26 results about "Rhodopsin" patented technology

The invention relates to the technical field of biomedicine, discloses mutant photo-induced ion channel ChR-2 protein, and further discloses a nucleic acid construct, an expression vector, a cell, related application and a computer model. The light-sensitive channel ChR2 protein mutant obtained by the invention has stronger light current, and the light-sensitive capability of the light-sensitive channel ChR2 protein mutant is at least improved by 100 times; besides, the invention also obtains a nucleotide sequence for coding the light-sensitive channel ChR2 protein mutant, constructs a recombinant expression vector, and obtains the light-sensitive channel ChR2 protein with higher expression quantity and stronger light sensitivity, and the light-sensitive channel ChR2 protein is very suitable for expression in cells of mammals (especially human); according to the invention, the rhodopsin in different channels is systematically studied by modifying the position G224 in the helix 6 of seven transmembrane helix motifs, which proves that the mutation of the position G224 in the helix 6 in WT ChR2 accelerates the photosensitivity of the channels, and the considered position is homologous in the helix 6 of the rhodopsin in different channels.

Described herein are pharmacologic correctors of rhodopsin, methods of making such compounds, pharmaceutical compositions and medicaments comprising such compounds, and methods of using such compounds in treating disease.

The invention relates to the technical field of biological medicine, in particular to application of aronia melanocarpa extract in prevention and / or treatment of retinal diseases. The invention discovers that the aronia melanocarpa extract effectively protects the functions of photoreceptor cells and bipolar cells by remarkably improving the expression of rhodopsin (RGO) and stem inhibition protein (SAG) genes in the retina and inhibiting the up-regulation of inflammatory factors TNF-alpha at the same time; in addition, cell apoptosis caused by light damage can be relieved by reducing TUNEL positive cells of the retinal outer nuclear layer (ONL), and therefore the structural integrity of the retina is maintained on the cellular level. Through the mechanisms, the aronia melanocarpa extract recovers normal electrophysiological reactions of photoreceptors and bipolar cells and protects the retina from further injury. The invention provides an effective strategy and theoretical basis for application of the aronia melanocarpa extract in prevention and treatment of retinal diseases caused by light damage.

The present invention relates to a fusion protein optogenetically activated by blue light, and a use thereof, wherein the fusion protein comprises: an extracellular domain of rhodopsin; a transmembrane domain of rhodopsin; and an intracellular domain of a G-protein coupled estrogen receptor (GPER) bound to the transmembrane domain. Specifically, the invention relates to a fusion protein that is activated by blue light, phosphorylates extracellular signal-regulated kinases (ERKs), inhibits apoptosis, and induces programmed necrosis.

The invention relates to the field of bioengineering and technology, in particular to an engineering modified strain, a method for improving the intracellular ATP level of the strain and application of the engineering modified strain. The engineering modified bacterium comprises a coding gene of the rhodopsin, wherein at least part of the rhodopsin is positioned on a biological membrane of the engineering modified bacterium. The engineering modified strain provided by the embodiment of the invention has the capability of obviously improving the intracellular ATP content, the intracellular ATP content is obviously improved compared with that of an original strain, and the engineering modified strain can be applied to promoting saccharomyces cerevisiae to synthesize a series of natural products.

A voltage indicator is described, including a voltage-sensitive rhodopsin domain having mutations to replace canonical counterion charge residues with neutral residues, and a capture protein that binds a fluorescent element, wherein the capture protein is provided together with the voltage-sensitive rhodopsin domain in a fusion protein.

The disclosure relates to a fusion protein including a transcription enhancer and a dCas9 protein, a complex for epigenetic regulation including the fusion protein and one or more guide RNAs (gRNAs), etc.The fusion protein or complex according to an aspect may induce apoptosis of colorectal cancer cells or compensate for rhodopsin deficiency by activating the gene EGFL8, opsin mw, etc., and may be utilized as a pharmaceutical composition or the like for preventing or treating cancer or ocular diseases.

Provided are: a nucleic acid including a nucleic acid sequence encoding a chimeric protein including at least part of an ion-transporting receptor rhodopsin and at least part of a G protein-coupled receptor rhodopsin and a nucleic acid sequence encoding a signal sequence; and a nucleic acid including a nucleic acid sequence encoding a chimeric protein including at least part of an ion channeling receptor rhodopsin and at least part of a G protein-coupled receptor rhodopsin; and a nucleic acid construct including the nucleic acid sequences. The use of the nucleic acids or nucleic acid constructs prevents and suppresses the progress of retinal diseases, and enhances the visual cognitive behavioral function and visual function.

