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Chemical crosslinkers trap αS in intact cells as a 60 kDa species, around 4 times the size of its monomeric state (14.5 kDa). What does this mean?


Normally, αS switches between membrane-associated and cytoplasmic forms. We have engineered αS to accumulate in a monomeric form at membranes, with striking effects on cell biology. What can we learn about αS in health and disease?


We have found a ‘short-cut’ for αS to readily form round cytoplasmic inclusions in cultured cells. This insight will be used for high throughput screens to achieve ‘inclusion reduction’.


Human αS has two homologs, β-synuclein and γ-synuclein. Is there an interplay between the three synuclein family members?

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