The journey of RNA polymerase II (Pol II) as it transcribes a gene is anything but a smooth
ride. Transcript elongation is discontinuous and can be perturbed by intrinsic regulatory …

To ward off against the catastrophic consequences of persistent DNA double-strand breaks
(DSBs), eukaryotic cells have developed a set of complex signaling networks that detect …

The SWI/SNF family of ATP-dependent chromatin remodeling complexes is implicated in
multiple DNA damage response mechanisms and frequently mutated in cancer. The BAF …

DNA damage shuts down genome-wide transcription to prevent transcriptional mutagenesis
and to initiate repair signalling, but the mechanism to stall elongating RNA polymerase II …

DNA double‐strand break (DSB) is a serious type of DNA damage and is known to trigger
multiple responses within cells. In these responses, novel relationships among DSB, DSB …

DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is a pleiotropic protein kinase
that plays critical roles in cellular processes fundamental to cancer. DNA-PKcs expression …

Genome integrity is constantly challenged by endogenous and exogenous insults that cause
DNA damage. To cope with these threats, cells have a surveillance mechanism, known as …

Transcription-blocking DNA lesions (TBLs) in genomic DNA are triggered by a wide variety
of DNA-damaging agents. Such lesions cause stalling of elongating RNA polymerase II …

Defective double-strand break (DSB) repair leads to genomic instabilities that may augment
carcinogenesis. DSBs trigger transient transcriptional silencing in the vicinity of …

A DNA double-strand break (DSB) jeopardizes genome integrity and endangers cell
viability. Actively transcribed genes are particularly detrimental if broken and need to be …