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Chak Shun Yu on Muck Rack

Chak Shun Yu

As seen in: Illumination, Nature, Cell Chemical Biology
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Articles

Assessment of mitochondrial lipid peroxidation in cells and zebrafish using a targeted mass spectrometry probe

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By Shinpei Uno, Stuart Caldwell, Hiran A. Prag, Chak Shun Yu, María Torres-López, Andrew James, Ana Lopez, Ana López, Angeleen Fleming, David Rubinsztein, Richard Hartley, Michael Murphy, Taylor A. Woetzel
| Cell Chemical Biology Verified
Keywords mitochondria lipid peroxidation, ferroptosis oxidative stress exomarker Introduction Mitochondria are both a major source of reactive oxygen species (ROS) and a significant target for oxidative damage in a range of pathologies.1,2 Lipid peroxidation is one of the most significant components of mitochondrial oxidative damage.
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Simultaneous and sensitive quantification of protein and low molecular weight persulfides, polysulfides and H2S in biological samples - Nature Communications

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By Chak Shun Yu, Stefan Warrington, Stuart Caldwell, Dunja Aksentijevic, Andrew James, Thomas Krieg, Richard Hartley
| Nature Verified
Abstract H2S reversibly modifies low molecular weight (LMWSH) and protein (PrSH) thiols to form persulfides (RSS−) and polysulfides (RS(S)nS−) for antioxidant defence and regulation of activity. However, our understanding of the biological significance of these processes is hampered by our inability to quantify these modifications.
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An inherited mitochondrial DNA mutation remodels inflammatory cytokine responses in macrophages and in vivo in mice - Nature Communications

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By Eloise Marques, Stephen P. Burr, Alva M. Casey, Richard J. Stopforth, Chak Shun Yu, Keira Turner, James Stewart, Julien Prudent, Valerie O’Donnell, Clare E. Bryant, Patrick F. Chinnery, Arthur Kaser, Alexander Von Kriegsheim, Robbin Kramer
| Nature Verified
Abstract Impaired mitochondrial bioenergetics in macrophages promotes hyperinflammatory cytokine responses, but whether inherited mtDNA mutations drive similar phenotypes is unknown. Here, we profiled macrophages harbouring a heteroplasmic mitochondrial tRNAAla mutation (m.5019A>G) to address this question.
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