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joannapaulson.bsky.social

@joannapaulson.bsky.social
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Reposted by @joannapaulson.bsky.social
Nitika Taneja @TanejaLab @nitikataneja.bsky.social · 01/07/2026
Very excited to share our new Nature study! We discovered that replication stress stabilizes CTCF-dependent chromatin loops enclosing stressed nascent DNA, where G9a-mediated heterochromatin protects it from nucleolytic degradation. rdcu.be/frzLg Huge thanks to all our collaborators and co-authors!
nature.com
Replication-stress-induced chromatin loops protect fork stability - Nature
Replication stress induces the formation of transient chromatin loops that enclose de novo heterochromatin-enriched stalled replication forks.
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Reposted by @joannapaulson.bsky.social
Nitika Taneja @TanejaLab @nitikataneja.bsky.social · 19/12/2025
Delighted to be part of this work from the Lopes lab identifying nucleoplasmic Lamin A/C as a key regulator of replication fork plasticity, acting via de novo heterochromatin and ADP-ribosylation to control RECQ1-mediated fork restart. Now in Nature Comm. 🎉Special efforts: @joannapaulson.bsky.social
rdcu.be
Nucleoplasmic Lamin A/C controls replication fork restart upon stress by modulating local H3K9me3 and ADP-ribosylation levels
Nature Communications - Replication fork plasticity upon genotoxic stress is modulated by nuclear architectural components by elusive mechanisms. Here the authors implicate Lamin A/C – best...
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Reposted by @joannapaulson.bsky.social
Nitika Taneja @TanejaLab @nitikataneja.bsky.social · 19/01/2025
Happy to have contributed(along with PhD students @joannapaulson.bsky.social & Collin Bakker) to such great work from @lopeslab.bsky.social and team! www.biorxiv.org/content/10.1...
biorxiv.org
Nucleoplasmic Lamin A/C controls replication fork restart upon stress by modulating local H3K9me3 and ADP-ribosylation levels
Mild replication interference is a consolidated strategy for cancer chemotherapy. Tolerance to mild replication stress (RS) relies on active fork slowing, mediated by transient fork reversal and RECQ1...
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