Source 1primary paper2019
Toolkit/opto-iTrkB
opto-iTrkB
Also known as: iLID opto-iTrkB
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
opto-iTrkB, also called iLID opto-iTrkB, is a blue-light-activated TrkB receptor tyrosine kinase construct built on the improved Light-Induced Dimerizer system. In the reported design, cytosolic inactive iLID-RTK is recruited to tdnano under blue light, which drives receptor dimerization and activates downstream ERK and Akt signaling.
Usefulness & Problems
Why this is useful
This construct enables optical control of TrkB pathway activation with light-dependent recruitment and dimerization rather than constitutive receptor activity. It is useful for studying RTK signaling dynamics because ERK and Akt activation was reported for opto-iTrkB only when the tdnano partner was present.
Problem solved
opto-iTrkB addresses the problem of controlling TrkB receptor activation with spatially and temporally defined light input. The reported design specifically solves how to keep the RTK monomeric and inactive in the dark, then activate it by blue-light-triggered recruitment to a dimerizing scaffold.
Problem links
Need conditional control of signaling activity
Derivedopto-iTrkB, also referred to as iLID opto-iTrkB, is a light-activated TrkB receptor construct built on the improved Light-Induced Dimerizer system. In the reported design, blue light recruits cytosolic, inactive iLID-RTK molecules to tdnano, driving receptor dimerization and enabling downstream ERK and Akt signaling.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Mechanisms
induced dimerizationinduced dimerizationlight-induced recruitmentlight-induced recruitmentreceptor tyrosine kinase activationreceptor tyrosine kinase activationTechniques
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 uses the improved Light-Induced Dimerizer system and requires the tdnano component for reported signaling output. The evidence indicates that iLID-RTK is cytosolic in the dark and is recruited under blue light, but the supplied material does not provide additional construct architecture, expression, or delivery details.
The supplied evidence is limited to one 2019 source and provides only a brief activity statement for opto-iTrkB. Multi-day and population-level compatibility was stated for opto-iTrkA in PC12 cells, but equivalent validation was not provided here for opto-iTrkB.
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 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 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.
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.
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.
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
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 source1 linked approval claimfirst-pass slug opto-itrkb
and opto-iTrkB are capable of reproducing downstream ERK and Akt signaling
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:
Comparisons
Source-backed strengths
The source reports a clear dark-state mechanism in which iLID-RTK is cytosolic, monomeric, and inactive, which supports low basal signaling by design. It also reports that blue light with tdnano recruits two copies of iLID-RTK to drive dimerization and that opto-iTrkB reproduces downstream ERK and Akt signaling under these conditions.
Compared with eOPN3
opto-iTrkB and eOPN3 address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling
Compared with opto-iTrkA
opto-iTrkB and opto-iTrkA 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
Compared with tandem-dimer nano (tdnano)
opto-iTrkB and tandem-dimer nano (tdnano) address a similar problem space because they share signaling.
Shared frame: shared target processes: signaling; shared mechanisms: induced dimerization, light-induced recruitment
Strengths here: looks easier to implement in practice.
Ranked Citations
- 1.