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In conclusion, in the present report, a novel missense mutation in GRK1 gene in homozygous state was reported in an Italian patient affected with Oguchi disease.
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 Regulates Endothelial Cell Migration and Angiogenesis Through RhoA/Rho Kinase Signaling.
In the Ca(2+)/NCS-1.D2R peptide complex, the C-terminal region adopts a 310 helix-turn-310 helix, whereas in the GRK1 peptide complex it forms an a-helix
The identification of the c.1607_1610delCGGA mutation in a patient with Oguchi disease confirms the pathogenicity of this variant.
Rho-kinase 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 mutations suggests either reduced bipolar or ganglion cell numbers or altered synaptic structure in the inner retina.
Defects in GRK1 or GRK7 cause patients to suffer from an inability to properly deactivate rhodopsin 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 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
RhoK activation in brain microvascular endothelial cells could be a cause of blood-brain barrier impairment during HIV-1 encephalitis.
A novel homozygous GRK1 mutation (p.P391H) was found in 2 Japanese siblings with Oguchi disease.
Conserved bicoid homeodomain factors thus appear to be the key factors governing localization of GRK1 Enhancer/Promoter activity in retina and photoreceptors.
The authors found two different novel mutations in Japanese patients. The results indicate that a considerable number of GRK1 mutations exist in the Japanese population.
A GRK1 region close to its C-terminus also seemed to be the binding site for S-modulin/recoverin.
Genetic mapping supported the diagnosis of typical Oguchi disease in a Pakistani family and also resulted in the identification of a novel nonsense mutation (c.614C>A; p.S205X) in exon 1 of GRK1.
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 rd8 mutation.
Rods and cones share the same isoforms of recoverin and GRK1, and photoactivation also triggers a calcium decline in cones
Knockout of Unc119 partially reversed the transport defect of GRK1 in cone photoreceptors caused by deletion of Pde6d.
rhodopsin kinase may modulate the decay of light-activated PDE*, 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 expression, inhibits RhoA/Rho kinase 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.
The conserved short enhancer/promoter immediately upstream of the Rk gene contains the key elements required for appropriate response to spatial and temporal cues during photoreceptor cell differentiation and fate determination.
Nrl and Grk1 have roles in photoresponse recovery and age-related degeneration
transport of prenylated proteins, particularly GRK1 and cone phosphodiesterase, to rod and cone outer segments
PKA and GRK phosphorylation of the beta(2)AR has distinct roles for agonist dose-dependent coupling to G(i) proteins in cardiac myocytes
study revealed that arrestin, in addition to its role in quenching the activity of rhodopsin, can tune the kinetics of rhodopsin phosphorylation by competing with GRK1
The C-terminal segment in GCAP2 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 + via recoverin.
crystalline dimer interface was disrupted with a L166K mutation and the structure of GRK1-L166K was determined in complex with Mg(2+) . ATP to 2.5 A resolution
A novel rhodopsin-kinase-binding site within the C-terminal region of recoverin.
similar to transducin activation, rhodopsin phosphorylation by GRK1 and high affinity arrestin-1 binding only requires a rhodopsin monomer
Recoverin and rhodopsin kinase have roles in a Ca2+-dependent feedback loop in membrane rafts from rod outer segments
an interaction surface for the recoverin target rhodopsin kinase is constituted upon Ca2+ binding to the non-acylated mutant
Recoverin binds exclusively to an amphipathic peptide at the N terminus of rhodopsin kinase
Ca(2+)-bound recoverin is bound between rhodopsin and RK in a ternary complex on rod outer segment disk membranes, thereby blocking RK interaction with rhodopsin at high Ca(2+)
key elements of rhodopsin kinase in different ligand states are involved in G protein-coupled receptor kinase activation
In situ hybridization and immunohistochemical studies localizes both GRK1B and GRK7-1 in the cone outer segments.
Specifically phosphorylates the activated forms of G protein-coupled receptors (By similarity).
, G-protein receptor kinase 1
, G-protein coupled receptor kinase 1
, G protein-coupled receptpr kinase 1
, G-protein-coupled receptor kinase 1a
, G protein-coupled receptor kinase 1 b
, G-protein-coupled receptor kinase 1b