Kathryn Miller‐Jensen

Interferon-β paracrine signaling mediates synergy between TLR3 and TRIF-independent TLR pathways

This study investigates how TLR2 and TLR3 signaling in macrophages synergistically activate cytokines, showing that IFN-β paracrine signaling mediates some of this synergy.

Interplay between cytokine and FGF2 signaling in induction of entosis and vasculogenic mimicry response in glioblastoma

This study investigates the role of cytokine and FGF2 signaling in inducing entosis and vasculogenic mimicry in glioblastoma, linking macrophage activity to alternative vascularization mechanisms.

Multiomics reveals age-dependent metabolic reprogramming of macrophages by wound bed niche secreted signals

This paper identifies age-dependent metabolic reprogramming in wound macrophages driven by niche secreted signals using multi-omics approaches.

Mapping intratumoral myeloid-T cell interactomes at single-cell resolution reveals targets for overcoming checkpoint inhibitor resistance

The paper develops a computational method to analyze single-cell RNA-seq data to study cell-cell interactions in tumors, showing that CD40 agonist enhances immune checkpoint blockade by modulating myeloid-T cell interactions.

A transcriptional cycling model recapitulates chromatin-dependent features of noisy inducible transcription

The paper develops a transcriptional cycling model to study how chromatin states influence transcriptional noise and viral activation in response to environmental cues.

TNF stimulation primarily modulates transcriptional burst size of NF-κB-regulated genes

The paper investigates how TNF stimulation affects transcriptional noise in NF-κB-regulated genes, finding that it primarily increases burst size rather than frequency.

Fold-change detection of NF-κB at target genes with different transcript outputs

The paper investigates fold-change detection of NF-κB at low and high abundance target genes in single cells and finds that transcriptional noise and promoter-bound NF-κB levels differ from model predictions.

Systems analysis by mass cytometry identifies susceptibility of latent HIV-infected T cells to targeting of p38 and mTOR pathways