About

Terry Furey is a Professor of Genetics and Biology at the University of North Carolina at Chapel Hill, serving as the Chair of the CFAC Genomics Core Subcommittee. His research focuses on chromatin and gene regulation, complex traits, inflammatory bowel disease (IBD), toxicogenomics, computational biology, and single-cell genomics. He investigates how chromatin structures influence gene transcription and regulation, integrating high-throughput sequence-based assays with gene expression, transcription factor binding, and epigenetic data to understand the complex processes involved. Furey's work on IBD involves partnering with other researchers to uncover molecular determinants of disease phenotypes, particularly examining how changes in gene expression and chromatin landscapes in intestinal cell types contribute to inflammation. His research also explores environmental toxicogenomics, specifically how exposure to inhalational toxicants like ozone affects cellular function through alterations in chromatin architecture and transcriptional profiles. Using human tissue and mouse models, he aims to identify how genetic variation influences these molecular changes, providing insights into health complications related to environmental exposures.

Research topics

• Biology
• Genetics
• Medicine
• Computer Science
• Internal medicine
• Cell biology
• Endocrinology
• Pathology
• Computational biology
• Cancer research
• Gastroenterology
• Immunology
• Molecular biology

Selected publications

• Myeloid Cell Adhesion Molecule 1 (CADM1) Promotes Proinflammatory Signaling in Human Inflammatory Bowel Diseases.

  UNC Libraries · 2026-01-09

  articleOpen access

  Cytotoxic T cells have been postulated to facilitate the destruction of intestinal epithelium in inflammatory bowel diseases (IBDs). CADM1, which encodes a membrane adhesion protein that can bind the T cell receptor CRTAM, was markedly up regulated in colons of IBD patients compared with non-IBD (NIBD) patients.We performed comprehensive small RNA and RNA profiling on colon tissue from IBD and NIBD control patients in addition to characterizing the serum cleaved ectodomain of CADM1 (sCADM1) function in lamina propria mononuclear cells isolated from these patients. Last, a conditional loss-of-function mouse was developed to assess Cadm1 function in the myeloid compartment during chemical-induced colitis.We identified CADM1 enrichment in multiple immune cell clusters including macrophages and dendritic cells in the colons of IBD patients. Increased numbers of CADM1+ myeloid cells were measured adjacent to CD8+ T cells within colons of ulcerative colitis patients compared with NIBD patients. Conditional deletion of Cadm1 in myeloid cells resulted in reduced numbers of activated T cell populations and protected mice from chemical-induced colitis. Similarly, administration of a Cadm1 "neutralizing" antibody, which binds its extracellular domain reduced tissue inflammation and breakdown of the intestinal epithelium and crypts after induction of colitis in mice. Last, serum levels of sCADM1 were elevated in IBD patients compared with NIBD control subjects and treatment of lamina propria mononuclear cells with recombinant sCADM1 enhanced inflammatory STAT3 phosphorylation.CADM1 is a mediator of proinflammatory signaling cascades in the colon and a potential therapeutic target for the IBDs.

  PublisherDOI

• Fatty Acid Oxidation Suppression Reprograms Fibroblasts in Fibrostenotic Crohn’s Disease

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-10

  articleOpen access

  Abstract Fibrostenotic complications represent a major cause of morbidity in Crohn’s disease (CD), yet the cellular mechanisms that drive intestinal fibrosis independent of active inflammation remain poorly understood. Here, we identify impaired fatty acid oxidation (FAO) as a defining metabolic feature of fibroblasts in fibrostenotic CD. Untargeted lipidomics of non-inflamed colonic tissue from CD patients demonstrated enrichment of triacylglycerols and long-chain acylcarnitines, suggesting altered lipid utilization. Across three independent RNA-sequencing cohorts, including treatment-naïve pediatric ileal biopsies, FAO genes ( CPT1A, CPT2, SLC25A20 ) were selectively downregulated in patients with or destined to develop fibrostenotic disease. Single-cell RNA-sequencing localized these transcriptional alterations specifically to fibroblasts within strictured ileum. Primary fibroblasts derived from fibrostenotic CD exhibited increased neutral lipid accumulation, impaired mitochondrial fatty acid trafficking, and diminished responsiveness to PPARγ-mediated suppression of TGFβ-induced myofibroblast activation. Together, these findings demonstrate that FAO impairment is a conserved, fibroblast-specific metabolic program associated with intestinal fibrosis in CD and suggest that metabolic modulation of stromal cells represents a potential therapeutic strategy for fibrostenotic disease.

