Source 1primary paper2019
Toolkit/iLID-RTK
iLID-RTK
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
iLID-RTK is a blue-light-controlled, multi-component receptor tyrosine kinase switch built from the iLID and tdnano system. In darkness it is cytosolic, monomeric, and inactive, while blue light recruits two iLID-RTK molecules to tdnano to drive RTK dimerization and activation.
Usefulness & Problems
Why this is useful
This system enables optical control of receptor tyrosine kinase signaling by coupling blue light to inducible receptor dimerization. Reported opto-iTrkA and opto-iTrkB constructs reproduce downstream ERK and Akt signaling only when tdnano is present, indicating utility for conditional pathway activation with spatial and temporal light input.
Problem solved
It addresses the problem of activating RTKs on demand without constitutive receptor clustering in the dark state. The design specifically solves how to keep the receptor module cytosolic, monomeric, and inactive until blue-light-triggered recruitment to a dimerizing scaffold occurs.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
Heterodimerizationlight-induced heterodimerizationreceptor tyrosine kinase activationrecruitment-driven dimerizationTechniques
No technique tags yet.
Target processes
No target processes tagged yet.
Input: Light
Implementation Constraints
The switch is multi-component and requires both an iLID-RTK construct and the tdnano partner for activity. Blue light is the input modality, and activation depends on light-driven recruitment of two iLID-RTK copies to tdnano; PC12-cell compatibility was reported for opto-iTrkA during multi-day and population-level activation.
The evidence provided comes from a single 2019 source and focuses on neurotrophin receptor implementations, specifically opto-iTrkA and opto-iTrkB. Quantitative performance metrics, reversibility kinetics, spectral constraints beyond blue light, and validation across diverse cell types or in vivo settings are not provided in the supplied evidence.
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 ilid-rtk
In the absence of light, the iLID-RTK is cytosolic, monomeric and inactive.
Source:
mechanismsupports
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.
Source:
mechanismsupports
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.
Source:
Comparisons
Source-backed strengths
The reported dark state is explicitly cytosolic, monomeric, and inactive, supporting low basal activity. In the cited study, opto-iTrkA was compatible with multi-day and population-level activation in PC12 cells, and opto-iTrkA/opto-iTrkB reproduced ERK and Akt signaling only in the presence of tdnano.
Ranked Citations
- 1.