Source 1primary paper2022Cell Death Discovery
Toolkit/re-engineered MLKL membrane recruitment tool
re-engineered MLKL membrane recruitment tool
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
The re-engineered MLKL membrane recruitment tool is a single-component optogenetic system derived from MLKL that preserves light-mediated plasma membrane recruitment while blocking MLKL-associated cell-killing activity. It is intended to modulate protein function through light-controlled localization at the plasma membrane.
Usefulness & Problems
Why this is useful
This tool provides optical control over protein localization at the plasma membrane using an MLKL-derived single-component design. It is useful where plasma membrane recruitment is desired without the confounding cytotoxicity associated with native or death-inducing light-activated MLKL variants.
Problem solved
It addresses the problem that MLKL-based light activation can couple membrane recruitment to rapid cell death. The re-engineered variant separates light-mediated plasma membrane recruitment from MLKL cell-killing capacity.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
light-mediated membrane recruitmentmembrane recruitmentMembrane RecruitmentOligomerizationTechniques
No technique tags yet.
Target processes
localizationInput: Light
Implementation Constraints
The tool is based on engineered MLKL domains and is described as single-component. The available evidence supports light-mediated plasma membrane recruitment, but does not specify construct architecture, illumination parameters, expression system, or cofactor requirements.
The supplied evidence does not report quantitative performance metrics, kinetics, reversibility, wavelength dependence, or validation across multiple cargos or cell types. Independent replication is not provided in the supplied evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
A light-activated version of MLKL was engineered that rapidly oligomerizes, is recruited to the plasma membrane upon light exposure, and induces rapid cell death.
we engineered a light-activated version of MLKL that rapidly oligomerizes and is recruited to the plasma membrane in cells exposed to light, inducing rapid cell death
A light-activated version of MLKL was engineered that rapidly oligomerizes, is recruited to the plasma membrane upon light exposure, and induces rapid cell death.
we engineered a light-activated version of MLKL that rapidly oligomerizes and is recruited to the plasma membrane in cells exposed to light, inducing rapid cell death
A light-activated version of MLKL was engineered that rapidly oligomerizes, is recruited to the plasma membrane upon light exposure, and induces rapid cell death.
we engineered a light-activated version of MLKL that rapidly oligomerizes and is recruited to the plasma membrane in cells exposed to light, inducing rapid cell death
A light-activated version of MLKL was engineered that rapidly oligomerizes, is recruited to the plasma membrane upon light exposure, and induces rapid cell death.
we engineered a light-activated version of MLKL that rapidly oligomerizes and is recruited to the plasma membrane in cells exposed to light, inducing rapid cell death
A light-activated version of MLKL was engineered that rapidly oligomerizes, is recruited to the plasma membrane upon light exposure, and induces rapid cell death.
we engineered a light-activated version of MLKL that rapidly oligomerizes and is recruited to the plasma membrane in cells exposed to light, inducing rapid cell death
A light-activated version of MLKL was engineered that rapidly oligomerizes, is recruited to the plasma membrane upon light exposure, and induces rapid cell death.
we engineered a light-activated version of MLKL that rapidly oligomerizes and is recruited to the plasma membrane in cells exposed to light, inducing rapid cell death
A light-activated version of MLKL was engineered that rapidly oligomerizes, is recruited to the plasma membrane upon light exposure, and induces rapid cell death.
we engineered a light-activated version of MLKL that rapidly oligomerizes and is recruited to the plasma membrane in cells exposed to light, inducing rapid cell death
MLKL was re-engineered to block cell-killing capacity while retaining light-mediated membrane recruitment, yielding a single-component optogenetic tool for modulation of protein function at the plasma membrane.
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
MLKL was re-engineered to block cell-killing capacity while retaining light-mediated membrane recruitment, yielding a single-component optogenetic tool for modulation of protein function at the plasma membrane.
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
MLKL was re-engineered to block cell-killing capacity while retaining light-mediated membrane recruitment, yielding a single-component optogenetic tool for modulation of protein function at the plasma membrane.
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
MLKL was re-engineered to block cell-killing capacity while retaining light-mediated membrane recruitment, yielding a single-component optogenetic tool for modulation of protein function at the plasma membrane.
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
MLKL was re-engineered to block cell-killing capacity while retaining light-mediated membrane recruitment, yielding a single-component optogenetic tool for modulation of protein function at the plasma membrane.
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
MLKL was re-engineered to block cell-killing capacity while retaining light-mediated membrane recruitment, yielding a single-component optogenetic tool for modulation of protein function at the plasma membrane.
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
MLKL was re-engineered to block cell-killing capacity while retaining light-mediated membrane recruitment, yielding a single-component optogenetic tool for modulation of protein function at the plasma membrane.
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
The light-activated MLKL tool was used to study signaling responses of non-dying bystander cells.
used to study signaling responses of non-dying bystander cells
The light-activated MLKL tool was used to study signaling responses of non-dying bystander cells.
used to study signaling responses of non-dying bystander cells
The light-activated MLKL tool was used to study signaling responses of non-dying bystander cells.
used to study signaling responses of non-dying bystander cells
The light-activated MLKL tool was used to study signaling responses of non-dying bystander cells.
used to study signaling responses of non-dying bystander cells
The light-activated MLKL tool was used to study signaling responses of non-dying bystander cells.
used to study signaling responses of non-dying bystander cells
The light-activated MLKL tool was used to study signaling responses of non-dying bystander cells.
used to study signaling responses of non-dying bystander cells
The light-activated MLKL tool was used to study signaling responses of non-dying bystander cells.
used to study signaling responses of non-dying bystander cells
The light-activated MLKL tool was used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death.
used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death
The light-activated MLKL tool was used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death.
used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death
The light-activated MLKL tool was used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death.
used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death
The light-activated MLKL tool was used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death.
used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death
The light-activated MLKL tool was used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death.
used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death
The light-activated MLKL tool was used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death.
used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death
The light-activated MLKL tool was used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death.
used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death
The light-activated MLKL tool can be controlled spatially and temporally.
We demonstrate this tool can be controlled spatially and temporally
The light-activated MLKL tool can be controlled spatially and temporally.
We demonstrate this tool can be controlled spatially and temporally
The light-activated MLKL tool can be controlled spatially and temporally.
We demonstrate this tool can be controlled spatially and temporally
The light-activated MLKL tool can be controlled spatially and temporally.
We demonstrate this tool can be controlled spatially and temporally
The light-activated MLKL tool can be controlled spatially and temporally.
We demonstrate this tool can be controlled spatially and temporally
The light-activated MLKL tool can be controlled spatially and temporally.
We demonstrate this tool can be controlled spatially and temporally
The light-activated MLKL tool can be controlled spatially and temporally.
We demonstrate this tool can be controlled spatially and temporally
Approval Evidence
1 source1 linked approval claimfirst-pass slug re-engineered-mlkl-membrane-recruitment-tool
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
Source:
engineered functionsupports
MLKL was re-engineered to block cell-killing capacity while retaining light-mediated membrane recruitment, yielding a single-component optogenetic tool for modulation of protein function at the plasma membrane.
we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane
Source:
Comparisons
Source-backed strengths
The reported strength is that the construct retains light-mediated membrane recruitment after engineering to block cell-killing activity. The source specifically describes it as a single-component optogenetic tool for modulation of protein function at the plasma membrane.
Ranked Citations
- 1.