Article
Biology
Bo-Ruei Chen, Yinan Wang, Anthony Tubbs, Dali Zong, Faith C. Fowler, Nicholas Zolnerowich, Wei Wu, Amelia Bennett, Chun-Chin Chen, Wendy Feng, Andre Nussenzweig, Jessica K. Tyler, Barry P. Sleckman
Summary: This study identifies LIN37 as a factor that prevents DNA end resection and homologous recombination in non-cycling quiescent cells independently of 53BP1. Loss of LIN37 leads to the expression of HR proteins and promotes DNA end resection in these cells, indicating a unique pathway for DNA end protection in quiescent cells.
Article
Cell Biology
Nicole B. Averbeck, Carina Barent, Burkhard Jakob, Tatyana Syzonenko, Marco Durante, Gisela Taucher-Scholz
Summary: DNA double-strand breaks (DSBs) are the molecular origin of the biological effects of ionizing radiation. The ubiquitin ligase RNF138 plays a crucial role in regulating the resection of DSBs in G1 phase, allowing the recruitment of the resection factor CtIP to these DSBs in a radiation-dependent manner.
Article
Immunology
Kristen L. Hoek, Michael J. Greer, Kathleen G. McClanahan, Ali Nazmi, M. Blanca Piazuelo, Kshipra Singh, Keith T. Wilson, Danyvid Olivares-Villagomez
Summary: Activation and differentiation of CD4(+) T cells are crucial for immune responses, with granzyme B playing a role in modulating IL-17 production and potentially influencing cell differentiation and disease onset in adoptive transfer models of intestinal inflammation.
MUCOSAL IMMUNOLOGY
(2021)
Article
Genetics & Heredity
Dongju Park, Mehdi Gharghabi, Morgan S. Schrock, Rebecca Plow, Teresa Druck, Charles Yungvirt, C. Marcelo Aldaz, Kay Huebner
Summary: Down regulation of Wwox protein expression occurs in many cancers, contributing to insensitivity to ionizing radiation (IR) and platinum drug treatments. Patients with reduced Wwox expression in their cancer tissue show decreased overall survival following these treatments, in accord with our earlier finding that reduced Wwox protein expression in cancers is associated with changes in choice of DNA double-strand break (DSB) repair pathway.