Pelin Yaşar

This paper presents a protocol using single-molecule imaging to measure how endocrine disruptors affect transcriptional bursting in human breast cancer cells.

The paper shows that hormone response magnitude in mammary organoids and ER+ cancer cells varies independently of receptor abundance and follows distinct activation dynamics.

The paper identifies H3K27me3 chromatin heterogeneity as a mechanism underlying variable TFF1 expression and endocrine resistance in ER+ breast cancer.

The paper identifies CXXC5 as a ubiquitinated protein degraded by the ubiquitin-proteasome pathway, independent of cell cycle phases.

The paper investigates how altered ERα function and cofactor recruitment affect transcriptional bursting in estrogen responsive genes, finding gene-specific reductions in active alleles in BPA-treated cells.