Source 1primary paper2024Advanced Science
Toolkit/URMT
URMT
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
URMT is a 980 nm near-infrared light-controlled multicomponent nanoplatform for tumor applications that combines a UCNP-based photodynamic nanosystem with an engineered enzyme-activatable antisense oligonucleotide. It is surface-functionalized with triphenylphosphonium (TPP) for mitochondrial targeting and enables coupled photodynamic action and enzyme-activated gene regulation.
Usefulness & Problems
Why this is useful
URMT is useful for achieving spatiotemporally controlled therapeutic activity by linking near-infrared light activation to mitochondrial photodynamic damage and subsequent gene regulation. The reported system is positioned for precise and specific gene regulation in targeted tumor treatment and for augmenting antitumor effects through combination action.
Problem solved
URMT addresses the problem of coordinating external light control with intracellular, enzyme-dependent activation of a gene-regulatory payload in tumors. Specifically, it couples 980 nm NIR-triggered ROS generation and APE1 relocalization to mitochondria with APE1-mediated cleavage of AP-site-containing oligonucleotides to release functional single strands.
Published Workflows
Objective: Develop a 980 nm NIR light-controlled nanosystem for combined tumor therapy that couples photodynamic mitochondrial damage with enzyme-activated gene regulation to improve spatiotemporal precision.
Why it works: The strategy is designed so that 980 nm NIR light triggers ROS generation from the UCNP-based photodynamic system, ROS induces APE1 translocation to mitochondria, and APE1 then cleaves AP-site-containing DNA to release functional strands for gene regulation. This couples externally controlled photodynamic activation with endogenous enzyme-responsive oligonucleotide activation.
NIR-triggered ROS generationAPE1 translocation from nucleus to mitochondriaAPE1 cleavage at AP sitesrelease of functional single strands for gene regulationmitochondrial damageupconversion nanoparticle-based photodynamic nanosystem designenzyme-activatable antisense oligonucleotide engineeringTPP surface functionalizationNIR light activation
Steps
- 1.Engineer an enzyme-activatable antisense oligonucleotideengineered oligonucleotide component within URMT
Create an antisense component that can be activated by enzyme cleavage for downstream gene regulation.
The activatable oligonucleotide provides the gene-regulation logic that is later coupled to the photodynamic nanosystem.
- 2.Combine the activatable antisense oligonucleotide with a UCNP-based photodynamic nanosystemassembled hybrid nanosystem
Integrate light-triggered photodynamic function with the enzyme-activatable gene-regulation component.
The photodynamic module is needed to generate ROS under NIR light, which is the upstream trigger for the enzyme-activation mechanism.
- 3.Surface functionalize the hybrid nanosystem with TPP for mitochondrial targetingmitochondria-targeted final nanoplatform
Add mitochondrial targeting capability to the hybrid nanosystem.
Mitochondrial targeting is added after hybrid system construction to localize photodynamic damage and align the platform with the intended mitochondrial mechanism.
- 4.Activate URMT with 980 nm NIR light to generate ROSlight-activated therapeutic nanosystem
Trigger the photodynamic function that initiates the downstream activation cascade.
ROS generation is the immediate upstream event that enables APE1 translocation and therefore must occur before enzyme-mediated strand release.
- 5.Use ROS-induced APE1 mitochondrial translocation and AP-site cleavage to release functional single strands for gene regulationenzyme-activated gene-regulation system
Convert the photodynamic trigger into gene-regulatory output through endogenous APE1 cleavage.
This step depends on prior ROS generation because the abstract states ROS induces APE1 translocation, which then enables AP-site cleavage and strand release.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
enzyme-activated oligonucleotide cleavagelight-triggered subcellular relocalizationmitochondrial targetingPhotocleavagephotodynamic ros generationTechniques
No technique tags yet.
Target processes
localizationInput: Light
Implementation Constraints
URMT is constructed from a UCNP-based photodynamic nanosystem and an engineered antisense oligonucleotide containing AP sites that can be recognized and cleaved by APE1. The platform is surface-functionalized with TPP for mitochondrial targeting, and its activation requires 980 nm NIR illumination to generate ROS and induce APE1 translocation from the nucleus to mitochondria.
