K. Yusa

Genome-scale CRISPR-Cas9 screen identifies novel host factors as potential therapeutic targets for SARS-CoV-2 infection.

The paper identifies TRIM28, TRIM33, EHMT1, and EHMT2 as novel host factors involved in SARS-CoV-2 infection and shows that EHMT1/2 inhibition reduces viral growth and disease severity.

B1 SINE-binding ZFP266 impedes reprogramming through suppression of chromatin opening mediated by pioneering factors

This study identifies ZFP266 as a reprogramming roadblock gene that suppresses chromatin opening by binding SINEs near pioneer factor binding sites, and shows that replacing its KRAB domain with a co-activator domain enhances reprogramming.

KAT7 is a therapeutic vulnerability of MLL-rearranged acute myeloid leukemia

This study identifies KAT7 as a critical therapeutic target in MLL-rearranged AML by showing its role in maintaining acetylation marks and supporting cell proliferation.

Agreement between two large pan-cancer CRISPR-Cas9 gene dependency datasets

This study compares two large pan-cancer CRISPR-Cas9 screens, finding high concordance in gene dependencies despite differences in protocols and reagents.

Functional linkage of gene fusions to cancer cell fitness assessed by pharmacological and CRISPR/Cas9 screening

The paper functionally links gene fusions to cancer cell fitness using drug sensitivity and CRISPR-Cas9 data, identifying rare functional fusions and novel therapeutic targets.

Prioritisation of oncology therapeutic targets using CRISPR-Cas9 screening

This study uses CRISPR-Cas9 screens in cancer cell lines to identify and prioritize new oncology therapeutic targets based on gene fitness, biomarkers, and tractability.

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

The paper identifies how ATM counteracts toxic non-homologous end-joining at broken replication forks by showing that loss of NHEJ components or BRCA1-A complex confers resistance to DNA-damaging agents in ATM-deficient cells.

Genome-wide and high-density CRISPR-Cas9 screens identify point mutations in PARP1 causing PARP inhibitor resistance

The paper identifies PARP1 point mutations causing PARP inhibitor resistance through CRISPR-Cas9 screens and shows their impact on PARP1 trapping and chemotherapy sensitivity.