Source 1primary paper2018ACS Synthetic Biology
Toolkit/light-inducible TrkA activation strategies
light-inducible TrkA activation strategies
Also known as: light-inducible activation of TrkA, optical activation of TrkA
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Light-inducible TrkA activation strategies comprise four engineered optical designs for activating TrkA signaling without nerve growth factor. The reported approaches use light to drive plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA, recapitulating native NGF/TrkA-associated functions.
Usefulness & Problems
Why this is useful
These strategies provide an optical method to control TrkA signaling in the absence of NGF. Reported utility includes promotion of neurite growth in PC12 cells and support of dorsal root ganglion neuron survival.
Source:
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Source:
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
Source:
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Problem solved
These designs address the problem of activating TrkA signaling without exogenous NGF while enabling light-dependent control. The source specifically frames them as strategies for light-inducible TrkA activation and functional recapitulation of NGF/TrkA outputs.
Source:
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Problem links
Need conditional control of signaling activity
DerivedLight-inducible TrkA activation strategies are four engineered optical designs for activating TrkA signaling in the absence of nerve growth factor (NGF). The reported approaches use light to induce plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA, thereby recapitulating native NGF/TrkA functions.
Need inducible protein relocalization or recruitment
DerivedLight-inducible TrkA activation strategies are four engineered optical designs for activating TrkA signaling in the absence of nerve growth factor (NGF). The reported approaches use light to induce plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA, thereby recapitulating native NGF/TrkA functions.
Need precise spatiotemporal control with light input
DerivedLight-inducible TrkA activation strategies are four engineered optical designs for activating TrkA signaling in the absence of nerve growth factor (NGF). The reported approaches use light to induce plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA, thereby recapitulating native NGF/TrkA functions.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
HeterodimerizationHeterodimerizationHeterodimerizationmembrane recruitmentmembrane recruitmentMembrane RecruitmentTechniques
Computational DesignTarget processes
localizationsignalingInput: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: multi component delivery burdenimplementation constraint: spectral hardware requirementoperating role: regulatorswitch architecture: multi componentswitch architecture: recruitment
The reported designs are multi-component optical strategies centered on the intracellular domain of TrkA. Practical implementation details beyond light-induced plasma membrane recruitment and homo-interaction are not specified in the supplied evidence.
The supplied evidence is limited to a single 2018 source and does not provide detailed quantitative performance metrics, illumination parameters, or comparative benchmarking among the four strategies. Independent replication and validation outside the reported cell contexts are not documented in the provided evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Approval Evidence
1 source6 linked approval claimsfirst-pass slug light-inducible-trka-activation-strategies
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF.
Source:
cell survivalsupports
This optical TrkA activation approach supports survival of dorsal root ganglion neurons in the absence of NGF.
supports survival of dorsal root ganglion neurons in the absence of NGF
Source:
cellular effectsupports
This optical TrkA activation approach promotes neurite growth in PC12 cells.
promotes neurite growth in PC12 cells
Source:
functional recapitulationsupports
Optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA successfully recapitulates native NGF/TrkA functions.
We demonstrate successful recapitulation of native NGF/TrkA functions by optical induction of plasma membrane recruitment and homo-interaction of the intracellular domain of TrkA.
Source:
pathway activationsupports
This optical TrkA activation approach activates PI3K/AKT and Raf/ERK signaling pathways.
This approach activates PI3K/AKT and Raf/ERK signaling pathways
Source:
tool designsupports
The paper presents four strategies for light-inducible activation of TrkA in the absence of NGF.
Here we present the design and evaluation of four strategies for light-inducible activation of TrkA in the absence of NGF. Our strategies involve the light-sensitive protein Arabidopsis cryptochrome 2 and its binding partner CIB1.
Source:
use casesupports
Light-based activation of TrkA provides high spatial and temporal resolution for investigating NGF/TrkA signaling.
This ability to activate TrkA using light bestows high spatial and temporal resolution for investigating NGF/TrkA signaling.
Source:
Comparisons
Source-backed strengths
The study reports design and evaluation of four distinct strategies rather than a single construct. Functional validation includes neurite growth in PC12 cells, survival of dorsal root ganglion neurons without NGF, and recapitulation of native NGF/TrkA functions through optical induction of membrane recruitment and homo-interaction of TrkA intracellular domains.
Compared with fusion proteins with large N-terminal anchors
light-inducible TrkA activation strategies and fusion proteins with large N-terminal anchors address a similar problem space because they share localization, signaling.
Shared frame: same top-level item type; shared target processes: localization, signaling; shared mechanisms: heterodimerization; same primary input modality: light
Compared with iLID/SspB
light-inducible TrkA activation strategies and iLID/SspB address a similar problem space because they share localization, signaling.
Shared frame: same top-level item type; shared target processes: localization, signaling; shared mechanisms: heterodimerization, membrane recruitment, membrane_recruitment; same primary input modality: light
Relative tradeoffs: appears more independently replicated; looks easier to implement in practice.
Compared with LOVpep/ePDZb
light-inducible TrkA activation strategies and LOVpep/ePDZb address a similar problem space because they share localization, signaling.
Shared frame: same top-level item type; shared target processes: localization, signaling; shared mechanisms: heterodimerization; same primary input modality: light
Relative tradeoffs: appears more independently replicated; looks easier to implement in practice.
Ranked Citations
- 1.