Microbial type rhodopsins, such as the light-gated cation-selective membrane channel, channelrhodopsin-2 (Chop2 / ChR2) or the ion pump halorhodopsin (HaloR) are expressed in retinal ganglion cells upon transduction using recombinant AAV vectors. Selective targeting of these transgenes for expression in discrete subcellular regions or sites is achieved by including a sorting motif in the vector that can target either the central area or surround (off-center) area of these cells. Nucleic acid molecules comprising nucleotide sequences encoding such rhodopsins and sorting motifs and their use in methods of differential expression of the transgene are disclosed. These compositions and methods provide significant improvements for restoring visual perception and various aspects of vision, particular in patients with retinal disease.

The invention discloses a visual purple protein maximum absorption light wavelength prediction method based on a graph neural network. Comprising the following steps: generating a three-dimensional structure model according to an amino acid sequence of a to-be-predicted rhodopsin protein; generating a ligand pocket graph according to the three-dimensional structure model of the visual purple protein to be predicted; and inputting the ligand pocket graph into a pre-trained maximum absorption wavelength prediction model to obtain a maximum absorption wavelength prediction value. The method can make full use of protein three-dimensional structure information, accurately characterizes the ligand binding pocket microenvironment, has high prediction precision and strong generalization ability, and has important scientific significance and application value.

To provide a modified channel rhodopsin having high ion permeability (photoreactivity).SOLUTION: A third extracellular domain counting from the N-terminal side of three extracellular domains possessed by channel rhodopsin derived from volvox is replaced with an extracellular domain corresponding to channel rhodopsin-2 derived from Chlamydomonas reinhardtii.SELECTED DRAWING: Figure 2

The present disclosure provides systems, methods, and compositions for modifying a target nucleic acid. Particularly, the present invention relates to modifying sequences in the 5' UTR near the Kozak sequence to silence a gene, for example, mutating a target rhodopsin allele start codon or deleting a region of the target rhodopsin allele comprising at least a portion of the start codon.

An object of the present invention is to provide a modified channel rhodopsin capable of opening and closing an ion channel by irradiation with light at different wavelengths, and / or having high ion permeability (photoreactivity). The solution is to substitute a C-terminal region of a channel rhodopsin obtained by substituting an N-terminal region of a Volvox carteri-derived channel rhodopsin by an N-terminal region of a Chlamydomonas reinhardtii-derived channel rhodopsin-1, by a C-terminal region of a Chlamydomonas reinhardtii-derived channel rhodopsin-2 or a C-terminal region of a Tetraselmis striata-derived channel rhodopsin.

A quantum dot (QD)-rhodopsin bioconjugate system uses Förster resonance energy transfer (FRET)-mediated induction of cellular membrane depolarization via optical activation of ion channel proteins channelrhodopsin (ChR).

To provide prevention and suppression of progression of retinal diseases, improvement in visual cognitive behavioral function, and strengthening of visual function.SOLUTION: A chimeric protein of two types of rhodopsins, an ion-transporting rhodopsin and a G protein-coupled receptor rhodopsin, and a nucleic acid encoding the chimeric protein are provided for the prevention and suppression of progression of retinal diseases, improvement in visual cognitive behavioral functions (e.g., improvement in light-dark determination functions, improvement in bright spot evading functions, and / or crisis avoidance functions), and enhancement of visual functions (e.g., improvement in visual acuity). The present invention also provides a method for preventing or suppressing progression of a disease, disorder or symptom of the retina, for improving a visual cognitive behavioral function (e.g., improvement in light-dark determination functions, improvement in bright spot evading functions, and / or crisis avoidance functions), or for enhancing visual functions (e.g., improvement in visual acuity), in a subject. The method comprises the step of administering an effective amount of a nucleic acid encoding a chimeric protein of an ion-transporting receptor rhodopsin and a G protein-coupled receptor rhodopsin to the subject.SELECTED DRAWING: None

The invention provides a light-driven proton concentration regulated engineered yeast strain, and belongs to the technical field of genetic engineering and optogenetics. The invention provides a fusion gene. The fusion gene comprises a coding gene of a visual purple protein and a coding gene of a plasma membrane localization signal peptide. As a light-driven proton pump, the rhodopsin protein can absorb light energy under an illumination condition and pump protons into cells from outside the cells. The fusion gene provided by the invention is constructed to a host bacterium through a genetic engineering means, the rhodopsin is positioned on a plasma membrane of a cell, and the function of a light-driven proton pump can be realized under an illumination condition, so that extracellular protons are pumped into the cell, and accurate regulation and control of intracellular pH are realized. The strategy not only provides a new means for metabolism regulation, but also provides a brand new solution for pH regulation in industrial fermentation and metabolic engineering, and is expected to promote cell growth and production of metabolites.

The invention relates to the technical field of microorganisms, in particular to a microbial system for enhancing acetic acid metabolism and a construction method and application thereof. The microbial system comprises microorganisms capable of growing with acetic acid as a carbon source, and ACS genes are overexpressed in the microorganisms and used for converting acetic acid into acetyl coenzyme A; visual purple protein is expressed on a microbial cell membrane and is used for forming a transmembrane proton gradient under visible light irradiation by utilizing a light-driven proton pump function so as to drive ATP synthase to synthesize ATP; cdS nano-particles are loaded on the surfaces of the microorganisms or in the cells and are used for supplementing NADPH / NADH and assisting ATP regeneration. Through the synergistic effect of ACS gene overexpression, a light-driven proton pump and a CdS hybridization module in microorganisms, a light energy-ATP-NADPH dual-energy supply system is formed, and the problem of insufficient energy and reducing power in acetic acid metabolism is remarkably relieved.

