Source 1primary paper2011Science
Toolkit/melanopsin
melanopsin
Also known as: melanopsin, Opn4
Taxonomy: Mechanism Branch / Component. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Melanopsin (Opn4) is a light-responsive opsin used as an optogenetic protein domain to activate Gq-linked signaling. Supplied evidence indicates that melanopsin can be functionally linked to an NFAT control circuit and that light-driven activation in cardiomyocytes modulates beating rate and local pacemaker activity.
Usefulness & Problems
Why this is useful
Melanopsin is useful as an optical actuator for probing spatial and temporal aspects of Gq signaling in cardiovascular research. The supplied evidence also links Opn4 to wavelength-specific pulmonary artery photorelaxation and direct interaction with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
Source:
Melanopsin is presented as an optogenetic tool that enables light-induced Gq activation in cardiomyocytes. In the abstract, this activation increases beating rate and generates local pacemaker activity.
Source:
optogenetic activation of Gq signalling
Source:
investigation of spatial aspects of Gq signalling
Source:
investigation of temporal aspects of Gq signalling in cardiovascular research
Problem solved
This tool helps solve the problem of controllably activating Gq signaling with light in cardiomyocytes and related cardiovascular contexts. The evidence supports its use for studying how timed and localized Gq activation affects beating rate, pacemaker activity, and vascular light responses.
Source:
It provides a way to investigate spatial and temporal aspects of Gq signalling in a cardiovascular context using light. This addresses the need for controllable activation of Gq signalling in cardiomyocytes.
Source:
enables light-induced control of Gq signalling in cardiomyocytes
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Component: A low-level protein part used inside a larger architecture that realizes a mechanism.
Target processes
recombinationsignalingInput: Light
Implementation Constraints
The available evidence indicates that target cells such as cardiomyocytes must express melanopsin and be exposed to light. Melanopsin signal transduction has been functionally linked to an NFAT control circuit, and Opn4, Opn3, and GRK2 were detected in rat pulmonary arteries and pulmonary arterial smooth muscle cells, but no additional cofactor, vector, or hardware details are provided.
The supplied evidence does not provide quantitative performance metrics, spectral parameters, kinetics, or construct-level design details. It also does not establish broader in vivo translation, delivery strategies, or comparative benchmarking against alternative Gq-control methods.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2primary paper2017American Journal of Physiology-Lung Cellular and Molecular Physiology
Source 3primary paper2014Cardiovascular Research
Source 4review2017Cell Calcium
Ranked Claims
Wavelength-specific pulmonary artery photorelaxation is attenuated in Opn4 knockout tissue and further reduced after Opn3 knockdown.
Wavelength-specific photorelaxation was attenuated in PAs from Opn4-/- mice and further reduced following shRNA-mediated knockdown of Opn3.
Wavelength-specific pulmonary artery photorelaxation is attenuated in Opn4 knockout tissue and further reduced after Opn3 knockdown.
Wavelength-specific photorelaxation was attenuated in PAs from Opn4-/- mice and further reduced following shRNA-mediated knockdown of Opn3.
Wavelength-specific pulmonary artery photorelaxation is attenuated in Opn4 knockout tissue and further reduced after Opn3 knockdown.
Wavelength-specific photorelaxation was attenuated in PAs from Opn4-/- mice and further reduced following shRNA-mediated knockdown of Opn3.
Wavelength-specific pulmonary artery photorelaxation is attenuated in Opn4 knockout tissue and further reduced after Opn3 knockdown.
Wavelength-specific photorelaxation was attenuated in PAs from Opn4-/- mice and further reduced following shRNA-mediated knockdown of Opn3.
Wavelength-specific pulmonary artery photorelaxation is attenuated in Opn4 knockout tissue and further reduced after Opn3 knockdown.
Wavelength-specific photorelaxation was attenuated in PAs from Opn4-/- mice and further reduced following shRNA-mediated knockdown of Opn3.
Wavelength-specific pulmonary artery photorelaxation is attenuated in Opn4 knockout tissue and further reduced after Opn3 knockdown.
Wavelength-specific photorelaxation was attenuated in PAs from Opn4-/- mice and further reduced following shRNA-mediated knockdown of Opn3.
Wavelength-specific pulmonary artery photorelaxation is attenuated in Opn4 knockout tissue and further reduced after Opn3 knockdown.
Wavelength-specific photorelaxation was attenuated in PAs from Opn4-/- mice and further reduced following shRNA-mediated knockdown of Opn3.
