Toolkit/Opto-Casp8-V1
Opto-Casp8-V1
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Opto-Casp8-V1 is a blue light-responsive caspase-8 optogenetic construct built in the context of Arabidopsis cryptochrome 2/CIB1N-based apoptosis control. Under blue light, related GFP-PHR-caspase8 and Flag-CIB1N-caspase8 fusion components show light-dependent interaction and cleavage, and Opto-Casp8-V1 is reported to undergo less efficient self-cleavage and consumption than Opto-Casp8-V2.
Usefulness & Problems
Why this is useful
This construct provides optical control over caspase-8-associated cell death signaling using blue light. The cited study also reports blue light-controlled regulation of inflammasome activation and induction of pyroptosis when apoptosis and necroptosis mechanisms are compromised, indicating utility for probing death-pathway crosstalk.
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-V1 addresses the need for conditional, light-gated control of caspase-8 signaling rather than constitutive activation. The available evidence specifically supports blue light-dependent activation-associated interaction and cleavage in a CRY2/CIB1N fusion context.
Problem links
Need conditional recombination or state switching
DerivedOpto-Casp8-V1 is a blue light-responsive caspase-8 optogenetic construct reported in the context of Arabidopsis cryptochrome 2-based apoptosis control. Under blue light, related PHR/CIB1N-caspase-8 fusion components undergo light-dependent interaction and cleavage, and Opto-Casp8-V1 is specifically reported to be less efficiently self-cleaved and consumed than Opto-Casp8-V2.
Need precise spatiotemporal control with light input
DerivedOpto-Casp8-V1 is a blue light-responsive caspase-8 optogenetic construct reported in the context of Arabidopsis cryptochrome 2-based apoptosis control. Under blue light, related PHR/CIB1N-caspase-8 fusion components undergo light-dependent interaction and cleavage, and Opto-Casp8-V1 is specifically reported to be less efficiently self-cleaved and consumed than Opto-Casp8-V2.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Mechanisms
light-induced protein interactionlight-induced protein interactionPhotocleavageself-cleavage/proteolytic activationself-cleavage/proteolytic activationTechniques
No technique tags yet.
Target processes
recombinationInput: Light
Implementation Constraints
The construct is described in an Arabidopsis cryptochrome 2-based optogenetic framework using PHR and CIB1N fusion components linked to caspase-8. The supplied evidence supports blue light as the input and mentions GFP-PHR-caspase8 and Flag-CIB1N-caspase8 constructs, but does not provide sequence architecture, expression system details, or illumination parameters.
The evidence is limited and primarily comparative, with the clearest direct statement being that Opto-Casp8-V1 is less efficiently self-cleaved and consumed than Opto-Casp8-V2 under blue light. Independent replication, quantitative performance metrics, and detailed implementation parameters are not provided in the supplied evidence.
Validation
Observations
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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.
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.
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.
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.
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.
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.
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.
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.
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.
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 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 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.
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.
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
Opto-Casp8-V2 exhibited significantly more efficient self-cleavage and consumption than Opto-Casp8-V1 under blue light
Source:
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:
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:
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:
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:
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:
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
The reported system shows blue light-dependent cleavage and stronger interaction in co-immunoprecipitation assays for GFP-PHR-caspase8 and Flag-CIB1N-caspase8. Opto-Casp8-V1 is part of a comparative construct series, establishing that its behavior can be benchmarked against Opto-Casp8-V2 under the same blue light conditions.
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.
Compared with GFP-PHR-caspase8/Flag-CIB1N-caspase8
Opto-Casp8-V1 and GFP-PHR-caspase8/Flag-CIB1N-caspase8 address a similar problem space because they share recombination.
Shared frame: shared target processes: recombination; shared mechanisms: photocleavage; same primary input modality: light
Strengths here: looks easier to implement in practice.
Compared with Opto-Casp8-V2
Opto-Casp8-V1 and Opto-Casp8-V2 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 PA-Cre 3.0
Opto-Casp8-V1 and PA-Cre 3.0 address a similar problem space because they share recombination.
Shared frame: shared target processes: recombination; shared mechanisms: photocleavage; same primary input modality: light
Strengths here: looks easier to implement in practice.
Ranked Citations
- 1.