RHO Proteins) and RK in a ternary complex on rod outer segment disk membranes, thereby blocking RK interaction with rhodopsin (show RHO Proteins) at high Ca(2 (show CA2 Proteins)+)
key elements of rhodopsin kinase in different ligand states are involved in G protein-coupled receptor (show GPBAR1 Proteins) kinase activation
We conclude that, in addition to their well-established roles in Meta II inactivation, Grk1 and Arr1 can modulate the kinetics of Meta III decay and rod dark adaptation in vivo.
The retinal phenotype of Grk1-/- mice is compromised by a Crb1 (show CRB1 Proteins) rd8 mutation.
Rods and cones share the same isoforms of recoverin (show RCVRN Proteins) and GRK1, and photoactivation also triggers a calcium decline in cones
Knockout of Unc119 (show UNC119 Proteins) partially reversed the transport defect of GRK1 in cone photoreceptors caused by deletion of Pde6d (show PDE6D Proteins).
rhodopsin kinase may modulate the decay of light-activated PDE (show TWIST1 Proteins)*, which may be responsible for the quickening of response recovery in background light.
Altering the expression of GRK1 from 0.3- to 3-fold that in wild-type rods had little effect on the single photon response amplitude.
phototransduction does not play a direct role in the light-dependent dephosphorylation of GRK1.
PLCdelta3 negatively regulates RhoA (show RHOA Proteins) expression, inhibits RhoA (show RHOA Proteins)/Rho kinase (show ROCK2 Proteins) signaling, and thereby promotes neurite extension.
The results of this study demonstrated a light-independent mechanism for retinal degeneration in the absence of GRK1, suggesting a second, not previously recognized role for that kinase.
Nrl (show NRL Proteins) and Grk1 have roles in photoresponse recovery and age-related degeneration
Specifically phosphorylates the activated forms of G protein-coupled receptors (By similarity).
, rhodopsin kinase
, G-protein-coupled receptor kinase 1a
, G-protein coupled receptor kinase 1
, G-protein receptor kinase 1
, G protein-coupled receptpr kinase 1