Source 1primary paper2020Frontiers in Cellular Neuroscience
Toolkit/recombinant AAV1/2 viral particles
recombinant AAV1/2 viral particles
Also known as: AAV1/2, rAAVs
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Recombinant AAV1/2 viral particles are a viral gene delivery harness used to express the LOV2-PAH1 optogenetic REST inhibitor in HEK293T cells, primary neurons, and mouse hippocampal neurons in vivo. In the cited study, these particles enabled efficient hippocampal neuronal transduction and subsequent functional testing of the delivered cargo.
Usefulness & Problems
Why this is useful
This delivery system is useful for introducing optogenetic or other genetic payloads into cultured cells and neurons, including hippocampal neurons in vivo. The cited evidence specifically supports its use for expressing LOV2-PAH1 in contexts relevant to neuronal gene regulation and seizure-related studies.
Source:
To study the impact of REST modulation on seizure propensity, we developed a tool for its negative modulation in vivo. The tool is composed of the paired-amphipathic helix 1 (PAH1) domain ... fused to the light-oxygen-voltage sensing 2 (LOV2) domain
Source:
These data support the validity of our tool to modulate REST activity in vivo
Problem solved
Recombinant AAV1/2 addresses the practical problem of delivering a genetically encoded REST-modulating probe into HEK293T cells, primary neurons, and mouse hippocampus. In the cited work, this enabled in vivo and in vitro expression of LOV2-PAH1 for testing its effects on neuronal gene expression.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A delivery strategy grouped with the mechanism branch because it determines how a system is instantiated and deployed in context.
Techniques
No technique tags yet.
Target processes
No target processes tagged yet.
Implementation Constraints
The cited study used recombinant AAV1/2 particles to deliver the LOV2-PAH1 construct into HEK293T cells, primary neurons, and mouse hippocampus. Beyond this application context, the supplied evidence does not report construct architecture, promoter choice, viral production parameters, or dosing conditions.
The available evidence is limited to a single study and a single cargo context, LOV2-PAH1. No quantitative transduction metrics, packaging details, tropism comparisons, dose information, or broader validation across tissues or species are provided in the supplied evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Recombinant AAV1/2 viral particles enabled LOV2-PAH1 expression in HEK293T cells and primary neurons and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles enabled LOV2-PAH1 expression in HEK293T cells and primary neurons and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles enabled LOV2-PAH1 expression in HEK293T cells and primary neurons and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles enabled LOV2-PAH1 expression in HEK293T cells and primary neurons and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles enabled LOV2-PAH1 expression in HEK293T cells and primary neurons and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles enabled LOV2-PAH1 expression in HEK293T cells and primary neurons and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles enabled LOV2-PAH1 expression in HEK293T cells and primary neurons and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Expression of the open LOV2-PAH1 probe increased expression of several neuronal genes in mouse hippocampus.
mRNA expression analysis revealed an increased expression of several neuronal genes in the hippocampi of mice expressing the open probe.
Expression of the open LOV2-PAH1 probe increased expression of several neuronal genes in mouse hippocampus.
mRNA expression analysis revealed an increased expression of several neuronal genes in the hippocampi of mice expressing the open probe.
Expression of the open LOV2-PAH1 probe increased expression of several neuronal genes in mouse hippocampus.
mRNA expression analysis revealed an increased expression of several neuronal genes in the hippocampi of mice expressing the open probe.
Expression of the open LOV2-PAH1 probe increased expression of several neuronal genes in mouse hippocampus.
mRNA expression analysis revealed an increased expression of several neuronal genes in the hippocampi of mice expressing the open probe.
Expression of the open LOV2-PAH1 probe increased expression of several neuronal genes in mouse hippocampus.
mRNA expression analysis revealed an increased expression of several neuronal genes in the hippocampi of mice expressing the open probe.
Expression of the open LOV2-PAH1 probe increased expression of several neuronal genes in mouse hippocampus.
mRNA expression analysis revealed an increased expression of several neuronal genes in the hippocampi of mice expressing the open probe.
Expression of the open LOV2-PAH1 probe increased expression of several neuronal genes in mouse hippocampus.
mRNA expression analysis revealed an increased expression of several neuronal genes in the hippocampi of mice expressing the open probe.
PAH1 is described as a competitive inhibitor of REST activation by mSin3, and the LOV2 domain is used as a molecular switch to hide or expose the PAH1 inhibitor.
PAH1 domain, a competitive inhibitor of REST activation by mSin3, fused to the light-oxygen-voltage sensing 2 (LOV2) domain ... a molecular switch to alternatively hide or expose the PAH1 inhibitor
PAH1 is described as a competitive inhibitor of REST activation by mSin3, and the LOV2 domain is used as a molecular switch to hide or expose the PAH1 inhibitor.
PAH1 domain, a competitive inhibitor of REST activation by mSin3, fused to the light-oxygen-voltage sensing 2 (LOV2) domain ... a molecular switch to alternatively hide or expose the PAH1 inhibitor
PAH1 is described as a competitive inhibitor of REST activation by mSin3, and the LOV2 domain is used as a molecular switch to hide or expose the PAH1 inhibitor.
