Zhigang Cai

The paper introduces CauNagi, a causal machine learning tool, to identify causal drivers of VEXAS syndrome using single-cell transcriptomic data, revealing key regulatory hubs involved in myeloid dysfunction.

This paper uses single-cell RNA sequencing to analyze cellular changes in Lynch Syndrome colorectal cancer, identifying cancer stem cells, immune infiltration, and mutation burden during malignant transition.

This study shows that neutrophil loss of Uba1 in mice causes VEXAS-like autoinflammatory disease, with symptoms including increased neutrophils, cytokines, and vacuoles.

This study uses scRNA-seq to show that loss of Morrbid reduces osteoclasts and inflammation in a mouse model of CRMO, suggesting it as a therapeutic target for osteomyelitis.

This study uses single-cell and spatial transcriptomics to analyze granuloma formation in a natural CGD mouse model and identifies therapeutic targets.

This study shows that Zbtb33 knockout in mice does not induce clonal hematopoiesis but influences tumor immunity and the tumor microenvironment.

This study introduces a computational pipeline to quantify hematopoietic cell plasticity using single-cell RNA-seq data and identifies factors influencing plasticity under genetic and environmental stress.

This study shows that clonal hematopoiesis driven by TET2 mutations interacts with inflammatory signals like PTX3/IL-1β to promote colitis and leukemia through a gut-bone marrow axis.