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data provide the first evidence that T17M rhodopsin mutant disrupts C3 secretion via the induction of ROS (显示 ROS1 蛋白) and the suppression of TWIST1 (显示 TWIST1 蛋白).
Wild-type opsin mainly formed oligomers. Only a minor population formed aggregates. The G188R opsin mutant mainly formed aggregates. When wild-type opsin and G188R opsin were coexpressed in cells, properly folded wild-type opsin did not aggregate with G188R opsin and was trafficked normally to the cell membrane. The autosomal dominant phenotype due to misfolded opsin mutants is not due to WT-mutant physical interaction.
Data suggest that retinitis pigmentosa-associated mutation G51A behaves differently in human rhodopsin compared to bovine rhodopsin; human rhodopsin is more thermally stable than ancestral ancestrally reconstructed mammalian rhodopsin.
The metformin-rescued P23H rhodopsin was still intrinsically unstable and led to increased structural instability of the rod outer segments. These data suggest that improving the traffic of misfolding rhodopsin mutants is unlikely to be a practical therapy, but also highlights the potential of altering translation through AMPK (显示 PRKAA1 蛋白) to improve protein function in other protein misfolding diseases
Study reports an X-ray free electron laser crystal structure of the rhodopsin-arrestin (显示 SAG 蛋白) complex, in which the phosphorylated C terminus of rhodopsin forms an extended intermolecular beta sheet with the N-terminal beta strands of arrestin (显示 SAG 蛋白). Phosphorylation was detected at rhodopsin C-terminal tail residues T336 and S338.
results suggest that nonsense-mediated mRNA decay modulates the severity of retinitis pigmentosa in patients with nonsense mutations in the rhodopsin gene
both the charged G90D(2.57) and the hydrophobic T94I(2.61) mutation alter the dark state by weakening the interaction between the Schiff base (SB) and its counterion E113(3.28) We propose that this interference with the tight regulation of the dim light photoreceptor rhodopsin increases background noise in the visual system and causes the loss of night vision characteristic for CSNB (显示 CSN2 蛋白) patients.
a recurrent missense mutation (c.403C > T, p.R135W) in the rhodopsin (RHO) gene cosegregated with all retinitis pigmentosa affected individuals in the family.
Autosomal recessive retinitis pigmentosa with homozygous rhodopsin mutation E150K and non-coding cis-regulatory variants in CRX-binding regions of SAMD7.
Functional role of positively selected amino acid substitutions in mammalian rhodopsin evolution has been uncovered for a large number of mammalian species.
overexpression of full-length rhodopsin or its cytoplasmic tail domain, but not of rhodopsin lacking the cytoplasmic tail, exacerbated rod degeneration in kif3a (显示 KIF3A 蛋白) mutants, implying an important role of the cytoplasmic tail in rod degeneration.
expression as well as the protein localization of rhodopsin in the zebrafish from larval to adult stage were demonstrated; results demonstrated the involvement of rhodopsin in the zebrafish pineal gland physiology particularly in light capture during the zebrafish lifespan
Mitogen-associated protein kinase (显示 TGFB3 蛋白) and protein kinase A regulate rhodopsin transcription through parallel signal transduction pathways
we show that OPN2 and OPN4 (显示 OPN4 蛋白) participate in immediate pigment darkening induced by UVA in murine normal and malignant melanocytes through a conserved common pathway
Photoactivation of rhodopsin increases near-Infrared backscattering from rods and causes lengthening of their rod outer segment.
Specific visible radiation facilitates lipolysis in mature 3T3-L1 adipocytes via rhodopsin-dependent beta3-adrenergic signaling.
Rab8a (显示 RAB8A 蛋白) and Rab11a (显示 RAB11A 蛋白) Are Dispensable for Rhodopsin Transport in Mouse Photoreceptors
This study demonstrated that Rhodopsin Phosphorylation on Dark Adaptation in Mouse Rods.
Findings indicate that Rho and ROCK knockout may improve the behavior of mice and prevent MPTP (显示 PTPN2 蛋白)-induced dopaminergic neurons damage by regulating Sema3A (显示 SEMA3A 蛋白), PlexinA and NRP-1 (显示 NRP1 蛋白) in a mouse model of Parkinson's disease.
The authors elucidated this dependency by showing that guanylate cyclase-1 is a novel rhodopsin-binding protein.
