Source 1primary paper2016Scientific Reports
Toolkit/OptoCNK1
OptoCNK1
Also known as: optogenetic clustering of CNK1
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
OptoCNK1 is an optogenetic CNK1 clustering construct implemented in MCF7 cells to stimulate CNK1 independently of upstream effectors. Light-induced CNK1 clustering was reported to selectively engage RAF-MEK-ERK or AKT signaling as a function of applied light intensity, with corresponding effects on cell fate.
Usefulness & Problems
Why this is useful
This construct is useful for probing how CNK1 organization controls downstream signaling without confounding activation from upstream inputs. In MCF7 cells, it enabled intensity-dependent interrogation of ERK-associated differentiation versus AKT-associated proliferation.
Problem solved
OptoCNK1 addresses the problem of stimulating CNK1 while uncoupling it from upstream effectors. It also provides a way to test how different extents of light-driven CNK1 clustering bias signaling output between RAF-MEK-ERK and AKT pathways.
Problem links
Need precise spatiotemporal control with light input
DerivedOptoCNK1 is an optogenetic CNK1 clustering construct implemented in MCF7 cells to stimulate CNK1 independently of upstream effectors. Light-induced CNK1 clustering was reported to differentially engage RAF-MEK-ERK or AKT signaling as a function of light intensity, thereby influencing cell fate decisions.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Mechanisms
intensity-dependent pathway selectionintensity-dependent pathway selectionlight-induced protein clusteringlight-induced protein clusteringTechniques
No technique tags yet.
Target processes
No target processes tagged yet.
Input: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementoperating role: actuator
The available evidence states that OptoCNK1 was implemented in MCF7 cells and used to stimulate CNK1 uncoupled from upstream effectors. Practical details such as the light-responsive domain, illumination wavelength, expression strategy, and construct design are not provided in the supplied evidence.
The supplied evidence is limited to one study in MCF7 cells and does not establish performance across other cell types or experimental contexts. The evidence provided does not specify construct architecture, photoreceptor module, wavelength, dynamic range, reversibility, or quantitative activation thresholds.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Approval Evidence
1 source2 linked approval claimsfirst-pass slug optocnk1
Using an optogenetic approach to stimulate CNK1 uncoupled from upstream effectors... OptoCNK1 implemented in MCF7 cells
Source:
cell fate effectsupports
In MCF7 cells, OptoCNK1 induces differentiation at low light intensity with ERK activity, whereas higher light intensity stimulates AKT signalling and promotes cell proliferation.
OptoCNK1 implemented in MCF7 cells induces differentiation at low light intensity stimulating ERK activity whereas stimulation of AKT signalling by higher light intensity promotes cell proliferation
Source:
mechanismsupports
Selective clusters of CNK1 stimulate either RAF-MEK-ERK signalling or AKT signalling depending on applied light intensity.
we identified selective clusters of CNK1 that either stimulate RAF-MEK-ERK or AKT signalling depending on the light intensity applied
Source:
Comparisons
Source-backed strengths
The reported strength of OptoCNK1 is that a single light-controlled construct could differentially activate distinct signaling programs depending on light intensity. In MCF7 cells, low light intensity was associated with ERK activity and differentiation, whereas higher light intensity stimulated AKT signaling and promoted proliferation.
Compared with alkynyl-functionalized photocleavable linker
OptoCNK1 and alkynyl-functionalized photocleavable linker address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Compared with cyp-14A5 promoter
OptoCNK1 and cyp-14A5 promoter address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Compared with red light-inducible recombinase library
OptoCNK1 and red light-inducible recombinase library address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Ranked Citations
- 1.