Arnab Ray Chaudhuri
@Arnab_RC1
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Associate Professor, Department of Molecular Genetics, Erasmus University Medical Center
Rotterdam, The Netherlands
Joined July 2019
RT @durocherlab: JOB ALERT 🚨 We are hiring TWO principal investigators in cell, molecular, systems, or chemical biology in Toronto, Canada.….
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RT @Fusion_Conf: @Arnab_RC1 we are looking forward to your presentation at the #DRRSC26 🌟.Please share this with your followers to let them….
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RT @DrSagarSengupta: Happy to present our work in @embojournal where we show how p53 acts as a transcriptional repressor by directly recrui….
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RT @ShyamKSharan: Congratulations @SounakSahu, Mélissa Galloux, members of our BRCA Variant Analysis Unit @theNCI for this outstanding work….
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RT @Sanjiba06972691: Excited to share the latest preprint from our lab.Mitochondrial genome-encoded mitomiRs regulate cellular plasticity a….
biorxiv.org
Ferroptosis is a distinct form of regulated cell death promoted by iron-dependent lipid peroxidation. The metabolic plasticity of cancer cells determines their sensitivity to ferroptosis. Although...
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RT @luijsterburglab: New paper with @KokicGoran and @SvejstrupLab in Cell Press! We show that STK19 facilitates the clearance of lesion-sta….
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RT @TychoMevissen: Excited that our work on transcription-coupled DNA repair is now published @CellCellPress! We recapitulated TC-NER in Xe….
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RT @Marteijnlab: 🚨 New publication in @MolecularCell ! We reveal STK19 as essential transcription-coupled DNA repair factor, stabilizing th….
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Our study show that maintaining a fine balance of RAD51 levels by positive and negative regulation is critical for efficient HR, maintenance of genome stability and cellular viability.
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This suggests that HR defects in BRCA2-deficient cells are primarily due to RAD51 removal by FIGNL1 rather than defective RAD51 loading. Furthermore, we identified the MMS22L-TONSL complex as responsible for loading RAD51 in BRCA2/FIGNL1 double-deficient cells.
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We demonstrate for the first time that defective RAD51 loading at DSBs and subsequent HR defects in BRCA2-deficient cells can be rescued by the loss of the anti-recombinase FIGNL1.
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What is the primary cause of homologous recombination deficiency observed upon loss of BRCA2? Is it due to the defect in RAD51 loading by BRCA2?.
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A tour de force by @RaviprasadKV1 and tremendous collaborative efforts by @AnanyaAcharya, @Satheesh_NCI, @Little_Carm, and twitterless Nupur Nagar. Amazing collaboration with with labs of @ CejkaLab, @ShyamKSharan, @KMPoluri, @AmelieFT, Kannar and Lebbink labs.
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Very excited to present the latest preprint from our lab! "FIGNL1 inhibits homologous recombination in BRCA2 deficient cells by dissociating RAD51 filaments" .
biorxiv.org
Homologous recombination (HR) deficiency upon BRCA2 loss arises from defects in the formation of RAD51 nucleoprotein filaments. Here, we demonstrate that loss of the anti-recombinase FIGNL1 retains...
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RT @davidkcortez: The Cortez lab ( is looking for new postdocs or senior scientists. If you are interested in genom….
lab.vanderbilt.edu
OPEN POSITIONS FOR POSTDOCS OR SENIOR SCIENTISTS Billions of base pairs of DNA must be replicated trillions of times during a human lifetime. Adding to the difficulty, thousands of DNA lesions happen...
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RT @nussenza: A high-resolution view of how replication-coupled DNA breaks are generated, processed and repaired. Congrats to @pavani_rapha….
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RT @SarahLa47195747: The team has a postdoctoral position open in Molecular & Cellular Genetics, to study replication fork repair pathways….
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RT @Tanejalab: Join our dynamic lab! PhD positions available: explore chromatin organization upon replication stress #Oncode. Also, Postdoc….
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