Source 1primary paper2023eLife
Toolkit/Opto-RhoGEFs
Opto-RhoGEFs
Also known as: optogenetically recruitable RhoGEFs
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Opto-RhoGEFs are optogenetically recruitable Rho guanine nucleotide exchange factor systems for light-controlled, reversible regulation of Rho GTPase activity. In a 2023 eLife study, they were used to control endothelial cell morphology and vascular endothelial barrier strength from global to subcellular scales.
Usefulness & Problems
Why this is useful
This tool is useful for perturbing Rho GTPase signaling with spatial and temporal precision using light. The cited study showed control over endothelial cell size, roundness, local extension, contraction, and monolayer barrier strength.
Source:
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
Source:
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
Problem solved
Opto-RhoGEFs address the problem of reversibly controlling Rho GTPase-dependent cell behavior at global and subcellular scales. In endothelial systems, they enabled temporal control of morphology and barrier regulation that was described as cell-cell overlap-dependent and VE-cadherin-independent.
Source:
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
HeterodimerizationTechniques
No technique tags yet.
Target processes
localizationrecombinationsignalingInput: Light
Implementation Constraints
The available evidence indicates that these are multi-component, optogenetically recruitable RhoGEF systems activated by light. However, the supplied material does not specify the light-responsive domains, expression strategy, cofactors, or construct design details needed for implementation.
The provided evidence is limited to a single 2023 study and application in endothelial cells. The specific photoreceptor components, wavelengths, construct architecture, and quantitative performance metrics are not given in the supplied evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Observations
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c4 during normalization. In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism. Derived from claim c4. Quoted text: The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c5 during normalization. Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction. Derived from claim c5. Quoted text: Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c4 during normalization. In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism. Derived from claim c4. Quoted text: The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c5 during normalization. Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction. Derived from claim c5. Quoted text: Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c4 during normalization. In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism. Derived from claim c4. Quoted text: The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c5 during normalization. Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction. Derived from claim c5. Quoted text: Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c4 during normalization. In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism. Derived from claim c4. Quoted text: The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c5 during normalization. Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction. Derived from claim c5. Quoted text: Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c4 during normalization. In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism. Derived from claim c4. Quoted text: The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c5 during normalization. Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction. Derived from claim c5. Quoted text: Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c4 during normalization. In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism. Derived from claim c4. Quoted text: The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c5 during normalization. Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction. Derived from claim c5. Quoted text: Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c4 during normalization. In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism. Derived from claim c4. Quoted text: The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
successMammalian Cell Lineapplication demoendothelial cells
Inferred from claim c5 during normalization. Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction. Derived from claim c5. Quoted text: Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
Supporting Sources
Ranked Claims
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
iLID-based Opto-RhoGEFs allow reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID-based Opto-RhoGEFs allow reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID-based Opto-RhoGEFs allow reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID-based Opto-RhoGEFs allow reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID-based Opto-RhoGEFs allow reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID-based Opto-RhoGEFs allow reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID-based Opto-RhoGEFs allow reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID enables reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID enables reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID enables reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID enables reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID enables reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID enables reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
iLID enables reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
The iLID membrane tag was optimized and HaloTag was applied to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was applied to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was applied to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was applied to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was applied to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was applied to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was applied to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for activating Cdc42, Rac, and Rho, respectively.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for activating Cdc42, Rac, and Rho, respectively.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for activating Cdc42, Rac, and Rho, respectively.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for activating Cdc42, Rac, and Rho, respectively.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for activating Cdc42, Rac, and Rho, respectively.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for activating Cdc42, Rac, and Rho, respectively.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for activating Cdc42, Rac, and Rho, respectively.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for optogenetic control of Rho GTPase signaling.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for optogenetic control of Rho GTPase signaling.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for optogenetic control of Rho GTPase signaling.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for optogenetic control of Rho GTPase signaling.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for optogenetic control of Rho GTPase signaling.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for optogenetic control of Rho GTPase signaling.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for optogenetic control of Rho GTPase signaling.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
The iLID membrane tag was optimized and HaloTag was added to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was added to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was added to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was added to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was added to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was added to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
The iLID membrane tag was optimized and HaloTag was added to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
Approval Evidence
1 source12 linked approval claimsfirst-pass slug opto-rhogefs
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs)
Source:
application resultsupports
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
application resultsupports
In an endothelial cell monolayer, Opto-RhoGEFs demonstrated precise temporal control of vascular barrier strength through a cell-cell overlap-dependent and VE-cadherin-independent mechanism.
The resulting optogenetically recruitable RhoGEFs (Opto-RhoGEFs) were tested in an endothelial cell monolayer and demonstrated precise temporal control of vascular barrier strength by a cell-cell overlap-dependent, VE-cadherin-independent, mechanism.
Source:
application resultsupports
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
application resultsupports
Opto-RhoGEFs enabled precise optogenetic control of endothelial cell morphology, including cell size, cell roundness, local extension, and cell contraction.
Furthermore, Opto-RhoGEFs enabled precise optogenetic control in endothelial cells over morphological features such as cell size, cell roundness, local extension, and cell contraction.
Source:
biological findingsupports
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Source:
capabilitysupports
iLID-based Opto-RhoGEFs allow reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
Source:
mechanism of actionsupports
iLID enables reversible, non-invasive, subcellular activation of Rho GTPase signaling by recruiting a GEF to a specific area at the plasma membrane.
This tool allows for Rho GTPase activation at the subcellular level in a reversible and non-invasive manner by recruiting a GEF to a specific area at the plasma membrane
Source:
mechanistic conclusionsupports
Membrane protrusions at the junction region can rapidly increase endothelial barrier integrity independently of VE-cadherin.
found that membrane protrusions at the junction region can rapidly increase barrier integrity independent of VE-cadherin
Source:
optimizationsupports
The iLID membrane tag was optimized and HaloTag was applied to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
Source:
tool constructionsupports
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for activating Cdc42, Rac, and Rho, respectively.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
Source:
tool designsupports
GEF domains from ITSN1, TIAM1, and p63RhoGEF were integrated into iLID to create Opto-RhoGEFs for optogenetic control of Rho GTPase signaling.
Guanine-nucleotide exchange factor (GEF) domains from ITSN1, TIAM1, and p63RhoGEF, activating Cdc42, Rac, and Rho, respectively, were integrated into the optogenetic recruitment tool improved light-induced dimer (iLID).
Source:
tool optimizationsupports
The iLID membrane tag was optimized and HaloTag was added to increase flexibility for multiplex imaging.
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
Source:
Comparisons
Source-backed strengths
The reported strengths are reversibility and precise control across global to subcellular spatial scales. In the cited application, Opto-RhoGEFs modulated multiple endothelial morphological outputs and precisely controlled vascular barrier strength in a monolayer context.
Source:
The membrane tag of iLID was optimized and a HaloTag was applied to gain more flexibility for multiplex imaging.
Ranked Citations
- 1.