ARTEMIS stabilizes the genome and modulates proliferative responses in multipotent mesenchymal cells |
| |
Authors: | Sarah A Maas Nina M Donghia Kathleen Tompkins Oded Foreman Kevin D Mills |
| |
Institution: | (1) The Jackson Laboratory, 600 Main Street, 04609 Bar Harbor, ME, USA;(2) Adnexus Therapeutics, 02453 Waltham, MA, USA;(3) Division of Infectious Diseases, University of North Carolina, NC27599 Chapel Hill, USA;(4) The Jackson Laboratory, 4910 Raley Road, 95838 Sacramento, CA, USA;(5) Main Medical Center Research Institute, Scarborough, Maine, USA |
| |
Abstract: | Background Unrepaired DNA double-stranded breaks (DSBs) cause chromosomal rearrangements, loss of genetic information, neoplastic transformation
or cell death. The nonhomologous end joining (NHEJ) pathway, catalyzing sequence-independent direct rejoining of DSBs, is
a crucial mechanism for repairing both stochastically occurring and developmentally programmed DSBs. In lymphocytes, NHEJ
is critical for both development and genome stability. NHEJ defects lead to severe combined immunodeficiency (SCID) and lymphoid
cancer predisposition in both mice and humans. While NHEJ has been thoroughly investigated in lymphocytes, the importance
of NHEJ in other cell types, especially with regard to tumor suppression, is less well documented. We previously reported
evidence that the NHEJ pathway functions to suppress a range of nonlymphoid tumor types, including various classes of sarcomas,
by unknown mechanisms. |
| |
Keywords: | |
本文献已被 SpringerLink 等数据库收录! |
|