TopBP1 activates the ATR-ATRIP complex.

By A. Kumagai, Joon Lee, H. Yoo, W. G. Dunphy. Cell, 2006

795 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/036cff946b13d41e55d9db9dd64d1a2b1e93f6d1

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Citations in the corpus

The DNA Damage Response: Making it safe to play with knives (2010, background): “…of the RAD17-RFC2-5 clamp loader, which loads the PCNA-related RAD9-HUS1-RAD1 (9-1-1) heterotrimer bound to the ATRactivating TOPBP1 protein and stimulates ATR kinase activity (Cimprich and Cortez, 2008; Ellison and Stillman, 2003; Kumagai et al., 2006; Mordes et al., 2008; Zou et al., 2003).”
The DNA damage response: ten years after. (2007, background): “In addition to its role in DNA replication, TopBP1 binds the 911 complex and contains a domain that can bind ATRIP and stimulate ATR kinase activity (Kumagai et al., 2006).”
A vertebrate gene, ticrr, is an essential checkpoint and replication regulator. (2010, neutral): “Once recruited, TopBP1 promotes ATR activation (Kumagai et al. 2006).”
Surviving the breakup: the DNA damage checkpoint. (2006, background): “Very recent evidence demonstrates that Xenopus ATR is catalytically activated by DNA damage with the help of TopBP1 (72, 160).”
DNA damage-induced cell death: from specific DNA lesions to the DNA damage response and apoptosis. (2013, background): “TopBP1 directly activates the ATR-ATRIP complex, most likely via a conformational change of the ATR-ATRIP complex [104].”
DNA damage sensing by the ATM and ATR kinases. (2013, background): “Vertebrate TopBP1 and yeast Dpb11, as well as the yeast Ddc1 subunit of 9-1- 1, stimulate ATR or Mec1 through a bipartite ATR/Mec1-activation domain (Kumagai et al. 2006; Navadgi-Patil and Burgers 2009; Navadgi-Patil et al. 2011), suggesting that the basic mechanism for ATR stimulation may be…”
Continued primer synthesis at stalled replication forks contributes to checkpoint activation (2010, background): “This leads to phosphorylation of many proteins, including Chk1, one of the primary effectors of ATR and a necessary component of the arrest response (Kumagai et al., 2006; Segurado and Tercero, 2009).”
Treslin Collaborates with TopBP1 in Triggering the Initiation of DNA Replication (2010, background): “We chose this construct because it lacks a key region required for activation of ATR, but nonetheless contains all of the regions necessary to support DNA replication (Hashimoto et al., 2006; Kumagai et al., 2006; Yan et al., 2006).”
Phosphorylation-dependent assembly of DNA damage response systems and the central roles of TOPBP1 (2021, background): “While the interaction with ATR is mediated by a predominantly unstructured ATR-activating domain (AAD) near the C-terminus of TOPBP1/Dpb11/Rad4 [103-105], the link to 9-1-1 is mediated by binding of the phosphorylated C-terminus of RAD9/Ddc1/Rad9 [101, 106, 107] to one or other of the upstream BRCT ”