The supplied evidence is limited to a single 2024 study and does not provide detailed quantitative performance metrics, comparative benchmarking, or broad validation across models. The available claims also do not specify delivery efficiency, off-target effects, long-term safety, or the exact gene targets regulated by the released single strands.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
URMT is constructed from an engineered enzyme-activatable antisense oligonucleotide combined with a UCNP-based photodynamic nanosystem and surface functionalized with TPP for mitochondrial targeting.
URMT is constructed by engineering an enzyme-activatable antisense oligonucleotide, which combined with an upconversion nanoparticle (UCNP)-based photodynamic nanosystem, followed by the surface functionalization of triphenylphosphine (TPP), a mitochondria-targeting ligand.
URMT is constructed from an engineered enzyme-activatable antisense oligonucleotide combined with a UCNP-based photodynamic nanosystem and surface functionalized with TPP for mitochondrial targeting.
URMT is constructed by engineering an enzyme-activatable antisense oligonucleotide, which combined with an upconversion nanoparticle (UCNP)-based photodynamic nanosystem, followed by the surface functionalization of triphenylphosphine (TPP), a mitochondria-targeting ligand.
URMT is constructed from an engineered enzyme-activatable antisense oligonucleotide combined with a UCNP-based photodynamic nanosystem and surface functionalized with TPP for mitochondrial targeting.
URMT is constructed by engineering an enzyme-activatable antisense oligonucleotide, which combined with an upconversion nanoparticle (UCNP)-based photodynamic nanosystem, followed by the surface functionalization of triphenylphosphine (TPP), a mitochondria-targeting ligand.
URMT is constructed from an engineered enzyme-activatable antisense oligonucleotide combined with a UCNP-based photodynamic nanosystem and surface functionalized with TPP for mitochondrial targeting.
URMT is constructed by engineering an enzyme-activatable antisense oligonucleotide, which combined with an upconversion nanoparticle (UCNP)-based photodynamic nanosystem, followed by the surface functionalization of triphenylphosphine (TPP), a mitochondria-targeting ligand.
URMT is constructed from an engineered enzyme-activatable antisense oligonucleotide combined with a UCNP-based photodynamic nanosystem and surface functionalized with TPP for mitochondrial targeting.
URMT is constructed by engineering an enzyme-activatable antisense oligonucleotide, which combined with an upconversion nanoparticle (UCNP)-based photodynamic nanosystem, followed by the surface functionalization of triphenylphosphine (TPP), a mitochondria-targeting ligand.
APE1 recognizes AP sites in DNA double strands and cleaves them to release functional single strands for gene regulation in the URMT strategy.
APE1 can recognize the basic apurinic/apyrimidinic (AP) sites in DNA double-strands and perform cleavage, thereby releasing the functional single-strands for gene regulation.
APE1 recognizes AP sites in DNA double strands and cleaves them to release functional single strands for gene regulation in the URMT strategy.
APE1 can recognize the basic apurinic/apyrimidinic (AP) sites in DNA double-strands and perform cleavage, thereby releasing the functional single-strands for gene regulation.
APE1 recognizes AP sites in DNA double strands and cleaves them to release functional single strands for gene regulation in the URMT strategy.
APE1 can recognize the basic apurinic/apyrimidinic (AP) sites in DNA double-strands and perform cleavage, thereby releasing the functional single-strands for gene regulation.
APE1 recognizes AP sites in DNA double strands and cleaves them to release functional single strands for gene regulation in the URMT strategy.
APE1 can recognize the basic apurinic/apyrimidinic (AP) sites in DNA double-strands and perform cleavage, thereby releasing the functional single-strands for gene regulation.
APE1 recognizes AP sites in DNA double strands and cleaves them to release functional single strands for gene regulation in the URMT strategy.
APE1 can recognize the basic apurinic/apyrimidinic (AP) sites in DNA double-strands and perform cleavage, thereby releasing the functional single-strands for gene regulation.
URMT generates ROS upon 980 nm NIR light activation, inducing APE1 translocation from the nucleus to mitochondria.
URMT allows for the 980 nm NIR light-activated generation of reactive oxygen species, which can induce the translocation of a DNA repair enzyme (namely apurinic/apyrimidinic endonuclease 1, APE1) from the nucleus to mitochondria.
URMT generates ROS upon 980 nm NIR light activation, inducing APE1 translocation from the nucleus to mitochondria.