Opsin 3 and Opsin 4 interact directly with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
where the opsins interact directly with GRK2, as demonstrated with a proximity ligation assay
Opsin 3 and Opsin 4 interact directly with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
where the opsins interact directly with GRK2, as demonstrated with a proximity ligation assay
Opsin 3 and Opsin 4 interact directly with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
where the opsins interact directly with GRK2, as demonstrated with a proximity ligation assay
Opsin 3 and Opsin 4 interact directly with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
where the opsins interact directly with GRK2, as demonstrated with a proximity ligation assay
Opsin 3 and Opsin 4 interact directly with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
where the opsins interact directly with GRK2, as demonstrated with a proximity ligation assay
Opsin 3 and Opsin 4 interact directly with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
where the opsins interact directly with GRK2, as demonstrated with a proximity ligation assay
Opsin 3 and Opsin 4 interact directly with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
where the opsins interact directly with GRK2, as demonstrated with a proximity ligation assay
Opsin 3, Opsin 4, and GRK2 are present in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
We discovered Opsin 3 (Opn3), Opn4, and G protein-coupled receptor kinase 2 (GRK2) in rat pulmonary arteries (PAs) and in pulmonary arterial smooth muscle cells (PASMCs)
Opsin 3, Opsin 4, and GRK2 are present in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
We discovered Opsin 3 (Opn3), Opn4, and G protein-coupled receptor kinase 2 (GRK2) in rat pulmonary arteries (PAs) and in pulmonary arterial smooth muscle cells (PASMCs)
Opsin 3, Opsin 4, and GRK2 are present in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
We discovered Opsin 3 (Opn3), Opn4, and G protein-coupled receptor kinase 2 (GRK2) in rat pulmonary arteries (PAs) and in pulmonary arterial smooth muscle cells (PASMCs)
Opsin 3, Opsin 4, and GRK2 are present in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
We discovered Opsin 3 (Opn3), Opn4, and G protein-coupled receptor kinase 2 (GRK2) in rat pulmonary arteries (PAs) and in pulmonary arterial smooth muscle cells (PASMCs)
Opsin 3, Opsin 4, and GRK2 are present in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
We discovered Opsin 3 (Opn3), Opn4, and G protein-coupled receptor kinase 2 (GRK2) in rat pulmonary arteries (PAs) and in pulmonary arterial smooth muscle cells (PASMCs)
Opsin 3, Opsin 4, and GRK2 are present in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
We discovered Opsin 3 (Opn3), Opn4, and G protein-coupled receptor kinase 2 (GRK2) in rat pulmonary arteries (PAs) and in pulmonary arterial smooth muscle cells (PASMCs)
Opsin 3, Opsin 4, and GRK2 are present in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
We discovered Opsin 3 (Opn3), Opn4, and G protein-coupled receptor kinase 2 (GRK2) in rat pulmonary arteries (PAs) and in pulmonary arterial smooth muscle cells (PASMCs)
This review covers an optogenetic toolkit for precise control of calcium signaling, including genetically encoded calcium actuators and multiple mechanistic classes such as STIM1/CRAC-based, GPCR-based, RTK-based, and channel-based approaches.
Functional Opsin 3 and Opsin 4 in pulmonary arteries constitute an endogenous optogenetic system that mediates photorelaxation in the pulmonary vasculature.
These findings show that functional Opn3 and Opn4 in PAs represent an endogenous "optogenetic system" that mediates photorelaxation in the pulmonary vasculature.
Functional Opsin 3 and Opsin 4 in pulmonary arteries constitute an endogenous optogenetic system that mediates photorelaxation in the pulmonary vasculature.
These findings show that functional Opn3 and Opn4 in PAs represent an endogenous "optogenetic system" that mediates photorelaxation in the pulmonary vasculature.
Functional Opsin 3 and Opsin 4 in pulmonary arteries constitute an endogenous optogenetic system that mediates photorelaxation in the pulmonary vasculature.
These findings show that functional Opn3 and Opn4 in PAs represent an endogenous "optogenetic system" that mediates photorelaxation in the pulmonary vasculature.
Functional Opsin 3 and Opsin 4 in pulmonary arteries constitute an endogenous optogenetic system that mediates photorelaxation in the pulmonary vasculature.
These findings show that functional Opn3 and Opn4 in PAs represent an endogenous "optogenetic system" that mediates photorelaxation in the pulmonary vasculature.
Functional Opsin 3 and Opsin 4 in pulmonary arteries constitute an endogenous optogenetic system that mediates photorelaxation in the pulmonary vasculature.
These findings show that functional Opn3 and Opn4 in PAs represent an endogenous "optogenetic system" that mediates photorelaxation in the pulmonary vasculature.
