Kosuke Yusa

BRCA2 loss triggers a downward spiral of genomic instability via ROS-dependent metabolic collapse

This paper shows BRCA2 loss causes genomic instability through ROS-dependent metabolic collapse, highlighting the role of glutathione metabolism and PARP inhibitors in cell death.

Precursor of chemically expanded hepatocytes (pre-cHep) with 1-million-fold expansion potential and liver repopulation capacity

The paper reports a method to reprogram primary human hepatocytes into proliferative pre-cHep cells with high expansion potential and liver repopulation capacity, offering an alternative to PHHs for drug testing and disease modeling.

CDK12/13 inhibitor, CTX-439, suppresses tumor growth and potentiates BCL-2 family blockade

This study develops CTX-439, a CDK12/13 inhibitor, showing anti-tumor effects and resistance mechanisms, and proposes combining it with BCL-2 family inhibitors for cancer treatment.

Hic2 fast-tracks iPS cell generation by suppressing KLF4-dependent epidermal detour

This paper identifies Hic2 as a gene that enhances iPSC generation by suppressing KLF4-dependent epidermal gene expression during reprogramming.

Inference of gene regulatory networks using time-series single-cell RNA-seq data with CRISPR perturbations

This paper introduces RENGE, a method for inferring gene regulatory networks from time-series scCRISPR data, which outperforms existing methods and produces GRNs consistent with known databases.

Minimal genome-wide human CRISPR-Cas9 library

The paper designs a smaller genome-wide CRISPR-Cas9 library with reduced size while maintaining sensitivity and specificity, enhancing its applicability in complex models.

JACKS: joint analysis of CRISPR/Cas9 knock-out screens

JACKS improves hit identification in CRISPR/Cas9 screens by jointly analyzing data from the same guide RNA library, reducing required cell numbers by 2.5-fold.

Tandem duplications lead to loss of fitness effects in CRISPR-Cas9 data

The paper shows that targeting tandem amplified regions in CRISPR-Cas9 screens reduces cellular fitness, while chromosomal duplications have minimal effects.

Unsupervised correction of gene-independent cell responses to CRISPR-Cas9 targeting

CRISPRcleanR reduces false positives in CRISPR-Cas9 screens by correcting gene-independent responses without assuming copy number status.

A screen for combination therapies in BRAF/NRAS wild type melanoma identifies nilotinib plus MEK inhibitor as a synergistic combination