Source 1primary paper2016Scientific Reports
Toolkit/anion channelrhodopsins
anion channelrhodopsins
Also known as: Acrs, ACRs, anti-CRISPR proteins, natural ACRs
Taxonomy: Mechanism Branch / Component. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Anion channelrhodopsins (ACRs) are natural light-gated anion-conducting microbial rhodopsins from cryptophyte algae used as optogenetic actuators. In cultured neonatal rat ventricular cardiomyocytes, their expression enables light-evoked inhibitory currents, suppression of electrical activity, and shortening of action potential duration when illumination is applied during repolarization.
Usefulness & Problems
Why this is useful
ACRs provide inhibitory cardiac optogenetic control at substantially lower light intensity than previously available optogenetic tools. This makes them useful for temporally precise optical suppression of cardiomyocyte electrical activity and for phase-specific modulation of repolarization.
Problem solved
This tool addresses the need for more efficient inhibitory optogenetic control in cardiac cells, specifically by producing inhibitory currents in cardiomyocytes at less than one-thousandth of the light intensity required by previously available tools. It also enables optical shortening of cardiac action potential duration when light is delivered during repolarization.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Component: A low-level protein part used inside a larger architecture that realizes a mechanism.
Techniques
Structural CharacterizationTarget processes
editingsignalingInput: Light
Implementation Constraints
Use requires expression of ACRs in the target cells and optical illumination. In the cited cardiac application, constructs were expressed in cultured neonatal rat ventricular cardiomyocytes, and action potential shortening required switching light on during the repolarization phase.
The supplied evidence is limited to cultured neonatal rat ventricular cardiomyocytes and does not establish in vivo performance or therapeutic efficacy. The evidence also does not define performance across diverse cardiac disorders, delivery strategies, or broader cell and organism contexts.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2review2017Annual Review of Biochemistry
Source 3primary paper2015Science
Source 4review2023Biomolecules
Ranked Claims
Anti-CRISPRs share very little structural or sequence resemblance to each other or to other proteins.
Anti-CRISPRs share very little structural or sequential resemblance to each other or to other proteins
Anti-CRISPRs share very little structural or sequence resemblance to each other or to other proteins.
Anti-CRISPRs share very little structural or sequential resemblance to each other or to other proteins
Anti-CRISPRs share very little structural or sequence resemblance to each other or to other proteins.
Anti-CRISPRs share very little structural or sequential resemblance to each other or to other proteins
Anti-CRISPRs share very little structural or sequence resemblance to each other or to other proteins.
Anti-CRISPRs share very little structural or sequential resemblance to each other or to other proteins
Anti-CRISPRs share very little structural or sequence resemblance to each other or to other proteins.
Anti-CRISPRs share very little structural or sequential resemblance to each other or to other proteins
Anti-CRISPRs share very little structural or sequence resemblance to each other or to other proteins.
Anti-CRISPRs share very little structural or sequential resemblance to each other or to other proteins
Anti-CRISPRs share very little structural or sequence resemblance to each other or to other proteins.
Anti-CRISPRs share very little structural or sequential resemblance to each other or to other proteins
Anti-CRISPRs can act as orthosteric inhibitors, allosteric inhibitors, or enzymes that irreversibly modify CRISPR-Cas components.
Acrs, which can act as orthosteric or allosteric inhibitors of CRISPR-Cas machinery, as well as enzymes that irreversibly modify CRISPR-Cas components.
Anti-CRISPRs can act as orthosteric inhibitors, allosteric inhibitors, or enzymes that irreversibly modify CRISPR-Cas components.
Acrs, which can act as orthosteric or allosteric inhibitors of CRISPR-Cas machinery, as well as enzymes that irreversibly modify CRISPR-Cas components.
Anti-CRISPRs can act as orthosteric inhibitors, allosteric inhibitors, or enzymes that irreversibly modify CRISPR-Cas components.
Acrs, which can act as orthosteric or allosteric inhibitors of CRISPR-Cas machinery, as well as enzymes that irreversibly modify CRISPR-Cas components.
Anti-CRISPRs can act as orthosteric inhibitors, allosteric inhibitors, or enzymes that irreversibly modify CRISPR-Cas components.
Acrs, which can act as orthosteric or allosteric inhibitors of CRISPR-Cas machinery, as well as enzymes that irreversibly modify CRISPR-Cas components.
