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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 (show RHO Proteins) bound to a pre-activated form of the mouse visual arrestin, determined by serial femtosecond X-ray laser crystallography
Sag (show RNF7 Proteins) is essential for embryonic vasculogenesis and tumor angiogenesis.
SAG (show RNF7 Proteins) knockdown caused the accumulation of proapoptotic Bax (show BAX Proteins) and SARM (show SARM1 Proteins), imbalance of Bcl-2 (show BCL2 Proteins)/Bax (show BAX Proteins) in the mitochondria, induction of cytosolic cytochrome c (show CYCS Proteins) 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 (show C7ORF49 Proteins)
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 (show TFAP2A Proteins) regulates photoreceptor survival in the vertebrate retina.
This is the first dominant-acting mutation identified in SAG (show DMBT1 Proteins), a founder mutation possibly originating in Mexico several centuries ago. The phenotype is clearly adRP (show PLIN2 Proteins) 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 (show DMBT1 Proteins) gene.
NEDD4-1 (show NEDD4 Proteins) overexpression sensitizes cancer cells to etoposide-induced apoptosis by reducing SAG (show DMBT1 Proteins) levels through targeted degradation. SAG (show DMBT1 Proteins) is added to a growing list of NEDD4-1 (show NEDD4 Proteins) substrates and mediates its biological function.
Sag (show DMBT1 Proteins) is a Kras-cooperating oncogene (show RAB1A Proteins) that promotes lung tumorigenesis
Based on their observed affinity for arrestin-1, P-opsin (show RHO Proteins) 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 (show DMBT1 Proteins) gene is the cause of Oguchi's disease in a Chinese family.
Identification of autoantibodies specific for two retinal antigens (CRALBP (show RLBP1 Proteins) 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 (show DMBT1 Proteins) gene.
maintenance of low levels of the active monomer is the biological role of arrestin-1 self-association
Conformational changes are involved in the arrestin-rhodopsin (show RHO Proteins) 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
Models suggest that the phosphorylated carboxy-terminal region of rhodopsin (show RHO Proteins), 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.
may act as a GTP/GDP-binding protein\; may play a role in signal transduction in the retina
S-antigen; retina and pineal gland (arrestin)
, -antigen; retina and pineal gland (arrestin)
, Arrestin Sb
, retinal S-antigen
, rod photoreceptor arrestin
, 48 kDa protein
, arrestin 1
, rod arrestin
, visual arrestin 1
, retinal S-antigen (48 KDa protein)
, arrestin, S-antigen