Associate Professor at the University of California Irvine
Irvine, California
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The Department of Biological Chemistry at UCI is seeking a tenure-track Assistant Professor!
This is a broad search across biomedical sciences, including genome stability. Join a dynamic department with great faculty benefits and year-round sunshine!
recruit.ap.uci.edu/JPF10441
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Rémi Buisson retweeted
Fellow RNA enthusiasts: I'm organizing an RNA symposium on Jan 16, 2026 at @UCIrvine and attendance is free! A great opportunity to discuss the latest discoveries in RNA! Come join us! Contact me if you'd like to sponsor us.
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Today, we report that APOBEC3B targets unprotected single-stranded DNA at replication forks upon ATR inhibition, triggering a reaction cascade involving UNG2 and APE1 that leads to fork collapse and hyperactivation of PARP1, causing replication catastrophe.science.org/doi/10.1126/scia…
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Many thanks to @pedroorteg
for leading this work, and to @maciejowskilab
and @abbygreenlab for their contributions to the story.
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A beautiful News & Views by @UnterholznerLab highlighting our latest paper in @NatureSMB, where we show that transcription stress triggers an inflammatory response through the release of IL-1α.
Free link: rdcu.be/ehkTV
nature.com/articles/s41594-0…
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Today, we report our new study demonstrating that PACT functions as an inhibitor rather than an activator of PKR, and works together with ADAR1 to suppress aberrant activation of PKR by self-derived double-stranded RNA. nature.com/articles/s41467-0…
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Rémi Buisson retweeted
🙌Way to show up! #UCIrvine research team @masrilab has made it to Round 4 of #STATMadness! We are getting so close to the semi-finals and the championship round. We have a shorter time frame. Submit your votes by Thursday, March 27 at 1 a.m. PT. Let’s go! bit.ly/43piMYT
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Today @NatureSMB, we report that the activation of NF-κB after DNA damage can occur through two distinct mechanisms. While ATM triggers NF-κB activation after DSBs, we found that IRAK1 induces NF-κB in response to DNA damage causing transcriptional stress. nature.com/articles/s41594-0…
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Our findings provide an alternative mechanism for damaged cells with impaired transcription to initiate an inflammatory response without relying on their own gene expression, a necessary step that injured cells depend on during canonical innate immune responses.
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Our detailed protocol by @AmbrocioSanchz , a graduate student in the lab, revealing our secret to performing perfect in vitro APOBEC deaminase reactions on DNA substrates at near-nucleotide resolution. authors.elsevier.com/a/1kDyI…
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New Lab Preprint!🥳 Using CRISPR-Translate, a genome-wide CRISPR-Cas9 knockout screening method developed by the lab exploiting translation levels as a readout, we reveal that PACT is an inhibitor of PKR and not an activator during RNA viral infections. biorxiv.org/content/10.1101/…
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Simultaneous deletion of PACT and ADAR1 results in synthetic lethality, which can be fully rescued in PKR-deficient cells. This suggests PACT cooperates with ADAR1 to suppress PKR activation from self-dsRNAs in uninfected cells.
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New Lab Preprint! We show that ATR inhibition leads to PARP1 hyperactivation at replication forks, driven by an APOBEC3B-initiated reaction cascade involving UNG2 and APE1, which targets unprotected single-stranded DNA at the forks. biorxiv.org/content/10.1101/…
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Our findings uncover the mechanisms behind replication fork collapse during replication catastrophe and show that APOBEC3B drives cell sensitivity caused by ATR and PARP inhibitors.
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Thanks to @pedroorteg for driving this project with the help of @AmbrocioSanchz and @ElodieBournique. Special thanks to @abbygreenlab for assistance with the DNA fiber assay!
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