Anti-CRISPRs can act as orthosteric inhibitors, allosteric inhibitors, or enzymes that irreversibly modify CRISPR-Cas components.
Acrs, which can act as orthosteric or allosteric inhibitors of CRISPR-Cas machinery, as well as enzymes that irreversibly modify CRISPR-Cas components.
Anti-CRISPRs can act as orthosteric inhibitors, allosteric inhibitors, or enzymes that irreversibly modify CRISPR-Cas components.
Acrs, which can act as orthosteric or allosteric inhibitors of CRISPR-Cas machinery, as well as enzymes that irreversibly modify CRISPR-Cas components.
Anti-CRISPRs can act as orthosteric inhibitors, allosteric inhibitors, or enzymes that irreversibly modify CRISPR-Cas components.
Acrs, which can act as orthosteric or allosteric inhibitors of CRISPR-Cas machinery, as well as enzymes that irreversibly modify CRISPR-Cas components.
Anti-CRISPR action toward Cas proteins can modulate conformation, dynamic allosteric signaling, nucleic acid binding, and cleavage ability.
their action toward Cas proteins modulates conformation, dynamic (allosteric) signaling, nucleic acid binding, and cleavage ability
Anti-CRISPR action toward Cas proteins can modulate conformation, dynamic allosteric signaling, nucleic acid binding, and cleavage ability.
their action toward Cas proteins modulates conformation, dynamic (allosteric) signaling, nucleic acid binding, and cleavage ability
Anti-CRISPR action toward Cas proteins can modulate conformation, dynamic allosteric signaling, nucleic acid binding, and cleavage ability.
their action toward Cas proteins modulates conformation, dynamic (allosteric) signaling, nucleic acid binding, and cleavage ability
Anti-CRISPR action toward Cas proteins can modulate conformation, dynamic allosteric signaling, nucleic acid binding, and cleavage ability.
their action toward Cas proteins modulates conformation, dynamic (allosteric) signaling, nucleic acid binding, and cleavage ability
Anti-CRISPR action toward Cas proteins can modulate conformation, dynamic allosteric signaling, nucleic acid binding, and cleavage ability.
their action toward Cas proteins modulates conformation, dynamic (allosteric) signaling, nucleic acid binding, and cleavage ability
Anti-CRISPR action toward Cas proteins can modulate conformation, dynamic allosteric signaling, nucleic acid binding, and cleavage ability.
their action toward Cas proteins modulates conformation, dynamic (allosteric) signaling, nucleic acid binding, and cleavage ability
Anti-CRISPR action toward Cas proteins can modulate conformation, dynamic allosteric signaling, nucleic acid binding, and cleavage ability.
their action toward Cas proteins modulates conformation, dynamic (allosteric) signaling, nucleic acid binding, and cleavage ability
Anti-CRISPR proteins have enabled the development of highly controllable and precise CRISPR-Cas tools.
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Anti-CRISPR proteins have enabled the development of highly controllable and precise CRISPR-Cas tools.
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Anti-CRISPR proteins have enabled the development of highly controllable and precise CRISPR-Cas tools.
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Anti-CRISPR proteins have enabled the development of highly controllable and precise CRISPR-Cas tools.
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Anti-CRISPR proteins have enabled the development of highly controllable and precise CRISPR-Cas tools.
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Anti-CRISPR proteins have enabled the development of highly controllable and precise CRISPR-Cas tools.
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Anti-CRISPR proteins have enabled the development of highly controllable and precise CRISPR-Cas tools.
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Cryptophyte cation channelrhodopsins are structurally distinct from green algae cation channelrhodopsins and from cryptophyte anion channelrhodopsins.
Cryptophyte anion channelrhodopsins enable efficient optogenetic neural suppression.
Green algae cation channelrhodopsins have been used extensively for neural activation.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
required light intensity relative to Arch 0.001 fold
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Anion channel rhodopsins are a family of light-gated anion channels from cryptophyte algae.
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
Anion channel rhodopsins are a family of light-gated anion channels from cryptophyte algae.
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
Anion channel rhodopsins are a family of light-gated anion channels from cryptophyte algae.
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
Anion channel rhodopsins are a family of light-gated anion channels from cryptophyte algae.
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
Anion channel rhodopsins are a family of light-gated anion channels from cryptophyte algae.
