HIGHLIGHTS
SUMMARY
So far, however, only SSiNGLe and GLOE-seq have been applied to generate profiles of endogenous mammalian SSBs and these efforts have been limited to very few cell types (Cao et_al, 2019; Sriramachandran et_al, 2020). An emerging theme from these studies is that a persistent DNA break first serves as a nucleation point for binding of various protein components of cellular DNA damage response that in turn leads to transcription activation via local chromatin remodeling (Ju et_al, 2006; Le May et_al, 2012; Trotter et_al, 2015) or changes in chromatin topology (Perillo et_al, 2008; Le . . .
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