Tomoya Isobe

Single-Cell Proteo-Transcriptomic Profiling Uncovers Post-Translational Regulatory Layers in Human Hematopoiesis

This paper uses single-cell proteo-transcriptomic profiling to reveal post-translational regulatory mechanisms in human hematopoiesis, showing that protein-RNA correlations and transcription factor dynamics provide insights into lineage commitment and fate decisions.

DNA barcoding-based paired daughter cell analysis reveals division preferences of hematopoietic stem cells

The paper develops a DNA barcoding-based method to analyze HSC daughter cell pairs, revealing biased division patterns toward symmetric divisions and linking these to molecular features.

LDB1-dependent enhancer connectivity defines T-cell leukemia identities and masks metabolic vulnerabilities

The paper identifies LDB1-dependent enhancer connectivity as critical for T-cell leukemia subtypes and reveals a metabolic vulnerability exploitable by statins.

MECOM promotes leukemia progression and inhibits mast cell differentiation through functional competition with GATA2

This study shows that MECOM mutations impair DNA binding and functionally antagonize GATA2, promoting leukemia and inhibiting mast cell differentiation.

Self-supervised learning for a gene program-centric view of cell states

Tripso, a self-supervised transformer model, identifies gene program-specific embeddings and discovers novel gene programs, revealing biological insights in hematopoietic development and disease.

Predicting how perturbations reshape cellular trajectories with PerturbGen

PerturbGen predicts how genetic perturbations affect cellular trajectories across time in human datasets, showing effects on immune responses, hematopoiesis, and skin development.

diffGEK: Differential Gene Expression Kinetics

diffGEK compares transcriptional kinetics across biological conditions to identify mechanistic differences in gene expression dynamics.

CH-related Mutant ASXL1 Promotes Atherosclerosis in Mice via Dysregulated Innate Immunity

This study shows that ASXL1 mutations in mice promote atherosclerosis by dysregulating innate immunity through impaired inhibition of NF-κB signaling.