Roderick L. Beijersbergen

The paper develops a validated TCR-pMHC database (TCRvdb) by assessing VDJdb entries with a high-throughput platform, finding only 50% of claims are functionally confirmed.

The paper constructs an atlas of human multi-protein complexes by integrating computational structure predictions with genetic dependency data, identifying 354 high-confidence complexes including novel ones.

The paper develops a high-throughput live-cell screening platform using time-lapse FRET-FLIM to study dynamic signaling phenotypes, demonstrating its effectiveness in identifying regulators of cAMP signaling.

The paper identifies YM155 as a β-catenin condensate inhibitor using a NECO screening platform, showing its anti-proliferative effect on WNT-driven colorectal cancer organoids.

The paper investigates the molecular and genomic effects of a global DNA damage tolerance defect, identifying type 3 deletions as a mutational signature of replication stress.

This paper identifies SLC25A23 as a vulnerability in senescent cancer cells and shows that salinomycin induces immunogenic cell death, enhancing immune destruction of these cells when combined with a DR5 agonistic antibody.

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

This study identifies 67 epigenetic drugs that modulate CRISPR-Cas9 editing efficiency and repair outcomes based on chromatin context in human cells.

The paper identifies Fpt1 as a chromatin-associated regulator that promotes RNA Polymerase III eviction from tRNA genes in response to nutrient changes in yeast.

This study identifies PAXIP1 and STAG2 as co-regulators of the Glucocorticoid Receptor (GR) that maintain 3D genome architecture and enable stress hormone-dependent transcription.

This study shows that Cas9 expression levels significantly affect the efficiency and speed of large-scale pooled CRISPR screens, with higher Cas9 expression improving performance.

The paper measures how chromatin context influences the balance between DNA repair pathways after Cas9-induced breaks in over 1,000 genomic locations.

This paper develops feedback-ISA (f-ISA) to model feedback mechanisms in signaling pathways, showing it can explain phosphorylation levels in MAPK and AKT pathways across breast cancer cell lines and conditions.