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
Anion channel rhodopsins are a family of light-gated anion channels from cryptophyte algae.
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
Anion channel rhodopsins are a family of light-gated anion channels from cryptophyte algae.
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
ACRs strictly conduct anions and exclude protons and larger cations.
ACRs strictly conducted anions, completely excluding protons and larger cations
ACRs strictly conduct anions and exclude protons and larger cations.
ACRs strictly conducted anions, completely excluding protons and larger cations
ACRs strictly conduct anions and exclude protons and larger cations.
ACRs strictly conducted anions, completely excluding protons and larger cations
ACRs strictly conduct anions and exclude protons and larger cations.
ACRs strictly conducted anions, completely excluding protons and larger cations
ACRs strictly conduct anions and exclude protons and larger cations.
ACRs strictly conducted anions, completely excluding protons and larger cations
ACRs strictly conduct anions and exclude protons and larger cations.
ACRs strictly conducted anions, completely excluding protons and larger cations
ACRs strictly conduct anions and exclude protons and larger cations.
ACRs strictly conducted anions, completely excluding protons and larger cations
ACRs provide membrane hyperpolarization and neuronal silencing through light-gated chloride conduction.
provide highly sensitive and efficient membrane hyperpolarization and neuronal silencing through light-gated chloride conduction
ACRs provide membrane hyperpolarization and neuronal silencing through light-gated chloride conduction.
provide highly sensitive and efficient membrane hyperpolarization and neuronal silencing through light-gated chloride conduction
ACRs provide membrane hyperpolarization and neuronal silencing through light-gated chloride conduction.
provide highly sensitive and efficient membrane hyperpolarization and neuronal silencing through light-gated chloride conduction
ACRs provide membrane hyperpolarization and neuronal silencing through light-gated chloride conduction.
provide highly sensitive and efficient membrane hyperpolarization and neuronal silencing through light-gated chloride conduction
ACRs provide membrane hyperpolarization and neuronal silencing through light-gated chloride conduction.
provide highly sensitive and efficient membrane hyperpolarization and neuronal silencing through light-gated chloride conduction
ACRs provide membrane hyperpolarization and neuronal silencing through light-gated chloride conduction.
provide highly sensitive and efficient membrane hyperpolarization and neuronal silencing through light-gated chloride conduction
ACRs provide membrane hyperpolarization and neuronal silencing through light-gated chloride conduction.
provide highly sensitive and efficient membrane hyperpolarization and neuronal silencing through light-gated chloride conduction
In cultured animal cells, ACRs hyperpolarized the membrane with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins.
hyperpolarized the membrane of cultured animal cells with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins
required light intensity relative to most efficient current optogenetic proteins one-thousandth
In cultured animal cells, ACRs hyperpolarized the membrane with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins.
hyperpolarized the membrane of cultured animal cells with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins
required light intensity relative to most efficient current optogenetic proteins one-thousandth
In cultured animal cells, ACRs hyperpolarized the membrane with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins.
hyperpolarized the membrane of cultured animal cells with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins
required light intensity relative to most efficient current optogenetic proteins one-thousandth
In cultured animal cells, ACRs hyperpolarized the membrane with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins.
hyperpolarized the membrane of cultured animal cells with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins
required light intensity relative to most efficient current optogenetic proteins one-thousandth
In cultured animal cells, ACRs hyperpolarized the membrane with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins.
hyperpolarized the membrane of cultured animal cells with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins
required light intensity relative to most efficient current optogenetic proteins one-thousandth
In cultured animal cells, ACRs hyperpolarized the membrane with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins.
hyperpolarized the membrane of cultured animal cells with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins
required light intensity relative to most efficient current optogenetic proteins one-thousandth
In cultured animal cells, ACRs hyperpolarized the membrane with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins.
hyperpolarized the membrane of cultured animal cells with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins
required light intensity relative to most efficient current optogenetic proteins one-thousandth
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Approval Evidence
4 sources15 linked approval claimsfirst-pass slugs anion-channel-rhodopsins, anion-channelrhodopsins, anti-crisprs
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Source:
We review the currently known functions and present more in-depth assessment of three functionally and structurally distinct types discovered over the past two years: (a) anion channelrhodopsins (ACRs) from cryptophyte algae, which enable efficient optogenetic neural suppression
Source:
Anion channelrhodopsins (ACRs) from cryptophyte algae expressed in cultured neonatal rat ventricular cardiomyocytes produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools
Source:
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
Source:
diversity of structure and sequencesupports
Anti-CRISPRs share very little structural or sequence resemblance to each other or to other proteins.