Eliminating Cngb1 (显示 CNGB1 蛋白) and reducing RDS (显示 PRPH2 蛋白) leads to additive defects in RDS (显示 PRPH2 蛋白) expression levels and rod electroretinogram (ERG (显示 ERG 蛋白)) function, (e.g., Cngb1 (显示 CNGB1 蛋白)-/-/rds (显示 PRPH2 蛋白)+/- versus rds (显示 PRPH2 蛋白)+/- or Cngb1 (显示 CNGB1 蛋白)-/-) but not to additive defects in rod ultrastructure.
These findings reveal that an early and significant pathophysiologic effect of endoplasmic reticulum stress in photoreceptors is the highly efficient elimination of misfolded rhodopsin protein.
Retinal degeneration in the P23H (proline-to-histidine) rhodopsin mutation is partially reversed, with regeneration of rod photoreceptors recovering normal morphology in a retinitis pigmentosa model.
the Xenopus rhodopsin gene has conserved transcriptional activators
The newly identified ciliary targeting VxPx motif present in rhodopsin binds the small GTPase (显示 RACGAP1 蛋白) Arf4 (显示 ARF4 蛋白) and regulates its association with the trans-Golgi network.
the rhodopsin is densely packed in the retina and the rhodopsin molecules are not aligned well.
Phototransduction, even when initiated by wild type rhodopsin, is altered in a way progressive with level of retinal degeneration. A model introduces idea of binding site for carboxy terminus of rhodopsin on rhodopsin kinase (显示 GRK1 蛋白).
the photoreceptor pathology associated with expression of these enigmatic Retinitis pigmentosa-associated rhodopsin pigments arises from their unexpected inability to dimerize via transmembrane helices 1 and 5
Rhodopsin mutant E113Q could have the potential for use as a template of anion biosensors at visible wavelength.
The study shows that, compared to the inactive 11-cis (显示 CISH 蛋白)-retinal case, trans-retinal rhodopsin is able to undergo protonated Schiff base (PSB) deprotonation due to a change in the conformation of the retinal and a consequent alteration in the hydrogen-bond (HB) network in which PSB and the counterion Glu113 are embedded.
These findings revealed a total water flux between the bulk and the protein inside in the Meta II state, and suggested that these pathways provide water molecules to the crucial sites of the activated rhodopsin.
Data suggest that a hetero-multimer complex forms between light-activated rhodopsin and light-activated heterotrimeric transducin (显示 GNAT1 蛋白) (T-alpha-1, Gnb1 (显示 GNB1 蛋白), Gngt1 (显示 GNGT1 蛋白)); the stoichiometry is 1:1 rhodopsin:transducin. The complex appears to form on native rod outer segment membranes upon light activation.
Study presents a comprehensive analysis of the kinetics and thermodynamics of the recombination reaction between opsin and 11-cis (显示 CISH 蛋白)-retinal (11CR) to form the mature visual pigment, Rho; and found that the lipid bilayer environment is important for ligand binding in Rho.
In response to light-induced isomerization of the retinal chromophore rhodopsin, hydrogen-bonding interactions involving these C=O groups are released, thus facilitating repacking of H5 and H7 onto the transmembrane core of the receptor.
rhodopsin can tolerate a second Lys (显示 LYZ 蛋白) in the retinal binding pocket and suggest that an evolutionary intermediate with two Lys (显示 LYZ 蛋白) could allow migration of the Schiff base Lys (显示 LYZ 蛋白) to a position other than the observed, highly conserved location in the seventh TM helix
multiconfigurational quantum chemistry is used to compare the isomerization mechanisms of the sensory rhodopsin from the cyanobacterium Anabaena PCC 7120 (ASR) and of the bovine rhodopsin (Rh).
The form-deprived experimental myopia groups showed an increased expression of rhodopsin and its mRNA compared to the controls.
Retinitis pigmentosa is an inherited progressive disease which is a major cause of blindness in western communities. It can be inherited as an autosomal dominant, autosomal recessive, or X-linked recessive disorder. In the autosomal dominant form,which comprises about 25% of total cases, approximately 30% of families have mutations in the gene encoding the rod photoreceptor-specific protein rhodopsin. This is the transmembrane protein which, when photoexcited, initiates the visual transduction cascade. Defects in this gene are also one of the causes of congenital stationary night blindness.
opsin 2, rod pigment
, Rhodopsin (retinitis pigmentosa 4, autosomal dominant)
, retinal rod opsin pigment rh1.1
, rod opsin
, L opsin
, LWS opsin
, Long Wavelength Sensitive opsin
, Red Opsin
, Rod Opsin
, opsin 2
, rhodopsin (opsin 2, rod pigment) (retinitis pigmentosa 4, autosomal dominant)