PAH1 domain, a competitive inhibitor of REST activation by mSin3, fused to the light-oxygen-voltage sensing 2 (LOV2) domain ... a molecular switch to alternatively hide or expose the PAH1 inhibitor
PAH1 is described as a competitive inhibitor of REST activation by mSin3, and the LOV2 domain is used as a molecular switch to hide or expose the PAH1 inhibitor.
PAH1 domain, a competitive inhibitor of REST activation by mSin3, fused to the light-oxygen-voltage sensing 2 (LOV2) domain ... a molecular switch to alternatively hide or expose the PAH1 inhibitor
PAH1 is described as a competitive inhibitor of REST activation by mSin3, and the LOV2 domain is used as a molecular switch to hide or expose the PAH1 inhibitor.
PAH1 domain, a competitive inhibitor of REST activation by mSin3, fused to the light-oxygen-voltage sensing 2 (LOV2) domain ... a molecular switch to alternatively hide or expose the PAH1 inhibitor
PAH1 is described as a competitive inhibitor of REST activation by mSin3, and the LOV2 domain is used as a molecular switch to hide or expose the PAH1 inhibitor.
PAH1 domain, a competitive inhibitor of REST activation by mSin3, fused to the light-oxygen-voltage sensing 2 (LOV2) domain ... a molecular switch to alternatively hide or expose the PAH1 inhibitor
PAH1 is described as a competitive inhibitor of REST activation by mSin3, and the LOV2 domain is used as a molecular switch to hide or expose the PAH1 inhibitor.
PAH1 domain, a competitive inhibitor of REST activation by mSin3, fused to the light-oxygen-voltage sensing 2 (LOV2) domain ... a molecular switch to alternatively hide or expose the PAH1 inhibitor
Mice expressing the active LOV2-PAH1 variant had fewer and less severe kainic acid-induced seizures than mice carrying the inactive probe.
Remarkably, mice expressing the active variant displayed a reduced number of KA-induced seizures, which were less severe compared to mice carrying the inactive probe.
Mice expressing the active LOV2-PAH1 variant had fewer and less severe kainic acid-induced seizures than mice carrying the inactive probe.
Remarkably, mice expressing the active variant displayed a reduced number of KA-induced seizures, which were less severe compared to mice carrying the inactive probe.
Mice expressing the active LOV2-PAH1 variant had fewer and less severe kainic acid-induced seizures than mice carrying the inactive probe.
Remarkably, mice expressing the active variant displayed a reduced number of KA-induced seizures, which were less severe compared to mice carrying the inactive probe.
Mice expressing the active LOV2-PAH1 variant had fewer and less severe kainic acid-induced seizures than mice carrying the inactive probe.
Remarkably, mice expressing the active variant displayed a reduced number of KA-induced seizures, which were less severe compared to mice carrying the inactive probe.
Mice expressing the active LOV2-PAH1 variant had fewer and less severe kainic acid-induced seizures than mice carrying the inactive probe.
Remarkably, mice expressing the active variant displayed a reduced number of KA-induced seizures, which were less severe compared to mice carrying the inactive probe.
Mice expressing the active LOV2-PAH1 variant had fewer and less severe kainic acid-induced seizures than mice carrying the inactive probe.
Remarkably, mice expressing the active variant displayed a reduced number of KA-induced seizures, which were less severe compared to mice carrying the inactive probe.
Mice expressing the active LOV2-PAH1 variant had fewer and less severe kainic acid-induced seizures than mice carrying the inactive probe.
Remarkably, mice expressing the active variant displayed a reduced number of KA-induced seizures, which were less severe compared to mice carrying the inactive probe.
The C450A and I539E light-independent AsLOV2 variants were used to mimic the closed inactive and open active states of LOV2-PAH1, respectively.
We employed the C450A and I539E light-independent AsLOV2 variants to mimic the closed (inactive) and open (active) states of LOV2-PAH1, respectively.
The C450A and I539E light-independent AsLOV2 variants were used to mimic the closed inactive and open active states of LOV2-PAH1, respectively.
We employed the C450A and I539E light-independent AsLOV2 variants to mimic the closed (inactive) and open (active) states of LOV2-PAH1, respectively.
The C450A and I539E light-independent AsLOV2 variants were used to mimic the closed inactive and open active states of LOV2-PAH1, respectively.
We employed the C450A and I539E light-independent AsLOV2 variants to mimic the closed (inactive) and open (active) states of LOV2-PAH1, respectively.
The C450A and I539E light-independent AsLOV2 variants were used to mimic the closed inactive and open active states of LOV2-PAH1, respectively.
We employed the C450A and I539E light-independent AsLOV2 variants to mimic the closed (inactive) and open (active) states of LOV2-PAH1, respectively.
The C450A and I539E light-independent AsLOV2 variants were used to mimic the closed inactive and open active states of LOV2-PAH1, respectively.
