Tracy Yamawaki

The paper identifies a compact regulatory logic governing fibroblast plasticity in fibrosis by analyzing enhancer repression and gene perturbations across multiple tissues.

This study shows that FAP-targeted BiTE(R) molecules, intended to reduce cardiac fibrosis, instead worsen heart function by triggering harmful immune responses.

Single-cell and spatial maps of human coronary arteries identify FAP as a marker of SMC-derived modulated cells; an anti-FAP BiTE reduced plaque burden in mouse models.

This study identifies RUNX1 as a key regulator of cardiac recovery by reprogramming macrophages, showing that its inhibition promotes heart function recovery in a chronic heart failure model.

The paper identifies bZIP transcription factors as key regulators of IL-2-induced Treg activation, linking chromatin accessibility changes to Th1/Th2 molecular phenotypes and metabolic pathways.

This paper links CAD GWAS variants to causal genes in SMCs using single-cell chromatin accessibility and Hi-C data, creating a scV2E2G map for disease mechanism discovery.

The paper identifies causal genes in heart disease GWAS loci by integrating Hi-C, chromatin accessibility, and transcriptomic data, revealing regulatory relationships in cardiac fibroblasts.

The paper introduces an imaging-free spatial transcriptomics technique called STRP-seq, validated on murine and lizard brains, revealing regional molecular anatomy.

The paper profiles small RNA expression in LPS-stimulated human monocytes and identifies a limited set of miRNAs upregulated during inflammation.