Gilad Barshad

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.

The paper identifies disease-driving SNPs in JIA risk haplotypes using functional genomic data and genotyping, and links them to target genes through chromatin interactions.

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

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.

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 uses a split mDHFR PCA assay to assess how disease-causing mutations in OXPHOS complex I subunits affect their physical interactions.

The paper examines co-expression of mitochondrial and nuclear OXPHOS genes across human tissues, finding positive co-expression in most tissues but negative correlation in ancient brain regions.