Source 1primary paper2019
Toolkit/opto-iTrkA
opto-iTrkA
Also known as: iLID opto-iTrkA
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
opto-iTrkA is an iLID-based light-activated TrkA construct engineered to control TrkA receptor signaling with blue light. The intracellular TrkA module is cytosolic, monomeric, and inactive in the dark, and activation requires light-driven recruitment in the presence of tdnano to reproduce downstream ERK and Akt signaling.
Usefulness & Problems
Why this is useful
This construct enables optical control of TrkA pathway activation with conditional dependence on a binding partner, tdnano. It is reported to be compatible with multi-day and population-level activation of TrkA in PC12 cells, supporting experiments that require repeated or extended stimulation.
Problem solved
opto-iTrkA addresses the problem of activating TrkA signaling with light rather than constitutive or ligand-based stimulation. The reported design also constrains signaling output by requiring tdnano for downstream ERK and Akt activation.
Problem links
Need conditional control of signaling activity
Derivedopto-iTrkA is an iLID-based light-activated TrkA construct engineered to control TrkA receptor signaling with blue light. The intracellular TrkA module is cytosolic, monomeric, and inactive in the dark, and activation requires light-driven recruitment in the presence of tdnano to reproduce downstream ERK and Akt signaling.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Techniques
No technique tags yet.
Target processes
signalingImplementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: regulatorswitch architecture: recruitment
The construct is described as iLID-based and requires blue light for activation. Reported activity depends on the presence of tdnano, and compatibility was specifically noted for PC12 cells in multi-day and population-level activation experiments.
The supplied evidence comes from a single 2019 source and provides limited quantitative performance details. No independent replication, kinetic parameters, dynamic range, or validation outside PC12 cells are provided in the evidence set.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
opto-iTrkA and opto-iTrkB reproduce downstream ERK and Akt signaling only in the presence of tdnano.
We demonstrate that iLID opto-iTrkA and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.
opto-iTrkA and opto-iTrkB reproduce downstream ERK and Akt signaling only in the presence of tdnano.
We demonstrate that iLID opto-iTrkA and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.
opto-iTrkA and opto-iTrkB reproduce downstream ERK and Akt signaling only in the presence of tdnano.
We demonstrate that iLID opto-iTrkA and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.
opto-iTrkA and opto-iTrkB reproduce downstream ERK and Akt signaling only in the presence of tdnano.
We demonstrate that iLID opto-iTrkA and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.
opto-iTrkA and opto-iTrkB reproduce downstream ERK and Akt signaling only in the presence of tdnano.
We demonstrate that iLID opto-iTrkA and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.
opto-iTrkA and opto-iTrkB reproduce downstream ERK and Akt signaling only in the presence of tdnano.
We demonstrate that iLID opto-iTrkA and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.
opto-iTrkA and opto-iTrkB reproduce downstream ERK and Akt signaling only in the presence of tdnano.
We demonstrate that iLID opto-iTrkA and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.
opto-iTrkA is compatible with multi-day and population-level activation of TrkA in PC12 cells.
We further show with our opto-iTrkA that the system is compatible with multi-day and population-level activation of TrkA in PC12 cells.
opto-iTrkA is compatible with multi-day and population-level activation of TrkA in PC12 cells.
We further show with our opto-iTrkA that the system is compatible with multi-day and population-level activation of TrkA in PC12 cells.
opto-iTrkA is compatible with multi-day and population-level activation of TrkA in PC12 cells.
We further show with our opto-iTrkA that the system is compatible with multi-day and population-level activation of TrkA in PC12 cells.
opto-iTrkA is compatible with multi-day and population-level activation of TrkA in PC12 cells.
We further show with our opto-iTrkA that the system is compatible with multi-day and population-level activation of TrkA in PC12 cells.
opto-iTrkA is compatible with multi-day and population-level activation of TrkA in PC12 cells.
We further show with our opto-iTrkA that the system is compatible with multi-day and population-level activation of TrkA in PC12 cells.
opto-iTrkA is compatible with multi-day and population-level activation of TrkA in PC12 cells.
We further show with our opto-iTrkA that the system is compatible with multi-day and population-level activation of TrkA in PC12 cells.
opto-iTrkA is compatible with multi-day and population-level activation of TrkA in PC12 cells.
