Edward J. Rice

The paper introduces a model-based framework to compare promoter-proximal pausing dynamics across biological contexts, revealing kinetic and distributional variations in pausing.

The paper identifies candidate causal SNPs and target genes in CD4+ T cells for juvenile idiopathic arthritis using GWAS data, chromatin accessibility, and functional assays.

This study investigates enhancer-promoter contact architecture and communication, finding that RNA polymerase II and PARP1 activity stabilize these contacts.

This study identifies a GDNF-RET-EGR1 positive feedback loop that promotes tamoxifen resistance in breast cancer by upregulating cyclin D1.

The paper investigates how A-MYB and BRDT regulate RNA polymerase II pause release during meiotic prophase I, linking transcriptional bursts to chromatin changes and recombination.

This study uses genetic variation in mice to show how DNA sequence affects RNA Polymerase II positioning and transcription dynamics across the genome.

The paper shows that RNA Pol II pausing is essential for proper pluripotency transitions in mouse embryos by maintaining balance between gene expression states.

The paper examines evolutionary changes in ANTXR2 expression in humans, finding regulatory changes and recent positive selection linked to adaptation to anthrax disease.

The paper predicts enhancer activity in sea urchin embryos using chromatin accessibility, transcription, and Pol II data, finding Pol II distribution is the best predictor for promoter-overlapping elements.

The paper introduces a method to estimate RNA half-lives using PRO-seq and RNA-seq data, finding correlations between RNA stability and splicing, miRNA binding, DNA methylation, and histone modifications.

A precision run-on sequencing (PRO-seq) variant with one streptavidin bead binding and on-bead enzymatic steps yields adapter-ligated cDNA in about 10 h and libraries from 0.05–0.25 × 10^6 cells.

The paper uses machine learning to show that transcription predicts histone marks and chromatin states, and that transcription is required for maintaining active and repressive histone modifications.

This study introduces ChRO-seq to map nascent transcription in glioblastoma and identifies enhancers and transcription factors driving GBM subtypes and clinical outcomes.

The paper compares nascent transcription in primates to identify evolutionary patterns in coding and non-coding transcription, finding that transcription factor binding sites and adaptive substitutions drive species-specific differences.

The paper uses deep sequencing to analyze mtDNA transcription in human and metazoan organisms, revealing conserved pausing sites and divergence across species.