www.nature.com/articles/s41...
www.nature.com/articles/s41...
In summary, the killswitch is a versatile tool that alters condensate material properties in live cells. It revealed that condensate composition and functions rely on their microenvironments, paving the way for new biology and therapeutic strategies
In summary, the killswitch is a versatile tool that alters condensate material properties in live cells. It revealed that condensate composition and functions rely on their microenvironments, paving the way for new biology and therapeutic strategies
In zebrafish embryos, killswitch targeted to transcriptional condensates via NANOG suppressed miRNA transcription. Across models, killswitch reveals functional consequences of changing condensate material property, without dissolving the structures themselves.
In zebrafish embryos, killswitch targeted to transcriptional condensates via NANOG suppressed miRNA transcription. Across models, killswitch reveals functional consequences of changing condensate material property, without dissolving the structures themselves.
In adenoviral 52K condensates, killswitch reduced dynamics and blocked recruitment of capsid protein IIIa, despite preserved binding interfaces. Viral progeny production dropped >90%. The KS thus uncovers hidden roles of condensate microenvironments for condensate regulation.
In adenoviral 52K condensates, killswitch reduced dynamics and blocked recruitment of capsid protein IIIa, despite preserved binding interfaces. Viral progeny production dropped >90%. The KS thus uncovers hidden roles of condensate microenvironments for condensate regulation.
Targeting BRD4::NUT condensates with killswitch disrupted RNA Pol II partitioning and reduced transcription. In NUP98::KDM5A-driven AML cells, killswitch caused proteasome-mediated degradation of fusion condensates and impaired leukemia cell growth.
Targeting BRD4::NUT condensates with killswitch disrupted RNA Pol II partitioning and reduced transcription. In NUP98::KDM5A-driven AML cells, killswitch caused proteasome-mediated degradation of fusion condensates and impaired leukemia cell growth.
To analyze compositional changes, we developed NuFANCI, a FACS-based method to isolate nuclear condensates. Applied to killswitch-targeted nucleoli, mass spectrometry revealed selective depletion of ~20 RNA-binding proteins, demonstrating condensate-material-property–dependent partitioning.
To analyze compositional changes, we developed NuFANCI, a FACS-based method to isolate nuclear condensates. Applied to killswitch-targeted nucleoli, mass spectrometry revealed selective depletion of ~20 RNA-binding proteins, demonstrating condensate-material-property–dependent partitioning.
Using the nanobody system, killswitch can be targeted to a wide range of endogenous condensates, including nucleoli, nuclear speckles, chromocenters, and disease-specific condensates.
Using the nanobody system, killswitch can be targeted to a wide range of endogenous condensates, including nucleoli, nuclear speckles, chromocenters, and disease-specific condensates.
Killswitch (KS) is a non-natural, self-associating micropeptide that can be genetically fused to condensate proteins or recruited via GFP-nanobody. It immobilizes scaffold proteins without affecting soluble pools—letting us perturb condensates selectively in live cells.
Killswitch (KS) is a non-natural, self-associating micropeptide that can be genetically fused to condensate proteins or recruited via GFP-nanobody. It immobilizes scaffold proteins without affecting soluble pools—letting us perturb condensates selectively in live cells.
In adenoviral 52K condensates, killswitch reduced dynamics and blocked recruitment of capsid protein IIIa, despite preserved binding interfaces. Viral progeny production dropped >90%. The KS thus uncovers hidden roles of condensate microenvironments for condensate regulation.
In adenoviral 52K condensates, killswitch reduced dynamics and blocked recruitment of capsid protein IIIa, despite preserved binding interfaces. Viral progeny production dropped >90%. The KS thus uncovers hidden roles of condensate microenvironments for condensate regulation.
Targeting BRD4::NUT condensates with killswitch disrupted RNA Pol II partitioning and reduced transcription. In NUP98::KDM5A-driven AML cells, killswitch caused proteasome-mediated degradation of fusion condensates and impaired leukemia cell growth.
Targeting BRD4::NUT condensates with killswitch disrupted RNA Pol II partitioning and reduced transcription. In NUP98::KDM5A-driven AML cells, killswitch caused proteasome-mediated degradation of fusion condensates and impaired leukemia cell growth.
To analyze compositional changes, we developed NuFANCI, a FACS-based method to isolate nuclear condensates. Applied to killswitch-targeted nucleoli, mass spectrometry revealed selective depletion of ~20 RNA-binding proteins, demonstrating condensate-material-property–dependent partitioning.
To analyze compositional changes, we developed NuFANCI, a FACS-based method to isolate nuclear condensates. Applied to killswitch-targeted nucleoli, mass spectrometry revealed selective depletion of ~20 RNA-binding proteins, demonstrating condensate-material-property–dependent partitioning.
Using the nanobody system, killswitch can be targeted to a wide range of endogenous condensates, including nucleoli, nuclear speckles, chromocenters, and disease-specific condensates.
Using the nanobody system, killswitch can be targeted to a wide range of endogenous condensates, including nucleoli, nuclear speckles, chromocenters, and disease-specific condensates.