  PublisherOA PDFDOI

• eQTL in diseased colon tissue identifies potential target genes associated with IBD

  Nature Communications · 2026-02-13

  articleOpen accessSenior author

  Genome-wide association studies (GWAS) have identified over 300 loci associated with the inflammatory bowel diseases (IBD), but putative causal genes for most loci are unknown. We conducted a disease-focused expression quantitative trait loci (eQTL) analysis using colon tissue from 252 IBD patients. We hypothesized IBD tissue could uncover IBD-associated regulatory variation undetectable in non-IBD cohorts. Here we show a total of 194 potential target genes for 108 IBD loci using eQTL from both IBD and non-IBD colon tissue. eQTL in IBD tissue were enriched for IBD GWAS colocalizations, provided evidence for genes such as ABO and TNFRSF14, and identified additional potential target genes compared to non-IBD tissue eQTL alone. Our results suggest disease state may alter the regulatory landscape and its characteristics, leading to increased effect sizes for some eQTL. These findings highlight the importance of diseased tissue eQTL studies for identifying potential consequences of IBD-associated variants.

  PublisherDOI

• WAD: a wavelet-based linear programming method using L1-minimal reconstruction loss for accessible chromatin data deconvolution

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-01

  preprintOpen accessSenior authorCorresponding

  Abstract Bulk tissue-based accessible chromatin studies provide summary annotations across all cell types within the tissue. These annotations can be skewed by varying proportions of individual cell types, especially in the context of disease studies. Estimated sample specific cell-type proportions can be used to mitigate effects of this variability while also addressing whether there exist significant alterations in cell proportions under certain conditions, like disease. We present WAD (Wavelet-based Accessible chromatin Deconvolution), a principled framework for robust estimation of cell type composition of bulk accessible chromatin data such as from the ATAC-seq assay. To determine informative reference cell profiles from single-cell accessible chromatin studies, WAD leverages wavelet-based denoising to suppress stochastic noise while preserving local chromatin continuity. Cell type proportion inference is reformulated as an L 1 -minimal linear programming problem, enabling scalable and interpretable solutions. Across 700 in silico pseudo-bulk mixtures generated from single-cell data, WAD achieved a consistently lower mean absolute error (MAE) and higher concordance ( r > 0.85) than existing machine learning-based methods. These results demonstrate that wavelet-based feature extraction provides a biologically grounded and computationally efficient approach to chromatin signal deconvolution. A complete implementation of WAD is available at https://github.com/chae-jh/WAD .

  PublisherOA PDFDOI

• Genome-Wide Uncertainty-Moderated Extraction of Signal Annotations from Multi-Sample Functional Genomics Data

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-08

  preprintOpen accessSenior authorCorresponding

  We present Consenrich, a simple but principled technique for genome-wide estimation of signals hidden in noisy multi-sample sequencing-based functional genomics datasets. Consenrich appeals to a sequential prediction-correction framework and models both the spatial dependencies between proximal loci and regional, sample-specific noise processes that corrupt sequencing data. Experiments reveal distinct improvement compared to benchmarks in a series of challenging estimation problems, where noisy functional genomics data samples must be reconciled. We further highlight the immediate practical appeal of this refined signal extraction for differential analyses between disease conditions and identification of functionally enriched genomic regions. A complete implementation of Consenrich is hosted at https://github.com/nolan-h-hamilton/Consenrich.

  PublisherOA PDFDOI

• Liver single-nucleus multiome profiling reveals cell-type mechanisms for cardiometabolic traits

  The American Journal of Human Genetics · 2025-12-02

  articleOpen access

  The liver is a central regulator of cardiometabolic physiology, coordinating processes such as lipid and glucose metabolism, protein synthesis, and detoxification. Genome-wide association studies (GWASs) have identified hundreds of genetic variants associated with cardiometabolic traits, yet their molecular mechanisms in liver cell types remain unclear. Using multiome gene expression and accessible chromatin sequencing on liver samples from 39 individuals, we profiled gene expression and chromatin accessibility in 68,398 nuclei across six primary liver cell types. We identified 306,706 accessible chromatin regions, including 70,884 regions that were undetected in bulk tissue analyses and predominantly represent less abundant cell types. To identify genetic effects on gene regulation in liver cell types, we mapped quantitative trait loci (QTLs) and detected 1,885 chromatin accessibility QTLs (caQTLs) and 67 expression QTLs (eQTLs). We integrated cell-type QTLs with GWAS signals and revealed cell types, genes, and chromatin regulatory elements involved in cardiometabolic traits, such as liver enzyme and cholesterol levels. Non-hepatocyte cell-type QTL analyses exposed previously obscured mechanisms, such as an eQTL for ADAMTS12 in liver sinusoidal endothelial cells potentially involved in liver fibrosis, demonstrating that single-nucleus approaches can capture regulatory events missed in bulk analyses. Furthermore, we predicted the cell type of action for bulk liver caQTLs colocalized with GWAS signals, enhancing mechanistic insights for complex trait associations. Our findings provide a high-resolution map of the hepatic regulatory landscape and advance the understanding of cellular contexts and molecular mechanisms underlying cardiometabolic traits.

