Brandon Hadland

This study uses behavioromic analysis to predict hematopoietic stem cell fate with high accuracy and identifies Activin signaling's role in cell behavior and fate.

This study identifies a developmental program for hematopoietic stem cell (HSC) dormancy established during embryogenesis through evasion of Notch signaling, revealing a mechanism for long-term regenerative potential.

This study shows that syndecan-2 in mesenchymal stromal cells, but not endothelial cells, supports HSC self-renewal and cytokine responses by modulating growth factor signaling.

This study shows that inhibiting farnesyltransferase reduces the ex vivo expansion of human and mouse hematopoietic stem cells.

This paper introduces a computer vision platform that detects live mutant blood cells with specific mutations using morphology recognition, without requiring nucleic acid sequencing.

The paper maps single-cell dynamics of endothelial-to-hematopoietic transition from iPSCs and identifies FGF signaling modulation to improve hematopoietic output.

This study investigates how hydrostatic pressure modulates endothelial cell responses to flow, showing pressure alters shear-induced signaling and transcriptional changes in human and mouse ECs.

This study uses sci-Plex to analyze how Activin and BMP4 gradients affect mesoderm patterning and hemogenic endothelial cell production in mouse embryonic stem cells.

The paper identifies rare fetal liver HSCs with unique features like differentiation latency and dormancy signatures using single cell RNA-sequencing and a niche-mimicking culture platform.

The paper shows that multipotent progenitors and HSC arise from distinct HE populations during mouse embryogenesis, identified through clonal assays and single-cell transcriptomics.

The paper identifies key signaling molecules involved in HSC development by analyzing single-cell transcriptomics data from AGM-derived cells and uses them to engineer a supportive niche for HSC generation.