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This is the first dominant-acting mutation identified in SAG, a founder mutation possibly originating in Mexico several centuries ago. The phenotype is clearly adRP and is distinct from the previously reported phenotypes of recessive null mutations, that is, Oguchi disease and recessive RP.
Macular dysfunction can occur in Oguchi disease with the 1147delA mutation in the SAG gene.
Based on their observed affinity for arrestin-1, P-opsin and inactive P-Rh very likely affect the physiological monomer-dimer-tetramer equilibrium of arrestin-1, and should therefore be taken into account when modeling photoreceptor function.
Compound heterozygosity of a nonsense R193X mutation and a heterozygous deletion of 3,224 bp encompassing exon 2 in the SAG gene is the cause of Oguchi's disease in a Chinese family.
Identification of autoantibodies specific for two retinal antigens (CRALBP and S-Ag) supports the concept of an autoimmunological origin of the disease.
the arrestin 1147delA, which has been known as a frequent cause of Oguchi disease, also may be related to the pathogenesis of autosomal recessive RP.
We describe a case of Oguchi disease with unusual findings caused by a putative heterozygous mutation in the SAG gene.
maintenance of low levels of the active monomer is the biological role of arrestin-1 self-association
Rhodopsin-arrestin complexes alter the morphology of endosomal compartments and severely damage receptor-mediated endocytic functions in retinitis pigmentosa.
The existence of 2 novel mutations of the arrestin gene in 2 unrelated Japanese patients strongly supports the previous data that arrestin gene mutations are associated with Oguchi's disease
Mutation 926delA of the SAG gene is the main cause of Oguchi disease in Japanese. This mutation appears to have been inherited from a single founder.
studies suggest that IRBP and S-Ag can initiate innate and, in sensitive individuals, adaptive immune response by attracting iDCs and T and B cells expressing CXCR3 and CXCR5
The tetramer form of arrestin increases the arrestin-binding capacity of microtubules while readily dissociating to supply active monomer when it is needed to quench rhodopsin signaling.
two models of interaction for the human S-arrestin/rhodopsin complex
ARRESTIN binds to different phosphorylated regions of the thyrotropin-releasing hormone receptor with distinct functional consequences.
S-Ag specific T cells are present in certain active Behcet's disease patients, and most of them are activated memory CD4(+) T cells.
Data indicate molecular dynamics simulations and site-directed fluorescence experiments on arrestin-1 interactions with rhodopsin, showing that loops within the C-edge of arrestin function as a membrane anchor.
Conformational changes are involved in the arrestin-rhodopsin binding interface through multiple docking modes.
K2A mutations in arrestin-1, -2, and -3 significantly reduced their binding to active phosphorhodopsin.
We hypothesize that, although arrestin requires at least a single Rho*P to bind the membrane, a single arrestin can actually interact with a pair of receptors
variant form of arrestin-1 binds rod outer segment membranes
Alpha-helix I plays an indirect role in receptor binding, likely keeping beta-strand I, which carries several phosphate-binding residues, in a position favorable for its interaction with receptor-attached phosphates.
Models suggest that the phosphorylated carboxy-terminal region of rhodopsin, Rh(330-348), undergoes significant conformational changes and becomes structured upon binding to arrestin.
arrestin and p44 bind differently to different phosphorylated rhodopsin species and that this may be due to a structural difference between p44's and arrestin's basal states.
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 G-protein coupled receptor, DRD4, requires ARR1 and ARR4 for desensitization and internalization.
ARR4 modulates essential functions in high acuity vision and downstream cellular signaling pathways that are not fulfilled or substituted by the coexpression of ARR1, despite its high expression levels in all mouse cones.
crystal structure of a constitutively active form of human rhodopsin bound to a pre-activated form of the mouse visual arrestin, determined by serial femtosecond X-ray laser crystallography
Sag is essential for embryonic vasculogenesis and tumor angiogenesis.
SAG knockdown caused the accumulation of proapoptotic Bax and SARM, imbalance of Bcl-2/Bax in the mitochondria, induction of cytosolic cytochrome c and activation of caspases, all of which led to disequilibrium between life and death of macrophages.
tetrameric visual arrestin 1 is a biomarker for retinal function in diabetic mice, assessed by MRI
The data suggest that monomeric arrestin-1 is cytotoxic and WT arrestin-1 protects rods by forming mixed oligomers with the mutant and/or competing with it for the binding to non-receptor partners.
Findings suggest a role for Bardet-Biedl syndrome 5 (BBS5) in regulating light-dependent translocation of arrestin1 (Arr1).
Visual arrestin interaction with clathrin adaptor AP-2 regulates photoreceptor survival in the vertebrate retina.
the 139-loop stabilizes basal conformation of arrestin-1 and acts as a brake, preventing its binding to non-preferred forms of rhodopsin.
a novel function of palmitoylation in shaping subcellular cAMP-PKA signaling in cardiomyocytes via modulating the recruitment of beta arrestin 2-PDE4D complexes to the agonist-stimulated beta(2)AR
Photoresponse recovery rates of mice with arrestin-1 content in the outer segment, were measured.
Physiological level of arrestin-1 expression in rods reflects the balance between short-term functional performance of photoreceptors and their long-term health.
siRNA silencing induces radiosensitization by increasing ROS levels and blocking NF-kappaB activation
study demonstrates a vital alternative function for Arr1 in the photoreceptor synapse and provides key insights into the potential molecular mechanisms of inherited retinal diseases, such as Oguchi disease and Arr1-associated retinitis pigmentosa.
Prolonged illumination up-regulates retinal arrestin and Guca1a/b: a novel mechanism for light adaptation.
may act as a GTP/GDP-binding protein\; may play a role in signal transduction in the retina
48 kDa protein
, arrestin 1
, retinal S-antigen (48 KDa protein)
, rod photoreceptor arrestin
, retinal S-antigen
, S-antigen; retina and pineal gland (arrestin)
, -antigen; retina and pineal gland (arrestin)
, Arrestin Sb
, arrestin, S-antigen
, rod arrestin
, visual arrestin 1