Source 1primary paper2023Journal of Controlled Release
Toolkit/AS1411 aptamer-modified cell membrane biomimetic core-shell system
AS1411 aptamer-modified cell membrane biomimetic core-shell system
Also known as: shell modified with AS1411 aptamers and photosensitizers
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
The AS1411 aptamer-modified cell membrane biomimetic core-shell system is a light-augmented delivery harness for CRISPR-Cas9 plasmid cargo (pCas9). It consists of a cell membrane-camouflaged shell modified with AS1411 aptamers and photosensitizers to promote tumor targeting, reactive oxygen species-mediated lysosomal escape, and light-controllable pCas9 release for enhanced gene editing.
Usefulness & Problems
Why this is useful
This system is useful as a tumor-directed, light-responsive nonviral delivery platform for CRISPR-Cas9 plasmids. The reported design combines cell membrane camouflage, AS1411-mediated targeting, and photosensitizer-enabled intracellular release steps that are intended to improve delivery performance for cancer gene editing applications.
Source:
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Source:
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Source:
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
Problem solved
It addresses the problem of in vivo CRISPR-Cas9 plasmid delivery to tumor cells, particularly the need for targeted delivery and efficient intracellular release after uptake. The source specifically frames the membrane-camouflaged, light-augmented system as a potential solution for in vivo CRISPR-Cas9 delivery and a feasible strategy for cancer therapy.
Source:
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Source:
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Source:
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
Problem links
Need controllable genome or transcript editing
DerivedThe AS1411 aptamer-modified cell membrane biomimetic core-shell system is a light-augmented delivery harness for CRISPR-Cas9 plasmid cargo. It uses a cell membrane-camouflaged shell bearing AS1411 aptamers and photosensitizers to promote tumor targeting, reactive oxygen species-mediated lysosomal escape, and pCas9 release for enhanced gene editing.
Need precise spatiotemporal control with light input
DerivedThe AS1411 aptamer-modified cell membrane biomimetic core-shell system is a light-augmented delivery harness for CRISPR-Cas9 plasmid cargo. It uses a cell membrane-camouflaged shell bearing AS1411 aptamers and photosensitizers to promote tumor targeting, reactive oxygen species-mediated lysosomal escape, and pCas9 release for enhanced gene editing.
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.
Mechanisms
cell membrane camouflagecell membrane camouflagelight-triggered cargo releaselight-triggered cargo releaselight-triggered lysosomal escapelight-triggered lysosomal escapereactive oxygen species generationreactive oxygen species generationtumor targeting via as1411 aptamer modificationtumor targeting via as1411 aptamer modificationTechniques
No technique tags yet.
Target processes
editingInput: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: externally suppliedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementoperating role: delivery
The construct is described as a core-shell system whose shell is camouflaged with a cell membrane and further modified with AS1411 aptamers and photosensitizers. Its function depends on laser irradiation to drive reactive oxygen species production, lysosomal escape, and pCas9 release, but the specific photosensitizer identity, membrane source, and irradiation conditions are not provided in the supplied evidence.
The evidence provided comes from a single 2023 source and includes only limited mechanistic and application-level details. Quantitative delivery efficiency, editing rates, light parameters, safety profile, and validation across multiple models are not described in the supplied evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
In H1299 cells, the biomimetic gene editing system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
Neoplastic H1299 cells were reprogrammed using the biomimetic gene editing system upon laser irradiation with reduced VEGF and Vimentin expression, leading to enhanced antimetastatic effects.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The membrane-camouflaged system combined with light augmentation provides a potential solution for in vivo delivery of CRISPR-Cas9 and a feasible strategy for cancer therapy.
Our approach of using a membrane-camouflaged system combined with light augmentation provides a potential solution for the in vivo delivery of CRISPR-Cas9 as well as a feasible strategy for cancer therapy.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
Genetic disruption of HIF-1α augmented the in vivo chemotherapeutic efficacy of paclitaxel.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
The authors developed a cell membrane biomimetic core-shell system for light-controllable precise gene editing.
Herein, we developed a cell membrane biomimetic core-shell system for light-controllable, precise gene editing.
Approval Evidence
1 source1 linked approval claimfirst-pass slug as1411-aptamer-modified-cell-membrane-biomimetic-core-shell-system
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production
Source:
mechanismsupports
The shell is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, producing light-controllable enhanced gene editing.
The shell of the system is camouflaged by a cell membrane and modified with AS1411 aptamers for tumor targeting and photosensitizers to induce lysosomal escape and pCas9 release through reactive oxygen species production, thereby producing light-controllable enhanced gene editing.
Source:
Comparisons
Source-backed strengths
The reported mechanism integrates tumor targeting with light-triggered reactive oxygen species production to induce lysosomal escape and pCas9 release, yielding light-controllable enhanced gene editing. In H1299 cells, the system with laser irradiation reprogrammed neoplastic cells and reduced VEGF and Vimentin expression, which was associated with enhanced antimetastatic effects.
Compared with APC
AS1411 aptamer-modified cell membrane biomimetic core-shell system and APC address a similar problem space because they share editing.
Shared frame: same top-level item type; shared target processes: editing; same primary input modality: light
Compared with cell membrane biomimetic core-shell system
AS1411 aptamer-modified cell membrane biomimetic core-shell system and cell membrane biomimetic core-shell system address a similar problem space because they share editing.
Shared frame: same top-level item type; shared target processes: editing; same primary input modality: light
Compared with light-emitting diode illumination
AS1411 aptamer-modified cell membrane biomimetic core-shell system and light-emitting diode illumination address a similar problem space because they share editing.
Shared frame: same top-level item type; shared target processes: editing; same primary input modality: light
Ranked Citations
- 1.