Browse the toolkit beneath workflows. The mechanism branch runs mechanism -> architecture -> component, while the technique branch runs from high-level approaches down to concrete methods.
9 items matching 1 filter
Mechanism Branch
Layer 1
Mechanisms
Top-level concepts: biophysical action modes such as heterodimerization, photocleavage, or RNA binding.
Layer 2
Architectures
Arrangements that realize or deploy mechanisms, including switches, construct patterns, and delivery strategies.
Layer 3
Components
Low-level parts and sequence-defined elements used inside architectures, including protein domains and RNA elements.
Technique Branch
Layer 1
Approaches
High-level engineering practices such as computational design, directed evolution, sequence verification, and functional assay.
Layer 2
Methods
Concrete methods used to design, build, verify, or characterize engineered systems.
Showing 1-9 of 9
PMC text for the anchor paper explicitly states that intraneural AAV6-hSyn-SwiChR-eYFP expression enabled transdermal optogenetic inhibition and sustained post-light inhibition of pain behaviors.
In this study, we developed a highly sensitive moderately K+-selective channelrhodopsin (HcKCR1-hs) by molecular engineering of the recently discovered Hyphochytrium catenoides kalium (potassium) channelrhodopsin 1.
Optogenetic control of contractility is a light-based engineering method proposed to spatially modulate cellular contractility and thereby influence cell migration behavior. In a one-dimensional active gel model, optogenetic activation or inhibition of contractility is predicted to switch cells between sessile and motile states at realistic parameter values.
Optogenetic inhibition of Delta is a light-controlled perturbation method reported in a 2019 EMBO Reports study to inhibit the Notch ligand Delta during tissue differentiation. The study links this intervention to revealing digital Notch signalling output.
The anchor paper explicitly states that it develops optoPAIN (Optogenetic Pain Assay in vivo) to examine bidirectional optogenetic and chemogenetic control of pain without physically contacting the animal.
We used a mouse model of temporal lobe epilepsy, on-line seizure detection, and responsive optogenetic intervention to investigate the potential for cerebellar control of spontaneous temporal lobe seizures.
Here we report the validation and further development of the channelrhodopsin pore model via crystal structure-guided engineering of next-generation light-activated chloride channels (iC++)
Explicitly supported component/tool names found in these sources include NpHR, ChR2, ArchT, closed-loop real-time seizure detection, and inhibitory luminopsins.
We designed a novel all-optical tool to simultaneously silence neuronal activity at arbitrary sites on the dorsal cortex, and monitor the consequences of the manipulation.