ArticleMolecular biology of the cell2006
Phosphorylation of Xenopus Rad1 and Hus1 defines a readout for ATR activation that is independent of Claspin and the Rad9 carboxy terminus.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Structure-function analysis of TOPBP1's role in ATR signaling using the DSB-mediated ATR activation in Xenopus egg extracts (DMAX) system.Scientific reports · 2021Article
- Biochemical analysis of TOPBP1 oligomerization.DNA repair · 2020Article
- APE1 senses DNA single-strand breaks for repair and signaling.Nucleic acids research · 2020Article
- APE2 promotes DNA damage response pathway from a single-strand break.Nucleic acids research · 2018Article
- DNA damage-specific deubiquitination regulates Rad18 functions to suppress mutagenesis.The Journal of cell biology · 2014Article
- A role for the MRN complex in ATR activation via TOPBP1 recruitment.Molecular cell · 2013Article
- The phosphorylation network for efficient activation of the DNA replication checkpoint in fission yeast.The Journal of biological chemistry · 2011Article
- Characterization of functional domains in human Claspin.Cell cycle (Georgetown, Tex.) · 2011Article
- Development of bimolecular fluorescence complementation using Dronpa for visualization of protein-protein interactions in cells.Molecular imaging and biology · 2010Article
- Tipin-replication protein A interaction mediates Chk1 phosphorylation by ATR in response to genotoxic stress.The Journal of biological chemistry · 2010Article
- Continued primer synthesis at stalled replication forks contributes to checkpoint activation.The Journal of cell biology · 2010Article
- The Fanconi anemia protein FANCM is controlled by FANCD2 and the ATR/ATM pathways.The Journal of biological chemistry · 2009Article
- A tale of two tails: activation of DNA damage checkpoint kinase Mec1/ATR by the 9-1-1 clamp and by Dpb11/TopBP1.DNA repair · 2009Review
- TopBP1 and DNA polymerase-alpha directly recruit the 9-1-1 complex to stalled DNA replication forks.The Journal of cell biology · 2009Article
- ATR signaling at a glance.Journal of cell science · 2009Article
- ATR: an essential regulator of genome integrity.Nature reviews. Molecular cell biology · 2008Review
- How ATR turns on: TopBP1 goes on ATRIP with ATR.Genes & development · 2008Article
- Undamaged DNA transmits and enhances DNA damage checkpoint signals in early embryos.Molecular and cellular biology · 2007Article
- The Rad9-Hus1-Rad1 (9-1-1) clamp activates checkpoint signaling via TopBP1.Genes & development · 2007Article
- The structural determinants of checkpoint activation.Genes & development · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The DNA damage checkpoint pathways sense and respond to DNA damage to ensure genomic stability. The ATR kinase is a central regulator of one such pathway and phosphorylates a number of proteins that have roles in cell cycle progression and DNA repair. Using the Xenopus egg extract system, we have investigated regulation of the Rad1/Hus1/Rad9 complex. We show here that phosphorylation of Rad1 and Hus1 occurs in an ATR- and TopBP1-dependent manner on T5 of Rad1 and S219 and T223 of Hus1. Mutation of these sites has no effect on the phosphorylation of Chk1 by ATR. Interestingly, phosphorylation of Rad1 is independent of Claspin and the Rad9 carboxy terminus, both of which are required for Chk1 phosphorylation. These data suggest that an active ATR signaling complex exists in the absence of the carboxy terminus of Rad9 and that this carboxy-terminal domain may be a specific requirement for Chk1 phosphorylation and not necessary for all ATR-mediated signaling events. Thus, Rad1 phosphorylation provides an alternate and early readout for the study of ATR activation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.