About

Danny T.Y. Wu, PhD, MSI, FAMIA, is an Associate Professor at the School of Information and Library Science (SILS) at the University of North Carolina at Chapel Hill. He is also a core faculty member of the Carolina Health Informatics Program (CHIP) and serves as volunteer faculty at the University of Cincinnati College of Medicine (UCCoM). Dr. Wu earned his PhD in Information from the University of Michigan School of Information (UMSI) in 2016, where he also completed his MS in Information Analysis and Retrieval in 2011. Prior to that, he obtained a BBA in Information Management from the College of Management at National Taiwan University in 2003. His academic and professional roles reflect a strong interdisciplinary focus on information science and health informatics, contributing to research and education at the intersection of these fields.

Research topics

• Biology
• Machine Learning
• Artificial Intelligence
• Data Mining
• Computer Science
• Genetics
• Chemistry
• Demography
• Algorithm
• Cell biology
• Psychiatry
• Biochemistry
• Computational biology
• Statistics
• Cancer research
• Internal medicine
• Medicine
• Mathematics
• Psychology
• Pediatrics
• Immunology

Selected publications

• The RING Finger E3 Ligase RNF25 Protects DNA Replication Forks Independently of its Canonical Roles in Ubiquitin Signaling

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-09 · 1 citations

  preprintOpen access

  The DNA damage response (DDR) mechanisms that allow cells to tolerate DNA replication stress are critically important for genome stability and cell viability. Using an unbiased genetic screen we identify a role for the RING finger E3 ubiquitin ligase RNF25 in promoting DNA replication stress tolerance. In response to DNA replication stress, RNF25-deficient cells generate aberrantly high levels of single-stranded DNA (ssDNA), accumulate in S-phase and show reduced mitotic entry. Using single-molecule DNA fiber analysis, we show that RNF25 protects reversed DNA replication forks generated by the fork remodeler HLTF from nucleolytic degradation by MRE11 and CtIP. Mechanistically, RNF25 interacts with the replication fork protection factor REV7 and recruits REV7 to nascent DNA after replication stress. The role of RNF25 in protecting replication forks is fully separable from its canonical functions in ubiquitin conjugation. This work reveals the RNF25-REV7 signaling axis as an important protective mechanism in cells experiencing replication stress.

  PublisherOA PDFDOI

• Same‐day emergencies in endodontic specialists' practice: Before, during and after the <scp>COVID</scp> ‐19 pandemic

  International Endodontic Journal · 2025-03-20

  articleOpen access

  AIM: The COVID-19 pandemic affected practice in endodontic offices. Same-day endodontic emergencies are cases with moderate or severe self-reported pain who request an unscheduled visit on the day they contact the office. The aims of this observational study were to: (A) analyse the rate of same-day endodontic emergencies in two endodontists' private offices, with respect to their demographic, aetiologic, diagnostic and procedural data; and (B) investigate the changes in characteristics of same-day emergencies between March 16 and May 31 annually over five years: 2019-2023. METHODOLOGY: Records of 5795 patients were reviewed and 892 same-day emergencies were identified. Overall and year-to-year comparisons of proportions of same-day emergencies, as well as demographic, aetiologic, diagnostic and procedural data were performed using chi-square test of independence followed by adjustments for multiple testing using the Benjamini-Hochberg method. RESULTS: The rate of same-day endodontic emergencies significantly increased during the initial outbreak of COVID-19 in 2020 and remained high in 2021 (p < .05; Q < .05). The rate of same-day emergencies in 2022 subsided to levels comparable to 2019 (p > .05). Year-to-year comparisons of aetiologic factors (caries, restorative, persistent infection and cracks) showed a significant increase only in the rate of cracks in 2020, 2021and 2022 compared with 2019 (p < .05), but this increase did not reach the significance level after adjusting for multiple comparisons throughout the 5 years (Q > .05). CONCLUSIONS: The COVID-19 pandemic was associated with a significant increase in the rate of same-day endodontic emergencies for 2 years. The spike in endodontic emergencies associated with the COVID-19 pandemic lasted well beyond the initial period of the outbreak. Further national and international studies are recommended to better understand the long-term impacts of pandemics of respiratory diseases on the public's oral health.

  PublisherOA PDFDOI

• High-dimensional Biomarker Identification for Interpretable Disease Prediction via Machine Learning Models

  UNC Libraries · 2025-05-08

  articleOpen access

  MOTIVATION: Omics features, often measured by high-throughput technologies, combined with clinical features, significantly impact the understanding of many complex human diseases. Integrating key omics biomarkers with clinical risk factors is essential for elucidating disease mechanisms, advancing early diagnosis, and enhancing precision medicine. However, the high dimensionality and intricate associations between disease outcomes and omics profiles present substantial analytical challenges. RESULTS: We propose a High-dimensional Feature Importance Test (HiFIT) framework to address these challenges. Specifically, we develop an ensemble data-driven biomarker identification tool, Hybrid Feature Screening (HFS), to construct a candidate feature set for downstream machine learning models. The pre-screened candidate features from HFS are further refined using a computationally efficient permutation-based feature importance test employing machine learning methods to flexibly model the potential complex associations between disease outcomes and molecular biomarkers. Through extensive numerical simulation studies and practical applications to microbiome-associated weight changes following bariatric surgery, as well as the examination of gene-expression-associated kidney pan-cancer survival data, we demonstrate HiFIT's superior performance in both outcome prediction and feature importance identification. AVAILABILITY AND IMPLEMENTATION: An R package implementing the HiFIT algorithm is available on GitHub (https://github.com/BZou-lab/HiFIT). SUPPLEMENTARY INFORMATION: Supplementary materials are available at Bioinformatics online.