We employed the C450A and I539E light-independent AsLOV2 variants to mimic the closed (inactive) and open (active) states of LOV2-PAH1, respectively.
The C450A and I539E light-independent AsLOV2 variants were used to mimic the closed inactive and open active states of LOV2-PAH1, respectively.
We employed the C450A and I539E light-independent AsLOV2 variants to mimic the closed (inactive) and open (active) states of LOV2-PAH1, respectively.
The C450A and I539E light-independent AsLOV2 variants were used to mimic the closed inactive and open active states of LOV2-PAH1, respectively.
We employed the C450A and I539E light-independent AsLOV2 variants to mimic the closed (inactive) and open (active) states of LOV2-PAH1, respectively.
The authors developed an in vivo REST negative-modulation tool composed of PAH1 fused to the AsLOV2 domain.
To study the impact of REST modulation on seizure propensity, we developed a tool for its negative modulation in vivo. The tool is composed of the paired-amphipathic helix 1 (PAH1) domain ... fused to the light-oxygen-voltage sensing 2 (LOV2) domain
The authors developed an in vivo REST negative-modulation tool composed of PAH1 fused to the AsLOV2 domain.
To study the impact of REST modulation on seizure propensity, we developed a tool for its negative modulation in vivo. The tool is composed of the paired-amphipathic helix 1 (PAH1) domain ... fused to the light-oxygen-voltage sensing 2 (LOV2) domain
The authors developed an in vivo REST negative-modulation tool composed of PAH1 fused to the AsLOV2 domain.
To study the impact of REST modulation on seizure propensity, we developed a tool for its negative modulation in vivo. The tool is composed of the paired-amphipathic helix 1 (PAH1) domain ... fused to the light-oxygen-voltage sensing 2 (LOV2) domain
The authors developed an in vivo REST negative-modulation tool composed of PAH1 fused to the AsLOV2 domain.
To study the impact of REST modulation on seizure propensity, we developed a tool for its negative modulation in vivo. The tool is composed of the paired-amphipathic helix 1 (PAH1) domain ... fused to the light-oxygen-voltage sensing 2 (LOV2) domain
The authors developed an in vivo REST negative-modulation tool composed of PAH1 fused to the AsLOV2 domain.
To study the impact of REST modulation on seizure propensity, we developed a tool for its negative modulation in vivo. The tool is composed of the paired-amphipathic helix 1 (PAH1) domain ... fused to the light-oxygen-voltage sensing 2 (LOV2) domain
The authors developed an in vivo REST negative-modulation tool composed of PAH1 fused to the AsLOV2 domain.
To study the impact of REST modulation on seizure propensity, we developed a tool for its negative modulation in vivo. The tool is composed of the paired-amphipathic helix 1 (PAH1) domain ... fused to the light-oxygen-voltage sensing 2 (LOV2) domain
The authors developed an in vivo REST negative-modulation tool composed of PAH1 fused to the AsLOV2 domain.
To study the impact of REST modulation on seizure propensity, we developed a tool for its negative modulation in vivo. The tool is composed of the paired-amphipathic helix 1 (PAH1) domain ... fused to the light-oxygen-voltage sensing 2 (LOV2) domain
The data support the validity of LOV2-PAH1 as a tool to modulate REST activity in vivo.
These data support the validity of our tool to modulate REST activity in vivo
The data support the validity of LOV2-PAH1 as a tool to modulate REST activity in vivo.
These data support the validity of our tool to modulate REST activity in vivo
The data support the validity of LOV2-PAH1 as a tool to modulate REST activity in vivo.
These data support the validity of our tool to modulate REST activity in vivo
The data support the validity of LOV2-PAH1 as a tool to modulate REST activity in vivo.
These data support the validity of our tool to modulate REST activity in vivo
The data support the validity of LOV2-PAH1 as a tool to modulate REST activity in vivo.
These data support the validity of our tool to modulate REST activity in vivo
The data support the validity of LOV2-PAH1 as a tool to modulate REST activity in vivo.
These data support the validity of our tool to modulate REST activity in vivo
The data support the validity of LOV2-PAH1 as a tool to modulate REST activity in vivo.
These data support the validity of our tool to modulate REST activity in vivo
Approval Evidence
1 source1 linked approval claimfirst-pass slug recombinant-aav1-2-viral-particles
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Source:
expression deliverysupports
Recombinant AAV1/2 viral particles enabled LOV2-PAH1 expression in HEK293T cells and primary neurons and efficiently transduced hippocampal neurons in vivo.
Recombinant AAV1/2 viral particles (rAAVs) allowed LOV2-PAH1 expression in HEK293T cells and primary neurons, and efficiently transduced hippocampal neurons in vivo.
Source:
Comparisons
Source-backed strengths
The reported strength is successful expression of LOV2-PAH1 in HEK293T cells and primary neurons together with efficient transduction of hippocampal neurons in vivo. The system also supported downstream biological readouts, as expression of the open LOV2-PAH1 probe increased expression of several neuronal genes in mouse hippocampus.
Ranked Citations