Journal
JOURNAL OF CELL BIOLOGY
Volume 218, Issue 4, Pages 1096-1107Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201809012
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Funding
- National Institutes of Health [RO1 CA204127]
- National Center for Advancing Translational Sciences, NIH Clinical and Translational Science Award program [UL1TR001866]
- National Institute of General Medical Sciences of the National Institutes of Health (Medical Scientist Training Program) [T32GM007739]
- William Randolph Hearst Foundation Fellowship at The Rockefeller University
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The replisome, the molecular machine dedicated to copying DNA, encounters a variety of obstacles during S phase. Without a proper response to this replication stress, the genome becomes unstable, leading to disease, including cancer. The immediate response is localized to the stalled replisome and includes protection of the nascent DNA. A number of recent studies have provided insight into the factors recruited to and responsible for protecting stalled replication forks. In response to replication stress, the SNF2 family of DNA translocases has emerged as being responsible for remodeling replication forks in vivo. The protection of stalled replication forks requires the cooperation of RAD51, BRCA1, BRCA2, and many other DNA damage response proteins. In the absence of these fork protection factors, fork remodeling renders them vulnerable to degradation by nucleases and helicases, ultimately compromising genome integrity. In this review, we focus on the recent progress in understanding the protection, processing, and remodeling of stalled replication forks in mammalian cells.
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