Rémi Buisson
@buissonlab.bsky.social
Associate Professor at University of California Irvine. APOBEC, innate immunity, DNA damage, RNA viruses, and scuba diving fanatic.
Thanks for the great description of our recent study!
May 20, 2025 at 4:00 PM
Thanks for the great description of our recent study!
Many thanks to @pedroorteg.bsky.social for leading this work, and to @johnmaciejowski.bsky.social and the Abby Green Lab for their contributions to the story.
April 16, 2025 at 9:19 PM
Many thanks to @pedroorteg.bsky.social for leading this work, and to @johnmaciejowski.bsky.social and the Abby Green Lab for their contributions to the story.
Thank you so much for this beautiful review of our paper!!
April 11, 2025 at 2:42 PM
Thank you so much for this beautiful review of our paper!!
So frustrating! For both reviewers and applicants…. So much work for nothing….
February 25, 2025 at 7:57 PM
So frustrating! For both reviewers and applicants…. So much work for nothing….
Free access to the paper: rdcu.be/d5pue
ATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage
Nature Structural & Molecular Biology - In this study, the authors show that DNA-damage-mediated transcriptional stress induces NF-κB through IRAK1, allowing damaged cells with impaired...
rdcu.be
January 6, 2025 at 3:17 PM
Free access to the paper: rdcu.be/d5pue
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.
January 6, 2025 at 3:17 PM
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.
Thank you very much! I am glad you liked our story!
January 6, 2025 at 2:55 PM
Thank you very much! I am glad you liked our story!
Félicitation !!!🥳
December 3, 2024 at 8:32 PM
Félicitation !!!🥳
We propose that both PACT and ADAR1 act as essential barriers against PKR, creating a threshold of tolerable levels to endogenous dsRNA in cells without activating PKR-mediated translation shutdown and cell death.
November 28, 2024 at 5:05 PM
We propose that both PACT and ADAR1 act as essential barriers against PKR, creating a threshold of tolerable levels to endogenous dsRNA in cells without activating PKR-mediated translation shutdown and cell death.
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.
November 28, 2024 at 5:05 PM
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.