Chowdhury Lab

Excited to share that Michelle Swift has been selected as an OCRA grantee! This support will help us study mechanisms of PARP inhibitor resistance in ovarian cancer and identify new therapeutic opportunities. ocrahope.org/research/curre…

Congratulations to @ChiaraMasnovo on receiving the @AmericanCancer Postdoctoral Fellowship! 🎉 Her project will be defining the DNA Repair Independent Mitotic Role of 53BP1 Mentor: Dipanjan Chowdhury Co-mentor: Alexander Spektor Well deserved recognition of outstanding work! 👏

Congratulations to @SusanKilgas on receiving the first place Best Poster Award at the DNA Damage Mutation and Cancer Gordon Research Conference for her poster on a novel layer of p53 regulation through TIRR 🎉

Congratulations to Michelle Swift on receiving the Best Short Talk Award at the #DRRSC26 Fusion Conference for her presentation on BRCA1/BARD1 regulation of DNA repair. 🎉 @Fusion_Conf

Excited to share our new paper from Sara J. Buhrlage lab & @ChowdhuryLab! We designed CAS-010, a selective, low nanomolar USP28 inhibitor that reduces p53 transcriptional activity, mimics p53 pathway loss & disrupts 53BP1-USP28 binding, offering new insights into USP28 function.

🧬 Grad students and postdocs in DNA repair/DDR: don’t forget to register for the 2026 GRS “Safeguarding the Genome” seminar — Feb 28–Mar 1, Ventura, CA. Keynote: @ChowdhuryLab. Abstracts due by Nov 23, 2025. Register here: 🔗 grc.org/dna-damage-mut…

📢 For all HaloTag lovers💙💚💛❤️💜🩶 we are excited to share that our work, in which we developed a new biotin-HaloTag ligand, is now published in @JCellBiol! Full link here: rupress.org/jcb/article-ab…

Excited to share our publication out in Science today! We define a role for the CST complex in DSB repair pathway choice. This study was conducted in close collaboration with Patrick Sung’s lab. Congratulations to Michelle Swift and all other authors! science.org/doi/10.1126/sc…

Thank you to @ChowdhuryLab (@Harvardmed, @DanaFarber) for joining us for a fantastic #WednedsayLectureSeries on "#DNA repair mechanisms in the context of cell cycle with implication in #cancer." 🧬 Hosted by the Si Lab.

📣 Excited to share our latest review on 53BP1’s function in replication stress, its role in fork protection, and the significance of 53BP1 nuclear bodies in this context! sciencedirect.com/science/articl…

@DanaFarber website blog published an article on our recent study of CDK5 in @Nature. For CDK5 curious readers: blog.dana-farber.org/insight/2024/1…

Special shout out to @KicksforCancer1 , Thank you for your support.

Enjoying New England fall weather with our annual lab hike! Celebrated recent achievements from the lab. Cheers to all of you 🍾

@ayoubnlab Thank you!

@ChowdhuryLab Very interesting work!!! Congratulations

📣Really excited to share our publication out in @NatureComms , where we show that the lncRNA NEAT1, regulated by the RBP TDP-43, destabilizes the TIRR/53BP1 complex in G1 phase of the cell cycle, affecting both the DSB repair-dependent and -independent functions of 53BP1.

@PeterLyLab @NatureComms @SusanKilgas @Alee_mSyed @SwiftMichelleL @ShrabastiRoych1 @APoetsch Thank you!

@ChowdhuryLab @NatureComms @SusanKilgas @Alee_mSyed @SwiftMichelleL @ShrabastiRoych1 @APoetsch Congrats on a very productive two-month span of papers!

@Chapman_lab_UK @auracarreiralab @SusanKilgas @Alee_mSyed @SwiftMichelleL @ShrabastiRoych1 @APoetsch Thank you, Ross!

@ChowdhuryLab @auracarreiralab @SusanKilgas @Alee_mSyed @SwiftMichelleL @ShrabastiRoych1 @APoetsch TIRRific work guys! Looking forward to reading this! Congratulations

Together, we show that the TDP-43-NEAT1 axis regulates the TIRR/53BP1 complex for the maintenance of genome integrity.

Finally, we showed that the RNA splicing factor TDP-43, implicated in neurodegenerative diseases and known to promote NEAT1 short isoform production, is hypostatic with NEAT1 with regards to 53BP1 function. TDP-43 loss phenocopies the impact of NEAT1 loss.

NEAT1 binding destabilizes the TIRR/53BP1 complex. NEAT1 short isoform is mostly present in G1 phase, which ensures the cell cycle-dependency of TIRR/53BP1 complex dissociation, and consequently 53BP1’s availability in G1 for DSB repair.