Anna G. Manjón

This study shows that transcription inhibition rapidly and reversibly rewires chromatin-nuclear lamina contacts through distinct Lamin A and LBR tethering mechanisms.

The paper identifies TOP2B as a regulator of genome-nuclear lamina interactions, showing its role in partitioning genomic regions between the nuclear lamina and interior, with LBR playing a complementary role.

The paper shows that DSBs in LADs cause megabase-scale detachment from the nuclear lamina, which is necessary for efficient repair.

The paper shows that homologous recombination (HR) promotes mitotic death, which suppresses the innate immune response by preventing immunogenic cell death.

A multiplexed screen reveals how dozens of proteins sense the local chromatin context to tune the balance between two DNA repair pathways.

The paper shows that disrupting nuclear lamina association promotes ABCB1 gene derepression and taxol resistance in RPE cells.

This study reports that lentiviral-based CRISPR-Cas9 vectors can integrate into the target genomic location, unexpectedly activating the target gene.

The paper develops TRANSACT, a transfer learning framework for predicting clinical drug response, outperforming existing methods on multiple datasets.