Key Resource Table: Molecular analysis of network vulnerability to α-synuclein pathology reveals PAKs as therapeutic targets for Parkinson’s disease
Output Details
- Biochemistry
- Human
- in situ
- In Vitro
- In Vivo
- Mass Spectrometry
- Mouse
- Spatial Transcriptomics
- Surgical
Meet the Authors
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Naman Vatsa
External Collaborator
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J Kate Brynildsen
External Collaborator
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Thomas Goralski
External Collaborator
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Kevin Kurgat
External Collaborator
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Lindsay Meyerdirk
External Collaborator
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Libby Breton
External Collaborator
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Daniella DeWeerd
External Collaborator
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Laura Brasseur
External Collaborator
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Lisa Turner
External Collaborator
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Katelyn Becker
External Collaborator
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Kristin L. Gallik
External Collaborator
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Christine Isaguirre
External Collaborator
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Ryan Sheldon
External Collaborator
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Danielle (Dani) Bassett
External Collaborator
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Related Research
Network analysis of α-synuclein pathology progression reveals p21-activated kinases as regulators of vulnerability
Misfolded α-synuclein accumulation in PD leads to pathogenic processes. We mapped α-synuclein pathology in mice to identify vulnerable regions and potential therapeutic targets, highlighting group II PAK inhibitors as promising for treating PD.
Microscopy-based bead protein-protein interaction assay.
Protocol for microscopy-based bead protein-protein interaction assay using GST- or mCherry-tagged baits and fluorescently-tagged preys. Requires purified proteins, monitors interactions in equilibrium, and allows quantification of fluorescent signal.
GUV assay
This protocol describes the preparation of GUVs for the reconstitution of LC3 lipidation reaction through the steps of PI3P production by PI3KC3-C1, WIPI2 recruitment and LC3 lipidation with PE. Screen reader support enabled.