Source 1primary paper2020Journal of Molecular Biology
Toolkit/OptoRAF1
OptoRAF1
Also known as: CRY2/CIB1-based optogenetic RAF1 system, optogenetic RAF1 system
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
OptoRAF1 is a blue light-responsive optogenetic RAF1 system built on the CRY2/CIB1 dimerizer pair. It reversibly activates the RAF/MEK/ERK pathway by recruiting RAF1 to the plasma membrane.
Usefulness & Problems
Why this is useful
This tool provides temporal control over RAF/MEK/ERK signaling with light rather than constitutive or chemically induced pathway activation. In mouse neural progenitor cells, it has been used to modulate proliferation, astrocytogenesis-associated gene expression, and neurite growth.
Source:
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Problem solved
OptoRAF1 addresses the need to perturb RAF signaling reversibly and with precise timing in living cells. The cited study specifically used it to test how early versus delayed RAF activation influences fate-related responses in mouse neural progenitor cells.
Problem links
Need conditional recombination or state switching
DerivedOptoRAF1 is a blue light-responsive, CRY2/CIB1-based optogenetic RAF1 system that reversibly activates the RAF/MEK/ERK pathway by recruiting RAF1 to the plasma membrane. It has been used in mouse neural progenitor cells to control RAF signaling with temporal precision.
Need inducible protein relocalization or recruitment
DerivedOptoRAF1 is a blue light-responsive, CRY2/CIB1-based optogenetic RAF1 system that reversibly activates the RAF/MEK/ERK pathway by recruiting RAF1 to the plasma membrane. It has been used in mouse neural progenitor cells to control RAF signaling with temporal precision.
Need precise spatiotemporal control with light input
DerivedOptoRAF1 is a blue light-responsive, CRY2/CIB1-based optogenetic RAF1 system that reversibly activates the RAF/MEK/ERK pathway by recruiting RAF1 to the plasma membrane. It has been used in mouse neural progenitor cells to control RAF signaling with temporal precision.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
HeterodimerizationHeterodimerizationHeterodimerizationmembrane recruitmentmembrane recruitmentMembrane RecruitmentTechniques
No technique tags yet.
Target processes
localizationrecombinationInput: 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: actuatoroperating role: regulatorswitch architecture: multi componentswitch architecture: recruitment
The mechanism described requires the blue light-sensitive CRY2/CIB1 protein dimerizer system and a design that enables plasma membrane recruitment of RAF1. Beyond domain fusion-based construction and blue light input, the supplied evidence does not specify wavelengths, expression strategy, membrane anchor design, or delivery method.
The supplied evidence is limited to a single 2020 study in mouse neural progenitor cells. Quantitative performance metrics, construct architecture details, illumination parameters, and validation in other cell types or organisms are not provided in the supplied evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Observations
successMammalian Cell Lineapplication demomouseneural progenitor cells
Inferred from claim c2 during normalization. Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes. Derived from claim c2. Quoted text: We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
mixedMammalian Cell Lineapplication demomousedifferentiated neural progenitor
Inferred from claim c3 during normalization. Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window. Derived from claim c3. Quoted text: However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Source:
mixedMammalian Cell Lineapplication demomouse
Inferred from claim c4 during normalization. OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth. Derived from claim c4. Quoted text: In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Source:
successMammalian Cell Lineapplication demomouseneural progenitor cells
Inferred from claim c2 during normalization. Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes. Derived from claim c2. Quoted text: We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
mixedMammalian Cell Lineapplication demomousedifferentiated neural progenitor
Inferred from claim c3 during normalization. Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window. Derived from claim c3. Quoted text: However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Source:
mixedMammalian Cell Lineapplication demomouse
Inferred from claim c4 during normalization. OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth. Derived from claim c4. Quoted text: In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Source:
successMammalian Cell Lineapplication demomouseneural progenitor cells
Inferred from claim c2 during normalization. Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes. Derived from claim c2. Quoted text: We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
mixedMammalian Cell Lineapplication demomousedifferentiated neural progenitor
Inferred from claim c3 during normalization. Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window. Derived from claim c3. Quoted text: However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Source:
mixedMammalian Cell Lineapplication demomouse
Inferred from claim c4 during normalization. OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth. Derived from claim c4. Quoted text: In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Source:
successMammalian Cell Lineapplication demomouseneural progenitor cells
Inferred from claim c2 during normalization. Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes. Derived from claim c2. Quoted text: We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
mixedMammalian Cell Lineapplication demomousedifferentiated neural progenitor