  PublisherDOI

• The RING finger E3 ligase RNF25 protects DNA replication forks independently of its canonical roles in ubiquitin signaling

  Nature Communications · 2025-08-05 · 2 citations

  articleOpen access

  The DNA damage response (DDR) mechanisms that allow cells to tolerate DNA replication stress are critically important for genome stability and cell viability. Using an unbiased genetic screen, we identify a role for the RING finger E3 ubiquitin ligase RNF25 in promoting DNA replication stress tolerance. In response to DNA replication stress, RNF25-deficient cells generate aberrantly high levels of single-stranded DNA (ssDNA), accumulate in S-phase and show reduced mitotic entry. Using single-molecule DNA fiber analysis, we show that RNF25 protects reversed DNA replication forks generated by the fork remodeler HLTF from nucleolytic degradation by MRE11 and CtIP. Mechanistically, RNF25 interacts with the replication fork protection factor REV7 and recruits REV7 to nascent DNA after replication stress. The role of RNF25 in protecting replication forks is fully separable from its canonical functions in ubiquitin conjugation. This work reveals the RNF25-REV7 signaling axis as an important protective mechanism in cells experiencing replication stress.

  PublisherDOI

• Impact of HLA-DPB1 and DPA1-DPB1 linkage mismatch on survival in HLA-14/14 matched unrelated donor HSCT: establishment and clinical validation of a predictive model based on NGS technology

  Human Immunology · 2025-09-01

  article
  PublisherDOI

• Berberine Ameliorates Pulmonary Fibrosis by Inactivating the Thrombospondin 2/Smad Homolog 2/3 Pathway

  Chemical Biology & Drug Design · 2025-04-01 · 3 citations

  article

  Pulmonary fibrosis (PF) is a progressive and irreversible lung disease. Previous studies have shown that berberine (BBR) ameliorates PF; however, the mechanism of BBR regulating PF remains unclear. mRNA expression of thrombospondin 2 (THBS2) was analyzed by quantitative real-time polymerase chain reaction. Protein expression level was detected by western blotting assay or immunohistochemistry assay. Cell function was analyzed using cell counting kit-8 assay, 5Ethynyl-2'-deoxyuridine assay, transwell invasion assay, wound-healing assay, enzyme-linked immunosorbent assays, and colorimetric assay. PF mouse model was established using bleomycin (BLM) to analyze the effect of BBR on PF. The results showed that THBS2 expression was upregulated in the lung tissues of BLM-induced PF mice and transforming growth factor-β1 (TGF-β1)-induced HLF cells. BBR ameliorated BLM-induced PF in vivo. TGF-β1 treatment induced HLF cell proliferation, invasion, migration, inflammation response, and oxidative stress, accompanied by increases in collagen I, fibronectin, and α-SMA protein expression; however, these effects were attenuated after THBS2 silencing. In addition, BBR attenuated TGF-β1-induced pro-fibrotic phenotypes of HLF cells and BLM-induced PF through the inactivation of the THBS2/Smad2/3 pathway. Thus, BBR inhibited BLM-induced PF by inactivating the THBS2/Smad2/3 pathway, providing a theoretical basis for PF treatment with BBR.

  PublisherDOI

• Fundamentals of Omics Applications in the Study of Common Oral Diseases

  Springer series on biofilms · 2025-01-01

  book-chapterSenior author
  PublisherDOI

• CD38⁺ Endothelial Remodeling Defines Spatially Diverse Vasculopathy Programs in Rapidly Advancing Oral Inflammation

