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Catalog
ASAP is committed to accelerating the pace of discovery and informing a path to a cure for Parkinson’s disease through collaboration, research-enabling resources, and data sharing. We’ve created this catalog to showcase the research outputs and tools developed by ASAP-funded programs.
Global ubiquitylation analysis of mitochondria in primary neurons identifies physiological Parkin targets following activation of PINK1
Published: Mutations in PINK1 and Parkin are implicated in PD via abherrant mitophagy. The authors identified ubiquitylated substrates of endogenous Parkin in mouse neurons by proteomic analysis. They identified and validated 22 protein targets of Parkin that are conserved in human neurons providing a functional Parkin landscape in neuronal cells. View original preprint.
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Global ubiquitylation analysis of mitochondria in primary neurons identifies endogenous Parkin targets following activation of PINK1
Published: Loss-of-function mutations in Parkin cause disruption of mitophagy and are associated with PD. Yet, much of the biology surrounding Parkin function has taken place in artificial cell systems. The authors used human neurons to identify and validate 22 protein targets of Parkin, providing a functional Parkin landscape in neuronal cells.
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In situ structural analysis reveals membrane shape transitions during autophagosome formation
Preprint: A hallmark of PD is the failure of quality control mechanisms in the cell, such as autophagy. The authors combined cell biology with correlative cryo-electron tomography in yeast cells to show a high resolution stepwise structural progression of autophagosome biogenesis. Further, they revealed the organelle interactome for growing autophagosomes.
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Combinatorial selective ER-phagy remodels the ER during neurogenesis
The molecular inventory of ER proteome remodeling and versatile genetic toolkit provides a quantitative framework for understanding contributions of individual ER-phagy receptors for reshaping ER during cell state transitions.
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Global lipidomics of WT and GRN-/- cells & mouse models, including plus and minus GRN addback
This dataset contains:
– Global lipidomics of WT and GRN-/- HeLa cells, including plus and minus GRN addback.
– Global lipidomics of WT and NPC1-/- HeLa cells.
– Global lipidomics of WT and GRN-/- HeLa cells, including plus and minus GRN addback.
Global lipidomics of WT and GRN mutant mouse brain tissue.
https://www.nature.com/articles/s41467-022-33500-9
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Code for extraction of any user-defined information from uniprot
Code for extraction of any user-defined information from Uniprot.
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Cryo-ET of S. cerevisiae during starvation (tomograms)
Cryo-ET of S. cerevisiae during starvation (tomograms). Accession number:
https://www.ebi.ac.uk/emdb/EMD-15526
https://www.ebi.ac.uk/emdb/EMD-15545
https://www.ebi.ac.uk/emdb/EMD-15546
https://www.ebi.ac.uk/emdb/EMD-15547
https://www.ebi.ac.uk/emdb/EMD-15549
https://www.ebi.ac.uk/emdb/EMD-15548
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Gene editing of YIPF4 in hESCs V3
This protocol describes the creation of YIPF4 knockout cell lines in H9 hESC cells using CRISPR-Cas9.
Associated with preprint:
https://doi.org/10.1101/2022.12.06.519342
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The chaperone Clusterin in neurodegeneration−friend or foe?
Review: The authors review the diverse functions of Clusterin in the pathogenesis of neurodegenerative diseases, focusing on evidence that Clusterin may act either as a suppressor or enhancer of pathology.
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Global proteomic analysis of WT and GRN-/- HeLa cells
Global proteomic analysis of WT and GRN-/- HeLa cells. https://www.nature.com/articles/s41467-022-33500-9
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H9 ES AAVS-NGN2; FBXO7-/-
H9 ES cells with AAVS1-NGN2 in which FBXO7 has been deleted using CRISPR.
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Characterizing spatial and temporal properties of ER-phagy receptors
Associated with preprint:
https://doi.org/10.1101/2023.06.26.546565
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Mechanisms underlying ubiquitin-driven selective mitochondrial and bacterial autophagy
Review: The authors review recent efforts to understand the biochemical mechanisms and principles by which cargo are marked with ubiquitin and how ubiquitin-binding cargo receptors use conserved structural modules to recruit the autophagosome initiation machinery, with a particular focus on mitochondria and intracellular bacteria as cargo.
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Evaluation of mtKeima foci in induced neurons (iNeurons)
Associated with preprint: https://www.biorxiv.org/content/10.1101/2022.11.02.514817v1
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