We further show with our opto-iTrkA that the system is compatible with multi-day and population-level activation of TrkA in PC12 cells.
In the absence of light, iLID-RTK is cytosolic, monomeric, and inactive.
In the absence of light, the iLID-RTK is cytosolic, monomeric and inactive.
In the absence of light, iLID-RTK is cytosolic, monomeric, and inactive.
In the absence of light, the iLID-RTK is cytosolic, monomeric and inactive.
In the absence of light, iLID-RTK is cytosolic, monomeric, and inactive.
In the absence of light, the iLID-RTK is cytosolic, monomeric and inactive.
In the absence of light, iLID-RTK is cytosolic, monomeric, and inactive.
In the absence of light, the iLID-RTK is cytosolic, monomeric and inactive.
In the absence of light, iLID-RTK is cytosolic, monomeric, and inactive.
In the absence of light, the iLID-RTK is cytosolic, monomeric and inactive.
In the absence of light, iLID-RTK is cytosolic, monomeric, and inactive.
In the absence of light, the iLID-RTK is cytosolic, monomeric and inactive.
In the absence of light, iLID-RTK is cytosolic, monomeric, and inactive.
In the absence of light, the iLID-RTK is cytosolic, monomeric and inactive.
Under blue light, the iLID plus tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID + tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID plus tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID + tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID plus tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID + tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID plus tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID + tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID plus tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID + tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID plus tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID + tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID plus tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Under blue light, the iLID + tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing and activating the RTK.
Genetic targeting of tdnano enables RTK activation at a specific subcellular location even with whole-cell illumination.
By leveraging genetic targeting of tdnano, we achieve RTK activation at a specific subcellular location even with whole-cell illumination
Genetic targeting of tdnano enables RTK activation at a specific subcellular location even with whole-cell illumination.
By leveraging genetic targeting of tdnano, we achieve RTK activation at a specific subcellular location even with whole-cell illumination
Genetic targeting of tdnano enables RTK activation at a specific subcellular location even with whole-cell illumination.
By leveraging genetic targeting of tdnano, we achieve RTK activation at a specific subcellular location even with whole-cell illumination
Genetic targeting of tdnano enables RTK activation at a specific subcellular location even with whole-cell illumination.
By leveraging genetic targeting of tdnano, we achieve RTK activation at a specific subcellular location even with whole-cell illumination
Genetic targeting of tdnano enables RTK activation at a specific subcellular location even with whole-cell illumination.
By leveraging genetic targeting of tdnano, we achieve RTK activation at a specific subcellular location even with whole-cell illumination
Genetic targeting of tdnano enables RTK activation at a specific subcellular location even with whole-cell illumination.
By leveraging genetic targeting of tdnano, we achieve RTK activation at a specific subcellular location even with whole-cell illumination
Genetic targeting of tdnano enables RTK activation at a specific subcellular location even with whole-cell illumination.
By leveraging genetic targeting of tdnano, we achieve RTK activation at a specific subcellular location even with whole-cell illumination
Approval Evidence
1 source2 linked approval claimsfirst-pass slug opto-itrka
We demonstrate that iLID opto-iTrkA
Source:
activitysupports
opto-iTrkA and opto-iTrkB reproduce downstream ERK and Akt signaling only in the presence of tdnano.
We demonstrate that iLID opto-iTrkA and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.
Source:
compatibilitysupports
opto-iTrkA is compatible with multi-day and population-level activation of TrkA in PC12 cells.
We further show with our opto-iTrkA that the system is compatible with multi-day and population-level activation of TrkA in PC12 cells.
Source:
Comparisons
Source-backed strengths
Source claims indicate that opto-iTrkA reproduces downstream ERK and Akt signaling only in the presence of tdnano, consistent with partner-dependent activation. It is also reported to support multi-day and population-level TrkA activation in PC12 cells, suggesting utility beyond acute single-cell stimulation.
Compared with kinase translocation reporters
opto-iTrkA and kinase translocation reporters address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling
opto-iTrkA and novel fluorescent biosensor for mitochondrial outer membrane rupture address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling
Compared with opto-iTrkB
opto-iTrkA and opto-iTrkB address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling; shared mechanisms: induced dimerization, light-induced recruitment, receptor tyrosine kinase activation
Ranked Citations
- 1.