Source 1primary paper2023Research Square (Research Square)
Toolkit/Opto-Casp8-V2
Opto-Casp8-V2
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Opto-Casp8-V2 is a blue light-responsive optogenetic caspase-8 construct built from the Arabidopsis cryptochrome 2 system. Under blue light, it shows more efficient self-cleavage and consumption than Opto-Casp8-V1 and more strongly promotes caspase-associated cell death outputs.
Usefulness & Problems
Why this is useful
This construct enables optical control of caspase-8-dependent death signaling with blue light. Reported applications include stronger induction of apoptosis-related outputs than the earlier V1 design and regulation of inflammasome activation and pyroptosis when apoptosis and necroptosis are compromised.
Source:
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
Source:
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
Problem solved
Opto-Casp8-V2 addresses the need for conditional, light-gated activation of caspase-8 signaling in mammalian cells. The reported optimization over Opto-Casp8-V1 specifically improves blue light-triggered self-cleavage and construct consumption, which is associated with stronger downstream cell death responses.
Problem links
Need conditional recombination or state switching
DerivedOpto-Casp8-V2 is a blue light-responsive optogenetic caspase-8 construct built from the Arabidopsis cryptochrome 2 system. Under blue light, it shows more efficient self-cleavage and consumption than Opto-Casp8-V1 and more strongly promotes caspase-associated cell death outputs.
Need precise spatiotemporal control with light input
DerivedOpto-Casp8-V2 is a blue light-responsive optogenetic caspase-8 construct built from the Arabidopsis cryptochrome 2 system. Under blue light, it shows more efficient self-cleavage and consumption than Opto-Casp8-V1 and more strongly promotes caspase-associated cell death outputs.
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
recombinationInput: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementoperating role: regulatorswitch architecture: cleavage
The construct is described as derived from the Arabidopsis cryptochrome 2 system and uses blue light as the input modality. Evidence mentions GFP-PHR-caspase8 and Flag-CIB1N-caspase8 components, indicating a fusion-based design involving CRY2-PHR and CIB1N-linked caspase-8 modules, but detailed construct architecture and expression conditions are not supplied here.
The evidence provided is limited to a single 2023 Research Square source and a small set of reported claims. Quantitative performance metrics, illumination parameters, cell-type scope, and independent replication are not provided in the supplied evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Observations
successMammalian Cell Linemechanistic demo
Inferred from claim c2 during normalization. Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation. Derived from claim c2. Quoted text: After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Source:
successMammalian Cell Linemechanistic demo
Inferred from claim c2 during normalization. Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation. Derived from claim c2. Quoted text: After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Source:
successMammalian Cell Linemechanistic demo
Inferred from claim c2 during normalization. Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation. Derived from claim c2. Quoted text: After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Source:
successMammalian Cell Linemechanistic demo
Inferred from claim c2 during normalization. Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation. Derived from claim c2. Quoted text: After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Source:
successMammalian Cell Linemechanistic demo
Inferred from claim c2 during normalization. Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation. Derived from claim c2. Quoted text: After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Source:
successMammalian Cell Linemechanistic demo
Inferred from claim c2 during normalization. Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation. Derived from claim c2. Quoted text: After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Source:
successMammalian Cell Linemechanistic demo
Inferred from claim c2 during normalization. Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation. Derived from claim c2. Quoted text: After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c5 during normalization. Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death. Derived from claim c5. Quoted text: Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c7 during normalization. Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised. Derived from claim c7. Quoted text: Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c4 during normalization. Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly. Derived from claim c4. Quoted text: Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c5 during normalization. Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death. Derived from claim c5. Quoted text: Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c7 during normalization. Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised. Derived from claim c7. Quoted text: Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c4 during normalization. Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly. Derived from claim c4. Quoted text: Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c5 during normalization. Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death. Derived from claim c5. Quoted text: Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c7 during normalization. Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised. Derived from claim c7. Quoted text: Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c4 during normalization. Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly. Derived from claim c4. Quoted text: Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c5 during normalization. Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death. Derived from claim c5. Quoted text: Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c7 during normalization. Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised. Derived from claim c7. Quoted text: Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c4 during normalization. Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly. Derived from claim c4. Quoted text: Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c5 during normalization. Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death. Derived from claim c5. Quoted text: Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c5 during normalization. Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death. Derived from claim c5. Quoted text: Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c7 during normalization. Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised. Derived from claim c7. Quoted text: Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c4 during normalization. Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly. Derived from claim c4. Quoted text: Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c7 during normalization. Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised. Derived from claim c7. Quoted text: Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c4 during normalization. Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly. Derived from claim c4. Quoted text: Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c5 during normalization. Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death. Derived from claim c5. Quoted text: Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c7 during normalization. Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised. Derived from claim c7. Quoted text: Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Source:
successMammalian Cell Lineapplication demo
Inferred from claim c4 during normalization. Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly. Derived from claim c4. Quoted text: Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Source:
Supporting Sources
Ranked Claims
Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly.
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly.
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly.
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly.
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly.
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly.
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly.
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised.
Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised.
Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised.
Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised.
Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised.
Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised.
Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised.
Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
GFP-PHR-caspase8 and Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and showed stronger interaction in co-immunoprecipitation assays.
The proteins GFP-PHR-caspase8/Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and interacted more strongly in co-immunoprecipitation assays.