Inferred from claim c3 during normalization. Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window. Derived from claim c3. Quoted text: However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Source:
mixedMammalian Cell Lineapplication demomouse
Inferred from claim c4 during normalization. OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth. Derived from claim c4. Quoted text: In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Source:
successMammalian Cell Lineapplication demomouseneural progenitor cells
Inferred from claim c2 during normalization. Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes. Derived from claim c2. Quoted text: We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
mixedMammalian Cell Lineapplication demomousedifferentiated neural progenitor
Inferred from claim c3 during normalization. Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window. Derived from claim c3. Quoted text: However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Source:
mixedMammalian Cell Lineapplication demomouse
Inferred from claim c4 during normalization. OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth. Derived from claim c4. Quoted text: In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Source:
successMammalian Cell Lineapplication demomouseneural progenitor cells
Inferred from claim c2 during normalization. Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes. Derived from claim c2. Quoted text: We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
mixedMammalian Cell Lineapplication demomousedifferentiated neural progenitor
Inferred from claim c3 during normalization. Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window. Derived from claim c3. Quoted text: However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Source:
mixedMammalian Cell Lineapplication demomouse
Inferred from claim c4 during normalization. OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth. Derived from claim c4. Quoted text: In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Source:
successMammalian Cell Lineapplication demomouseneural progenitor cells
Inferred from claim c2 during normalization. Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes. Derived from claim c2. Quoted text: We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
mixedMammalian Cell Lineapplication demomousedifferentiated neural progenitor
Inferred from claim c3 during normalization. Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window. Derived from claim c3. Quoted text: However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Source:
mixedMammalian Cell Lineapplication demomouse
Inferred from claim c4 during normalization. OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth. Derived from claim c4. Quoted text: In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Source:
Supporting Sources
Ranked Claims
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Approval Evidence
1 source4 linked approval claimsfirst-pass slug optoraf1
using an optogenetic RAF1 system (OptoRAF1). OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
Source:
functional effectsupports
Early light-induced OptoRAF1 activation in mouse neural progenitor cells promotes cell proliferation and increases expression of glial markers and glia-enriched genes.
We found that early light-induced OptoRAF1 activation in neural progenitor cells promotes cell proliferation and increased expression of glial markers and glia-enriched genes.
Source:
functional specificitymixed
OptoRAF1 activation does not significantly affect neurogenesis but promotes neuronal neurite growth.
In addition, activation of OptoRAF1 did not have a significant effect on neurogenesis, but was able to promote neuronal neurite growth.
Source:
mechanism of actionsupports
OptoRAF1 enables reversible activation of the RAF/MEK/ERK pathway by blue light-driven plasma membrane recruitment of RAF1 using the CRY2/CIB1 dimerizer system.
OptoRAF1 allows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 based on blue light-sensitive protein dimerizer CRY2/CIB1.
Source:
timing dependencesupports
Delayed OptoRAF1 activation in differentiated mouse neural progenitors has little effect on glial marker expression, indicating that RAF1 promotes astrocytogenesis only within a short time window.
However, delayed OptoRAF1 activation in differentiated neural progenitor had little effect on glia marker expression, suggesting that RAF1 is required to promote astrocytogenesis only within a short time window.
Source:
Comparisons
Source-backed strengths
The reported system is reversible and directly couples blue light input to plasma membrane recruitment of RAF1 through CRY2/CIB1. In mouse neural progenitor cells, early activation promoted cell proliferation, increased glial markers and glia-enriched genes, and promoted neuronal neurite growth while not significantly affecting neurogenesis.
Compared with Cry2/CIB
OptoRAF1 and Cry2/CIB address a similar problem space because they share localization, recombination.
Shared frame: same top-level item type; shared target processes: localization, recombination; shared mechanisms: heterodimerization; same primary input modality: light
OptoRAF1 and CRY2-talin/CIBN-CAAX optogenetic plasma membrane recruitment system address a similar problem space because they share localization, recombination.
Shared frame: same top-level item type; shared target processes: localization, recombination; shared mechanisms: heterodimerization, membrane_recruitment; same primary input modality: light
Strengths here: appears more independently replicated; looks easier to implement in practice.
Compared with iLID/SspB
OptoRAF1 and iLID/SspB address a similar problem space because they share localization, recombination.
Shared frame: same top-level item type; shared target processes: localization, recombination; shared mechanisms: heterodimerization, membrane recruitment, membrane_recruitment; same primary input modality: light
Relative tradeoffs: appears more independently replicated.
Ranked Citations
- 1.