Source 1primary paper2019Nano Letters
Toolkit/near-infrared light-activated DNA agonist nanodevice
near-infrared light-activated DNA agonist nanodevice
Also known as: NIR-DA, NIR-DA system
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
The near-infrared light-activated DNA agonist nanodevice (NIR-DA) is a multicomponent, nongenetic system for remote optical control of receptor tyrosine kinase signaling in live cells and animals. Upon near-infrared illumination, an active DNA agonist is released and dimerizes DNA-modified chimeric or native receptor tyrosine kinases at the cell surface, triggering downstream signaling.
Usefulness & Problems
Why this is useful
NIR-DA is useful for remotely manipulating cell signaling and phenotype in deep tissues without genetic encoding of a photosensor. Reported applications include control of cytoskeletal remodeling, cell polarization, directional migration, and in vivo regulation of skeletal muscle satellite cell migration and myogenesis.
Source:
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
Source:
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Problem solved
This tool addresses the problem of achieving non-genetic, remotely actuated control of receptor tyrosine kinase signaling in live cells and animals. It specifically enables near-infrared-triggered activation of cell-surface RTKs through a DNA agonist strategy rather than direct genetic optogenetic modification.
Problem links
Need conditional control of signaling activity
DerivedThe near-infrared light-activated DNA agonist nanodevice (NIR-DA) is a multicomponent, nongenetic system for remote control of receptor tyrosine kinase signaling in live cells and animals. Upon near-infrared illumination, a DNA agonist is released from gold nanorods and activates signaling by dimerizing DNA-modified chimeric or native receptor tyrosine kinases on the cell surface.
Need precise spatiotemporal control with light input
DerivedThe near-infrared light-activated DNA agonist nanodevice (NIR-DA) is a multicomponent, nongenetic system for remote control of receptor tyrosine kinase signaling in live cells and animals. Upon near-infrared illumination, a DNA agonist is released from gold nanorods and activates signaling by dimerizing DNA-modified chimeric or native receptor tyrosine kinases on the cell surface.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
HeterodimerizationHeterodimerizationHeterodimerizationphotothermal releasephotothermal releasereceptor tyrosine kinase dimerizationreceptor tyrosine kinase dimerizationTechniques
No technique tags yet.
Target processes
signalingInput: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: multi component delivery burdenimplementation constraint: spectral hardware requirementoperating role: regulatorswitch architecture: multi componentswitch architecture: recruitment
The reported system is a multicomponent DNA nanodevice that uses near-infrared light as the input modality and has been described as releasing a DNA agonist from gold nanorods upon illumination. The active agonist acts on DNA-modified chimeric or native receptor tyrosine kinases on the cell surface; however, the provided evidence does not specify construct sequences, conjugation chemistry, or illumination parameters.
The supplied evidence is limited to a single 2019 study and does not provide quantitative performance metrics such as activation kinetics, dynamic range, wavelength window, reversibility, or tissue penetration depth. Practical constraints of the multicomponent nanodevice, including delivery, receptor modification requirements, and nanoparticle handling, are implied but not fully characterized in the provided evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Approval Evidence
1 source6 linked approval claimsfirst-pass slug near-infrared-light-activated-dna-agonist-nanodevice
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Source:
cell behavior controlsupports
Activation of RTK signaling by the NIR-DA system enables control of cytoskeletal remodeling, cell polarization, and directional migration.
Such NIR-DA activation of RTK signaling enables the control of cytoskeletal remodeling, cell polarization, and directional migration.
Source:
in vivo applicationsupports
The NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis.
Furthermore, we demonstrate that the NIR-DA system can be used in vivo to mediate RTK signaling and skeletal muscle satellite cell migration and myogenesis, which are critical cellular behaviors in the process of skeletal muscle regeneration.
Source:
mechanismsupports
The active DNA agonist dimerizes DNA-modified chimeric or native receptor tyrosine kinase on cell surfaces and activates downstream signal transduction in live cells.
The active DNA agonist dimerizes the DNA-modified chimeric or native receptor tyrosine kinase (RTK) on cell surfaces and activates downstream signal transduction in live cells.
Source:
mechanismsupports
Upon near-infrared light treatment, the DNA agonist is released from gold nanorods through an LSPR-based photothermal effect and becomes active.
Upon NIR light treatment, the DNA agonist is released through the localized surface plasmon resonance (LSPR)-based photothermal effect of AuNRs and becomes active.
Source:
platform positioningsupports
The NIR-DA system is presented as a platform for exogenous modulation of deep tissues for applications such as regenerative medicine.
Thus, the NIR-DA system offers a powerful and versatile platform for exogenous modulation of deep tissues for purposes such as regenerative medicine.
Source:
tool introductionsupports
The paper reports a near-infrared light-activated DNA agonist nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Here we report a novel near-infrared light-activated DNA agonist (NIR-DA) nanodevice for nongenetic manipulation of cell signaling and phenotype in deep tissues.
Source:
Comparisons
Source-backed strengths
The system is reported to function in live cells and in vivo, indicating utility beyond cell-free or purely in vitro settings. It enables remote near-infrared control of RTK-dependent behaviors, including cytoskeletal remodeling, polarization, directional migration, satellite cell migration, and myogenesis.
Compared with fusion proteins with large N-terminal anchors
near-infrared light-activated DNA agonist nanodevice and fusion proteins with large N-terminal anchors address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling; shared mechanisms: heterodimerization; same primary input modality: light
Compared with LOVpep/ePDZb
near-infrared light-activated DNA agonist nanodevice and LOVpep/ePDZb address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling; shared mechanisms: heterodimerization; same primary input modality: light
Relative tradeoffs: appears more independently replicated; looks easier to implement in practice.
Compared with tandem-dimer nano (tdnano)
near-infrared light-activated DNA agonist nanodevice and tandem-dimer nano (tdnano) address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling; shared mechanisms: heterodimerization; same primary input modality: light
Ranked Citations
- 1.