Herpes simplex ICP4 preferentially binds to and delineates the viral genome, ultimately resulting in robust viral transcription at the expense of the host.

Inactivation of KAP1 by mTOR-mediated phosphorylation releases human cytomegalovirus from latency, and has the potential to be used as a therapy to purge the virus from transplant organs.

Direct estimation of the Hurst exponent shows that endosomes and lysosomes reside in regimes of persistent and anti-persistent motion with heavy-tailed residence time distributions and motion correlated with endocytic function.

SARS-CoV-2 infection reduces the intracellular levels of a human tRNA modification enzyme and alters host tRNA modification profiles.

The HCMV virion envelope is derived from the host exosome membrane, and exosome machinery and export pathways facilitate virion egress.

VPS13A is associated with the endoplasmic reticulum, mitochondria and lipid droplets and is required for cellular processes that require interaction between these organells.

WRNIP1 has been identified as a pivotal factor in preventing the pathological persistence of R-loop-induced transcription-replication conflicts and the accumulation of DNA damage, thereby ensuring genome integrity.

After DNA damage induction, transcription is blocked and XAB2 is released from R-loops allowing a subset of XAB2 molecules to interact with UV-stalled RNAP2 and participating to the TC-NER process.

The function and distribution of kinesin motors on exocytotic vesicles is dissected and visualized through a combination of gene knockout experiments, high-resolution microscopy and advanced data analysis.

Late effects of radiation therapy in mice can be prevented by treatment with either senolytics navitoclax or quercetin plus dasatinib or the senostatic metformin.