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-08-01 · 1 citations

  preprintOpen access

  Oral inflammatory diseases affect nearly half of the global population. Among them, newly defined peri-implantitis and high-grade periodontitis represent rapidly advancing inflammatory disease types, marked by relatively rapid tissue destruction. Despite their prevalence, the cell mechanisms and spatial architecture driving this severity remain poorly understood. Focusing first on peri-implantitis versus low- and moderate-grade periodontitis, we applied microbial profiling, single-cell RNA sequencing (scRNA-seq), and spatial proteomics (sp-proteomics) to uncover shared pathogenic programs linked to accelerated niche breakdown. Furthermore, to preserve spatial fidelity, each tissue was anatomically orientated along the tooth- or implant-epithelial interface, analogous sites of disease origination. Laser capture microdissection followed by microbiome analysis of unique tissue compartments revealed reduced bacterial load and diversity in peri-implantitis stroma. We then expanded our version-1 Human Periodontal Atlas by integrating newly generated peri-implantitis scRNAseq data (36-total samples; 121395-cells), revealing widespread transcriptional alterations, including oxidative stress, hypoxic, and NAD+ metabolism-associated signatures, primarily in a subpopulation of TNFRSF6B+/ICAM1+ post-capillary venules. We then performed high-resolution sp-proteomics (15-total samples; 337260-cells) and analyzed VEC states and associated neighborhoods via AstroSuite using newly developed tri-wise spatial analysis. This revealed CD34+-VEC loss and CD38+-VEC expansion almost exclusively in peri-implantitis. We extended this analysis to high-grade periodontitis. Mucosal biopsies from four lesion-affected and four unaffected sites within the same individuals (1:1 matched; 8 samples; 225137-cells) again demonstrated spatially restricted CD38+-VEC remodeling exclusively in affected tissues, with similar vasculopathy front patterning. The findings nominate spatially distinct vasculopathy patterning as a hallmark of rapidly advancing oral inflammation and a targetable therapeutic axis.

  PublisherOA PDFDOI

• High-dimensional biomarker identification for interpretable disease prediction via machine learning models

  Bioinformatics · 2025-04-25 · 5 citations

  articleOpen access

  MOTIVATION: Omics features, often measured by high-throughput technologies, combined with clinical features, significantly impact the understanding of many complex human diseases. Integrating key omics biomarkers with clinical risk factors is essential for elucidating disease mechanisms, advancing early diagnosis, and enhancing precision medicine. However, the high dimensionality and intricate associations between disease outcomes and omics profiles present substantial analytical challenges. RESULTS: We propose a high-dimensional feature importance test (HiFIT) framework to address these challenges. Specifically, we develop an ensemble data-driven biomarker identification tool, Hybrid Feature Screening (HFS), to construct a candidate feature set for downstream machine learning models. The pre-screened candidate features from HFS are further refined using a computationally efficient permutation-based feature importance test employing machine learning methods to flexibly model the potential complex associations between disease outcomes and molecular biomarkers. Through extensive numerical simulation studies and practical applications to microbiome-associated weight changes following bariatric surgery, as well as the examination of gene-expression-associated kidney pan-cancer survival data, we demonstrate HiFIT's superior performance in both outcome prediction and feature importance identification. AVAILABILITY AND IMPLEMENTATION: An R package implementing the HiFIT algorithm is available on GitHub (https://github.com/BZou-lab/HiFIT).

  PublisherOA PDFDOI

• Rad18 mediates specific mutational signatures and shapes the genomic landscape of carcinogen-induced tumors in vivo

  UNC Libraries · 2025-11-18

  articleOpen access

  The E3 ubiquitin ligase Rad18 promotes a damage-tolerant and error-prone mode of DNA replication termed trans-lesion synthesis that is pathologically activated in cancer. However, the impact of vertebrate <em>Rad18</em> on cancer genomes is not known. To determine how Rad18 affects mutagenesis <em>in vivo</em>, we have developed and implemented a novel computational pipeline to analyze genomes of carcinogen (7, 12-Dimethylbenz[a]anthracene, DMBA)-induced skin tumors from <em>Rad18^+/+</em> and <em>Rad18^- ^/ ^-</em> mice. We show that <em>Rad18</em> mediates specific mutational signatures characterized by high levels of A(T)&gt;T(A) single nucleotide variations (SNVs). In <em>Rad18^- ^/-</em> tumors, an alternative mutation pattern arises, which is characterized by increased numbers of deletions &gt;4 bp. Comparison with annotated human mutational signatures shows that COSMIC signature 22 predominates in <em>Rad18^+/+</em> tumors whereas <em>Rad18^- ^/ ^-</em> tumors are characterized by increased contribution of COSMIC signature 3 (a hallmark of BRCA-mutant tumors). Analysis of The Cancer Genome Atlas shows that <em>RAD18</em> expression is strongly associated with high SNV burdens, suggesting RAD18 also promotes mutagenesis in human cancers. Taken together, our results show Rad18 promotes mutagenesis <em>in vivo</em>, modulates DNA repair pathway choice in neoplastic cells, and mediates specific mutational signatures that are present in human tumors.

  PublisherDOI

Recent grants

• Investigating the microbial basis of early childhood caries via metagenomics and metatranscriptomics analyses

  NIH · $299k · 2019–2022

Frequent coauthors

• Michael I. Love

  University of North Carolina at Chapel Hill

  30 shared

• Kimon Divaris

  28 shared

• Qisheng Gu

  28 shared

• Katherine A. Hoadley

  27 shared

• C. Ryan Miller

  University of Alabama at Birmingham

  27 shared

• Melissa A. Troester

  University of North Carolina at Chapel Hill

  27 shared

• Markia A. Smith

  26 shared

• Andrea Walens

  26 shared

Labs

• Equity in Making (EITM) LabPI

Awards & honors

• Fellow of the American Medical Informatics Association (FAMI…