URMT allows for the 980 nm NIR light-activated generation of reactive oxygen species, which can induce the translocation of a DNA repair enzyme (namely apurinic/apyrimidinic endonuclease 1, APE1) from the nucleus to mitochondria.
URMT generates ROS upon 980 nm NIR light activation, inducing APE1 translocation from the nucleus to mitochondria.
URMT allows for the 980 nm NIR light-activated generation of reactive oxygen species, which can induce the translocation of a DNA repair enzyme (namely apurinic/apyrimidinic endonuclease 1, APE1) from the nucleus to mitochondria.
URMT generates ROS upon 980 nm NIR light activation, inducing APE1 translocation from the nucleus to mitochondria.
URMT allows for the 980 nm NIR light-activated generation of reactive oxygen species, which can induce the translocation of a DNA repair enzyme (namely apurinic/apyrimidinic endonuclease 1, APE1) from the nucleus to mitochondria.
URMT generates ROS upon 980 nm NIR light activation, inducing APE1 translocation from the nucleus to mitochondria.
URMT allows for the 980 nm NIR light-activated generation of reactive oxygen species, which can induce the translocation of a DNA repair enzyme (namely apurinic/apyrimidinic endonuclease 1, APE1) from the nucleus to mitochondria.
The reported approach offers high spatiotemporal precision and has potential for precise and specific gene regulation for targeted tumor treatment.
Altogether, the approach reported in this study offers high spatiotemporal precision and shows the potential to achieve precise and specific gene regulation for targeted tumor treatment.
The reported approach offers high spatiotemporal precision and has potential for precise and specific gene regulation for targeted tumor treatment.
Altogether, the approach reported in this study offers high spatiotemporal precision and shows the potential to achieve precise and specific gene regulation for targeted tumor treatment.
The reported approach offers high spatiotemporal precision and has potential for precise and specific gene regulation for targeted tumor treatment.
Altogether, the approach reported in this study offers high spatiotemporal precision and shows the potential to achieve precise and specific gene regulation for targeted tumor treatment.
The reported approach offers high spatiotemporal precision and has potential for precise and specific gene regulation for targeted tumor treatment.
Altogether, the approach reported in this study offers high spatiotemporal precision and shows the potential to achieve precise and specific gene regulation for targeted tumor treatment.
The reported approach offers high spatiotemporal precision and has potential for precise and specific gene regulation for targeted tumor treatment.
Altogether, the approach reported in this study offers high spatiotemporal precision and shows the potential to achieve precise and specific gene regulation for targeted tumor treatment.
The combined NIR light-controlled mitochondrial damage and enzyme-activated gene regulation strategy produces an augmented antitumor effect.
Overall, an augmented antitumor effect is observed due to NIR light-controlled mitochondrial damage and enzyme-activated gene regulation.
The combined NIR light-controlled mitochondrial damage and enzyme-activated gene regulation strategy produces an augmented antitumor effect.
Overall, an augmented antitumor effect is observed due to NIR light-controlled mitochondrial damage and enzyme-activated gene regulation.
The combined NIR light-controlled mitochondrial damage and enzyme-activated gene regulation strategy produces an augmented antitumor effect.
Overall, an augmented antitumor effect is observed due to NIR light-controlled mitochondrial damage and enzyme-activated gene regulation.
The combined NIR light-controlled mitochondrial damage and enzyme-activated gene regulation strategy produces an augmented antitumor effect.
Overall, an augmented antitumor effect is observed due to NIR light-controlled mitochondrial damage and enzyme-activated gene regulation.
The combined NIR light-controlled mitochondrial damage and enzyme-activated gene regulation strategy produces an augmented antitumor effect.
Overall, an augmented antitumor effect is observed due to NIR light-controlled mitochondrial damage and enzyme-activated gene regulation.
URMT is a 980 nm NIR light-controlled nanoplatform developed for spatiotemporally controlled photodynamic therapy and enzyme-activated gene expression regulation in tumors.
Herein, a 980 nm near-infrared (NIR) light-controlled nanoplatform, namely URMT, is developed, which can allow spatiotemporally controlled photodynamic therapy and trigger the enzyme-activated gene expression regulation in tumors.
URMT is a 980 nm NIR light-controlled nanoplatform developed for spatiotemporally controlled photodynamic therapy and enzyme-activated gene expression regulation in tumors.