The present invention relates to a method for tracking outer segment protein trafficking in vivo. Using the photoconvertible fluorescent protein Dendra2, the process and turnover dynamics of outer segment protein trafficking in mice are dynamically tracked. By tracing the source and destination of ectopically accumulated Rhodopsin, the pathways and paths that trigger cell death are revealed. Theoretically, the results will contribute to the development of theories of Rhodopsin trafficking and membrane turnover, further elucidate the processes and modes of abnormal Rhodopsin trafficking in retinal degenerative disease models, and potentially identify new modes of transport. Clinically, the results may reveal cell death pathways in patients with late-stage retinal degenerative diseases, providing new targets and directions for drug development.

Described herein are pharmacologic correctors of rhodopsin, methods of making such compounds, pharmaceutical compositions and medicaments comprising such compounds, and methods of using such compounds in treating disease.

Described herein are pharmacologic correctors of rhodopsin, methods of making such compounds, pharmaceutical compositions and medicaments comprising such compounds, and methods of using such compounds in treating disease.

Provided are a chimeric protein of two types of rhodopsins, an ion-transporting rhodopsin and a G protein-coupled receptor rhodopsin, and a nucleic acid encoding the same, for the prevention and suppression of progression of retinal diseases, the improvement in visual cognitive behavioral functions (e.g., improvement in light-dark determination functions, improvement in bright spot evading functions, and / or crisis avoidance functions), and the enhancement of visual functions (e.g., improvement in visual acuity). The present invention also provides a method for preventing or suppressing the progression of a disease, disorder or symptom of the retina, for improving a visual cognitive behavioral function (e.g., improvement in light-dark determination functions, improvement in bright spot evading functions, and / or crisis avoidance functions), or for enhancing visual functions (e.g., improvement in visual acuity), in a subject, where the method comprises the step of administering an effective amount of a nucleic acid encoding a chimeric protein of an ion-transporting receptor rhodopsin and a G protein-coupled receptor rhodopsin to the subject.

The invention relates to an electromicrobial system for synthesis of hydrogen, comprising: a gram-negative bacterial cell modified for synthesis of hydrogen, wherein the bacterial cell comprises: i) inner membrane-bound rhodopsin for proton-pumping, ii) membrane-bound hydrogenase, and iii) optionally an electron mediator located in the periplasm and / or on the outer membrane of the bacterial cell; and an electron source for donation of electrons to the bacterial cell.

The present invention relates to an electro-microbial system for photoautotrophic CO2 immobilization, and related methods, uses and products, the system comprising: A) a recombinantly engineered bacterial cell modified for photoautotrophic CO2 immobilization wherein the bacterial cell comprises a membrane-binding rhodopsin molecule and a component for the CO2 immobilization pathway; and B) an electron source for donating electrons into an electron transport chain.

Microbial type rhodopsins, such as the light-gated cation-selective membrane channel, channelrhodopsin-2 (Chop2 / ChR2) or the ion pump halorhodopsin (HaloR) are expressed in retinal ganglion cells upon transduction using recombinant AAV vectors. Selective targeting of these transgenes for expression in discrete subcellular regions or sites is achieved by including a sorting motif in the vector that can target either the central area or surround (off-center) area of these cells. Nucleic acid molecules comprising nucleotide sequences encoding such rhodopsins and sorting motifs and their use in methods of differential expression of the transgene are disclosed. These compositions and methods provide significant improvements for restoring visual perception and various aspects of vision, particular in patients with retinal disease.

A method of treating a retinal disease in a subject in need thereof, the method comprising administering to the subject a vector that comprises a mirtron for knocking down expression of a target gene expressed in the retina and a gene therapy vector comprising a mirtron for rhodopsin knock-down.

The invention relates to a method for tracking transportation of an outer fragment protein in vivo, which comprises the following steps of: dynamically tracking the transportation process of the outer fragment protein in a mouse body and updating kinetics by utilizing photoconversion fluorescent protein Dendra2, and revealing a path and a path for triggering cell death by tracing the source and the destination of ectopic accumulation Rhodopsin. On the research theory, the research result contributes to the development of Rhodopsin transportation and a membrane disc updating theory, and a new transportation mode can be possibly found by further elaborating the Rhodopsin abnormal transportation process and mode of the retinal degenerative disease model. In clinical treatment, a cell death path of a retinal degenerative disease patient in a later disease course can be found, and a new target spot and a new direction are provided for development of drugs of the retinal degenerative disease.