Jane Tian

TL;DR: This work links two major theories on aging, DNA damage accumulation, and mitochondrial dysfunction through nuclear DNA damage-induced nuclear-mitochondrial signaling, and demonstrates that they are important pathophysiological determinants in premature aging of A-T, pointing to therapeutic interventions.

TL;DR: It is demonstrated that a modest decrement in base excision repair capacity can render the brain more vulnerable to AD-related molecular and cellular alterations.

TL;DR: RecQL4 is the first 3′–5′ RecQ helicase to be found in both human and mouse mitochondria, and the loss of RECQL4 alters mitochondrial integrity, and measurements of mitochondrial bioenergetics showed a reduction in the mitochondrial reserve capacity after lentiviral knockdown ofRECQL4 in two different primary cell lines.

TL;DR: It is shown that Polβ is a mitochondrial polymerase involved in mtDNA maintenance and is required for mitochondrial homeostasis.

TL;DR: It is reported that WRN regulates the pathway choice between classical (c)- and alternative (alt)-nonhomologous end joining (NHEJ) during DNA double-strand break (DSB) repair and shields DSBs from MRE11/CtIP-mediated resection to prevent large deletions and telomere fusions.