Anti-CRISPRs share very little structural or sequential resemblance to each other or to other proteins
Source:
mechanism of actionsupports
Anti-CRISPRs can act as orthosteric inhibitors, allosteric inhibitors, or enzymes that irreversibly modify CRISPR-Cas components.
Acrs, which can act as orthosteric or allosteric inhibitors of CRISPR-Cas machinery, as well as enzymes that irreversibly modify CRISPR-Cas components.
Source:
mechanistic effects on cassupports
Anti-CRISPR action toward Cas proteins can modulate conformation, dynamic allosteric signaling, nucleic acid binding, and cleavage ability.
their action toward Cas proteins modulates conformation, dynamic (allosteric) signaling, nucleic acid binding, and cleavage ability
Source:
tool enabling rolesupports
Anti-CRISPR proteins have enabled the development of highly controllable and precise CRISPR-Cas tools.
The discovery of protein inhibitors of CRISPR-Cas systems, called anti-CRISPRs (Acrs), has enabled the development of highly controllable and precise CRISPR-Cas tools.
Source:
structural distinctnesssupports
Cryptophyte cation channelrhodopsins are structurally distinct from green algae cation channelrhodopsins and from cryptophyte anion channelrhodopsins.
Source:
tool functionsupports
Cryptophyte anion channelrhodopsins enable efficient optogenetic neural suppression.
Source:
application potentialsupports
Optical shortening of cardiac action potentials may benefit pathophysiology research and development of optogenetic treatments for cardiac disorders such as long QT syndrome.
Optical shortening of cardiac action potentials may benefit pathophysiology research and the development of optogenetic treatments for cardiac disorders such as the long QT syndrome.
Source:
capabilitysupports
Anion channelrhodopsin expression allowed precisely controlled shortening of action potential duration by switching on light during the repolarization phase, which was not possible with previously used optogenetic tools.
ACR expression allowed precisely controlled shortening of the action potential duration by switching on the light during its repolarization phase, which was not possible with previously used optogenetic tools.
Source:
comparative performancesupports
In cultured neonatal rat ventricular cardiomyocytes, anion channelrhodopsins produced inhibitory currents at less than one-thousandth of the light intensity required by archaerhodopsin-3.
produced inhibitory currents at less than one-thousandth of the light intensity required by previously available optogenetic tools, such as the proton pump archaerhodopsin-3 (Arch)
Source:
functional performancesupports
Because of greater photocurrents, anion channelrhodopsins permitted complete inhibition of cardiomyocyte electrical activity under conditions in which archaerhodopsin-3 was inefficient.
Because of their greater photocurrents, ACRs permitted complete inhibition of cardiomyocyte electrical activity under conditions in which Arch was inefficient.
Source:
functional activitysupports
Anion channel rhodopsins are a family of light-gated anion channels from cryptophyte algae.
We describe anion channel rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae
Source:
ion selectivitysupports
ACRs strictly conduct anions and exclude protons and larger cations.
ACRs strictly conducted anions, completely excluding protons and larger cations
Source:
optogenetic functionsupports
ACRs provide membrane hyperpolarization and neuronal silencing through light-gated chloride conduction.
provide highly sensitive and efficient membrane hyperpolarization and neuronal silencing through light-gated chloride conduction
Source:
performance comparisonsupports
In cultured animal cells, ACRs hyperpolarized the membrane with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins.
hyperpolarized the membrane of cultured animal cells with much faster kinetics at less than one-thousandth of the light intensity required by the most efficient currently available optogenetic proteins
Source:
tool utilitysupports
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Natural ACRs provide optogenetic inhibition tools with unprecedented light sensitivity and temporal precision.
Source:
Comparisons
Source-backed strengths
In cultured neonatal rat ventricular cardiomyocytes, ACR expression produced inhibitory currents and suppressed electrical activity under illumination. The reported light requirement was less than one-thousandth of that required by previously available optogenetic tools, indicating markedly improved light sensitivity in this application.
Ranked Citations
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