GFP-PHR-caspase8 and Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and showed stronger interaction in co-immunoprecipitation assays.
The proteins GFP-PHR-caspase8/Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and interacted more strongly in co-immunoprecipitation assays.
GFP-PHR-caspase8 and Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and showed stronger interaction in co-immunoprecipitation assays.
The proteins GFP-PHR-caspase8/Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and interacted more strongly in co-immunoprecipitation assays.
GFP-PHR-caspase8 and Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and showed stronger interaction in co-immunoprecipitation assays.
The proteins GFP-PHR-caspase8/Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and interacted more strongly in co-immunoprecipitation assays.
GFP-PHR-caspase8 and Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and showed stronger interaction in co-immunoprecipitation assays.
The proteins GFP-PHR-caspase8/Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and interacted more strongly in co-immunoprecipitation assays.
GFP-PHR-caspase8 and Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and showed stronger interaction in co-immunoprecipitation assays.
The proteins GFP-PHR-caspase8/Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and interacted more strongly in co-immunoprecipitation assays.
GFP-PHR-caspase8 and Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and showed stronger interaction in co-immunoprecipitation assays.
The proteins GFP-PHR-caspase8/Flag-CIB1N-caspase8 were cleaved in a blue light-dependent manner and interacted more strongly in co-immunoprecipitation assays.
Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation.
After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation.
After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation.
After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation.
After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation.
After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation.
After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation.
After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
The optogenetic tool enables precise modulation of caspase-8 activity to induce cellular apoptosis.
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
The optogenetic tool enables precise modulation of caspase-8 activity to induce cellular apoptosis.
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
The optogenetic tool enables precise modulation of caspase-8 activity to induce cellular apoptosis.
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
The optogenetic tool enables precise modulation of caspase-8 activity to induce cellular apoptosis.
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
The optogenetic tool enables precise modulation of caspase-8 activity to induce cellular apoptosis.
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
The optogenetic tool enables precise modulation of caspase-8 activity to induce cellular apoptosis.
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
The optogenetic tool enables precise modulation of caspase-8 activity to induce cellular apoptosis.
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
The study developed an optogenetic approach that rapidly modulates caspase-8 activation in response to blue light.
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
The study developed an optogenetic approach that rapidly modulates caspase-8 activation in response to blue light.
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
The study developed an optogenetic approach that rapidly modulates caspase-8 activation in response to blue light.
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
The study developed an optogenetic approach that rapidly modulates caspase-8 activation in response to blue light.
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
The study developed an optogenetic approach that rapidly modulates caspase-8 activation in response to blue light.
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
The study developed an optogenetic approach that rapidly modulates caspase-8 activation in response to blue light.
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
The study developed an optogenetic approach that rapidly modulates caspase-8 activation in response to blue light.
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
Approval Evidence
1 source6 linked approval claimsfirst-pass slug opto-casp8-v2
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light
Source:
comparative performancesupports
Opto-Casp8-V2 showed more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light and promoted apoptosis more strongly.
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Source:
conditional functionsupports
Under blue light control, the tool regulates inflammasome activation and induces pyroptosis when apoptosis and necroptosis mechanisms are compromised.
Additionally, through blue light control, it regulates the activation of the inflammasome and induction of pyroptosis in cases where apoptosis and necroptosis mechanisms are compromised.
Source:
mechanistic effectsupports
Blue light exposure decreased precursor PHR-Caspase8 abundance and increased activated caspase-8 (P18) and caspase-3 accumulation.
After exposure to blue light, the abundance of the precursor protein PHR-Caspase8 decreased, while the activated forms of caspase8 (P18) and caspase3 accumulated.
Source:
phenotypic effectsupports
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced nuclear shrinkage, apoptotic body formation, and cell death.
Both Opto-Casp8-V1 and Opto-Casp8-V2 induced the shrinkage of numerous nuclei, leading to the formation of apoptotic bodies and ultimately promoting cell death.
Source:
tool functionsupports
The optogenetic tool enables precise modulation of caspase-8 activity to induce cellular apoptosis.
Our optogenetic tool enables precise modulation of Caspase-8 activity, inducing cellular apoptosis.
Source:
tool functionsupports
The study developed an optogenetic approach that rapidly modulates caspase-8 activation in response to blue light.
In this study, we developed an optogenetic approach to rapidly modulate the activation of caspase-8 in response to blue light.
Source:
Comparisons
Source-backed strengths
Compared with Opto-Casp8-V1, Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption under blue light. Blue light-dependent cleavage and stronger interaction were supported by co-immunoprecipitation data for GFP-PHR-caspase8 and Flag-CIB1N-caspase8, and the construct was reported to promote apoptosis more strongly.
Source:
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light, and was found to promote cell apoptosis more strongly.
Opto-Casp8-V2 and modular light-controlled skeletal muscle-powered bioactuator address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination; same primary input modality: light
Compared with Opto-Casp8-V1
Opto-Casp8-V2 and Opto-Casp8-V1 address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination; shared mechanisms: light-induced protein interaction, photocleavage; same primary input modality: light
Compared with pcVP16
Opto-Casp8-V2 and pcVP16 address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination; same primary input modality: light
Ranked Citations
- 1.