53BP1, a Mediator of the DNA Damage Checkpoint

By Bin Wang, S. Matsuoka, P. Carpenter, Stephen J. Elledge. Science, 2002

622 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/9536d0debfff5d261ce9ce38c9e06bf71ce38f75

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

In Oncology

Citations in the corpus

DNA damage sensing by the ATM and ATR kinases. (2013, background): “In addition to their functions in regulating DSB repair, Brca1 and 53BP1 contribute to the efficient phosphorylation of some ATM substrates and have been implicated in checkpoint activation (DiTullio et al. 2002; Wang et al. 2002; Fabbro et al. 2004; Kitagawa et al. 2004).”
DNA damage-induced apoptosis (2004, background): “53BP1, yet another ATM target, interacts with phospho-H2AX, CHK2, p53 and BRCA1, and is required for CHK2 activation, BRCA1 phosphorylation, p53 stabilization and BRCA1 focus formation after DNA damage (Fernandez-Capetillo et al., 2002; Wang et al., 2002).”
53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks (2010, neutral): “…are in transducing a subset of ATM dependent cell cycle checkpoints (DiTullio et al., 2002; Fernandez-Capetillo et al., 2002; Lee et al., 2009; Wang et al., 2002) and facilitating the joining of distal DSBs formed at dysfunctional telomeres and during lymphocyte antigen receptor recombination…”
RNF168 ubiquitinates K13-15 on H2A/H2AX to drive DNA damage signaling. (2012, background): “…to the ubiquitindependent signals necessary for the further recruitment of downstream regulators of the DSB response pathway, such as 53BP1 and the BRCA1 complex (Al-Hakim et al., 2010; Kim et al., 2007; Panier and Durocher, 2009; Sobhian et al., 2007; Wang et al., 2002; Yan et al., 2007).”
γ-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin (2008, background): “It has been, therefore, suggested that g-H2AX is involved in the amplification step required for optimal checkpoint response at relatively low levels of DNA damage (30,98,99).”
BRD4 and Cancer: going beyond transcriptional regulation (2018, background): “53BP1 is a large protein of 1972 amino acids that has no apparent enzymatic activity but when recruited to DSB specific histone code acts as a molecular scaffold that recruits additional DSB-responsive proteins to damaged chromatin [60, 61].”