Molecular analyses and unbiased CRISPR screens reveal that extensive end resection occurs in quiescent cells after inducing DNA double strand breaks, in a manner dependent on DNA-PK.

Experiments in mice have shown than an enzyme that repairs broken DNA inside the nucleus also has a central role in the innate immune system because it is able to detect foreign DNA outside the nucleus.

DNA-PK and PTEN protect breast cancer cells from lethal replication stress induced by the WEE1 inhibitor AZD1775 and constitute new potential biomarkers for AZD1775 sensitivity.

Mycobacterium tuberculosis (Mtb), effectors secreted through SecA2 pathway cause double strand breaks (DSBs) in the host DNA, which in turn activates ATM kinase to gain survival advantages, through Akt.

Transcription factors can read out both the sequence and the structure of the non-template DNA strand in the transcription bubble, expanding the repertoire of mechanisms to control transcription.

In concert phosphorylation site modification of both XRCC4 and XLF C-terminal disordered tails promotes disassembly of XRCC4/XLF DNA tethers during c-NHEJ.

Activated macrophages initiate a robust DNA damage response that depends on type I IFN and regulates their genetic program and inflammasome activation, establishing a mechanistic link between DNA damage responses and innate immunity.

The Pk^pk and Pk^sple isoforms of the Prickle protein determine right- or left-handed bristle morphogenesis by coupling Frizzled/Vang signaling to the Fat/Dachsous PCP directional signal in opposite directions.

Mutations in four members of the mevalonate pathway have been identified from 134 index porokeratosis patients, including some that correlate with specific clinical manifestations of the disease.

Hundreds of proteins are involved in the DNA damage response but only three sensors for DSB were known but now SIRT6 is identified as a fourth DSB sensor.