Benjamin David Singer

The paper investigates the role of maintenance DNA methylation in age-related changes in Treg cell transcriptional and DNA methylation signatures using UHRF1-deficient mice.

This study identifies distinct pneumonia endotypes based on pathogen-specific host responses in the lung, linking them to clinical outcomes and suggesting personalized treatment strategies.

The paper identifies transcriptional and methylation signatures in umbilical cord blood linked to BPD risk in preterm infants.

This paper introduces RREM-seq, an enzyme-based reduced representation DNA methylation sequencing method that enables high-resolution profiling of low-input samples, including clinical specimens.

This study shows that FOXP3+ Treg cells use TBET to control activated CD8+ T cells during influenza recovery, but not Trm cell generation.

This study shows AMPK is necessary for Treg cell adaptation to metabolic stress in tumors and lung injury but not for baseline immune homeostasis.

This study shows that DNA methylation via UHRF1 is essential for iTregs to promote lung recovery after viral pneumonia.

This study identifies CRAMP1 as a selective regulator of histone H1 expression by interacting with GON4L in the histone locus body.

The paper examines alveolar T cell responses in SARS-CoV-2 pneumonia patients, finding that early interferon signaling and targeting of structural proteins correlate with better clinical outcomes.

This study uses bulk RNA-seq to identify inflammatory phenotypes in ataxia telangiectasia by analyzing peripheral blood mononuclear cells.

The paper identifies a systemic age-dependent transcriptome imbalance driven by transcript length across multiple species and shows its correlation with splicing factors and environmental stressors.

The paper identifies cancer-specific CTCF binding patterns across six cancer types and shows they are linked to oncogenic transcriptional changes without always involving DNA methylation or mutations.

Single-cell RNA-seq of lung tissue from transplant donors, fibrosis patients, and a living patient identifies cell type-specific disease-associated molecular pathways in pulmonary fibrosis.