  PublisherDOI

• Subcutaneous adipose tissue splice quantitative trait loci reveal differences in isoform usage associated with cardiometabolic traits

  UNC Libraries · 2025-11-08

  articleOpen accessSenior author
  PublisherDOI

• A machine learning approach identifies 5-ASA and ulcerative colitis as being linked with higher COVID-19 mortality in patients with IBD

  UNC Libraries · 2025-06-25

  articleOpen access1st authorCorresponding
  PublisherDOI

• Reference-guided Genome Assembly of Long Non-coding RNA Transcripts Reveals Target Genes Associated With Crohn’s Disease

  Scientific Reports · 2025-10-01

  preprintOpen accessSenior authorCorresponding

  Abstract Crohn’s disease (CD) is highly heterogeneous in presentation and progression with no cure. Molecular phenotyping has been used to elucidate cellular and tissue-based alterations to characterize drivers and effects of disease. One currently understudied class of functional molecules is long non-coding RNAs (lncRNAs). Studying the full lncRNA landscape in IBD is challenging due in part to an incomplete lncRNA annotation and a lack of their functional characterization in tissues of interest. We used a genome-guided alignment strategy to assemble predicted lncRNA transcripts using short RNA-sequencing data from colon tissue of adult patient samples. When combining our predicted lncRNAs with previous lncRNA annotations, we determined 98 that were differentially expressed, recapitulating many from previous IBD studies while also uncovering new ones. We built gene co-expression networks to cluster lncRNAs with functionally characterized protein-coding genes. Clusters containing differential lncRNAs were correlated to disease status and associated with pathways related to the humoral immune response, metabolism, and tissue regeneration. We uncovered multiple differential lncRNAs whose expression significantly correlated with nearby differential protein-coding genes that have also been differentially expressed in other IBD datasets, such as PITX2 . We focused on a predicted lncRNA that is antisense to the PITX2-adjacent lncRNA PANCR , which we called PANCR-AS1 , and provide multiple lines of evidence that support PANCR-AS1 functioning as an enhancer of PITX2 expression. Overall, we determined lncRNAs that are potential contributors to CD pathogenesis. We developed a robust pipeline for identifying lncRNAs in diseased and non-diseased tissue that are absent from reference annotations. We also outlined a framework to pinpoint significant disease-associated lncRNAs with potential functional activity related to their nearby protein-coding genes.

  PublisherDOI

• Myeloid Cell Adhesion Molecule 1 (CADM1) Promotes Proinflammatory Signaling in Human Inflammatory Bowel Diseases

  Cellular and Molecular Gastroenterology and Hepatology · 2025-08-27 · 3 citations

  articleOpen access

  BACKGROUND & AIMS: Cytotoxic T cells have been postulated to facilitate the destruction of intestinal epithelium in inflammatory bowel diseases (IBDs). CADM1, which encodes a membrane adhesion protein that can bind the T cell receptor CRTAM, was markedly up regulated in colons of IBD patients compared with non-IBD (NIBD) patients. METHODS: We performed comprehensive small RNA and RNA profiling on colon tissue from IBD and NIBD control patients in addition to characterizing the serum cleaved ectodomain of CADM1 (sCADM1) function in lamina propria mononuclear cells isolated from these patients. Last, a conditional loss-of-function mouse was developed to assess Cadm1 function in the myeloid compartment during chemical-induced colitis. RESULTS: T cells within colons of ulcerative colitis patients compared with NIBD patients. Conditional deletion of Cadm1 in myeloid cells resulted in reduced numbers of activated T cell populations and protected mice from chemical-induced colitis. Similarly, administration of a Cadm1 "neutralizing" antibody, which binds its extracellular domain reduced tissue inflammation and breakdown of the intestinal epithelium and crypts after induction of colitis in mice. Last, serum levels of sCADM1 were elevated in IBD patients compared with NIBD control subjects and treatment of lamina propria mononuclear cells with recombinant sCADM1 enhanced inflammatory STAT3 phosphorylation. CONCLUSIONS: CADM1 is a mediator of proinflammatory signaling cascades in the colon and a potential therapeutic target for the IBDs.

  PublisherDOI

Recent grants

• High throughput functional studies of IBD-associated GWAS variants

  NIH · $2.6M · 2023–2027

• NIH Grant R01ES023195

  NIH · $2.2M · 2018

• Interpreting molecular role of DNA variants associated with Crohn's Disease through integrative analysis of open chromatin, epigenome and transcriptome data in diverse and relevant tissues and cells

  NIH · $588k · 2014–2017

• Integrative Genetic and Genomic Analyses in the Inflammatory Bowel Disease

  NIH · $901k · 2016–2020

Frequent coauthors

• Gregory E. Crawford

  Durham Technical Community College

  66 shared

• Shehzad Z. Sheikh

  University of North Carolina at Chapel Hill

  57 shared

• David Haussler

  University of California, Santa Cruz

  53 shared

• Lingyun Song

  51 shared

• W. James Kent

  University of California, Santa Cruz

  40 shared

• Krishna M. Roskin

  University of Cincinnati

  38 shared

• Nathan C. Sheffield

  University of Virginia

  37 shared

• Matthew R. Schaner

  University of North Carolina at Chapel Hill

  34 shared

Education

• Ph.D., Toxicology

  University of North Carolina at Chapel Hill

  1990

• M.S., Toxicology

  University of North Carolina at Chapel Hill

  1985

• B.S., Toxicology

  University of North Carolina at Chapel Hill

  1983