Microscopy-based bead protein-protein interaction assay
By taliag onAn assay to study protein-protein interaction
Assessing enrichment of proteins in the mitochondrial fraction in HEK cells
By taliag onThis is a method for measuring protein enrichment on mitochondria in various conditions. In the resulting Western blot, one can assess the level of contamination of other organelles in the enrichment prep.
Structural basis for membrane recruitment of ATG16L1 by WIPI2 in autophagy
By taliag onPublished: Autophagy is a conserved mechanism for the sequestration and degradation of cytosolic cargo. ATG16L1 and WIPI2 are essential for autophagy initiation. The authors showed through structural determination how ATG16L1 and WIPI2 interact and compared the other WIPI proteins showing the variety of mechanisms of membrane recruitment by WIPI proteins. View original preprint.
Global ubiquitylation analysis of mitochondria in primary neurons identifies endogenous Parkin targets following activation of PINK1
By Blythe Lloyd onPublished: 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.
Structural basis for the specificity of PPM1H phosphatase for Rab GTPases Figures
By Blythe Lloyd onRaw data associated with DOI: 10.15252/embr.202152675
Raw data associated with DOI: 10.7554/eLife.67900
By Blythe Lloyd onRaw data associated with DOI: 10.7554/eLife.67900
HyDrop Bead Generation & PCR Barcoding v1.0
By Blythe Lloyd onProtocol for producing dissolvable barcoded hydrogel beads used in HyDrop experiments.
Pathogenic LRRK2 control of primary cilia and Hedgehog signaling in neurons and astrocytes of mouse brain
By Michelle onPublished: Pathogenic mutations in LRRK2 are known to cause loss of primary cilia in neurons. The authors show that cilia loss is seen very early in mice harboring the most common LRRK2 mutation. Further, they show that this loss of cilia in astrocytes disrupted signaling pathways required for dopamine neuron maintenance. View original preprint.