Herein, a 980 nm near-infrared (NIR) light-controlled nanoplatform, namely URMT, is developed, which can allow spatiotemporally controlled photodynamic therapy and trigger the enzyme-activated gene expression regulation in tumors.
URMT is a 980 nm NIR light-controlled nanoplatform developed for spatiotemporally controlled photodynamic therapy and enzyme-activated gene expression regulation in tumors.
Herein, a 980 nm near-infrared (NIR) light-controlled nanoplatform, namely URMT, is developed, which can allow spatiotemporally controlled photodynamic therapy and trigger the enzyme-activated gene expression regulation in tumors.
URMT is a 980 nm NIR light-controlled nanoplatform developed for spatiotemporally controlled photodynamic therapy and enzyme-activated gene expression regulation in tumors.
Herein, a 980 nm near-infrared (NIR) light-controlled nanoplatform, namely URMT, is developed, which can allow spatiotemporally controlled photodynamic therapy and trigger the enzyme-activated gene expression regulation in tumors.
URMT is a 980 nm NIR light-controlled nanoplatform developed for spatiotemporally controlled photodynamic therapy and enzyme-activated gene expression regulation in tumors.
Herein, a 980 nm near-infrared (NIR) light-controlled nanoplatform, namely URMT, is developed, which can allow spatiotemporally controlled photodynamic therapy and trigger the enzyme-activated gene expression regulation in tumors.
Approval Evidence
1 source6 linked approval claimsfirst-pass slug urmt
Herein, a 980 nm near-infrared (NIR) light-controlled nanoplatform, namely URMT, is developed, which can allow spatiotemporally controlled photodynamic therapy and trigger the enzyme-activated gene expression regulation in tumors.
Source:
compositionsupports
URMT is constructed from an engineered enzyme-activatable antisense oligonucleotide combined with a UCNP-based photodynamic nanosystem and surface functionalized with TPP for mitochondrial targeting.
URMT is constructed by engineering an enzyme-activatable antisense oligonucleotide, which combined with an upconversion nanoparticle (UCNP)-based photodynamic nanosystem, followed by the surface functionalization of triphenylphosphine (TPP), a mitochondria-targeting ligand.
Source:
mechanismsupports
APE1 recognizes AP sites in DNA double strands and cleaves them to release functional single strands for gene regulation in the URMT strategy.
APE1 can recognize the basic apurinic/apyrimidinic (AP) sites in DNA double-strands and perform cleavage, thereby releasing the functional single-strands for gene regulation.
Source:
mechanismsupports
URMT generates ROS upon 980 nm NIR light activation, inducing APE1 translocation from the nucleus to mitochondria.
URMT allows for the 980 nm NIR light-activated generation of reactive oxygen species, which can induce the translocation of a DNA repair enzyme (namely apurinic/apyrimidinic endonuclease 1, APE1) from the nucleus to mitochondria.
Source:
performance propertysupports
The reported approach offers high spatiotemporal precision and has potential for precise and specific gene regulation for targeted tumor treatment.
Altogether, the approach reported in this study offers high spatiotemporal precision and shows the potential to achieve precise and specific gene regulation for targeted tumor treatment.
Source:
therapeutic effectsupports
The combined NIR light-controlled mitochondrial damage and enzyme-activated gene regulation strategy produces an augmented antitumor effect.
Overall, an augmented antitumor effect is observed due to NIR light-controlled mitochondrial damage and enzyme-activated gene regulation.
Source:
tool developmentsupports
URMT is a 980 nm NIR light-controlled nanoplatform developed for spatiotemporally controlled photodynamic therapy and enzyme-activated gene expression regulation in tumors.
Herein, a 980 nm near-infrared (NIR) light-controlled nanoplatform, namely URMT, is developed, which can allow spatiotemporally controlled photodynamic therapy and trigger the enzyme-activated gene expression regulation in tumors.
Source:
Comparisons
Source-backed strengths
The reported approach provides high spatiotemporal precision because activation is gated by 980 nm NIR light and by enzyme-dependent oligonucleotide cleavage. It also produced an augmented antitumor effect through the combination of NIR light-controlled mitochondrial damage and enzyme-activated gene regulation.
Ranked Citations
- 1.