Denisa Hathazi
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denisah.bsky.social
Denisa Hathazi
@denisah.bsky.social
Research Associate at University of Cambridge, at Horvath Lab.
Molecular scientist with a passion for metabolism and neuronal models
Congrats Jack!
🔥 Check out our new paper! @natcellbio.nature.com
Also thanks to @embo.org for their Postdoctoral Fellowship and especially to Mai and Heidi, I learned more than I could ever have imagined in Montreal 🇨🇦 🍁
New paper - MAPL strikes again! Interested in mitochondrial signalling, inflammation, lysosome biology, pyroptosis, and Parkinson's disease? Have a look, there's something for everyone! Feeling grateful! @mitocollier.bsky.social Funded by #CIHR, @asapresearch.parkinsonsroadmap.org.
rdcu.be/eKKz1 🇨🇦
October 14, 2025 at 3:31 PM
Reposted by Denisa Hathazi
How can mitophagy be an effective quality control mechanism if mtDNA mutations reach high enough levels to cause disease?

This question led us into a dark path, full of concepts of evolutionary genetics, germline stem cell biology and mito-nuclear compatibility.

www.science.org/doi/10.1126/...
Ubiquitin-mediated mitophagy regulates the inheritance of mitochondrial DNA mutations
Mitochondrial synthesis of adenosine triphosphate is essential for eukaryotic life but is dependent on the cooperation of two genomes: nuclear and mitochondrial DNA (mtDNA). mtDNA mutates ~15 times as...
www.science.org
October 10, 2025 at 8:45 AM
Reposted by Denisa Hathazi
'Skeetorial' of our latest paper: link.springer.com/article/10.1...

So proud of first author Christina Antoniou for this, now a postdoc with @melissa-gammons1.bsky.social.

(1) NMNAT2 is a repressor of SARM1 NADase in axons. A few people have NMNAT2 LoF mutations. Many more have low expression.
November 24, 2024 at 12:18 PM