Functional Opsin 3 and Opsin 4 in pulmonary arteries constitute an endogenous optogenetic system that mediates photorelaxation in the pulmonary vasculature.
These findings show that functional Opn3 and Opn4 in PAs represent an endogenous "optogenetic system" that mediates photorelaxation in the pulmonary vasculature.
Functional Opsin 3 and Opsin 4 in pulmonary arteries constitute an endogenous optogenetic system that mediates photorelaxation in the pulmonary vasculature.
These findings show that functional Opn3 and Opn4 in PAs represent an endogenous "optogenetic system" that mediates photorelaxation in the pulmonary vasculature.
Melanopsin and Opto-XRs are discussed in the review as GPCR-based optogenetic routes relevant to calcium signaling control.
Opto-RTKs are discussed in the review as receptor-tyrosine-kinase-based optogenetic tools within the calcium-control toolkit.
OptoSTIM1 and Opto-CRAC are discussed in the review as STIM1/CRAC-based optogenetic tools for controlling calcium signaling.
PACR is discussed in the review as a genetically encoded photoactivatable calcium releaser for optical control of calcium signaling.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
In mice carrying implants containing light-inducible transgenic cells, serum levels of secreted alkaline phosphatase could be remotely controlled by fiber optics or by direct transdermal illumination.
In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination.
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
The synthetic optogenetic transcription device enables light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice.
we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Light-controlled expression of glucagon-like peptide 1 attenuated glycemic excursions in type II diabetic mice.
Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice.
Approval Evidence
4 sources10 linked approval claimsfirst-pass slugs melanopsin, opsin-4
We recently demonstrated that blue light induces vasorelaxation in the systemic mouse circulation, a phenomenon mediated by the nonvisual G protein-coupled receptor melanopsin (Opsin 4; Opn4).
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The supplied review scaffold says the anchor review names melanopsin among GPCR-based optogenetic routes for calcium signaling control.
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We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
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By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells
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genetic dependencysupports
Wavelength-specific pulmonary artery photorelaxation is attenuated in Opn4 knockout tissue and further reduced after Opn3 knockdown.
Wavelength-specific photorelaxation was attenuated in PAs from Opn4-/- mice and further reduced following shRNA-mediated knockdown of Opn3.
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interactionsupports
Opsin 3 and Opsin 4 interact directly with GRK2 in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
where the opsins interact directly with GRK2, as demonstrated with a proximity ligation assay
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presencesupports
Opsin 3, Opsin 4, and GRK2 are present in rat pulmonary arteries and pulmonary arterial smooth muscle cells.
We discovered Opsin 3 (Opn3), Opn4, and G protein-coupled receptor kinase 2 (GRK2) in rat pulmonary arteries (PAs) and in pulmonary arterial smooth muscle cells (PASMCs)
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review scopesupports
This review covers an optogenetic toolkit for precise control of calcium signaling, including genetically encoded calcium actuators and multiple mechanistic classes such as STIM1/CRAC-based, GPCR-based, RTK-based, and channel-based approaches.
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summary modelsupports
Functional Opsin 3 and Opsin 4 in pulmonary arteries constitute an endogenous optogenetic system that mediates photorelaxation in the pulmonary vasculature.
These findings show that functional Opn3 and Opn4 in PAs represent an endogenous "optogenetic system" that mediates photorelaxation in the pulmonary vasculature.
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tool classificationsupports
Melanopsin and Opto-XRs are discussed in the review as GPCR-based optogenetic routes relevant to calcium signaling control.
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functional effectsupports
Light-induced Gq activation in melanopsin-expressing cardiomyocytes generates local pacemaker activity.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate and generates local pacemaker activity.
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functional effectsupports
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate.
Light-induced Gq activation in melanopsin-expressing cardiomyocytes increases beating rate
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tool positioningsupports
Melanopsin is proposed as an optogenetic tool for investigating spatial and temporal aspects of Gq signalling in cardiovascular research.
We propose that melanopsin is a powerful optogenetic tool for the investigation of spatial and temporal aspects of Gq signalling in cardiovascular research.
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designsupports
The authors designed a synthetic signaling cascade linking melanopsin signal transduction to an NFAT control circuit to enable light-inducible transgene expression.
By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression
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Comparisons
Source-backed strengths
Evidence from the supplied literature describes melanopsin as a powerful optogenetic tool for cardiovascular investigation of Gq signaling. Reported functional outcomes include modulation of cardiomyocyte beating rate, generation of local pacemaker activity, and genetic dependence of pulmonary photorelaxation on Opn4, with further reduction after Opn3 knockdown.
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light-induced activation modulates cardiomyocyte beating rate
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light-induced activation generates local pacemaker activity
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