Esashi Lab
@esashilab.bsky.social
Sir William Dunn School, University of Oxford, Interested in genome stability, homologous recombination, chromosome, centromeres
https://esashilab.wordpress.com/
https://esashilab.wordpress.com/
Thanks so much for coming, Sarah! We loved your talk - super exciting and inspiring. Can’t wait to catch up soon!
July 14, 2025 at 6:38 PM
Thanks so much for coming, Sarah! We loved your talk - super exciting and inspiring. Can’t wait to catch up soon!
Huge thanks to everyone involved and for the incredible support from the community.
This is our very first post on this platform, and we're looking forward to continuing to connect with you all!
This is our very first post on this platform, and we're looking forward to continuing to connect with you all!
February 25, 2025 at 5:56 PM
Huge thanks to everyone involved and for the incredible support from the community.
This is our very first post on this platform, and we're looking forward to continuing to connect with you all!
This is our very first post on this platform, and we're looking forward to continuing to connect with you all!
This study, conceived eight years ago, was made possible by a global collaboration across the UK, USA, Japan and Turkey. The dedicated team efforts of Emily and Lucia, relayed by Brian, Jacob, Emoke and Ramazan, and invaluable assistance from many others, brought this research to life.
February 25, 2025 at 5:56 PM
This study, conceived eight years ago, was made possible by a global collaboration across the UK, USA, Japan and Turkey. The dedicated team efforts of Emily and Lucia, relayed by Brian, Jacob, Emoke and Ramazan, and invaluable assistance from many others, brought this research to life.
Note that the phenotype varies between cell lines (HCT116 vs RPE1), but in the big picture, we propose that homologous recombination and mismatch repair factors engage in a ‘tug of war’ at centromeres to maintain their functional resilience.
February 25, 2025 at 5:56 PM
Note that the phenotype varies between cell lines (HCT116 vs RPE1), but in the big picture, we propose that homologous recombination and mismatch repair factors engage in a ‘tug of war’ at centromeres to maintain their functional resilience.