Kathleen M. Attwood

TL;DR: It is demonstrated that DSBs induced at the nuclear membrane (but not at nuclear pores or nuclear interior) fail to rapidly activate the DNA damage response (DDR) and repair by homologous recombination (HR), revealing a new level of regulation in DSB repair controlled by spatial organization of DNA within the nucleus.

TL;DR: It is suggested that polymeric actin is required for proper DNA double-strand break repair and may function through the stabilization of the Ku heterodimer at the DNA damage site.

TL;DR: This review explores how ubiquitination and sumoylation contribute to the “writing” of key post-translational modifications within chromatin that are in turn “read” by the DDR machinery and chromatin-remodeling factors, which act together to facilitate the efficient detection and repair of DNA damage.

TL;DR: Reduced KAP1 expression results in a constitutive increase in PML NB number in both human U2-OS cells and normal human diploid fibroblasts, which implicate KAP 1-dependent changes in chromatin structure as one possible mechanism by which ATM may regulate PMLNB number in response to DNA damage.

TL;DR: It is shown that modulation of the functions of a chaperone can affect signal transduction at the cell surface, and modulation of DRiP78 levels will affect receptor functions, such as cell migration in cells that endogenously express CCR5.